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    <title>Recent ucsdsom_ped_oapdeposits items</title>
    <link>https://escholarship.org/uc/ucsdsom_ped_oapdeposits/rss</link>
    <description>Recent eScholarship items from Department of Pediatrics - Open Access Policy Deposits</description>
    <pubDate>Fri, 26 Jun 2026 03:14:35 +0000</pubDate>
    <item>
      <title>Cats on dry kibble diet have significantly different microbiome than those on canned wet food</title>
      <link>https://escholarship.org/uc/item/6rn7083q</link>
      <description>Domestic cats (Felis catus) are understudied regarding how commercial diets impact their gut microbiomes. Here, we reanalyzed the 16S rRNA gene (V4) amplicon sequencing Kittybiome dataset, using new tools and techniques. Results demonstrated significant microbial composition differences between cats eating commercial dry kibble diets and those eating canned wet food. Kibble-fed cats showed enriched Prevotella, Bifidobacterium, and Megamonas amplicon sequencing variants (ASVs), linked to carbohydrate metabolism and metabolic disease.</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/6rn7083q</guid>
      <pubDate>Thu, 18 Jun 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Allaband, Celeste</name>
        <uri>https://orcid.org/0000-0003-1832-4858</uri>
      </author>
      <author>
        <name>Ganz, Holly H</name>
      </author>
      <author>
        <name>Rojas, Connie A</name>
      </author>
      <author>
        <name>Knight, Rob</name>
      </author>
    </item>
    <item>
      <title>Pre-Natal Exposure to Mouse Parvovirus at Day 5 and 12 Gestation Does Not Induce Immune Tolerance</title>
      <link>https://escholarship.org/uc/item/2nc2c34k</link>
      <description>Parvoviruses have a predilection for rapidly dividing cells such as occurs during embryonic development. Potentially, in utero exposure could lead to immune tolerance in progeny mice. To determine if MPV infection in utero results in immune tolerance, pregnant mice were inoculated by oral gavage with 50 ID50 MPV1e or sham inoculated with phosphate buffered saline at day 5 and 12 gestation. Offspring were fostered to MPV-negative recipient dams prior to development of a milk spot. After confirming the offspring were seronegative for MPV by serology and not shedding by fecal PCR, they were challenged with 50 ID50 MPV1e by oral gavage at weaning or sham inoculated. At 4 weeks post inoculation, all weanlings exposed in utero developed antibodies to MPV, and MPV was detected by fecal PCR. Similarly, all weanlings from sham-inoculated dams challenged with MPV developed antibodies and MPV was detected by fecal PCR. None of the sham inoculated weanling mice from MPV infected dams or sham...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/2nc2c34k</guid>
      <pubDate>Thu, 18 Jun 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Kendall, Lon V</name>
      </author>
      <author>
        <name>Allaband, Celeste</name>
        <uri>https://orcid.org/0000-0003-1832-4858</uri>
      </author>
      <author>
        <name>Henderson, Kenneth S</name>
      </author>
    </item>
    <item>
      <title>Streamlined extraction of nucleic acids and metabolites from low- and high-biomass samples using isopropanol and matrix tubes</title>
      <link>https://escholarship.org/uc/item/1d46360w</link>
      <description>An essential aspect of population-based research is collecting samples outside of a clinical setting. This is crucial because microbial populations are highly dynamic, varying significantly across hosts, environments, and time points, a variability that clinical sample collection alone cannot fully capture. At-home sample collection enables the inclusion of a larger and more diverse group of participants, accounting for differences in ethnicity, age, and other factors. However, managing large studies is challenging due to the complexities involved in sample acquisition, processing, and analysis. Building on our previous work demonstrating the effectiveness of single 1 mL barcoded, racked Matrix Tubes in reducing sample processing time and well-to-well contamination for paired DNA and metabolite extraction, we further validate this method against a previously benchmarked plate-based approach using the same extraction reagents. This validation focuses on samples from the built environment,...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/1d46360w</guid>
      <pubDate>Thu, 18 Jun 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Brennan, Caitriona</name>
        <uri>https://orcid.org/0000-0003-3943-6701</uri>
      </author>
      <author>
        <name>Shaffer, Justin P</name>
      </author>
      <author>
        <name>Belda-Ferre, Pedro</name>
      </author>
      <author>
        <name>Mohanty, Ipsita</name>
      </author>
      <author>
        <name>Weng, Yuhan</name>
      </author>
      <author>
        <name>Cantrell, Kalen</name>
      </author>
      <author>
        <name>Ackermann, Gail</name>
      </author>
      <author>
        <name>Allaband, Celeste</name>
        <uri>https://orcid.org/0000-0003-1832-4858</uri>
      </author>
      <author>
        <name>Bryant, MacKenzie</name>
      </author>
      <author>
        <name>Farmer, Sawyer</name>
      </author>
      <author>
        <name>González, Antonio</name>
      </author>
      <author>
        <name>McDonald, Daniel</name>
      </author>
      <author>
        <name>Martino, Cameron</name>
      </author>
      <author>
        <name>Meehan, Michael J</name>
      </author>
      <author>
        <name>Rahman, Gibraan</name>
      </author>
      <author>
        <name>Salido, Rodolfo A</name>
      </author>
      <author>
        <name>Schwartz, Tara</name>
      </author>
      <author>
        <name>Song, Jin</name>
      </author>
      <author>
        <name>Tribelhorn, Caitlin</name>
      </author>
      <author>
        <name>Tubb, Helena M</name>
      </author>
      <author>
        <name>Dorrestein, Pieter C</name>
      </author>
      <author>
        <name>Knight, Rob</name>
      </author>
    </item>
    <item>
      <title>Opioid Agonist Therapy Adherence Trajectories Among Commercially and Publicly Insured People Living With Hepatitis C in the United States</title>
      <link>https://escholarship.org/uc/item/47h0z536</link>
      <description>BACKGROUND: Hepatitis C virus (HCV) infection is a public health concern, with people living with opioid use disorder having a higher risk of infection. Despite the cooccurrence of HCV and opioid use disorder, little is known about the treatment patterns for the disorder in this population. This study characterized opioid agonist therapy adherence trajectories over 15 months following opioid agonist therapy initiation among people living with HCV and opioid use disorder and described the baseline characteristics of the patients within distinct opioid agonist therapy adherence trajectories.
METHODS: We used Merative MarketScan healthcare claims data from 2015 to 2019 to identify distinct medication treatment adherence trajectories via growth mixture modeling among 5,495 people who initiated opioid agonist therapy for opioid use disorder and were living with HCV.
RESULTS: Our models identified three distinct opioid agonist therapy adherence trajectories over the 15 months of follow-up....</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/47h0z536</guid>
      <pubDate>Wed, 3 Jun 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Psaras, Catherine</name>
      </author>
      <author>
        <name>Arah, Onyebuchi A</name>
        <uri>https://orcid.org/0000-0002-9067-1697</uri>
      </author>
      <author>
        <name>Chew, Kara W</name>
      </author>
      <author>
        <name>Lee, Sung-Jae</name>
      </author>
      <author>
        <name>Javanbakht, Marjan</name>
        <uri>https://orcid.org/0000-0003-0088-3803</uri>
      </author>
      <author>
        <name>Nianogo, Roch A</name>
      </author>
      <author>
        <name>Seamans, Marissa J</name>
      </author>
    </item>
    <item>
      <title>Regulation of axon outgrowth during mushroom body development by acetylated α-tubulin lysine 394 and tau</title>
      <link>https://escholarship.org/uc/item/9dv5h7gm</link>
      <description>Disruptions in the microtubule cytoskeleton play a role in various neurological diseases that afflict a large fraction of the population. Microtubule function is regulated by post-translational modifications like acetylation, and one consistently identified acetylation site in mammals and Drosophila melanogaster is α-tubulin lysine 394 (K394). Our previous research demonstrated that an acetylation-blocking point mutation-K394R-causes a decrease in microtubule stability in axon terminals at the developing neuromuscular junction. Here, we asked whether K394 acetylation regulates the development of additional neuronal structures. Using the central brain mushroom body as a model, we found that K394R results in β lobe overextension at the midline. The K394R phenotype manifests during metamorphosis and affects β lobe growth in a cell-autonomous manner. Our data suggest that the K394R phenotype may result from changes in Tau, a microtubule-associated protein enriched in the mushroom...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/9dv5h7gm</guid>
      <pubDate>Mon, 25 May 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Welch, Chloe J</name>
      </author>
      <author>
        <name>Mueller, Liam O’Connor</name>
      </author>
      <author>
        <name>Trujillo, Sophia P</name>
      </author>
      <author>
        <name>Wildonger, Jill</name>
        <uri>https://orcid.org/0000-0002-6462-5830</uri>
      </author>
    </item>
    <item>
      <title>In their own words: experiences surrounding masculinising chest surgery among transgender and gender-diverse adolescents – a secondary analysis of GENDER-Q data</title>
      <link>https://escholarship.org/uc/item/83s5c6gt</link>
      <description>Objective: 

                    Masculinising chest surgery, also known as top surgery, is the most requested gender-affirming procedure among transgender and gender-diverse (TGD) adolescents, yet research on patient experiences remains limited. This study explored the experiences of TGD adolescents who were seeking or had undergone masculinising chest surgery. 

                  
                  
                    Design: 

                    Qualitative secondary analysis using existing themes framework and data from the GENDER-Q (GQ) and GENDER-Q Youth (GQY) research programmes, which aim to develop comprehensive patient-reported outcome measures for gender-affirming care. 

                  
                  
                    Setting: 

                    Participants were sampled from five high-volume gender-affirming care clinics, three in Canada and two in the United States. Interviews were conducted online. 

                  
                  
        ...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/83s5c6gt</guid>
      <pubDate>Thu, 21 May 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Armstrong, Kathleen</name>
      </author>
      <author>
        <name>Quan, Ivy</name>
        <uri>https://orcid.org/0009-0004-6174-3104</uri>
      </author>
      <author>
        <name>Kennedy, Shelby L</name>
      </author>
      <author>
        <name>Kaur, Manraj N</name>
        <uri>https://orcid.org/0000-0002-1911-0395</uri>
      </author>
      <author>
        <name>Cornacchi, Sylvie D</name>
      </author>
      <author>
        <name>Rae, Charlene</name>
      </author>
      <author>
        <name>Johnson, Natasha</name>
      </author>
      <author>
        <name>Khatchadourian, Karine</name>
      </author>
      <author>
        <name>Marinkovic, Maja</name>
        <uri>https://orcid.org/0000-0001-8911-8010</uri>
      </author>
      <author>
        <name>Sequeira, Gina M</name>
      </author>
      <author>
        <name>Bradley, Brenda</name>
      </author>
      <author>
        <name>Cheung, Kevin</name>
      </author>
      <author>
        <name>Morrison, Shane D</name>
      </author>
      <author>
        <name>Klassen, Anne F</name>
        <uri>https://orcid.org/0000-0003-4720-0096</uri>
      </author>
    </item>
    <item>
      <title>Selfish: discovery of differential chromatin interactions via a self-similarity measure</title>
      <link>https://escholarship.org/uc/item/7k5638gx</link>
      <description>MOTIVATION: High-throughput conformation capture experiments, such as Hi-C provide genome-wide maps of chromatin interactions, enabling life scientists to investigate the role of the three-dimensional structure of genomes in gene regulation and other essential cellular functions. A fundamental problem in the analysis of Hi-C data is how to compare two contact maps derived from Hi-C experiments. Detecting similarities and differences between contact maps are critical in evaluating the reproducibility of replicate experiments and for identifying differential genomic regions with biological significance. Due to the complexity of chromatin conformations and the presence of technology-driven and sequence-specific biases, the comparative analysis of Hi-C data is analytically and computationally challenging.
RESULTS: We present a novel method called Selfish for the comparative analysis of Hi-C data that takes advantage of the structural self-similarity in contact maps. We define a novel...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/7k5638gx</guid>
      <pubDate>Thu, 21 May 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Ardakany, Abbas Roayaei</name>
      </author>
      <author>
        <name>Ay, Ferhat</name>
        <uri>https://orcid.org/0000-0002-0708-6914</uri>
      </author>
      <author>
        <name>Lonardi, Stefano</name>
        <uri>https://orcid.org/0000-0002-2696-7274</uri>
      </author>
    </item>
    <item>
      <title>Multi-strain analysis of Pseudomonas putida reveals the metabolic and genetic diversity of the species</title>
      <link>https://escholarship.org/uc/item/1bk2w52m</link>
      <description>&lt;i&gt;Pseudomonas putida&lt;/i&gt; is a gram-negative bacterial species increasingly utilized in biotechnology due to its robust growth, ability to degrade aromatic compounds, solvent tolerance, and genetic tractability. In this study, we report a comprehensive multi-strain analysis of 164 &lt;i&gt;P. putida&lt;/i&gt; strains based on the reconstruction of a pan&lt;i&gt;-&lt;/i&gt;putida metabolic network and the formulation of strain-specific genome-scale metabolic models (GEMs). We performed whole-genome sequencing and hybrid assembly for 40 strains, contributing a ~8% increase to the available genomic data for &lt;i&gt;P. putida&lt;/i&gt;. Furthermore, high-throughput phenotypic profiling using the Biolog phenotype microarray system for 24 strains on 190 unique carbon sources, along with 15 aromatic compounds not present on Biolog plates, yielded 4,920 unique strain-phenotype measurements. These data were leveraged to curate GEMs for 24 representative strains, including a refined model for strain KT2440, which comprised...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/1bk2w52m</guid>
      <pubDate>Thu, 14 May 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Mueller, Joshua</name>
      </author>
      <author>
        <name>Krishnan, Jayanth</name>
      </author>
      <author>
        <name>Wei, Qixing</name>
      </author>
      <author>
        <name>Hefner, Ying</name>
      </author>
      <author>
        <name>Monk, Jonathan M</name>
      </author>
      <author>
        <name>Verkler, Hans</name>
      </author>
      <author>
        <name>Tibocha-Bonilla, Juan D</name>
      </author>
      <author>
        <name>Ayala, Anthony</name>
      </author>
      <author>
        <name>Palsson, Bernhard O</name>
        <uri>https://orcid.org/0000-0003-2357-6785</uri>
      </author>
      <author>
        <name>Feist, Adam M</name>
        <uri>https://orcid.org/0000-0002-8630-4800</uri>
      </author>
      <author>
        <name>Niu, Wei</name>
      </author>
    </item>
    <item>
      <title>Ultrasound of the Rectus Femoris Muscle and Association with Pediatric Liver Failure - Preliminary One-Year Pilot Outcomes Data</title>
      <link>https://escholarship.org/uc/item/7cq3q7m6</link>
      <description>Ultrasound of the Rectus Femoris Muscle and Association with Pediatric Liver Failure - Preliminary One-Year Pilot Outcomes Data</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/7cq3q7m6</guid>
      <pubDate>Thu, 7 May 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Chu, C</name>
      </author>
      <author>
        <name>Yu, V</name>
      </author>
      <author>
        <name>Dodge, J</name>
      </author>
      <author>
        <name>Kasturi, S</name>
      </author>
      <author>
        <name>Acharya, P</name>
      </author>
      <author>
        <name>Rigual, D</name>
      </author>
      <author>
        <name>Terrault, N</name>
      </author>
    </item>
    <item>
      <title>Minimal correlation but complementary diagnostic utility for plasma cell-free RNA and proteins</title>
      <link>https://escholarship.org/uc/item/6w03495w</link>
      <description>BackgroundProteins and RNA circulate in plasma and can offer insights into human physiology. Yet, despite their clinical importance, direct comparisons between these analytes remain unexplored.Methods:Here, we measure and compare plasma cell-free RNA (cfRNA) and protein levels for 263 children diagnosed with inflammatory diseases, specifically either Kawasaki disease (KD) or Multisystem Inflammatory Syndrome in Children (MIS-C), by RNA sequencing (n = 108 KD and n = 47 MIS-C, mean age=4.2 years) and SomaScan proteomics (n = 70 KD and n = 101 MIS-C, mean age=6.8 years).ResultsHere we show that cell-free RNA and protein levels are largely uncorrelated across samples (feature-by-sample correlation coefficient 0.052; median feature-level correlation coefficient 0.009). Nonetheless, machine learning models based on either modality distinguish KD from MIS-C with similar high accuracy (median area under the curve greater than 0.93). Analysis of KD subtypes reveals distinct cell-free...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/6w03495w</guid>
      <pubDate>Thu, 23 Apr 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Bliss, Andrew</name>
      </author>
      <author>
        <name>Loy, Conor J</name>
      </author>
      <author>
        <name>Kim, Jihoon</name>
      </author>
      <author>
        <name>Shimizu, Chisato</name>
      </author>
      <author>
        <name>Lenz, Joan S</name>
      </author>
      <author>
        <name>Belcher, Emma</name>
      </author>
      <author>
        <name>Tremoulet, Adriana H</name>
      </author>
      <author>
        <name>Burns, Jane C</name>
        <uri>https://orcid.org/0000-0001-5679-1217</uri>
      </author>
      <author>
        <name>De Vlaminck, Iwijn</name>
      </author>
    </item>
    <item>
      <title>A mixed methods pilot study of a virtual therapeutic writing intervention for adolescent/young adults with cancer</title>
      <link>https://escholarship.org/uc/item/5g95b72q</link>
      <description>OBJECTIVE: To evaluate the feasibility and acceptability of a virtual therapeutic writing intervention for AYAs with cancer.
METHODS: A single-arm pilot study of the intervention was conducted at Rady Children's Hospital San Diego. The six-session intervention was facilitated by a writing coach over two to three months, during which time participants produced written work regarding their experiences with cancer. Primary outcomes were measures of acceptability and feasibility, assessed via quantitative and qualitative methods.
RESULTS: Study enrollment and retention rates were 75% and 83%, respectively. Participants rated all intervention sessions as highly enjoyable, helpful, useful, and satisfactory. Qualitatively, participants reported that the intervention helped them cope with their cancer and they would recommend the study to others with cancer.
CONCLUSIONS: This virtual therapeutic writing study is feasible and acceptable among AYAs with cancer. A randomized controlled trial...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/5g95b72q</guid>
      <pubDate>Thu, 23 Apr 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Rapoport, Chelsea S</name>
      </author>
      <author>
        <name>Choi, Alyssa K</name>
      </author>
      <author>
        <name>Radovsky, Siloh</name>
      </author>
      <author>
        <name>Chen, Melinda A</name>
      </author>
      <author>
        <name>Devereaux, Mary</name>
      </author>
      <author>
        <name>Korhummel, Megan</name>
      </author>
      <author>
        <name>O’Donnell, Shea</name>
      </author>
      <author>
        <name>Malcarne, Vanessa L</name>
      </author>
      <author>
        <name>Kuo, Dennis J</name>
      </author>
    </item>
    <item>
      <title>Intraosseous Venous Malformation of the Rib With EWSR1-NFATC1 Fusion Mimicking Malignancy: A Pediatric Case Report.</title>
      <link>https://escholarship.org/uc/item/4p11v2p9</link>
      <description>BACKGROUND: Intraosseous venous malformations are rare, benign vascular bone lesions that may mimic malignant sarcomas on imaging.
OBSERVATIONS: A 14-year-old male presented with fever and cough. Imaging revealed an incidental ossified rib mass with aggressive features. CT-guided biopsy was nondiagnostic, whereas open biopsy demonstrated a vascular lesion positive for CD31, FLI-1, and ERG. Molecular testing identified an EWSR1-NFATC1 fusion. Gross total resection was achieved, followed by prolonged disease-free survival, and the patient resumed full athletic activity 7 months after surgery.
CONCLUSIONS: This case highlights the value of open biopsy and molecular testing to prevent misdiagnosis and overtreatment of intraosseous venous malformations.</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/4p11v2p9</guid>
      <pubDate>Thu, 23 Apr 2026 00:00:00 +0000</pubDate>
      <author>
        <name>McCarty, Bridgette</name>
      </author>
      <author>
        <name>Gochnauer, Heather</name>
      </author>
      <author>
        <name>Longstaff, Xochitl</name>
      </author>
      <author>
        <name>Labib, Angelina</name>
      </author>
      <author>
        <name>Naheedy, John</name>
      </author>
      <author>
        <name>Kulatti, Art</name>
      </author>
      <author>
        <name>Mo, Jun Q</name>
      </author>
      <author>
        <name>Ellington, Natalie</name>
      </author>
      <author>
        <name>Ding, Hilda</name>
      </author>
      <author>
        <name>Lee, Karen</name>
      </author>
      <author>
        <name>Keller, Benjamin</name>
      </author>
      <author>
        <name>Eichenfield, Dawn</name>
      </author>
      <author>
        <name>Schiff, Deborah</name>
        <uri>https://orcid.org/0000-0003-3154-8987</uri>
      </author>
    </item>
    <item>
      <title>Correction: Breath-Focused Mindfulness and Compassion Training in Parent-Child Dyads: Pilot Intervention Study</title>
      <link>https://escholarship.org/uc/item/3kq3b2z9</link>
      <description>Correction: Breath-Focused Mindfulness and Compassion Training in Parent-Child Dyads: Pilot Intervention Study</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/3kq3b2z9</guid>
      <pubDate>Thu, 23 Apr 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Jaiswal, Satish</name>
        <uri>https://orcid.org/0000-0002-3617-1106</uri>
      </author>
      <author>
        <name>Nan, Jason</name>
      </author>
      <author>
        <name>Dizon, Seth</name>
      </author>
      <author>
        <name>Young, Jessica O</name>
      </author>
      <author>
        <name>Purpura, Suzanna R</name>
      </author>
      <author>
        <name>Manchanda, James K</name>
      </author>
      <author>
        <name>Ramanathan, Dhakshin</name>
      </author>
      <author>
        <name>Kuo, Dennis J</name>
      </author>
      <author>
        <name>Mishra, Jyoti</name>
      </author>
    </item>
    <item>
      <title>Glucocorticoids in Kawasaki Disease — Refining Indications and the Science</title>
      <link>https://escholarship.org/uc/item/1785z13h</link>
      <description>Kawasaki disease is the most common cause of acquired heart disease in children in the developed world.1 Although Kawasaki disease manifests with acute, transient systemic signs, its long-term morb...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/1785z13h</guid>
      <pubDate>Thu, 23 Apr 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Burns, Jane C</name>
        <uri>https://orcid.org/0000-0001-5679-1217</uri>
      </author>
      <author>
        <name>Newburger, Jane W</name>
      </author>
    </item>
    <item>
      <title>Application of Bone Mineral Density Study Guidelines across California Pediatric Oncology Survivorship Programs</title>
      <link>https://escholarship.org/uc/item/04p9h0wv</link>
      <description>INTRODUCTION Advances in the treatment of children and adolescents with cancer have resulted in an increased percentage of pediatric cancer survivors (PCSs). However, PCSs are at increased risk of bone health issues from prolonged therapy with corticosteroids, higher cumulative corticosteroid dose, hematopoietic stem cell transplant (HCT), total body irradiation and cranial/craniospinal radiation which can decrease bone mineral density (BMD). Low BMD in PCS is associated with osteoporosis and osteopenia in adult life. The Children's Oncology Group's (COG) long-term follow-up (LTFU) guidelines (Version 6.0) recommend a baseline evaluation of BMD by DXA (Dual-energy X-ray absorptiometry) for PCS who received corticosteroids or HCT at entry into LTFU clinic (2 to 5 years after completion of therapy). Based on Z-scores the guidelines may recommend evaluation for endocrine defects and/or consultation with a bone health specialist with a repeat DXA after 2 years and thereafter as clinically...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/04p9h0wv</guid>
      <pubDate>Thu, 23 Apr 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Joshirao, Mrinal</name>
      </author>
      <author>
        <name>Torno, Lilibeth</name>
      </author>
      <author>
        <name>Lin, Carol Hwang</name>
      </author>
      <author>
        <name>Panigrahi, Arun Ranjan</name>
      </author>
      <author>
        <name>Raphael, Robert</name>
      </author>
      <author>
        <name>Alvarez, Griselda</name>
        <uri>https://orcid.org/0000-0002-4806-1385</uri>
      </author>
      <author>
        <name>Goldsby, Robert</name>
      </author>
      <author>
        <name>Kuo, Dennis John</name>
      </author>
    </item>
    <item>
      <title>Correction: A microbial survey of the International Space Station (ISS)</title>
      <link>https://escholarship.org/uc/item/3ht0p7jb</link>
      <description>[This corrects the article DOI: 10.7717/peerj.4029.].</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/3ht0p7jb</guid>
      <pubDate>Tue, 21 Apr 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Lang, Jenna M</name>
      </author>
      <author>
        <name>Coil, David A</name>
        <uri>https://orcid.org/0000-0001-6049-8240</uri>
      </author>
      <author>
        <name>Neches, Russell Y</name>
        <uri>https://orcid.org/0000-0002-2055-8381</uri>
      </author>
      <author>
        <name>Brown, Wendy E</name>
      </author>
      <author>
        <name>Cavalier, Darlene</name>
      </author>
      <author>
        <name>Severance, Mark</name>
      </author>
      <author>
        <name>Hampton-Marcell, Jarrad T</name>
      </author>
      <author>
        <name>Gilbert, Jack A</name>
        <uri>https://orcid.org/0000-0001-7920-7001</uri>
      </author>
      <author>
        <name>Eisen, Jonathan A</name>
        <uri>https://orcid.org/0000-0002-0159-2197</uri>
      </author>
    </item>
    <item>
      <title>Peripheral rotavirus-specific T-cell responses following monovalent oral rotavirus vaccine in infants</title>
      <link>https://escholarship.org/uc/item/2f99x2ks</link>
      <description>Despite evidence of varying vaccine effectiveness, T cell responses to rotavirus (RV) vaccines remain incompletely studied. To address this research gap, RV-specific T cells in the blood of infants pre- and post-monovalent RV vaccination (RV1) were analyzed for memory recall and functionality using RV-specific peptide pool stimulation. We find that RV vaccine elicits heterogenous responses with respect to cellular and humoral immunity. T cell responses to RV vaccine are detectable in the periphery, though poorly functional. Vaccination induces Th2-biased conventional effector memory and central memory CD4 + T cells, as suggested by chemokine receptor profiles, though the response wanes by 8 months post vaccination. The presence of preexisting immunity results in no significant increase in either RV-specific IgA or T cells after vaccination. Our data provides the first in-depth assessment of RV-specific T cell responses induced by vaccine, demonstrating patterns of negative and...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/2f99x2ks</guid>
      <pubDate>Mon, 30 Mar 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Nicols, Alexander R</name>
      </author>
      <author>
        <name>Lee, Yesun</name>
      </author>
      <author>
        <name>Congrave-Wilson, Zion</name>
      </author>
      <author>
        <name>Kim, Minjun</name>
      </author>
      <author>
        <name>Cheng, Wesley A</name>
      </author>
      <author>
        <name>Jumarang, Jaycee</name>
      </author>
      <author>
        <name>Navarro, Jocelyn</name>
      </author>
      <author>
        <name>Navarro, Rafaella</name>
      </author>
      <author>
        <name>Rodriguez-Angeles, Yamile</name>
      </author>
      <author>
        <name>Durand, David</name>
      </author>
      <author>
        <name>Taylor, Zackary W</name>
      </author>
      <author>
        <name>De León, Ruth G</name>
      </author>
      <author>
        <name>Ochoa, Theresa J</name>
      </author>
      <author>
        <name>Sette, Alessandro</name>
      </author>
      <author>
        <name>da Silva Antunes, Ricardo</name>
      </author>
      <author>
        <name>Pannaraj, Pia S</name>
      </author>
    </item>
    <item>
      <title>Kaposiform Lymphangiomatosis Complicated by Kasabach–Merritt Phenomenon, Recurrent Pericardial Effusions, and Pneumococcal Meningitis</title>
      <link>https://escholarship.org/uc/item/0ft7c408</link>
      <description>Kaposiform lymphangiomatosis (KLA) is a rare disorder characterized by lymphatic anomalies—primarily intrathoracic—and systemic manifestations including coagulopathy, respiratory symptoms, and pleural and/or pericardial effusions. We present the case of a 12-year-old male with KLA complicated by Kasabach–Merritt phenomenon, recurrent pericardial effusions, multifocal bone lesions, and pneumococcal meningitis. Diagnosis was suspected based upon imaging that revealed abnormal pulmonary and mediastinal lymphatics, splenomegaly with low-attenuation lesions in the spleen, and multiple lytic bone lesions. A blood test (FoundationOne Liquid CDX) revealed an activating NRAS Q61R mutation that is frequently associated with KLA. The patient’s pericardial effusions and lytic bone lesions resolved, and Kasabach–Merritt phenomenon improved with combination therapy including sirolimus, zoledronic acid, prednisone, and trametinib.</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/0ft7c408</guid>
      <pubDate>Thu, 26 Mar 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Lee, Danny</name>
      </author>
      <author>
        <name>Ding, Hilda</name>
      </author>
      <author>
        <name>Kruk, Peter</name>
      </author>
      <author>
        <name>Schiff, Deborah E</name>
        <uri>https://orcid.org/0000-0003-3154-8987</uri>
      </author>
    </item>
    <item>
      <title>Kawasaki Disease and the Importance of Family History</title>
      <link>https://escholarship.org/uc/item/6gv810rk</link>
      <description>BACKGROUND: Kawasaki disease (KD), a coronary artery vasculitis, is rare in teenagers who nonetheless have an increased risk of coronary artery aneurysms.
CASE SUMMARY: A 19-year-old woman had a prolonged febrile illness that resolved without treatment. The diagnosis of KD was made at autopsy at 42 years of age after sudden cardiac death associated with calcified giant coronary artery aneurysm. An interview of the decedent's mother revealed a KD-compatible illness in the decedent's son at 5 years of age that also was not diagnosed.
DISCUSSION: Susceptibility to KD is influenced by host genetics, and first-degree relatives of an index case have a 10-fold increased relative risk of disease. Pathognomonic changes in the coronary arteries discovered at autopsy should prompt counseling of family members.
TAKE-HOME MESSAGES: KD should be considered in adolescents and young adults with prolonged unexplained fever and mucocutaneous findings, including rash, conjunctival injection, oral...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/6gv810rk</guid>
      <pubDate>Thu, 12 Mar 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Maadanian, Daniel H</name>
      </author>
      <author>
        <name>Shimizu, Chisato</name>
      </author>
      <author>
        <name>Burns, Jane C</name>
        <uri>https://orcid.org/0000-0001-5679-1217</uri>
      </author>
    </item>
    <item>
      <title>Lipid Peroxidation and Kawasaki Disease</title>
      <link>https://escholarship.org/uc/item/55t186g0</link>
      <description>Lipid Peroxidation and Kawasaki Disease</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/55t186g0</guid>
      <pubDate>Thu, 12 Mar 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Faro, FD</name>
      </author>
      <author>
        <name>Burns, JC</name>
        <uri>https://orcid.org/0000-0001-5679-1217</uri>
      </author>
    </item>
    <item>
      <title>Menstrual Dysfunction Is Associated With Elevated Liver Enzymes in Adolescent Females: A United States Population-Based Study</title>
      <link>https://escholarship.org/uc/item/8vk6k9c9</link>
      <description>Purpose Polycystic ovary syndrome and metabolic dysfunction–associated steatotic liver disease (MASLD) both emerge during adolescence; however, it remains unknown whether menstrual abnormalities and hyperandrogenism signals increased hepatic risk. Methods We analyzed 2011–2020 National Health and Nutrition Examination Survey data for 1,651 females aged 12–19 years in the United States who were at least 2 years postmenarche. Amenorrhea was defined as self-reported absence of menses in the past 12 months. Biochemical hyperandrogenism was defined as free androgen index ≥5. Elevated alanine aminotransferase (ALT; &amp;gt;22 U/L) was the primary hepatic outcome; suspected MASLD was defined as elevated ALT plus ≥1 cardiometabolic risk factor. Survey-weighted logistic regression models adjusted for age, race and ethnicity, and body mass index (BMI) percentile. Results Amenorrhea was reported by 2.8% of participants and was associated with higher odds of elevated ALT (adjusted odds ratio...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/8vk6k9c9</guid>
      <pubDate>Tue, 3 Mar 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Noon, Sheila L</name>
      </author>
      <author>
        <name>Chun, Lauren F</name>
      </author>
      <author>
        <name>Mackay, Gillian</name>
      </author>
      <author>
        <name>Schwimmer, Jeffrey B</name>
      </author>
    </item>
    <item>
      <title>Implementation of a Hybrid Closed-Loop Automated Insulin Delivery System in a 29-Day Infant With Neonatal Diabetes.</title>
      <link>https://escholarship.org/uc/item/9wq637cv</link>
      <description>Neonatal diabetes mellitus (NDM) often requires insulin treatment to maintain adequate glycemic control and support growth and development. Conventional insulin treatment regimens are particularly challenging in NDM due to young age, developmentally appropriate feeding variation, and heightened insulin sensitivity leading to very small insulin dosing. We present this case as-to our knowledge-the earliest implementation of a hybrid closed-loop (HCLS) automated insulin delivery system in an NDM patient. HCLS with U10 significantly improved glycemic control compared to conventional insulin delivery with minimization of hypoglycemia. The adaptive capabilities of HCLS allowed for developmentally appropriate, ad libitum feeding without carbohydrate quantification, resulting in a meaningful quality of life improvement. This case adds to evidence supporting safe and effective use of diabetes technology in very young children. It demonstrates that the benefits seen in older populations...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/9wq637cv</guid>
      <pubDate>Mon, 2 Mar 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Ghaben, Alexandra</name>
      </author>
      <author>
        <name>Byer-Mendoza, Christine</name>
      </author>
      <author>
        <name>McNamara, Kimberly</name>
      </author>
      <author>
        <name>Huber, Andrea</name>
      </author>
      <author>
        <name>Cymbaluk, Anna</name>
      </author>
      <author>
        <name>Singh, Puja</name>
      </author>
    </item>
    <item>
      <title>Milk as a Transmission Vehicle for Highly Pathogenic Avian Influenza A (H5N1).</title>
      <link>https://escholarship.org/uc/item/8jw3v054</link>
      <description>Highly pathogenic avian influenza A (H5N1) (H5N1 hereafter) is an emerging pathogen in mammals. The recent recognition of H5N1 in dairy cattle increases opportunities for human exposure and infection and may accelerate a trajectory toward sustained human-to-human transmission. Furthermore, the presence of virus at high concentration in unpasteurized milk raises new risks for humans, especially infants and children. Milk has been identified as a vehicle for viral transmission in and between mammalian species, including humans. Sialic acids (SAs) found on cell surfaces are important mediators of species susceptibility to specific influenza strains and play an important role in viral tropism. New data demonstrate that SA receptors with α2,3 linkages capable of binding avian influenza strains are present in human mammary tissue. The presence of SA receptors that can bind avian influenza and a comparative analysis of viral transmission risk of raw and pasteurized milk in several mammalian...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/8jw3v054</guid>
      <pubDate>Thu, 12 Feb 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Byington, Carrie L</name>
      </author>
      <author>
        <name>Stellwagen, Lisa</name>
      </author>
      <author>
        <name>Bode, Lars</name>
      </author>
      <author>
        <name>Hooshmand, Mitra</name>
      </author>
      <author>
        <name>Pizzo, Donald P</name>
      </author>
      <author>
        <name>Russo, Hana</name>
      </author>
      <author>
        <name>Gonias, Steven L</name>
      </author>
    </item>
    <item>
      <title>The IBEX knowledge-base a community resource enabling adoption and development of immunofluorescence imaging methods</title>
      <link>https://escholarship.org/uc/item/0bx351dn</link>
      <description>The iterative bleaching extends multiplexity (IBEX) Knowledge-Base is a central portal for researchers adopting IBEX and related 2D and 3D immunofluorescence imaging methods. The design of the Knowledge-Base is modeled after efforts in the open-source software community and includes three facets: a development platform (GitHub), static website, and service for data archiving. The Knowledge-Base facilitates the practice of open science throughout the research life cycle by providing validation data for recommended and non-recommended reagents, such as primary and secondary antibodies. In addition to reporting negative data, the Knowledge-Base empowers method adoption and evolution by providing a venue for sharing protocols, videos, datasets, software, and publications. A dedicated discussion forum fosters a sense of community among researchers while addressing questions not covered in published manuscripts. Together, scientists from around the world are advancing scientific discovery...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/0bx351dn</guid>
      <pubDate>Thu, 12 Feb 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Yaniv, Ziv</name>
      </author>
      <author>
        <name>Anidi, Ifeanyichukwu U</name>
      </author>
      <author>
        <name>Arakkal, Leanne</name>
      </author>
      <author>
        <name>Arroyo-Mejías, Armando J</name>
      </author>
      <author>
        <name>Beuschel, Rebecca T</name>
      </author>
      <author>
        <name>Börner, Katy</name>
      </author>
      <author>
        <name>Chu, Colin J</name>
      </author>
      <author>
        <name>Clark, Beatrice H</name>
      </author>
      <author>
        <name>Clatworthy, Menna R</name>
      </author>
      <author>
        <name>Colautti, Jake</name>
      </author>
      <author>
        <name>Coscia, Fabian</name>
      </author>
      <author>
        <name>Croteau, Joshua</name>
      </author>
      <author>
        <name>Denha, Saven</name>
      </author>
      <author>
        <name>Dever, Rose</name>
      </author>
      <author>
        <name>Dutra, Walderez O</name>
      </author>
      <author>
        <name>Fritzsche, Sonja</name>
      </author>
      <author>
        <name>Fullam, Spencer</name>
      </author>
      <author>
        <name>Gerner, Michael Y</name>
      </author>
      <author>
        <name>Gola, Anita</name>
      </author>
      <author>
        <name>Gollob, Kenneth J</name>
      </author>
      <author>
        <name>Hernandez, Jonathan M</name>
      </author>
      <author>
        <name>Hor, Jyh Liang</name>
      </author>
      <author>
        <name>Ichise, Hiroshi</name>
      </author>
      <author>
        <name>Jing, Zhixin</name>
      </author>
      <author>
        <name>Jonigk, Danny</name>
      </author>
      <author>
        <name>Kandov, Evelyn</name>
      </author>
      <author>
        <name>Kastenmüller, Wolfgang</name>
      </author>
      <author>
        <name>Koenig, Joshua FE</name>
      </author>
      <author>
        <name>Kothurkar, Aanandita</name>
      </author>
      <author>
        <name>Kortekaas, Rosa K</name>
      </author>
      <author>
        <name>Kreins, Alexandra Y</name>
      </author>
      <author>
        <name>Lamborn, Ian T</name>
      </author>
      <author>
        <name>Lin, Yuri</name>
      </author>
      <author>
        <name>Morais, Katia Luciano Pereira</name>
      </author>
      <author>
        <name>Lunich, Aleksandra</name>
      </author>
      <author>
        <name>Luz, Jean CS</name>
      </author>
      <author>
        <name>MacDonald, Ryan B</name>
      </author>
      <author>
        <name>Makranz, Chen</name>
      </author>
      <author>
        <name>Maltez, Vivien I</name>
      </author>
      <author>
        <name>McDonough, John E</name>
      </author>
      <author>
        <name>Moriarty, Ryan V</name>
      </author>
      <author>
        <name>Ocampo-Godinez, Juan M</name>
      </author>
      <author>
        <name>Olyntho, Vitoria Murakami</name>
      </author>
      <author>
        <name>Oxenius, Annette</name>
      </author>
      <author>
        <name>Padhan, Kartika</name>
      </author>
      <author>
        <name>Remmert, Kirsten</name>
      </author>
      <author>
        <name>Richoz, Nathan</name>
      </author>
      <author>
        <name>Schrom, Edward C</name>
      </author>
      <author>
        <name>Shang, Wanjing</name>
      </author>
      <author>
        <name>Shi, Lihong</name>
      </author>
      <author>
        <name>Shih, Rochelle M</name>
      </author>
      <author>
        <name>Speranza, Emily</name>
      </author>
      <author>
        <name>Stierli, Salome</name>
      </author>
      <author>
        <name>Teichmann, Sarah A</name>
      </author>
      <author>
        <name>Verse, Tibor Z</name>
      </author>
      <author>
        <name>Vierhout, Megan</name>
      </author>
      <author>
        <name>Wachter, Brianna T</name>
      </author>
      <author>
        <name>Wade-Vallance, Adam K</name>
      </author>
      <author>
        <name>Williams, Margaret</name>
      </author>
      <author>
        <name>Zangger, Nathan</name>
      </author>
      <author>
        <name>Germain, Ronald N</name>
      </author>
      <author>
        <name>Radtke, Andrea J</name>
      </author>
    </item>
    <item>
      <title>Social Determinants of Health and Pediatric Long COVID in the US</title>
      <link>https://escholarship.org/uc/item/3tz3m4qn</link>
      <description>Importance: Millions of children worldwide are experiencing prolonged symptoms after SARS-CoV-2 infection, yet social risk factors for developing long COVID are largely unknown. As child health is influenced by the environment in which they live and interact, adverse social determinants of health (SDOH) may contribute to the development of pediatric long COVID.
Objective: To identify whether adverse SDOH are associated with increased odds of long COVID in school-aged children and adolescents in the US.
Design, Setting, and Participants: This cross-sectional analysis of a multicenter, longitudinal, meta-cohort study encompassed 52 sites (health care and community settings) across the US. School-aged children (6-11 years; n = 903) and adolescents (12-17 years; n = 3681) with SARS-CoV-2 infection history were included. Those with an unknown date of first infection, history of multisystem inflammatory syndrome in children, or symptom surveys with less than 50% of questions completed...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/3tz3m4qn</guid>
      <pubDate>Thu, 29 Jan 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Rhee, Kyung E</name>
      </author>
      <author>
        <name>Thaweethai, Tanayott</name>
      </author>
      <author>
        <name>Pant, Deepti B</name>
      </author>
      <author>
        <name>Stein, Cheryl R</name>
      </author>
      <author>
        <name>Salisbury, Amy L</name>
      </author>
      <author>
        <name>Kinser, Patricia A</name>
      </author>
      <author>
        <name>Kleinman, Lawrence C</name>
      </author>
      <author>
        <name>Gallagher, Richard</name>
      </author>
      <author>
        <name>Warburton, David</name>
      </author>
      <author>
        <name>Mohandas, Sindhu</name>
      </author>
      <author>
        <name>Snowden, Jessica N</name>
      </author>
      <author>
        <name>Stockwell, Melissa S</name>
      </author>
      <author>
        <name>Tantisira, Kelan G</name>
      </author>
      <author>
        <name>Flaherman, Valerie J</name>
      </author>
      <author>
        <name>Teufel, Ronald J</name>
      </author>
      <author>
        <name>Castro, Leah</name>
      </author>
      <author>
        <name>Chung, Alicia</name>
      </author>
      <author>
        <name>Espinoza Esparza, Jocelyn</name>
      </author>
      <author>
        <name>Hockett, Christine W</name>
      </author>
      <author>
        <name>Isidoro-Chino, Maria</name>
      </author>
      <author>
        <name>Krishnan, Anita</name>
      </author>
      <author>
        <name>McCormack, Lacey A</name>
      </author>
      <author>
        <name>Nabower, Aleisha M</name>
      </author>
      <author>
        <name>Nahin, Erica R</name>
      </author>
      <author>
        <name>Rosas, Johana M</name>
      </author>
      <author>
        <name>Siddiqui, Sarwat</name>
      </author>
      <author>
        <name>Szmuszkovicz, Jacqueline R</name>
      </author>
      <author>
        <name>Vangeepuram, Nita</name>
      </author>
      <author>
        <name>Zimmerman, Emily</name>
      </author>
      <author>
        <name>Brown, Heather-Elizabeth</name>
      </author>
      <author>
        <name>Carmilani, Megan</name>
      </author>
      <author>
        <name>Coombs, K</name>
      </author>
      <author>
        <name>Fisher, Liza</name>
      </author>
      <author>
        <name>Witvliet, Margot Gage</name>
      </author>
      <author>
        <name>Wood, John C</name>
      </author>
      <author>
        <name>Milner, Joshua D</name>
      </author>
      <author>
        <name>Rosenzweig, Erika B</name>
      </author>
      <author>
        <name>Irby, Katherine</name>
      </author>
      <author>
        <name>Karlson, Elizabeth W</name>
      </author>
      <author>
        <name>Qian, Zihan</name>
      </author>
      <author>
        <name>Lamendola-Essel, Michelle F</name>
      </author>
      <author>
        <name>Hasson, Denise C</name>
      </author>
      <author>
        <name>Katz, Stuart D</name>
      </author>
      <author>
        <name>Yin, H Shonna</name>
      </author>
      <author>
        <name>Foulkes, Andrea S</name>
      </author>
      <author>
        <name>Gross, Rachel S</name>
      </author>
      <author>
        <name>Irby, Katherine</name>
      </author>
      <author>
        <name>Zani, Kathleen</name>
      </author>
      <author>
        <name>Arthur, Lindsay R</name>
      </author>
      <author>
        <name>Brown, Ann Marie</name>
      </author>
      <author>
        <name>Evans, Danielle N</name>
      </author>
      <author>
        <name>Hill, Trenesha</name>
      </author>
      <author>
        <name>Hobart-Porter, Laura</name>
      </author>
      <author>
        <name>Howard, Lee</name>
      </author>
      <author>
        <name>Hummel, Kathy</name>
      </author>
      <author>
        <name>Krehbiel, Hannah</name>
      </author>
      <author>
        <name>Yount, Phaedra</name>
      </author>
      <author>
        <name>Elliott, Amy</name>
      </author>
      <author>
        <name>Adam, Grace</name>
      </author>
      <author>
        <name>Angal, Jyoti</name>
      </author>
      <author>
        <name>Barber, Maria</name>
      </author>
      <author>
        <name>Clark, Katelynne</name>
      </author>
      <author>
        <name>Dos Reis, Clayton</name>
      </author>
      <author>
        <name>Freesemann, Mandy</name>
      </author>
      <author>
        <name>Friedrich, Christa</name>
      </author>
      <author>
        <name>Hockett, Christine</name>
      </author>
      <author>
        <name>Johannsen, Rachel</name>
      </author>
      <author>
        <name>Johnson-Vonk, Emily</name>
      </author>
      <author>
        <name>Kaiser, Cassidy</name>
      </author>
      <author>
        <name>Kruse, Alexa</name>
      </author>
      <author>
        <name>Lang, Jennifer</name>
      </author>
      <author>
        <name>Lim, Peter</name>
      </author>
      <author>
        <name>McCoy, Meggie</name>
      </author>
      <author>
        <name>Miller, Lorie</name>
      </author>
      <author>
        <name>Petereit (Cerkovnik), Shelby</name>
      </author>
      <author>
        <name>RiChard (Werpy), Jaime</name>
      </author>
      <author>
        <name>Seiler, Jessica</name>
      </author>
      <author>
        <name>Sundleaf, Bret</name>
      </author>
      <author>
        <name>Svendsen, Joshua</name>
      </author>
      <author>
        <name>Trosper, Billy</name>
      </author>
      <author>
        <name>Vermeulen, Olivia</name>
      </author>
      <author>
        <name>Young, Scott</name>
      </author>
      <author>
        <name>Palumbo, Paul</name>
      </author>
      <author>
        <name>Dabney, Sean</name>
      </author>
      <author>
        <name>Fahrner, Marie-Christine</name>
      </author>
      <author>
        <name>Gallagher, Torrey</name>
      </author>
      <author>
        <name>Martini, Karilyn</name>
      </author>
      <author>
        <name>McNally, Mary</name>
      </author>
      <author>
        <name>Vivensi Stiverson, Sarah</name>
      </author>
      <author>
        <name>Kosut, Jessica S</name>
      </author>
      <author>
        <name>Balaraman, Venkataraman</name>
      </author>
      <author>
        <name>Cheung, JoAnn</name>
      </author>
      <author>
        <name>Hong, Travis KF</name>
      </author>
      <author>
        <name>Kalua, Shanelle</name>
      </author>
      <author>
        <name>Minami, Evan</name>
      </author>
      <author>
        <name>Siu, Andrea</name>
      </author>
      <author>
        <name>Tong, Micah</name>
      </author>
      <author>
        <name>Teufel II, Ronald J</name>
      </author>
      <author>
        <name>Atz, Andy</name>
      </author>
      <author>
        <name>Dantas, Marina</name>
      </author>
    </item>
    <item>
      <title>Evaluating the Test-Negative Design for COVID-19 Vaccine Effectiveness Using Randomized Trial Data</title>
      <link>https://escholarship.org/uc/item/6pn6p9gr</link>
      <description>Importance: The test-negative design (TND) has been widely used to assess postmarketing COVID-19 vaccine effectiveness but requires further evaluation for this application.
Objective: To determine whether the TND reliably evaluates vaccine effectiveness against symptomatic COVID-19 using placebo-controlled vaccine efficacy randomized clinical trials (RCTs).
Design, Setting, and Participants: This secondary cross-protocol analysis constructed TND study datasets from study sites in 16 countries across 5 continents using the blinded phase cohorts of 5 harmonized phase 3 COVID-19 Prevention Network RCTs: COVE (Coronavirus Vaccine Efficacy and Safety), AZD1222, ENSEMBLE, PREVENT-19 (Prefusion Protein Subunit Vaccine Efficacy Novavax Trial COVID-19), and VAT00008. Participants included adults who received the intended number of doses, experienced COVID-19-like symptoms, and obtained SARS-CoV-2 testing. Start dates ranged from July 27, 2020, to October 19, 2021; data cutoff dates ranged...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/6pn6p9gr</guid>
      <pubDate>Wed, 28 Jan 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Andrews, Leah IB</name>
      </author>
      <author>
        <name>Halloran, M Elizabeth</name>
      </author>
      <author>
        <name>Neuzil, Kathleen M</name>
      </author>
      <author>
        <name>van der Laan, Lars</name>
      </author>
      <author>
        <name>Huang, Yunda</name>
      </author>
      <author>
        <name>Andriesen, Jessica</name>
      </author>
      <author>
        <name>Patel, Mayur</name>
      </author>
      <author>
        <name>Fisher, Leigh H</name>
      </author>
      <author>
        <name>Janes, Holly</name>
      </author>
      <author>
        <name>Rouphael, Nadine</name>
      </author>
      <author>
        <name>Walsh, Stephen R</name>
      </author>
      <author>
        <name>Theodore, Deborah A</name>
      </author>
      <author>
        <name>Tieu, Hong-Van</name>
      </author>
      <author>
        <name>Sobieszczyk, Magdalena</name>
      </author>
      <author>
        <name>El Sahly, Hana M</name>
      </author>
      <author>
        <name>Baden, Lindsey R</name>
      </author>
      <author>
        <name>Falsey, Ann R</name>
      </author>
      <author>
        <name>Campbell, Thomas B</name>
      </author>
      <author>
        <name>Kelley, Colleen F</name>
      </author>
      <author>
        <name>Healy, Catherine Mary</name>
      </author>
      <author>
        <name>Immergluck, Lilly</name>
      </author>
      <author>
        <name>Luft, Benjamin</name>
      </author>
      <author>
        <name>Hirsch, Ian</name>
      </author>
      <author>
        <name>de Bruyn, Guy</name>
      </author>
      <author>
        <name>Truyers, Carla</name>
      </author>
      <author>
        <name>Priddy, Frances</name>
      </author>
      <author>
        <name>Sumner, Kelsey M</name>
      </author>
      <author>
        <name>Flannery, Brendan</name>
      </author>
      <author>
        <name>Follmann, Dean</name>
      </author>
      <author>
        <name>Gilbert, Peter B</name>
      </author>
      <author>
        <name>Abad, Vanessa</name>
      </author>
      <author>
        <name>Abalos, Karina</name>
      </author>
      <author>
        <name>Abate, Getahun</name>
      </author>
      <author>
        <name>Abbas, Anum</name>
      </author>
      <author>
        <name>Accini, Jose</name>
      </author>
      <author>
        <name>Ackerman, Ronald</name>
      </author>
      <author>
        <name>Ackerman, Jamie</name>
      </author>
      <author>
        <name>Ackermann, Jeremy</name>
      </author>
      <author>
        <name>Adams, Atoya</name>
      </author>
      <author>
        <name>Adams, Michael R</name>
      </author>
      <author>
        <name>Adams, Mark S</name>
      </author>
      <author>
        <name>Adams, Michael</name>
      </author>
      <author>
        <name>Adelglass, Jeffrey M</name>
      </author>
      <author>
        <name>Afework, Sarah</name>
      </author>
      <author>
        <name>Ahmad, Nina</name>
      </author>
      <author>
        <name>Akamine, Christine</name>
      </author>
      <author>
        <name>Ake, Julie A</name>
      </author>
      <author>
        <name>Albert, Gary</name>
      </author>
      <author>
        <name>Alcaide, Maria L</name>
      </author>
      <author>
        <name>Alderson, Nathan</name>
      </author>
      <author>
        <name>Aleman, Lily</name>
      </author>
      <author>
        <name>Alemán, José O</name>
      </author>
      <author>
        <name>Al-Ibrahim, Mohamed S</name>
      </author>
      <author>
        <name>Allaw, Mohammed</name>
      </author>
      <author>
        <name>Allen, Leland N</name>
      </author>
      <author>
        <name>Allen, Mary</name>
      </author>
      <author>
        <name>Aloysia, Naveena</name>
      </author>
      <author>
        <name>Alvarado, Hilario</name>
      </author>
      <author>
        <name>Alvarez León, Winniberg Stephany</name>
      </author>
      <author>
        <name>Amador, Carmen</name>
      </author>
      <author>
        <name>Amuasi, John Humphrey</name>
      </author>
      <author>
        <name>Andersen, James</name>
      </author>
      <author>
        <name>Anderson, Evan J</name>
      </author>
      <author>
        <name>Anderson, Corey G</name>
      </author>
      <author>
        <name>Anderson, Victoria R</name>
      </author>
      <author>
        <name>Andes, David R</name>
      </author>
      <author>
        <name>Andrasik, Michele P</name>
      </author>
      <author>
        <name>Andree, Stephanie</name>
      </author>
      <author>
        <name>Andrews, Jeb</name>
      </author>
      <author>
        <name>Andriesen, Jessica G</name>
      </author>
      <author>
        <name>Andriulis, Victoria</name>
      </author>
      <author>
        <name>Áñez, Germán</name>
      </author>
      <author>
        <name>Angeles Ceregido, Maria</name>
      </author>
      <author>
        <name>Ansah, Nana Akosua</name>
      </author>
      <author>
        <name>Ansel, Jessica L</name>
      </author>
      <author>
        <name>Anthony, Codi M</name>
      </author>
      <author>
        <name>Antony, Johannes</name>
      </author>
      <author>
        <name>Antwi, Mohammed</name>
      </author>
      <author>
        <name>Arduino, Roberto C</name>
      </author>
      <author>
        <name>Aristy, Florida</name>
      </author>
      <author>
        <name>Arnold, Valerie K</name>
      </author>
      <author>
        <name>Arrazcaeta, Alicia</name>
      </author>
      <author>
        <name>Arroyo, Hugo Macareno</name>
      </author>
      <author>
        <name>Asante, Kwaku Poku</name>
      </author>
      <author>
        <name>Atmar, Robert L</name>
      </author>
      <author>
        <name>August, Allison</name>
      </author>
      <author>
        <name>Avworo, Ayoade</name>
      </author>
      <author>
        <name>Bacher, Christina</name>
      </author>
      <author>
        <name>Bäcker, Martín</name>
      </author>
      <author>
        <name>Baden, Lindsay R</name>
      </author>
      <author>
        <name>Badillo, Diana</name>
      </author>
      <author>
        <name>Bainbridge, Emma</name>
      </author>
      <author>
        <name>Baka, Michele</name>
      </author>
      <author>
        <name>Baker, Sherrie</name>
      </author>
      <author>
        <name>Balani, Bindu</name>
      </author>
      <author>
        <name>Ball, Brandy</name>
      </author>
      <author>
        <name>Baron, Mira</name>
      </author>
      <author>
        <name>Barouch, Dan H</name>
      </author>
      <author>
        <name>Barranco-Santana, Elizabeth</name>
      </author>
      <author>
        <name>Barrat Hernández, Alejandro Quintín</name>
      </author>
    </item>
    <item>
      <title>Hepatic Glycogenosis Resulting in Hyperammonemia in a Young Adult With Type 1 Diabetes Mellitus</title>
      <link>https://escholarship.org/uc/item/8qj674j5</link>
      <description>Abstract&lt;p&gt;A 19-year-old male individual with poorly controlled type 1 diabetes mellitus (T1DM) of 16 years duration presented with diabetic ketoacidosis (DKA) and was found to have hepatomegaly with disproportionately elevated transaminases, hyperammonemia, and lactic acidosis, which persisted after DKA resolution. Autoimmune, infectious, metabolic, and toxic causes were excluded. Liver elastography demonstrated homogeneous, nonsteatotic, noncirrhotic enlargement. Histology revealed hepatocytes with pale or clear cytoplasm and glycogenated nuclei. Total clinical picture is consistent with Mauriac syndrome—a rare complication exclusively observed in people with T1DM with poor glycemic control, resulting in pubertal and growth delay, cushingoid facies, lactic acidosis, transaminitis, and hyperlipidemia. Although prevalence of suboptimal management of T1DM remains common, even with modern insulin delivery mechanisms, Mauriac syndrome remains rare and poorly characterized. We highlight...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/8qj674j5</guid>
      <pubDate>Thu, 15 Jan 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Dinh, Cong B</name>
        <uri>https://orcid.org/0000-0002-3026-0992</uri>
      </author>
      <author>
        <name>Ghaben, Alexandra L</name>
        <uri>https://orcid.org/0000-0001-7377-7820</uri>
      </author>
      <author>
        <name>Newfield, Ron S</name>
      </author>
    </item>
    <item>
      <title>A resource to empirically establish drug exposure records directly from untargeted metabolomics data</title>
      <link>https://escholarship.org/uc/item/49v5w2g8</link>
      <description>Despite extensive efforts, extracting medication exposure information from clinical records remains challenging. To complement this approach, here we show the Global Natural Product Social Molecular Networking (GNPS) Drug Library, a tandem mass spectrometry (MS/MS) based resource designed for drug screening with untargeted metabolomics. This resource integrates MS/MS references of drugs and their metabolites/analogs with standardized vocabularies on their exposure sources, pharmacologic classes, therapeutic indications, and mechanisms of action. It enables direct analysis of drug exposure and metabolism from untargeted metabolomics data, supporting flexible summarization at multiple ontology levels to align with different research goals. We demonstrate its application by stratifying participants in a human immunodeficiency virus (HIV) cohort based on detected drug exposures. We uncover drug-associated alterations in microbiota-derived N-acyl lipids that are not captured when stratifying...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/49v5w2g8</guid>
      <pubDate>Mon, 15 Dec 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Zhao, Haoqi Nina</name>
      </author>
      <author>
        <name>Kvitne, Kine Eide</name>
      </author>
      <author>
        <name>Brungs, Corinna</name>
      </author>
      <author>
        <name>Mohan, Siddharth</name>
      </author>
      <author>
        <name>Charron-Lamoureux, Vincent</name>
      </author>
      <author>
        <name>Bittremieux, Wout</name>
      </author>
      <author>
        <name>Tang, Runbang</name>
      </author>
      <author>
        <name>Schmid, Robin</name>
      </author>
      <author>
        <name>Lamichhane, Santosh</name>
      </author>
      <author>
        <name>Xing, Shipei</name>
      </author>
      <author>
        <name>El Abiead, Yasin</name>
      </author>
      <author>
        <name>Andalibi, Mohammadsobhan S</name>
      </author>
      <author>
        <name>Mannochio-Russo, Helena</name>
      </author>
      <author>
        <name>Ambre, Madison</name>
      </author>
      <author>
        <name>Avalon, Nicole E</name>
      </author>
      <author>
        <name>Bryant, MacKenzie</name>
      </author>
      <author>
        <name>Burnett, Lindsey A</name>
      </author>
      <author>
        <name>Caraballo-Rodríguez, Andrés Mauricio</name>
      </author>
      <author>
        <name>Maya, Martin Casas</name>
      </author>
      <author>
        <name>Chin, Loryn</name>
      </author>
      <author>
        <name>Corominas, Lluís</name>
      </author>
      <author>
        <name>Ellis, Ronald J</name>
      </author>
      <author>
        <name>Franklin, Donald</name>
      </author>
      <author>
        <name>Girod, Sagan</name>
      </author>
      <author>
        <name>Gomes, Paulo Wender P</name>
      </author>
      <author>
        <name>Hansen, Lauren</name>
      </author>
      <author>
        <name>Heaton, Robert K</name>
      </author>
      <author>
        <name>Iudicello, Jennifer E</name>
      </author>
      <author>
        <name>Jarmusch, Alan K</name>
      </author>
      <author>
        <name>Khatib, Lora</name>
      </author>
      <author>
        <name>Letendre, Scott</name>
        <uri>https://orcid.org/0000-0003-3490-4975</uri>
      </author>
      <author>
        <name>Magyari, Sarolt</name>
      </author>
      <author>
        <name>McDonald, Daniel</name>
      </author>
      <author>
        <name>Mohanty, Ipsita</name>
      </author>
      <author>
        <name>Cumsille, Andrés</name>
      </author>
      <author>
        <name>Moore, David J</name>
        <uri>https://orcid.org/0000-0002-2199-1662</uri>
      </author>
      <author>
        <name>Rajkumar, Prajit</name>
      </author>
      <author>
        <name>Ross, Dylan H</name>
      </author>
      <author>
        <name>Sapre, Harshada</name>
      </author>
      <author>
        <name>Shahneh, Mohammad Reza Zare</name>
      </author>
      <author>
        <name>Gil-Solsona, Ruben</name>
      </author>
      <author>
        <name>Thomas, Sydney P</name>
      </author>
      <author>
        <name>Tribelhorn, Caitlin</name>
      </author>
      <author>
        <name>Tubb, Helena M</name>
      </author>
      <author>
        <name>Walker, Corinn</name>
      </author>
      <author>
        <name>Wang, Crystal X</name>
      </author>
      <author>
        <name>Zemlin, Jasmine</name>
      </author>
      <author>
        <name>Zuffa, Simone</name>
        <uri>https://orcid.org/0000-0001-7237-3402</uri>
      </author>
      <author>
        <name>Wishart, David S</name>
      </author>
      <author>
        <name>Gago-Ferrero, Pablo</name>
      </author>
      <author>
        <name>Kaddurah-Daouk, Rima</name>
      </author>
      <author>
        <name>Wang, Mingxun</name>
      </author>
      <author>
        <name>Raffatellu, Manuela</name>
        <uri>https://orcid.org/0000-0001-6487-4215</uri>
      </author>
      <author>
        <name>Zengler, Karsten</name>
      </author>
      <author>
        <name>Pluskal, Tomáš</name>
      </author>
      <author>
        <name>Xu, Libin</name>
      </author>
      <author>
        <name>Knight, Rob</name>
      </author>
      <author>
        <name>Tsunoda, Shirley M</name>
        <uri>https://orcid.org/0000-0002-3974-8038</uri>
      </author>
      <author>
        <name>Dorrestein, Pieter C</name>
      </author>
    </item>
    <item>
      <title>BMI Percentile Cutoffs for Overweight and Obesity Are Set Too High in Terms of Adiposity and Metabolic Markers for Asian Children and Adolescents</title>
      <link>https://escholarship.org/uc/item/5mh86751</link>
      <description>OBJECTIVES: Asian adults develop metabolic complications at lower body mass indices (BMIs) compared with other ethnic groups, leading to lower BMI cutoffs for overweight and obesity. However, it remains unclear whether such adjustments are warranted in Asian children and adolescents. We aimed to determine whether lower BMI percentile cutoffs should be considered for overweight and obesity among Asian children and adolescents in the United States.
METHODS: We analysed nationally representative data from U.S. children and adolescents from NHANES, 2012-2020. Metabolic parameters-including truncal fat percentage, glycemic markers, lipid profiles and liver disease markers-were compared between Asian and non-Asian participants within the 85-95th percentile and ≥ 95th percentile ranges. Metabolic parameter-based matching analyses identified corresponding BMI percentiles between groups.
RESULTS: Asian children had more pronounced metabolic abnormalities than non-Asians in the overweight...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/5mh86751</guid>
      <pubDate>Sat, 13 Dec 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Hong, Suk‐Jin</name>
      </author>
      <author>
        <name>Zhang, Xinlian</name>
      </author>
      <author>
        <name>Hartmann, Phillipp</name>
        <uri>https://orcid.org/0000-0003-3658-3335</uri>
      </author>
    </item>
    <item>
      <title>Genome-resolved biogeography of Phaeocystales, cosmopolitan bloom-forming algae</title>
      <link>https://escholarship.org/uc/item/2xn6r56s</link>
      <description>Phaeocystales, comprising the genus Phaeocystis and an uncharacterized sister lineage, are nanoplanktonic haptophytes widespread in the global ocean. Several species form mucilaginous colonies and influence key biogeochemical cycles, yet their underlying diversity and ecological strategies remain underexplored. Here, we present new genomic data from 13 strains, including three high-quality reference genomes (N50 &amp;gt; 30 kbp), and integrate previous metagenome-assembled genomes to resolve a robust phylogeny. Divergence timing of P. antarctica aligns with Miocene cooling and Southern Ocean isolation. Genomic traits reveal metabolic flexibility, including mixotrophic nitrogen acquisition in temperate waters and gene expansions linked to polar nutrient adaptation. Concordantly, transcriptomic comparisons between temperate and polar Phaeocystis suggest Southern Ocean populations experience iron and B12 limitation. We also identify signatures of horizontal gene transfer and endogenous...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/2xn6r56s</guid>
      <pubDate>Wed, 10 Dec 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Füssy, Zoltán</name>
      </author>
      <author>
        <name>Lampe, Robert H</name>
      </author>
      <author>
        <name>Arrigo, Kevin R</name>
      </author>
      <author>
        <name>Barry, Kerrie</name>
        <uri>https://orcid.org/0000-0002-8999-6785</uri>
      </author>
      <author>
        <name>Brisbin, Margaret M</name>
      </author>
      <author>
        <name>Brussaard, Corina PD</name>
      </author>
      <author>
        <name>Decelle, Johan</name>
      </author>
      <author>
        <name>de Vargas, Colomban</name>
      </author>
      <author>
        <name>DiTullio, Giacomo R</name>
      </author>
      <author>
        <name>Elbourne, Liam DH</name>
      </author>
      <author>
        <name>Frischer, Marc E</name>
      </author>
      <author>
        <name>Goodstein, David M</name>
        <uri>https://orcid.org/0000-0001-6287-2697</uri>
      </author>
      <author>
        <name>Grigoriev, Igor V</name>
        <uri>https://orcid.org/0000-0002-3136-8903</uri>
      </author>
      <author>
        <name>Hayes, Richard D</name>
        <uri>https://orcid.org/0000-0002-5236-7918</uri>
      </author>
      <author>
        <name>Healey, Adam L</name>
      </author>
      <author>
        <name>James, Chase C</name>
      </author>
      <author>
        <name>Jenkins, Jerry W</name>
      </author>
      <author>
        <name>Juery, Caroline</name>
      </author>
      <author>
        <name>Kumar, Manish</name>
        <uri>https://orcid.org/0000-0001-8035-3399</uri>
      </author>
      <author>
        <name>Kustka, Adam B</name>
      </author>
      <author>
        <name>Maumus, Florian</name>
      </author>
      <author>
        <name>Novák Vanclová, Anna MG</name>
      </author>
      <author>
        <name>Oborník, Miroslav</name>
      </author>
      <author>
        <name>Paulsen, Ian T</name>
      </author>
      <author>
        <name>Probert, Ian</name>
      </author>
      <author>
        <name>Saito, Mak A</name>
      </author>
      <author>
        <name>Schmutz, Jeremy</name>
      </author>
      <author>
        <name>Skalický, Tomáš</name>
      </author>
      <author>
        <name>Tec-Campos, Diego</name>
      </author>
      <author>
        <name>Tomelka, Hannah</name>
      </author>
      <author>
        <name>Věchtová, Pavlína</name>
      </author>
      <author>
        <name>Venepally, Pratap</name>
      </author>
      <author>
        <name>Wilson-Mortier, Brendan</name>
      </author>
      <author>
        <name>Zengler, Karsten</name>
      </author>
      <author>
        <name>Zheng, Hong</name>
      </author>
      <author>
        <name>Allen, Andrew E</name>
        <uri>https://orcid.org/0000-0001-5911-6081</uri>
      </author>
    </item>
    <item>
      <title>Body Image in Men with HIV</title>
      <link>https://escholarship.org/uc/item/93r50159</link>
      <description>OBJECTIVE: To determine body image among HIV-infected men and to determine the relationship of lipodystrophy on body image.
METHODOLOGY: Self-report questionnaires on body image were distributed to HIV-infected men at the university-based HIV clinic. Two previously validated instruments, the Body Image Quality of Life (BIQLI) scale and the Situational Inventory of Body Image Dysphoria Short Form (SIBID-S) were used to measure body image effects. The presence of lipodystrophy was determined by both self-report and physician examination. Demographic characteristics, disease stage, health status, and quality of life were also ascertained. Analysis of responses was performed via both group comparisons and linear regression analyses.
RESULTS: One hundred ten men responded. Seventy-one percent identified their sexual orientation as men having sex with men (MSM). Forty-eight reported the presence of lipodystrophic characteristics; 62 reported no lipodystrophic changes. Agreement regarding...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/93r50159</guid>
      <pubDate>Fri, 5 Dec 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Huang, Jeannie S</name>
      </author>
      <author>
        <name>Lee, Daniel</name>
      </author>
      <author>
        <name>Becerra, Karen</name>
      </author>
      <author>
        <name>Santos, Rosanne</name>
      </author>
      <author>
        <name>Barber, Ed</name>
      </author>
      <author>
        <name>Mathews, W Christopher</name>
      </author>
    </item>
    <item>
      <title>Body image in women with HIV: a cross-sectional evaluation</title>
      <link>https://escholarship.org/uc/item/1mx7t2zd</link>
      <description>BackgroundHIV lipodystrophy syndrome is a recognized complication of potent antiretroviral therapy and is characterized by often dramatic changes in various body fat stores, both central and peripheral. Given prior findings of heightened body image dysphoria among HIV-infected men with lipodystrophy as compared to HIV-infected men without lipodystrophy, we sought to determine body image among HIV-infected and HIV-negative women and to determine the relationship of HIV and lipodystrophy with body image. Our a priori hypothesis was that women with HIV and lipodystrophy would have significantly poorer body image as compared to women without HIV and to women with HIV without lipodystrophy.Results116 women responded to two previously validated self-report instruments (Body Image Quality of Life Index (BIQLI) and the Situational Inventory of Body-Image Dysphoria – Short Form (SIBID-S)) on body image. 62 (53% subjects) HIV-infected women were recruited at the university-based HIV clinic....</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/1mx7t2zd</guid>
      <pubDate>Fri, 5 Dec 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Huang, Jeannie S</name>
      </author>
      <author>
        <name>Harrity, Shawn</name>
      </author>
      <author>
        <name>Lee, Daniel</name>
      </author>
      <author>
        <name>Becerra, Karen</name>
      </author>
      <author>
        <name>Santos, Rosanne</name>
      </author>
      <author>
        <name>Mathews, WChristopher</name>
      </author>
    </item>
    <item>
      <title>Frataxin Traps Low Abundance Quaternary Structure to Stimulate Human Fe-S Cluster Biosynthesis</title>
      <link>https://escholarship.org/uc/item/9sk03517</link>
      <description>Iron-sulfur clusters are essential protein cofactors synthesized in human mitochondria by an NFS1-ISD11-ACP-ISCU2-FXN assembly complex. Surprisingly, researchers have discovered three distinct quaternary structures for cysteine desulfurase subcomplexes, which display similar interactions between NFS1-ISD11-ACP protomeric units but distinct dimeric interfaces between the protomers. Although the role of these different architectures is unclear, possible functions include regulating activity and promoting the biosynthesis of distinct sulfur-containing biomolecules. Here, crystallography, native ion-mobility mass spectrometry, and chromatography methods reveal the Fe-S assembly subcomplex exists as an equilibrium mixture of these different quaternary structures. Our results suggest Friedreich's ataxia (FRDA) protein frataxin (FXN) functions as a "molecular lock" and shifts the equilibrium towards one of the architectures to stimulate the cysteine desulfurase activity and promote iron-sulfur...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/9sk03517</guid>
      <pubDate>Thu, 4 Dec 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Cory, Seth</name>
      </author>
      <author>
        <name>Lin, Cheng-Wei</name>
      </author>
      <author>
        <name>Havens, Steven</name>
      </author>
      <author>
        <name>Patra, Shachin</name>
      </author>
      <author>
        <name>Putnam, Christopher</name>
        <uri>https://orcid.org/0000-0002-6145-1265</uri>
      </author>
      <author>
        <name>Shirzadeh, Mehdi</name>
      </author>
      <author>
        <name>Russell, David</name>
      </author>
      <author>
        <name>Barondeau, David</name>
      </author>
    </item>
    <item>
      <title>Dual dysregulation of TNF/interferon signaling and classical monocytes are implicated in Reactive Infectious Mucocutaneous Eruptions</title>
      <link>https://escholarship.org/uc/item/9rh5t4b2</link>
      <description>Dual dysregulation of TNF/interferon signaling and classical monocytes are implicated in Reactive Infectious Mucocutaneous Eruptions</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/9rh5t4b2</guid>
      <pubDate>Thu, 4 Dec 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Tan, Zhehao</name>
      </author>
      <author>
        <name>Wu, Gio</name>
      </author>
      <author>
        <name>Figueroa, Daniela Salgado</name>
      </author>
      <author>
        <name>Dutta, Paramita</name>
      </author>
      <author>
        <name>Jaeger, Zachary</name>
      </author>
      <author>
        <name>Mazurie, Marissa</name>
      </author>
      <author>
        <name>Schairer, David</name>
      </author>
      <author>
        <name>Eichenfield, Dawn</name>
      </author>
      <author>
        <name>Tom, Wynnis L</name>
      </author>
      <author>
        <name>Galli, Lauren</name>
      </author>
      <author>
        <name>Eichenfield, Lawrence</name>
      </author>
      <author>
        <name>Geng, Bob</name>
      </author>
      <author>
        <name>Hinds, Brian</name>
      </author>
      <author>
        <name>Hoffman, Hal M</name>
      </author>
      <author>
        <name>Broderick, Lori</name>
      </author>
      <author>
        <name>Croker, Ben</name>
      </author>
      <author>
        <name>Ay, Ferhat</name>
        <uri>https://orcid.org/0000-0002-0708-6914</uri>
      </author>
      <author>
        <name>Oldenburg, Reid</name>
        <uri>https://orcid.org/0000-0003-1423-4927</uri>
      </author>
    </item>
    <item>
      <title>The Saccharomyces cerevisiae cell lysis mutant cly8 is a temperature-sensitive allele of ESP1</title>
      <link>https://escholarship.org/uc/item/8zv2g8hx</link>
      <description>The &lt;i&gt;Saccharomyces cerevisiae&lt;/i&gt; mutants designated &lt;i&gt;cly&lt;/i&gt; (cell lysis) cause cell lysis at elevated temperatures. The &lt;i&gt;cly8&lt;/i&gt; mutation, previously localized to an 80 kilobase region between &lt;i&gt;GCD2&lt;/i&gt; and &lt;i&gt;SPT6&lt;/i&gt; on the right arm of chromosome VII, has been used for mutation mapping and in recombination assays, but its genetic identity has remained unknown. Whole genome sequencing of &lt;i&gt;cly8&lt;/i&gt; mutant and &lt;i&gt;CLY8&lt;/i&gt; wild-type strains revealed four missense mutations specific to the &lt;i&gt;cly8&lt;/i&gt; mutant strain in the &lt;i&gt;GCD2&lt;/i&gt;-&lt;i&gt;SPT6&lt;/i&gt; interval, three of these missense mutations affected essential genes. The &lt;i&gt;esp1-G543E&lt;/i&gt; mutation, but not the two other missense mutations, recapitulated the temperature-sensitive growth, the cell lysis phenotype, and recessive nature of the &lt;i&gt;cly8&lt;/i&gt; mutation. The &lt;i&gt;ESP1&lt;/i&gt; gene encodes &lt;i&gt;S. cerevisiae&lt;/i&gt; separase and is required for normal chromosome segregation during mitosis. Shifting cells containing the &lt;i&gt;esp1-G543E&lt;/i&gt;...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/8zv2g8hx</guid>
      <pubDate>Thu, 4 Dec 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Putnam, Christopher D</name>
        <uri>https://orcid.org/0000-0002-6145-1265</uri>
      </author>
      <author>
        <name>Li, Bin-zhong</name>
      </author>
      <author>
        <name>Broderick, Lori</name>
      </author>
    </item>
    <item>
      <title>Time-resolved functional genomics using deep learning reveals a global hierarchical control of autophagy</title>
      <link>https://escholarship.org/uc/item/8gv1x71f</link>
      <description>Abstract  Recycling of cellular components through autophagy maintains homeostasis in dynamic nutrient environments, and its dysregulation is linked to several human disorders. Although extensive research has characterized the core mechanisms of autophagy, limited insight into its systems-wide dynamic control has hampered predictive modeling and effective in vivo manipulation. In this study, we mapped the genetic network that controls both the dynamic activation and inactivation of autophagy during nitrogen changes, using a combination of time-resolved high-content imaging, deep learning, and latent feature analysis. This approach generated a comprehensive genome-wide profiling repository, termed AutoDRY, categorizing 5919 mutants based on their nutrient response kinetics and differential contributions to autophagosome formation and clearance. Integrating these profiles with functional and genetic network data unveiled a hierarchical and multi-layered control of autophagy, identifying...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/8gv1x71f</guid>
      <pubDate>Thu, 4 Dec 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Chica, Nathalia</name>
      </author>
      <author>
        <name>Andersen, Aram N</name>
      </author>
      <author>
        <name>Orellana-Muñoz, Sara</name>
      </author>
      <author>
        <name>Garcia, Ignacio</name>
      </author>
      <author>
        <name>P, Aurélie Nguéa</name>
      </author>
      <author>
        <name>Nakken, Sigve</name>
      </author>
      <author>
        <name>Ayuda-Durán, Pilar</name>
      </author>
      <author>
        <name>Håkensbakken, Linda</name>
      </author>
      <author>
        <name>Schultz, Sebastian W</name>
      </author>
      <author>
        <name>Rødningen, Eline</name>
      </author>
      <author>
        <name>Putnam, Christopher D</name>
        <uri>https://orcid.org/0000-0002-6145-1265</uri>
      </author>
      <author>
        <name>Zucknick, Manuela</name>
      </author>
      <author>
        <name>Rusten, Tor Erik</name>
      </author>
      <author>
        <name>Enserink, Jorrit M</name>
      </author>
    </item>
    <item>
      <title>Perspective on Improving Environmental Monitoring of Biothreats</title>
      <link>https://escholarship.org/uc/item/8fm0b31b</link>
      <description>For more than a decade, the United States has performed environmental monitoring by collecting and analyzing air samples for a handful of biological threat agents (BTAs) in order to detect a possible biological attack. This effort has faced numerous technical challenges including timeliness, sampling efficiency, sensitivity, specificity, and robustness. The cost of city-wide environmental monitoring using conventional technology has also been a challenge. A large group of scientists with expertise in bioterrorism defense met to assess the objectives and current efficacy of environmental monitoring and to identify operational and technological changes that could enhance its efficacy and cost-effectiveness, thus enhancing its value. The highest priority operational change that was identified was to abandon the current concept of city-wide environmental monitoring because the operational costs were too high and its value was compromised by low detection sensitivity and other environmental...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/8fm0b31b</guid>
      <pubDate>Thu, 4 Dec 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Dunbar, John</name>
      </author>
      <author>
        <name>Pillai, Segaran</name>
      </author>
      <author>
        <name>Wunschel, David</name>
      </author>
      <author>
        <name>Dickens, Michael</name>
      </author>
      <author>
        <name>Morse, Stephen A</name>
      </author>
      <author>
        <name>Franz, David</name>
      </author>
      <author>
        <name>Bartko, Andrew</name>
        <uri>https://orcid.org/0000-0002-1237-2747</uri>
      </author>
      <author>
        <name>Challacombe, Jean</name>
      </author>
      <author>
        <name>Persons, Timothy</name>
      </author>
      <author>
        <name>Hughes, Molly A</name>
      </author>
      <author>
        <name>Blanke, Steve R</name>
      </author>
      <author>
        <name>Holland, Robin</name>
      </author>
      <author>
        <name>Hutchison, Janine</name>
      </author>
      <author>
        <name>Merkley, Eric D</name>
      </author>
      <author>
        <name>Campbell, Katrina</name>
      </author>
      <author>
        <name>Branda, Catherine S</name>
      </author>
      <author>
        <name>Sharma, Shashi</name>
      </author>
      <author>
        <name>Lindler, Luther</name>
      </author>
      <author>
        <name>Anderson, Kevin</name>
      </author>
      <author>
        <name>Hodge, David</name>
      </author>
    </item>
    <item>
      <title>Modulating NLRP3 splicing with antisense oligonucleotides to control pathological inflammation</title>
      <link>https://escholarship.org/uc/item/886752bx</link>
      <description>Inflammation has an essential role in healing. However, over-active inflammation disrupts normal cellular functions and can be life-threatening when not resolved. The NLR family pyrin domain-containing 3 (NLRP3) inflammasome, a component of the innate immune system, is an intracellular multiprotein complex that senses stress-associated signals, and, for this reason is a promising therapeutic target for treating unresolved, pathogenic inflammation. Alternative splicing of NLRP3 RNA has been suggested as a regulatory mechanism for inflammasome activation, as some spliced isoforms encode NLRP3 proteins with compromised function. Here, we take advantage of this natural regulatory mechanism and devise a way to control pathogenic inflammation using splice-switching antisense oligonucleotides (ASOs). To identify and induce NLRP3 isoforms lacking inflammatory activity, we tested a series of ASOs, each targeting a different exon, to determine the most effective strategy for downregulating...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/886752bx</guid>
      <pubDate>Thu, 4 Dec 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Klein, Roni</name>
      </author>
      <author>
        <name>Onyuru, Janset</name>
      </author>
      <author>
        <name>Centa, Jessica L</name>
      </author>
      <author>
        <name>Viera, Estela M</name>
      </author>
      <author>
        <name>Putnam, Christopher D</name>
        <uri>https://orcid.org/0000-0002-6145-1265</uri>
      </author>
      <author>
        <name>Hoffman, Hal M</name>
      </author>
      <author>
        <name>Hastings, Michelle L</name>
      </author>
    </item>
    <item>
      <title>Modulating NLRP3 splicing with antisense oligonucleotides to control pathological inflammation</title>
      <link>https://escholarship.org/uc/item/73r7t9w9</link>
      <description>Inflammation has an essential role in healing. However, over-active inflammation disrupts normal cellular functions and can be life-threatening when not resolved. The NLR family pyrin domain-containing 3 (NLRP3) inflammasome, a component of the innate immune system, is an intracellular multiprotein complex that senses stress-associated signals, and, for this reason is a promising therapeutic target for treating unresolved, pathogenic inflammation. Alternative splicing of &lt;i&gt;NLRP3&lt;/i&gt; RNA has been suggested as a regulatory mechanism for inflammasome activation, as some spliced isoforms encode NLRP3 proteins with compromised function. Here, we take advantage of this natural regulatory mechanism and devise a way to control pathogenic inflammation using splice-switching antisense oligonucleotides (ASOs). To identify and induce NLRP3 isoforms lacking inflammatory activity, we tested a series of ASOs, each targeting a different exon, to determine the most effective strategy for down-regulating...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/73r7t9w9</guid>
      <pubDate>Thu, 4 Dec 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Klein, Roni</name>
      </author>
      <author>
        <name>Onyuru, Janset</name>
      </author>
      <author>
        <name>Centa, Jessica L</name>
      </author>
      <author>
        <name>Viera, Estela M</name>
      </author>
      <author>
        <name>Duelli, Fox J</name>
      </author>
      <author>
        <name>Putnam, Christopher D</name>
        <uri>https://orcid.org/0000-0002-6145-1265</uri>
      </author>
      <author>
        <name>Hoffman, Hal M</name>
      </author>
      <author>
        <name>Hastings, Michelle L</name>
      </author>
    </item>
    <item>
      <title>Identification of different classes of genome instability suppressor genes through analysis of DNA damage response markers</title>
      <link>https://escholarship.org/uc/item/70k2c273</link>
      <description>ABSTRACT  Genetic studies in Saccharomyces cerevisiae have identified 266 genes and predicted an additional 38 genes that suppress the accumulation of spontaneous gross chromosomal rearrangements (GCRs). Here we identified mutations that induce two DNA damage response (DDR) markers, Hug1 expression and Ddc2 foci, and combined these data with other published screens identifying mutations inducing other DDR markers, including Rad52 foci and Rnr3 expression. Together, these data identify four categories of mutations: most mutations were DDR- GCR-, 356 were DDR+ GCR-, 72 were DDR- GCR+, and 157 were DDR+ GCR+. These results indicate that induction of DDR markers alone, while allowing DDR analysis, is not a reliable indicator of increased genome instability. They also guide further analysis of mechanistically distinct groups of GCR-inducing mutations, such as mutations that increase levels of GCR-inducing DNA damage and mutations that result in mis-repair of normal levels of DNA damage...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/70k2c273</guid>
      <pubDate>Thu, 4 Dec 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Li, Bin-Zhong</name>
      </author>
      <author>
        <name>Kolodner, Richard D</name>
      </author>
      <author>
        <name>Putnam, Christopher D</name>
        <uri>https://orcid.org/0000-0002-6145-1265</uri>
      </author>
    </item>
    <item>
      <title>Mutations of Complement Factor I and Potential Mechanisms of Neuroinflammation in Acute Hemorrhagic Leukoencephalitis</title>
      <link>https://escholarship.org/uc/item/6899n4qb</link>
      <description>PurposeAcute Hemorrhagic Leukoencephalitis (AHLE) is a rare demyelinating disorder of acute onset, rapid deterioration and significant morbidity and mortality. Most often described as a post-infectious complication of an upper respiratory illness, its precise pathophysiology remains unclear. We describe two pediatric patients with AHLE with partial complement factor I (FI) deficiency whose successful treatment included the interleukin-1 (IL-1) receptor antagonist, anakinra, implicating a role for FI and IL-1 in this disorder.MethodsExtensive clinical workup of two patients presenting with AHLE revealed complement abnormalities, specifically related to the alternative pathway and its regulator, FI. Aggressive management with steroids, immunoglobulin, and anakinra ultimately led to improvement of clinical status and near return to neurologic baseline in both patients. Genetic sequencing of the FI coding regions of the patients and their families was performed. In vitro protein expression...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/6899n4qb</guid>
      <pubDate>Thu, 4 Dec 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Broderick, Lori</name>
      </author>
      <author>
        <name>Gandhi, Chhavi</name>
      </author>
      <author>
        <name>Mueller, James L</name>
      </author>
      <author>
        <name>Putnam, Christopher D</name>
        <uri>https://orcid.org/0000-0002-6145-1265</uri>
      </author>
      <author>
        <name>Shayan, Katayoon</name>
      </author>
      <author>
        <name>Giclas, Patricia C</name>
      </author>
      <author>
        <name>Peterson, Karin S</name>
      </author>
      <author>
        <name>Aceves, Seema S</name>
      </author>
      <author>
        <name>Sheets, Robert M</name>
      </author>
      <author>
        <name>Peterson, Bradley M</name>
      </author>
      <author>
        <name>Newbury, Robert O</name>
      </author>
      <author>
        <name>Hoffman, Hal M</name>
      </author>
      <author>
        <name>Bastian, John F</name>
      </author>
    </item>
    <item>
      <title>Engineered Disulfide-forming Amino Acid Substitutions Interfere with a Conformational Change in the Mismatch Recognition Complex Msh2-Msh6 Required for Mismatch Repair*</title>
      <link>https://escholarship.org/uc/item/5zj73456</link>
      <description>ATP binding causes the mispair-bound Msh2-Msh6 mismatch recognition complex to slide along the DNA away from the mismatch, and ATP is required for the mispair-dependent interaction between Msh2-Msh6 and Mlh1-Pms1. It has been inferred from these observations that ATP induces conformational changes in Msh2-Msh6; however, the nature of these conformational changes and their requirement in mismatch repair are poorly understood. Here we show that ATP induces a conformational change within the C-terminal region of Msh6 that protects the trypsin cleavage site after Msh6 residue Arg(1124). An engineered disulfide bond within this region prevented the ATP-driven conformational change and resulted in an Msh2-Msh6 complex that bound mispaired bases but could not form sliding clamps or bind Mlh1-Pms1. The engineered disulfide bond also reduced mismatch repair efficiency in vivo, indicating that this ATP-driven conformational change plays a role in mismatch repair.</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/5zj73456</guid>
      <pubDate>Thu, 4 Dec 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Hargreaves, Victoria V</name>
      </author>
      <author>
        <name>Putnam, Christopher D</name>
        <uri>https://orcid.org/0000-0002-6145-1265</uri>
      </author>
      <author>
        <name>Kolodner, Richard D</name>
      </author>
    </item>
    <item>
      <title>Novel mutation in NLRP3 Exon 7 results in sensorineural hearing loss without chronic inflammation</title>
      <link>https://escholarship.org/uc/item/5vn964c3</link>
      <description>Novel mutation in NLRP3 Exon 7 results in sensorineural hearing loss without chronic inflammation</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/5vn964c3</guid>
      <pubDate>Thu, 4 Dec 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Broderick, L</name>
      </author>
      <author>
        <name>Grevich, S Cherukumilli</name>
      </author>
      <author>
        <name>Putnam, C</name>
        <uri>https://orcid.org/0000-0002-6145-1265</uri>
      </author>
      <author>
        <name>Hoffman, H</name>
      </author>
    </item>
    <item>
      <title>Distinct SUMO Ligases Cooperate with Esc2 and Slx5 to Suppress Duplication-Mediated Genome Rearrangements</title>
      <link>https://escholarship.org/uc/item/5d6408p6</link>
      <description>Suppression of duplication-mediated gross chromosomal rearrangements (GCRs) is essential to maintain genome integrity in eukaryotes. Here we report that SUMO ligase Mms21 has a strong role in suppressing GCRs in Saccharomyces cerevisiae, while Siz1 and Siz2 have weaker and partially redundant roles. Understanding the functions of these enzymes has been hampered by a paucity of knowledge of their substrate specificity in vivo. Using a new quantitative SUMO-proteomics technology, we found that Siz1 and Siz2 redundantly control the abundances of most sumoylated substrates, while Mms21 more specifically regulates sumoylation of RNA polymerase-I and the SMC-family proteins. Interestingly, Esc2, a SUMO-like domain-containing protein, specifically promotes the accumulation of sumoylated Mms21-specific substrates and functions with Mms21 to suppress GCRs. On the other hand, the Slx5-Slx8 complex, a SUMO-targeted ubiquitin ligase, suppresses the accumulation of sumoylated Mms21-specific...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/5d6408p6</guid>
      <pubDate>Thu, 4 Dec 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Albuquerque, Claudio P</name>
      </author>
      <author>
        <name>Wang, Guoliang</name>
      </author>
      <author>
        <name>Lee, Nancy S</name>
      </author>
      <author>
        <name>Kolodner, Richard D</name>
      </author>
      <author>
        <name>Putnam, Christopher D</name>
        <uri>https://orcid.org/0000-0002-6145-1265</uri>
      </author>
      <author>
        <name>Zhou, Huilin</name>
      </author>
    </item>
    <item>
      <title>Author Correction: Greengenes2 unifies microbial data in a single reference tree</title>
      <link>https://escholarship.org/uc/item/53h570rh</link>
      <description>Author Correction: Greengenes2 unifies microbial data in a single reference tree</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/53h570rh</guid>
      <pubDate>Thu, 4 Dec 2025 00:00:00 +0000</pubDate>
      <author>
        <name>McDonald, Daniel</name>
      </author>
      <author>
        <name>Jiang, Yueyu</name>
      </author>
      <author>
        <name>Balaban, Metin</name>
      </author>
      <author>
        <name>Cantrell, Kalen</name>
      </author>
      <author>
        <name>Zhu, Qiyun</name>
      </author>
      <author>
        <name>Gonzalez, Antonio</name>
      </author>
      <author>
        <name>Morton, James T</name>
      </author>
      <author>
        <name>Nicolaou, Giorgia</name>
      </author>
      <author>
        <name>Parks, Donovan H</name>
      </author>
      <author>
        <name>Karst, Søren M</name>
      </author>
      <author>
        <name>Albertsen, Mads</name>
      </author>
      <author>
        <name>Hugenholtz, Philip</name>
      </author>
      <author>
        <name>DeSantis, Todd</name>
      </author>
      <author>
        <name>Song, Se Jin</name>
      </author>
      <author>
        <name>Bartko, Andrew</name>
        <uri>https://orcid.org/0000-0002-1237-2747</uri>
      </author>
      <author>
        <name>Havulinna, Aki S</name>
      </author>
      <author>
        <name>Jousilahti, Pekka</name>
      </author>
      <author>
        <name>Cheng, Susan</name>
      </author>
      <author>
        <name>Inouye, Michael</name>
      </author>
      <author>
        <name>Niiranen, Teemu</name>
      </author>
      <author>
        <name>Jain, Mohit</name>
      </author>
      <author>
        <name>Salomaa, Veikko</name>
      </author>
      <author>
        <name>Lahti, Leo</name>
      </author>
      <author>
        <name>Mirarab, Siavash</name>
      </author>
      <author>
        <name>Knight, Rob</name>
        <uri>https://orcid.org/0000-0002-0975-9019</uri>
      </author>
    </item>
    <item>
      <title>Calculating fast differential genome coverages among metagenomic sources using micov</title>
      <link>https://escholarship.org/uc/item/2bn2r3m0</link>
      <description>Breadth of coverage, the proportion of a reference genome covered by at least one sequencing read, is critical for interpreting metagenomic data, informing analyses from genome assembly to taxonomic profiling. However, existing tools typically summarize coverage breadth at the whole-genome or aggregate-sample level, missing informative variation along genomes and between sample groups. Here we introduce MIcrobiome COVerage (micov), a tool that computes and compares per-sample breadth of coverage across many genomes and samples. micov offers two key advances: (1) rapid cumulative coverage breadth calculations specific to each sample type, and (2) detection of differential coverage breadth along genomes. Applying micov to three metagenomic datasets, we show that it identifies a genomic region in Prevotella copri that explains variation in community composition independent of host country of origin, uncovers dietary association with a partially annotated region in an uncharacterized...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/2bn2r3m0</guid>
      <pubDate>Thu, 4 Dec 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Weng, Yuhan</name>
      </author>
      <author>
        <name>Guccione, Caitlin</name>
      </author>
      <author>
        <name>McDonald, Daniel</name>
      </author>
      <author>
        <name>Oles, Renee</name>
      </author>
      <author>
        <name>Devkota, Suzanne</name>
        <uri>https://orcid.org/0000-0001-5575-9362</uri>
      </author>
      <author>
        <name>Kopylova, Evguenia</name>
      </author>
      <author>
        <name>Sepich-Poore, Gregory D</name>
      </author>
      <author>
        <name>Salido, Rodolfo A</name>
      </author>
      <author>
        <name>Din, M Omar</name>
      </author>
      <author>
        <name>Song, Se Jin</name>
      </author>
      <author>
        <name>Curtius, Kit</name>
      </author>
      <author>
        <name>Chu, Hiutung</name>
      </author>
      <author>
        <name>Bartko, Andrew</name>
        <uri>https://orcid.org/0000-0002-1237-2747</uri>
      </author>
      <author>
        <name>Hasty, Jeff</name>
      </author>
      <author>
        <name>Knight, Rob</name>
      </author>
    </item>
    <item>
      <title>Bioinformatic identification of genes suppressing genome instability</title>
      <link>https://escholarship.org/uc/item/196777bj</link>
      <description>Unbiased forward genetic screens for mutations causing increased gross chromosomal rearrangement (GCR) rates in Saccharomyces cerevisiae are hampered by the difficulty in reliably using qualitative GCR assays to detect mutants with small but significantly increased GCR rates. We therefore developed a bioinformatic procedure using genome-wide functional genomics screens to identify and prioritize candidate GCR-suppressing genes on the basis of the shared drug sensitivity suppression and similar genetic interactions as known GCR suppressors. The number of known suppressors was increased from 75 to 110 by testing 87 predicted genes, which identified unanticipated pathways in this process. This analysis explicitly dealt with the lack of concordance among high-throughput datasets to increase the reliability of phenotypic predictions. Additionally, shared phenotypes in one assay were imperfect predictors for shared phenotypes in other assays, indicating that although genome-wide datasets...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/196777bj</guid>
      <pubDate>Thu, 4 Dec 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Putnam, Christopher D</name>
        <uri>https://orcid.org/0000-0002-6145-1265</uri>
      </author>
      <author>
        <name>Allen-Soltero, Stephanie R</name>
      </author>
      <author>
        <name>Martinez, Sandra L</name>
      </author>
      <author>
        <name>Chan, Jason E</name>
      </author>
      <author>
        <name>Hayes, Tikvah K</name>
      </author>
      <author>
        <name>Kolodner, Richard D</name>
      </author>
    </item>
    <item>
      <title>SUMO E3 ligase Mms21 prevents spontaneous DNA damage induced genome rearrangements</title>
      <link>https://escholarship.org/uc/item/1749x3kg</link>
      <description>Abstract  Mms21, a subunit of the Smc5/6 complex, possesses an E3 ligase activity for the Small Ubiquitin-like MOdifier (SUMO), which has a major, but poorly understood role in genome maintenance. Here we show mutations that inactivate the E3 ligase activity of Mms21 cause Rad52- and Pol32-dependent break-induced replication (BIR), which specifically requires the Rrm3 DNA helicase. Interestingly, mutations affecting both Mms21 and the Sgs1 helicase, but not sumoylation of Sgs1, cause further accumulation of genome rearrangements, indicating the distinct roles of Mms21 and Sgs1 in suppressing genome rearrangements. Whole genome sequencing further revealed that the Mre11 endonuclease prevents microhomology-mediated translocations and hairpin-mediated inverted duplications in the mms21 mutant. Consistent with the accumulation of endogenous DNA lesions, mms21 cells accumulate spontaneous Ddc2 foci and display a hyper-activated DNA damage checkpoint. Together, these findings support...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/1749x3kg</guid>
      <pubDate>Thu, 4 Dec 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Liang, Jason</name>
      </author>
      <author>
        <name>Li, Bin-zhong</name>
      </author>
      <author>
        <name>Tan, Alexander P</name>
      </author>
      <author>
        <name>Kolodner, Richard D</name>
      </author>
      <author>
        <name>Putnam, Christopher D</name>
        <uri>https://orcid.org/0000-0002-6145-1265</uri>
      </author>
      <author>
        <name>Zhou, Huilin</name>
      </author>
    </item>
    <item>
      <title>Temporal nutrition analysis associates dietary regularity and quality with gut microbiome diversity: insights from the Food &amp;amp; You digital cohort</title>
      <link>https://escholarship.org/uc/item/1438s2bd</link>
      <description>The gut microbiota is profoundly influenced by dietary choices, with emerging evidence linking it to various health outcomes. Here, we investigate diet-microbiota associations using detailed temporal nutrition intake data captured through real-time food logging via a smartphone app and gut microbiota profiles from 16S rDNA sequencing in ~ 1,000 participants from a digital cohort on personalized nutrition (“Food &amp;amp; You” - clinicaltrials.gov NCT03848299). The primary outcome of the parental trial was to investigate post-meal glucose response variations between individuals in function of their individual factors such as diet, microbiome composition and lifestyle. Our analysis reaffirms that high-quality diets rich in vegetables, fruits, nuts, micronutrients, and favorable dietary indices like HEI (calculated both as standard HEI and daily HEI to capture day-to-day diet quality regularity) correlate with increased microbial diversity and improved stool quality, while fast food-rich...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/1438s2bd</guid>
      <pubDate>Thu, 4 Dec 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Singh, Rohan</name>
      </author>
      <author>
        <name>McDonald, Daniel</name>
      </author>
      <author>
        <name>Hernandez, Alejandra Rios</name>
      </author>
      <author>
        <name>Song, Se Jin</name>
      </author>
      <author>
        <name>Bartko, Andrew</name>
        <uri>https://orcid.org/0000-0002-1237-2747</uri>
      </author>
      <author>
        <name>Knight, Rob</name>
      </author>
      <author>
        <name>Salathé, Marcel</name>
      </author>
    </item>
    <item>
      <title>A three-country analysis of the gut microbiome indicates taxon associations with diet vary by taxon resolution and population</title>
      <link>https://escholarship.org/uc/item/0k84d543</link>
      <description>Emerging research suggests that diet plays a vital role in shaping the composition and function of the gut microbiota. Although substantial efforts have been made to identify general patterns linking diet to the gut microbiome, much of this research has been concentrated on a small number of countries. Additionally, both diet and the gut microbiome have highly complex and individualized configurations, and there is growing evidence that tailoring diets to individual gut microbiota profiles may optimize the path toward improving or maintaining health and preventing disease. Using fecal metagenomic data from 1,177 individuals across three countries, we examine the relationship between diet and bacterial genera, focusing on &lt;i&gt;Prevotella&lt;/i&gt; and &lt;i&gt;Faecalibacterium&lt;/i&gt;, which have gained significant attention for their potential roles in human health and strong associations with dietary patterns. We find that these two genera in particular show significant associations with many...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/0k84d543</guid>
      <pubDate>Thu, 4 Dec 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Khatib, Lora</name>
      </author>
      <author>
        <name>Song, Jin</name>
      </author>
      <author>
        <name>Dilmore, Amanda H</name>
      </author>
      <author>
        <name>Sanders, Jon G</name>
      </author>
      <author>
        <name>Brennan, Caitriona</name>
        <uri>https://orcid.org/0000-0003-3943-6701</uri>
      </author>
      <author>
        <name>Hernandez, Alejandra Rios</name>
      </author>
      <author>
        <name>Myers, Tyler</name>
      </author>
      <author>
        <name>Oles, Renee</name>
      </author>
      <author>
        <name>Farmer, Sawyer</name>
      </author>
      <author>
        <name>Cowart, Charles</name>
      </author>
      <author>
        <name>Birmingham, Amanda</name>
      </author>
      <author>
        <name>Diaz, Edgar A</name>
      </author>
      <author>
        <name>Nizet, Oliver</name>
      </author>
      <author>
        <name>Gilbert, Kat</name>
      </author>
      <author>
        <name>Litwin, Nicole</name>
      </author>
      <author>
        <name>Das, Promi</name>
      </author>
      <author>
        <name>Nowinski, Brent</name>
      </author>
      <author>
        <name>Bryant, Mackenzie</name>
      </author>
      <author>
        <name>Tribelhorn, Caitlin</name>
      </author>
      <author>
        <name>Sanders-Bodai, Karenina</name>
      </author>
      <author>
        <name>Chaumont, Soline</name>
      </author>
      <author>
        <name>Knol, Jan</name>
      </author>
      <author>
        <name>Roeselers, Guus</name>
      </author>
      <author>
        <name>Laiola, Manolo</name>
      </author>
      <author>
        <name>Shetty, Sudarshan A</name>
      </author>
      <author>
        <name>Veiga, Patrick</name>
      </author>
      <author>
        <name>Tap, Julien</name>
      </author>
      <author>
        <name>Derrien, Muriel</name>
      </author>
      <author>
        <name>Koutnikova, Hana</name>
      </author>
      <author>
        <name>Cotillard, Aurélie</name>
      </author>
      <author>
        <name>Lay, Christophe</name>
      </author>
      <author>
        <name>Tovar, Armando R</name>
      </author>
      <author>
        <name>Torres, Nimbe</name>
      </author>
      <author>
        <name>Arteaga, Liliana</name>
      </author>
      <author>
        <name>González, Antonio</name>
      </author>
      <author>
        <name>McDonald, Daniel</name>
      </author>
      <author>
        <name>Bartko, Andrew</name>
        <uri>https://orcid.org/0000-0002-1237-2747</uri>
      </author>
      <author>
        <name>Knight, Rob</name>
      </author>
    </item>
    <item>
      <title>Chronological age estimation from human microbiomes with transformer-based Robust Principal Component Analysis</title>
      <link>https://escholarship.org/uc/item/0g3589d0</link>
      <description>Deep learning for microbiome analysis has shown potential for understanding microbial communities and human phenotypes. Here, we propose an approach, Transformer-based Robust Principal Component Analysis(TRPCA), which leverages the strengths of transformer architectures and interpretability of Robust Principal Component Analysis. To investigate benefits of TRPCA over conventional machine learning models, we benchmarked performance on age prediction from three body sites(skin, oral, gut), with 16S rRNA gene amplicon(16S) and whole-genome sequencing(WGS) data. We demonstrated prediction of age from longitudinal samples and combined classification and regression tasks via multi-task learning(MTL). TRPCA improves age prediction accuracy from human microbiome samples, achieving the largest reduction in Mean Absolute Error for WGS skin (MAE: 8.03, 28% reduction) and 16S skin (MAE: 5.09, 14% reduction) samples, compared to conventional approaches. Additionally, TRPCA’s MTL approach achieves...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/0g3589d0</guid>
      <pubDate>Thu, 4 Dec 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Myers, Tyler</name>
      </author>
      <author>
        <name>Song, Se Jin</name>
      </author>
      <author>
        <name>Chen, Yang</name>
      </author>
      <author>
        <name>De Pessemier, Britta</name>
      </author>
      <author>
        <name>Khatib, Lora</name>
      </author>
      <author>
        <name>McDonald, Daniel</name>
      </author>
      <author>
        <name>Huang, Shi</name>
      </author>
      <author>
        <name>Gallo, Richard</name>
        <uri>https://orcid.org/0000-0002-1401-7861</uri>
      </author>
      <author>
        <name>Callewaert, Chris</name>
      </author>
      <author>
        <name>Havulinna, Aki S</name>
      </author>
      <author>
        <name>Lahti, Leo</name>
      </author>
      <author>
        <name>Roeselers, Guus</name>
      </author>
      <author>
        <name>Laiola, Manolo</name>
      </author>
      <author>
        <name>Shetty, Sudarshan A</name>
      </author>
      <author>
        <name>Kelley, Scott T</name>
      </author>
      <author>
        <name>Knight, Rob</name>
      </author>
      <author>
        <name>Bartko, Andrew</name>
        <uri>https://orcid.org/0000-0002-1237-2747</uri>
      </author>
    </item>
    <item>
      <title>Calculating fast differential genome coverages among metagenomic sources using micov</title>
      <link>https://escholarship.org/uc/item/9pv8623j</link>
      <description>Breadth of coverage, the proportion of a reference genome covered by at least one sequencing read, is critical for interpreting metagenomic data, informing analyses from genome assembly to taxonomic profiling. However, existing tools typically summarize coverage breadth at the whole-genome or aggregate-sample level, missing informative variation along genomes and between sample groups. Here we introduce MIcrobiome COVerage (micov), a tool that computes and compares per-sample breadth of coverage across many genomes and samples. micov offers two key advances: (1) rapid cumulative coverage breadth calculations specific to each sample type, and (2) detection of differential coverage breadth along genomes. Applying micov to three metagenomic datasets, we show that it identifies a genomic region in Prevotella copri that explains variation in community composition independent of host country of origin, uncovers dietary association with a partially annotated region in an uncharacterized...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/9pv8623j</guid>
      <pubDate>Wed, 26 Nov 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Weng, Yuhan</name>
      </author>
      <author>
        <name>Guccione, Caitlin</name>
      </author>
      <author>
        <name>McDonald, Daniel</name>
      </author>
      <author>
        <name>Oles, Renee</name>
      </author>
      <author>
        <name>Devkota, Suzanne</name>
        <uri>https://orcid.org/0000-0001-5575-9362</uri>
      </author>
      <author>
        <name>Kopylova, Evguenia</name>
      </author>
      <author>
        <name>Sepich-Poore, Gregory D</name>
      </author>
      <author>
        <name>Salido, Rodolfo A</name>
      </author>
      <author>
        <name>Din, M Omar</name>
      </author>
      <author>
        <name>Song, Se Jin</name>
      </author>
      <author>
        <name>Curtius, Kit</name>
      </author>
      <author>
        <name>Chu, Hiutung</name>
      </author>
      <author>
        <name>Bartko, Andrew</name>
        <uri>https://orcid.org/0000-0002-1237-2747</uri>
      </author>
      <author>
        <name>Hasty, Jeff</name>
      </author>
      <author>
        <name>Knight, Rob</name>
      </author>
    </item>
    <item>
      <title>Proximity of Maternal Time of Immigration to Child's Birth Is Associated With Autism Spectrum Disorder With Early Learning Delay Among Immigrant Populations in the United States: Findings From the Study to Explore Early Development</title>
      <link>https://escholarship.org/uc/item/3fp7d3zv</link>
      <description>Our objective was to examine the relationship between the timing of parental US immigration and autism spectrum disorder (ASD) without early learning delay (ELD), ASD with ELD, and ELD alone among US-born children. We analyzed data from a multi-site case-control study that recruited children aged 2-5 years with ASD or non-ASD developmental disorders and same-age population controls. Parental demographics were collected from caregivers at study enrollment. Mullen Scales of Early Learning ≤ 70 was used to define ELD. Among children with a non-US-born parent (N = 1048), we used multinomial logistic regression to examine time from parental immigration to the child's birth in relation to ASD alone, ASD with ELD (ASD + ELD), and ELD alone compared to population controls. Having a non-US-born mother (regardless of the father's birthplace) versus a non-US-born father only was evaluated as a potential effect modifier. Among those with a non-US-born mother, closer proximity of maternal...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/3fp7d3zv</guid>
      <pubDate>Thu, 20 Nov 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Aiona, Kaylynn</name>
      </author>
      <author>
        <name>Crume, Tessa</name>
      </author>
      <author>
        <name>Reyes, Nuri</name>
      </author>
      <author>
        <name>Schmiege, Sarah J</name>
      </author>
      <author>
        <name>Young, Janine</name>
      </author>
      <author>
        <name>Holst, Brady</name>
      </author>
      <author>
        <name>Durkin, Maureen S</name>
      </author>
      <author>
        <name>Magallanes, Melissa</name>
      </author>
      <author>
        <name>DiGuiseppi, Carolyn</name>
      </author>
    </item>
    <item>
      <title>Transcriptional regulatory networks of the human gut symbiont Bacteroides thetaiotaomicron are uncovered using machine learning</title>
      <link>https://escholarship.org/uc/item/5js9c563</link>
      <description>Bacteroides thetaiotaomicron VPI-5482 is a prominent human gut symbiont of increasing importance to human health and therapeutic applications. Despite its significance, the transcriptional regulatory network (TRN) governing its survival and resilience in vivo remains poorly understood. Here, we present BtModulome, a comprehensive transcriptional regulatory framework derived from independent component analysis of 461 RNA-seq datasets spanning diverse niche-specific conditions and genetic backgrounds. This analysis revealed the BtModulome consisting of 110 independently modulated gene sets (iModulons), explaining 72.9% of the variance in the RNA-seq dataset. We validated strong associations with 39 known regulators and identified 311 novel regulator-regulon relationships, accounting for 22.4% expansion of the known TRN of B. thetaiotaomicron. In addition, we functionally characterized 11 ECF-σs, including SigW-1, which orchestrates arylsulfatase expression critical for host colonization,...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/5js9c563</guid>
      <pubDate>Wed, 19 Nov 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Kim, Kangsan</name>
      </author>
      <author>
        <name>Choe, Donghui</name>
      </author>
      <author>
        <name>Kim, Sun Chang</name>
      </author>
      <author>
        <name>Yim, Sung Sun</name>
      </author>
      <author>
        <name>Jeong, Ki Jun</name>
      </author>
      <author>
        <name>Palsson, Bernhard</name>
        <uri>https://orcid.org/0000-0003-2357-6785</uri>
      </author>
      <author>
        <name>Cho, Suhyung</name>
      </author>
      <author>
        <name>Cho, Byung-Kwan</name>
      </author>
    </item>
    <item>
      <title>The Neuroimmune Landscape of the Lysosomal Storage Disorder Sanfilippo Syndrome</title>
      <link>https://escholarship.org/uc/item/47j046js</link>
      <description>Lysosomal storage disorders (LSDs) such as Sanfilippo syndrome (Mucopolysaccharidosis type III) are characterized by impaired lysosomal degradation due to inherited in lysosomal proteins. This dysfunction leads to the accumulation of undegraded substrates, such as heparan sulfate, ultimately leading to progressive neuroinflammation and neurodegeneration. Despite well-defined genetic causes, no disease-modifying therapies exist for Sanfilippo syndrome. While microglia, the brain's resident immune cells, can play both protective and pathogenic roles, the contribution of neuroinflammation to LSD pathology remains underexplored. This review examines the contribution of neuroinflammation to Sanfilippo syndrome, emphasizing emerging mechanisms involving TLR4 signaling, inflammasome activation, the cGAS-STING pathway, and lysosomal biogenesis regulators such as TFE family transcription factors. We also discuss the potential of cellular therapies to modulate neuroimmune responses and...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/47j046js</guid>
      <pubDate>Thu, 6 Nov 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Badell‐Grau, Rafael A</name>
      </author>
      <author>
        <name>Schlachetzki, Johannes CM</name>
      </author>
    </item>
    <item>
      <title>Clinically Significant Neuroimaging Findings Among Pediatric Patients Presenting to the Emergency Department With Symptoms of Psychosis: A Multicenter Retrospective Study</title>
      <link>https://escholarship.org/uc/item/4hd4389v</link>
      <description>BACKGROUND: The clinical utility of diagnostic neuroimaging for pediatric patients presenting to the emergency department (ED) for psychosis remains unclear. We sought to estimate the prevalence of and characteristics associated with clinically significant neuroimaging findings among pediatric patients presenting to the ED with symptoms of psychosis who had neuroimaging performed.
METHODS: This retrospective cross-sectional study included visits by patients 5 to &amp;lt; 18 years old presenting with symptoms of psychosis to 28 EDs affiliated with the Pediatric Emergency Medicine Collaborative Research Committee from 2016 to 2019 and had neuroimaging performed. We estimated the rate of clinically significant neuroimaging findings, defined as those resulting in further testing, treatment, or medical admission, overall and by imaging modality. Multivariable logistic regression models examined presenting features associated with clinically significant findings.
RESULTS: Clinically significant...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/4hd4389v</guid>
      <pubDate>Fri, 31 Oct 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Hoffmann, Jennifer A</name>
      </author>
      <author>
        <name>Parikh, Tapan K</name>
      </author>
      <author>
        <name>Lorenz, Doug</name>
      </author>
      <author>
        <name>Goldman, Michael P</name>
      </author>
      <author>
        <name>Powers, Emily M</name>
      </author>
      <author>
        <name>Patel, Shilpa J</name>
      </author>
      <author>
        <name>Lavina, Ilana S</name>
      </author>
      <author>
        <name>Heyming, Theodore W</name>
      </author>
      <author>
        <name>England, Jasmin T</name>
      </author>
      <author>
        <name>Saidinejad, Mohsen</name>
      </author>
      <author>
        <name>Claudius, Ilene</name>
      </author>
      <author>
        <name>Ghosh, Pallavi</name>
      </author>
      <author>
        <name>Shapiro, Daniel J</name>
      </author>
      <author>
        <name>Swan, Tricia B</name>
      </author>
      <author>
        <name>Bouvay, Kamali L</name>
      </author>
      <author>
        <name>Kurowski, Eileen Murtagh</name>
      </author>
      <author>
        <name>Smith, Nadine M</name>
      </author>
      <author>
        <name>Davis, Justin R</name>
      </author>
      <author>
        <name>Moxam, Alexander B</name>
      </author>
      <author>
        <name>Muhrer, Eli J</name>
      </author>
      <author>
        <name>Shenoi, Rohit P</name>
      </author>
      <author>
        <name>Portillo, Elyse N</name>
      </author>
      <author>
        <name>Kaplan, Ron L</name>
      </author>
      <author>
        <name>Uspal, Neil G</name>
      </author>
      <author>
        <name>Lapus, Robert M</name>
      </author>
      <author>
        <name>Vo, Andrea T</name>
      </author>
      <author>
        <name>Fenster, Daniel B</name>
      </author>
      <author>
        <name>Barrocas, Danielle B</name>
      </author>
      <author>
        <name>Liu, Deborah R</name>
      </author>
      <author>
        <name>Chaudhari, Pradip P</name>
      </author>
      <author>
        <name>Cafferty, Rachel</name>
      </author>
      <author>
        <name>Freedman, Stephen B</name>
      </author>
      <author>
        <name>Rose, Jerri A</name>
      </author>
      <author>
        <name>Evers, Megan F</name>
      </author>
      <author>
        <name>Metcalf, Ashley M</name>
      </author>
      <author>
        <name>Saleh, Fareed</name>
      </author>
      <author>
        <name>Dunnick, Jennifer</name>
      </author>
      <author>
        <name>Pitetti, Raymond D</name>
      </author>
      <author>
        <name>Nathani, Yashas R</name>
      </author>
      <author>
        <name>Waseem, Muhammad</name>
      </author>
      <author>
        <name>Florin, Todd A</name>
      </author>
      <author>
        <name>Group, the Pediatric Emergency Medicine Collaborative Research Committee Psychosis Study</name>
      </author>
    </item>
    <item>
      <title>Mitochondrial Lon Peptidase 1 Controls Diaphragm and Lung Development in a Context-Dependent Manner</title>
      <link>https://escholarship.org/uc/item/9rj5q555</link>
      <description>Congenital Diaphragmatic Hernia (CDH) is a rare neonatal disorder causing diaphragmatic defects and cardiopulmonary hypoplasia, traditionally attributed to mechanical compression from organ herniation. However, emerging evidence suggests genetic mutations may independently impair lung development, prompting debate over CDH etiology. Here, we investigated the requirement of mitochondrial function guarded by LON peptidase 1 (&lt;i&gt;Lonp1&lt;/i&gt;), a CDH risk gene, in either diaphragm or lung development. &lt;i&gt;Lonp1&lt;/i&gt; loss in skeletal muscles of the diaphragm led to its thinning and membranization, recapitulating the pathology of sac-type CDH. On the other hand, lung-specific inactivation caused severe hypoplasia with defective branching morphogenesis, independent of diaphragm anomalies. Molecularly, &lt;i&gt;Lonp1&lt;/i&gt; disruption dysregulated key transcription factors and signaling pathways known to be critical for early lung development. Our findings here revealed that mitochondrial defects contribute...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/9rj5q555</guid>
      <pubDate>Thu, 23 Oct 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Xu, Le</name>
        <uri>https://orcid.org/0000-0001-6321-5023</uri>
      </author>
      <author>
        <name>Tan, Chunting</name>
      </author>
      <author>
        <name>Talaba, Nicole</name>
      </author>
      <author>
        <name>Sou, Andrew</name>
      </author>
      <author>
        <name>Shen, Yufeng</name>
      </author>
      <author>
        <name>Chung, Wendy K</name>
      </author>
      <author>
        <name>McCulley, David J</name>
      </author>
      <author>
        <name>Sun, Xin</name>
      </author>
    </item>
    <item>
      <title>Abatacept Prevents Severe Acute Graft‐Versus‐Host Disease Without Increasing Graft Failure Risk in Pediatric Bone Marrow Failure Syndromes</title>
      <link>https://escholarship.org/uc/item/7xj4x0h3</link>
      <description>BACKGROUND: Pediatric patients with inherited or acquired bone marrow failure syndromes (BMFS) often require an allogeneic hematopoietic stem cell transplant (HSCT) to cure the hematological manifestations. Amongst these, those without a matched sibling donor (MSD), are at increased risk for graft failure and are known to tolerate graft-versus-host disease (GVHD) poorly. Abatacept (ABA) is Food and Drug Administration (FDA)-approved for the prevention of acute GVHD.
OBJECTIVES: Our primary objective was to investigate the cumulative incidence (CI) of severe acute (Grade III-IV) GVHD in patients with BMFS undergoing a matched unrelated donor (MUD) or mismatched related or unrelated donor (MMRD/MMUD) HSCT with ABA added to standard GVHD prophylaxis of calcineurin inhibitor and methotrexate or mycophenolate mofetil, and evaluate the incidence of graft failure. Secondary outcomes included overall survival (OS) and acute and chronic GVHD-free graft failure-free overall survival (GFS)...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/7xj4x0h3</guid>
      <pubDate>Thu, 23 Oct 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Hudda, Zahra</name>
      </author>
      <author>
        <name>Davies, Stella M</name>
      </author>
      <author>
        <name>Lane, Adam</name>
      </author>
      <author>
        <name>Schiff, Deborah E</name>
        <uri>https://orcid.org/0000-0003-3154-8987</uri>
      </author>
      <author>
        <name>Anderson, Eric J</name>
      </author>
      <author>
        <name>Mehta, Parinda A</name>
      </author>
      <author>
        <name>Myers, Kasiani C</name>
      </author>
      <author>
        <name>Gloude, Nicholas J</name>
      </author>
    </item>
    <item>
      <title>BRAF V600E-positive mononuclear cells in blood at diagnosis portend treatment failure and neurodegeneration in pediatric LCH</title>
      <link>https://escholarship.org/uc/item/06w1s0qx</link>
      <description>ABSTRACT: Langerhans cell histiocytosis (LCH) is a myeloid neoplastic disorder driven by mitogen-activated protein kinase (MAPK) activation in hematopoietic cells. Historically, LCH has been staged according to involvement of "risk organs" (bone marrow, liver, and spleen), based on risk of death. With improvements in supportive care and efficacy of MAPK pathway inhibitors, patients with LCH now rarely die. However, most patients with LCH with multisystem disease are not cured with current front-line chemotherapy, and treatment failure is associated with long-term morbidity, including LCH-associated neurodegeneration (LCH-ND). In this study, we evaluated the impact of extent of LCH at presentation, tumor genotype, and BRAFV600E in pretherapy peripheral blood mononuclear cells (PBMCs) and bone marrow on systemic and central nervous system outcomes in a cohort of 385 pediatric patients with LCH and 115 adults with LCH, followed up for a median of 4 years (range, 0.02-18 years). Five-year...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/06w1s0qx</guid>
      <pubDate>Thu, 23 Oct 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Lin, Howard</name>
      </author>
      <author>
        <name>Batajoo, Akanksha</name>
      </author>
      <author>
        <name>Peckham-Gregory, Erin</name>
      </author>
      <author>
        <name>Zinn, Daniel</name>
      </author>
      <author>
        <name>Eckstein, Olive S</name>
      </author>
      <author>
        <name>El-Mallawany, Nader Kim</name>
      </author>
      <author>
        <name>Gulati, Nitya</name>
      </author>
      <author>
        <name>Prudowsky, Zachary D</name>
      </author>
      <author>
        <name>Scull, Brooks</name>
      </author>
      <author>
        <name>Velazquez, Jessica</name>
      </author>
      <author>
        <name>Abhyankar, Harshal</name>
      </author>
      <author>
        <name>Simko, Stephen J</name>
      </author>
      <author>
        <name>Vakula, Daria</name>
      </author>
      <author>
        <name>Fleischmann, Ryan</name>
      </author>
      <author>
        <name>Karri, Vivekanudeep</name>
      </author>
      <author>
        <name>Hicks, M John</name>
      </author>
      <author>
        <name>Fisher, Kevin E</name>
      </author>
      <author>
        <name>Curry, Choladda V</name>
      </author>
      <author>
        <name>Roy, Angshumoy</name>
      </author>
      <author>
        <name>Schiff, Deborah</name>
        <uri>https://orcid.org/0000-0003-3154-8987</uri>
      </author>
      <author>
        <name>Heym, Kenneth M</name>
      </author>
      <author>
        <name>Scheurer, Michael E</name>
      </author>
      <author>
        <name>Parsons, D Williams</name>
      </author>
      <author>
        <name>Merad, Miriam</name>
      </author>
      <author>
        <name>Man, Tsz-Kwong</name>
      </author>
      <author>
        <name>McClain, Kenneth L</name>
      </author>
      <author>
        <name>Picarsic, Jennifer</name>
      </author>
      <author>
        <name>Allen, Carl E</name>
      </author>
    </item>
    <item>
      <title>Highly accurate assembly polishing with DeepPolisher</title>
      <link>https://escholarship.org/uc/item/13z6x363</link>
      <description>Accurate genome assemblies are essential for biological research, but even the highest-quality assemblies retain errors caused by the technologies used to construct them. Base-level errors are typically fixed with an additional polishing step that uses reads aligned to the draft assembly to identify necessary edits. However, current methods struggle to find a balance between over- and underpolishing. Here, we present an encoder-only transformer model for assembly polishing called DeepPolisher, which predicts corrections to the underlying sequence using Pacific Biosciences (PacBio) HiFi read alignments to a diploid assembly. Our pipeline introduces a method, PHAsing Reads in Areas Of Homozygosity (PHARAOH), which uses ultralong Oxford Nanopore Technologies (ONT) data to ensure alignments are accurately phased and to correctly introduce heterozygous edits in falsely homozygous regions. We demonstrate that the DeepPolisher pipeline can reduce assembly errors by approximately half,...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/13z6x363</guid>
      <pubDate>Wed, 22 Oct 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Mastoras, Mira</name>
      </author>
      <author>
        <name>Asri, Mobin</name>
      </author>
      <author>
        <name>Brambrink, Lucas</name>
      </author>
      <author>
        <name>Hebbar, Prajna</name>
      </author>
      <author>
        <name>Kolesnikov, Alexey</name>
      </author>
      <author>
        <name>Cook, Daniel E</name>
      </author>
      <author>
        <name>Nattestad, Maria</name>
      </author>
      <author>
        <name>Lucas, Julian</name>
      </author>
      <author>
        <name>Won, Taylor S</name>
      </author>
      <author>
        <name>Chang, Pi-Chuan</name>
      </author>
      <author>
        <name>Carroll, Andrew</name>
      </author>
      <author>
        <name>Paten, Benedict</name>
      </author>
      <author>
        <name>Shafin, Kishwar</name>
      </author>
      <author>
        <name>Consortium, and the Human Pangenome Reference</name>
      </author>
      <author>
        <name>Tayoun, Ahmad Abou</name>
      </author>
      <author>
        <name>Albracht, Derek</name>
      </author>
      <author>
        <name>Allen, Jamie</name>
      </author>
      <author>
        <name>Alsheikh-Ali, Alawi A</name>
      </author>
      <author>
        <name>Andrews, Casey</name>
      </author>
      <author>
        <name>Antipov, Dmitry</name>
      </author>
      <author>
        <name>Antonacci-Fulton, Lucinda</name>
      </author>
      <author>
        <name>Asri, Mobin</name>
      </author>
      <author>
        <name>Ayllon, Marcelo</name>
      </author>
      <author>
        <name>Balacco, Jennifer R</name>
      </author>
      <author>
        <name>Belter, Edward A</name>
      </author>
      <author>
        <name>Bender, Halle D</name>
      </author>
      <author>
        <name>Blair, Andrew P</name>
      </author>
      <author>
        <name>Buonaiuto, Silvia</name>
      </author>
      <author>
        <name>Bolognini, Davide</name>
      </author>
      <author>
        <name>Bonini, Katherine E</name>
      </author>
      <author>
        <name>Boucher, Christina</name>
      </author>
      <author>
        <name>Bourque, Guillaume</name>
      </author>
      <author>
        <name>Cao, Shuo</name>
      </author>
      <author>
        <name>Carroll, Andrew</name>
      </author>
      <author>
        <name>Mc Cartney, Ann M</name>
      </author>
      <author>
        <name>Cechova, Monika</name>
      </author>
      <author>
        <name>Chang, Pi-Chuan</name>
      </author>
      <author>
        <name>Chang, Xian</name>
      </author>
      <author>
        <name>Cheema, Jitender</name>
      </author>
      <author>
        <name>Cheng, Haoyu</name>
      </author>
      <author>
        <name>Ciofi, Claudio</name>
      </author>
      <author>
        <name>Cody, Sarah</name>
      </author>
      <author>
        <name>Colonna, Vincenza</name>
      </author>
      <author>
        <name>Conwell, Holland C</name>
      </author>
      <author>
        <name>Cook-Deegan, Robert</name>
      </author>
      <author>
        <name>Diekhans, Mark</name>
      </author>
      <author>
        <name>Diroma, Maria Angela</name>
      </author>
      <author>
        <name>Doerr, Daniel</name>
      </author>
      <author>
        <name>Dong, Zheng</name>
      </author>
      <author>
        <name>Durbin, Richard</name>
      </author>
      <author>
        <name>Ebler, Jana</name>
      </author>
      <author>
        <name>Eichler, Evan E</name>
      </author>
      <author>
        <name>Eizenga, Jordan M</name>
      </author>
      <author>
        <name>Eskandar, Parsa</name>
      </author>
      <author>
        <name>Ferro, Eddie</name>
      </author>
      <author>
        <name>Fiston-Lavier, Anna-Sophie</name>
      </author>
      <author>
        <name>Ford, Sarah M</name>
      </author>
      <author>
        <name>Ford, Willard W</name>
      </author>
      <author>
        <name>Formenti, Giulio</name>
      </author>
      <author>
        <name>Frankish, Adam</name>
      </author>
      <author>
        <name>Freeberg, Mallory A</name>
      </author>
      <author>
        <name>Fu, Qichen</name>
      </author>
      <author>
        <name>Fullerton, Stephanie M</name>
      </author>
      <author>
        <name>Fulton, Robert S</name>
      </author>
      <author>
        <name>Gao, Yan</name>
      </author>
      <author>
        <name>Garcia, Gage H</name>
      </author>
      <author>
        <name>Garcia, Obed A</name>
      </author>
      <author>
        <name>Gardner, Joshua MV</name>
      </author>
      <author>
        <name>Garg, Shilpa</name>
      </author>
      <author>
        <name>Garrison, Erik</name>
      </author>
      <author>
        <name>Garrison, Nanibaa' A</name>
      </author>
      <author>
        <name>Garza, John</name>
      </author>
      <author>
        <name>Ghorbani, Mohammadmersad</name>
      </author>
      <author>
        <name>Graves-Lindsay, Tina</name>
      </author>
      <author>
        <name>Green, Richard E</name>
      </author>
      <author>
        <name>Groza, Cristian</name>
      </author>
      <author>
        <name>Guarracino, Andrea</name>
      </author>
      <author>
        <name>Gymrek, Melissa</name>
        <uri>https://orcid.org/0000-0002-6086-3903</uri>
      </author>
      <author>
        <name>Haggerty, Leanne</name>
      </author>
      <author>
        <name>Hall, Ira M</name>
      </author>
      <author>
        <name>Hansen, Nancy F</name>
      </author>
      <author>
        <name>Hashmi, Mohammad Amiruddin</name>
      </author>
      <author>
        <name>Haeussler, Maximilian</name>
      </author>
      <author>
        <name>Haussler, David</name>
        <uri>https://orcid.org/0000-0003-1533-4575</uri>
      </author>
      <author>
        <name>Hebbar, Prajna</name>
      </author>
      <author>
        <name>Heringer, Peter</name>
      </author>
      <author>
        <name>Hickey, Glenn</name>
      </author>
      <author>
        <name>Hillaker, Todd L</name>
      </author>
      <author>
        <name>Hossain, S Nakib</name>
      </author>
      <author>
        <name>Huang, Neng</name>
      </author>
      <author>
        <name>Hunt, Sarah E</name>
      </author>
      <author>
        <name>Hunt, Toby</name>
      </author>
      <author>
        <name>Jafarzadeh, Nafiseh</name>
      </author>
      <author>
        <name>Jain, Nivesh</name>
      </author>
      <author>
        <name>Jarvis, Erich D</name>
      </author>
      <author>
        <name>Jiang, Juan</name>
      </author>
      <author>
        <name>LoTempio, Jonathan</name>
      </author>
      <author>
        <name>Kenny, Eimear E</name>
      </author>
      <author>
        <name>Kim, Juhyun</name>
      </author>
      <author>
        <name>Koo, Bonhwang</name>
      </author>
    </item>
    <item>
      <title>Sexual health outcomes following gender affirming metoidioplasty: a systematic review</title>
      <link>https://escholarship.org/uc/item/03t681fs</link>
      <description>INTRODUCTION: Numerous studies have evaluated urologic and aesthetic outcomes of genital gender affirming surgery. However, minimal data exist on sexual function of transmasculine individuals after genital gender affirming surgery, and studies often aggregate outcomes from different techniques. This paper aims to systematically review the literature on sexual health outcomes following metoidioplasty surgery.
OBJECTIVES: To synthesize and analyze the literature on sexual health following metoidioplasty, to identify areas of further investigation, and to improve shared decision making and sexual outcomes following metoidioplasty.
METHODS: Studies were systematically identified using PubMed, Embase, and Web of Science from database origins through July 30, 2025, in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analysis statement. Included sexual health outcomes were desire/arousal, sensation, orgasm, masturbation, erection, penetrative capacity, sexual...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/03t681fs</guid>
      <pubDate>Wed, 22 Oct 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Goldstein, Benjamin</name>
      </author>
      <author>
        <name>Uloko, Maria</name>
      </author>
      <author>
        <name>Okamuro, Kyle</name>
      </author>
      <author>
        <name>Moore, Maxwell</name>
      </author>
      <author>
        <name>Peters, Blair R</name>
      </author>
      <author>
        <name>Blumenthal, Jill</name>
      </author>
      <author>
        <name>Marinkovic, Maja</name>
        <uri>https://orcid.org/0000-0001-8911-8010</uri>
      </author>
      <author>
        <name>Anger, Jennifer</name>
      </author>
    </item>
    <item>
      <title>Transcriptional regulation by PHGDH drives amyloid pathology in Alzheimer’s disease</title>
      <link>https://escholarship.org/uc/item/98z6d74g</link>
      <description>Virtually all individuals aged 65 or older develop at least early pathology of Alzheimer's disease (AD), yet most lack disease-causing mutations in APP, PSEN, or MAPT, and many do not carry the APOE4 risk allele. This raises questions about AD development in the general population. Although transcriptional dysregulation has not traditionally been a hallmark of AD, recent studies reveal significant epigenomic changes in late-onset AD (LOAD) patients. We show that altered expression of the LOAD biomarker phosphoglycerate dehydrogenase (PHGDH) modulates AD pathology in mice and human brain organoids independent of its enzymatic activity. PHGDH has an uncharacterized role in transcriptional regulation, promoting the transcription of inhibitor of nuclear factor kappa-B kinase subunit alpha (IKKa) and high-mobility group box 1 (HMGB1) in astrocytes, which suppress autophagy and accelerate amyloid pathology. A blood-brain-barrier-permeable small-molecule inhibitor targeting PHGDH's transcriptional...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/98z6d74g</guid>
      <pubDate>Thu, 9 Oct 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Chen, Junchen</name>
      </author>
      <author>
        <name>Hadi, Fatemeh</name>
      </author>
      <author>
        <name>Wen, Xingzhao</name>
      </author>
      <author>
        <name>Zhao, Wenxin</name>
      </author>
      <author>
        <name>Xu, Ming</name>
      </author>
      <author>
        <name>Xue, Shuanghong</name>
      </author>
      <author>
        <name>Lin, Pei</name>
      </author>
      <author>
        <name>Calandrelli, Riccardo</name>
      </author>
      <author>
        <name>Richard, John Lalith Charles</name>
      </author>
      <author>
        <name>Song, Zhixuan</name>
      </author>
      <author>
        <name>Li, Jessica</name>
      </author>
      <author>
        <name>Amani, Alborz</name>
      </author>
      <author>
        <name>Liu, Yang</name>
      </author>
      <author>
        <name>Chen, Xu</name>
      </author>
      <author>
        <name>Zhong, Sheng</name>
      </author>
    </item>
    <item>
      <title>Genome-wide mapping of RNA-protein associations through sequencing</title>
      <link>https://escholarship.org/uc/item/6ks0z590</link>
      <description>RNA-protein interactions critically regulate gene expression and cellular processes, yet their comprehensive mapping remains challenging due to their structural diversity. We introduce PRIM-seq (protein-RNA interaction mapping by sequencing), a method for concurrent de novo identification of RNA-binding proteins and their associated RNAs. PRIM-seq generates unique chimeric DNA sequences by proximity ligation of RNAs with protein-linked DNA barcodes, which are subsequently decoded through sequencing. We apply PRIM-seq to two human cell lines and construct a human RNA-protein association network (HuRPA), encompassing &amp;gt;350,000 associations involving ~7,000 RNAs and ~11,000 proteins, including 2,610 proteins that each interact with at least 10 distinct RNAs. We experimentally validate the tumorigenesis-associated lincRNA LINC00339, the RNA with the highest number of protein associations in HuRPA, as a protein-associated RNA. We further validate the RNA-associating abilities of...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/6ks0z590</guid>
      <pubDate>Thu, 9 Oct 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Qi, Zhijie</name>
      </author>
      <author>
        <name>Xue, Shuanghong</name>
      </author>
      <author>
        <name>Chen, Junchen</name>
      </author>
      <author>
        <name>Zhao, Wenxin</name>
      </author>
      <author>
        <name>Johnson, Kara</name>
      </author>
      <author>
        <name>Wen, Xingzhao</name>
      </author>
      <author>
        <name>Charles Richard, John Lalith</name>
        <uri>https://orcid.org/0000-0002-1186-6390</uri>
      </author>
      <author>
        <name>Lin, Pei</name>
      </author>
      <author>
        <name>Zhong, Sheng</name>
      </author>
    </item>
    <item>
      <title>USP10/GSK3B-mediated inhibition of PTEN drives resistance to PI3K inhibitors in breast cancer</title>
      <link>https://escholarship.org/uc/item/5040q3cg</link>
      <description>Activating mutations in PIK3CA, the gene encoding the catalytic p110-alpha subunit of PI3K, are some of the most frequent genomic alterations in breast cancer. Alpelisib, a small-molecule inhibitor that targets p110-alpha, is a recommended drug for patients with PIK3CA-mutant advanced breast cancer. However, clinical success for PI3K inhibitors has been limited by their narrow therapeutic window. The lipid phosphatase PTEN is a potent tumour suppressor and a major negative regulator of the PI3K pathway. Unsurprisingly, inactivating mutations in PTEN correlate with tumour progression and resistance to PI3K inhibition due to persistent PI3K signalling. Here we demonstrate that PI3K inhibition leads rapidly to the inactivation of PTEN. Using a functional genetic screen we show that this effect is mediated by a USP10-GSK3-B signalling axis, in which USP10 stabilizes GSK3-B resulting in GSK3-B-mediated phosphorylation of the C-terminal tail of PTEN. This phosphorylation inhibits PTEN...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/5040q3cg</guid>
      <pubDate>Thu, 9 Oct 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Kumari, Nishi</name>
      </author>
      <author>
        <name>Wright, Sarah CE</name>
      </author>
      <author>
        <name>Witham, Christopher M</name>
      </author>
      <author>
        <name>Monserrat, Laia</name>
      </author>
      <author>
        <name>Palafox, Marta</name>
      </author>
      <author>
        <name>Richard, John Lalith Charles</name>
      </author>
      <author>
        <name>Costa, Carlotta</name>
      </author>
      <author>
        <name>Elkabets, Moshe</name>
      </author>
      <author>
        <name>Agostino, Mark</name>
      </author>
      <author>
        <name>Klemm, Theresa</name>
      </author>
      <author>
        <name>Eccles, Melissa K</name>
      </author>
      <author>
        <name>Garnham, Alexandra</name>
      </author>
      <author>
        <name>Wu, Ting</name>
      </author>
      <author>
        <name>Nilsson, Jonas A</name>
      </author>
      <author>
        <name>Walz, Nikita</name>
      </author>
      <author>
        <name>Venugopal, Veena</name>
      </author>
      <author>
        <name>Cerra, Anthony</name>
      </author>
      <author>
        <name>Vasilevski, Natali</name>
      </author>
      <author>
        <name>Bridgeman, Stephanie C</name>
      </author>
      <author>
        <name>Bassi, Sona</name>
      </author>
      <author>
        <name>Saei, Azad</name>
      </author>
      <author>
        <name>Helal, Moutaz</name>
      </author>
      <author>
        <name>Neundorf, Philipp</name>
      </author>
      <author>
        <name>Riedel, Angela</name>
      </author>
      <author>
        <name>Rosenfeldt, Mathias</name>
      </author>
      <author>
        <name>Gill, Jespal</name>
      </author>
      <author>
        <name>Pahor, Nikolett</name>
      </author>
      <author>
        <name>Hartmann, Oliver</name>
      </author>
      <author>
        <name>Chung, Jacky</name>
      </author>
      <author>
        <name>Sidhu, Sachdev S</name>
      </author>
      <author>
        <name>Moderau, Nina</name>
      </author>
      <author>
        <name>Jha, Sudhakar</name>
      </author>
      <author>
        <name>Rodon, Jordi</name>
      </author>
      <author>
        <name>Diefenbacher, Markus E</name>
      </author>
      <author>
        <name>Komander, David</name>
      </author>
      <author>
        <name>Serra, Violeta</name>
      </author>
      <author>
        <name>Eichhorn, Pieter</name>
      </author>
    </item>
    <item>
      <title>Urinary Abnormalities Differentiating Kawasaki Disease From Clinically Similar Febrile Illnesses</title>
      <link>https://escholarship.org/uc/item/35s308bm</link>
      <description>OBJECTIVE: 

                  To test the hypothesis that urinary abnormalities differ among Kawasaki disease (KD), multisystem inflammatory syndrome in children (MIS-C), and other pediatric febrile illnesses. 

               
               
                  METHODS: 

                  We conducted a cross-sectional analysis of dipstick and automated microscopic urinalyses from participants prospectively evaluated for KD and other causes of fever, for MIS-C, and for urinary tract infection (UTI). We compared urinary leukocyte (WBC) and bacterial counts and levels of bilirubin and urobilinogen among these groups. 

               
               
                  RESULTS: 

                  Urinalyses were available for 247 participants with KD, 61 participants with MIS-C, 143 febrile controls (FC), and 45 participants with UTI. Pyuria defined by laboratory reference range (male: &amp;gt;8 WBC/μL; female: &amp;gt;20 WBC/μL) occurred in 73.7%, 66.1%, 47.6%, and 93.3% of the KD, MIS-C,...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/35s308bm</guid>
      <pubDate>Thu, 9 Oct 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Kanegaye, John T</name>
      </author>
      <author>
        <name>Lyubasyuk, Vera</name>
      </author>
      <author>
        <name>Sivilay, Nipha</name>
      </author>
      <author>
        <name>Burns, Jane C</name>
        <uri>https://orcid.org/0000-0001-5679-1217</uri>
      </author>
      <author>
        <name>Tremoulet, Adriana H</name>
      </author>
    </item>
    <item>
      <title>Genetic variation in the activity of a TREM2–p53 signaling axis determines oxygen-induced lung injury</title>
      <link>https://escholarship.org/uc/item/22582970</link>
      <description>Bronchopulmonary dysplasia is a common complication of preterm birth, driven in part by the inflammatory effects of supplemental oxygen on the immature lung. Although oxygen therapy is essential, it contributes to disrupted lung development but not all infants are equally susceptible. Using genetically diverse mouse models, we found that hyperoxia-sensitive mice exhibit a distinct innate immune response compared to resilient strains. Notably, the hyperoxia-sensitive C57BL/6J strain showed selective upregulation of TREM2 on lung macrophages and monocytes. Deletion of TREM2 in myeloid cells led to reduced inflammation, preserved alveolar structure and sustained cell proliferation in the developing lung following oxygen exposure. Mechanistically, TREM2 loss limited p53 activation, favoring cell-cycle arrest over apoptosis. These results identify TREM2 as a key driver of immune-mediated lung injury in neonatal hyperoxia and suggest it may be a promising therapeutic target for preventing...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/22582970</guid>
      <pubDate>Thu, 9 Oct 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Abe, Yohei</name>
      </author>
      <author>
        <name>Spann, Nathanael J</name>
      </author>
      <author>
        <name>Tang, Wenxi</name>
      </author>
      <author>
        <name>Zeng, Fenghua</name>
      </author>
      <author>
        <name>Seymour, Cadence</name>
      </author>
      <author>
        <name>Jansky, Sean</name>
      </author>
      <author>
        <name>Guo, Jason L</name>
      </author>
      <author>
        <name>Huff, Robert</name>
      </author>
      <author>
        <name>Chanthavixay, Kelly</name>
      </author>
      <author>
        <name>Richard, John Lalith Charles</name>
      </author>
      <author>
        <name>Mooney, Miguel</name>
      </author>
      <author>
        <name>Dhar, Debanjan</name>
      </author>
      <author>
        <name>Ganguly, Souradipta</name>
      </author>
      <author>
        <name>Lopez, David M</name>
      </author>
      <author>
        <name>Longaker, Michael T</name>
      </author>
      <author>
        <name>Benner, Christopher</name>
        <uri>https://orcid.org/0000-0002-4618-0719</uri>
      </author>
      <author>
        <name>Glass, Christopher K</name>
        <uri>https://orcid.org/0000-0003-4344-3592</uri>
      </author>
      <author>
        <name>Sajti, Eniko</name>
        <uri>https://orcid.org/0000-0002-0531-7715</uri>
      </author>
    </item>
    <item>
      <title>Nanobioreactor detection of space-associated hematopoietic stem and progenitor cell aging</title>
      <link>https://escholarship.org/uc/item/6gx202cr</link>
      <description>Human hematopoietic stem and progenitor cell (HSPC) fitness declines following exposure to stressors that reduce survival, dormancy, telomere maintenance, and self-renewal, thereby accelerating aging. While previous National Aeronautics and Space Administration (NASA) research revealed immune dysfunction in low-earth orbit (LEO), the impact of spaceflight on human HSPC aging had not been studied. To study HSPC aging, our NASA-supported Integrated Space Stem Cell Orbital Research (ISSCOR) team developed bone marrow niche nanobioreactors with lentiviral bicistronic fluorescent, ubiquitination-based cell-cycle indicator (FUCCI2BL) reporter for real-time HSPC tracking in artificial intelligence (AI)-driven CubeLabs. In month-long International Space Station (ISS) missions (SpX-24, SpX-25, SpX-26, and SpX-27) compared with ground controls, FUCCI2BL reporter, whole-genome and transcriptome sequencing, and cytokine arrays demonstrated cell-cycle, inflammatory cytokine, mitochondrial...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/6gx202cr</guid>
      <pubDate>Thu, 25 Sep 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Pham, Jessica</name>
      </author>
      <author>
        <name>Isquith, Jane</name>
      </author>
      <author>
        <name>Balaian, Larisa</name>
      </author>
      <author>
        <name>Nandi, Shuvro P</name>
        <uri>https://orcid.org/0000-0003-4855-4697</uri>
      </author>
      <author>
        <name>Engstrom, Claire</name>
      </author>
      <author>
        <name>Mack, Karla</name>
      </author>
      <author>
        <name>van der Werf, Inge</name>
      </author>
      <author>
        <name>Chang, Patrick</name>
      </author>
      <author>
        <name>Stoudemire, Jana</name>
      </author>
      <author>
        <name>Ladel, Luisa</name>
      </author>
      <author>
        <name>Klacking, Emma</name>
        <uri>https://orcid.org/0009-0004-0239-2041</uri>
      </author>
      <author>
        <name>Ruiz, Antonio</name>
      </author>
      <author>
        <name>Chilin-Fuentes, Daisy</name>
      </author>
      <author>
        <name>Sneifer, Jenna</name>
      </author>
      <author>
        <name>Mays, David</name>
      </author>
      <author>
        <name>Gamble, Paul</name>
      </author>
      <author>
        <name>Giza, Shelby</name>
      </author>
      <author>
        <name>Janowitz, Jiya</name>
      </author>
      <author>
        <name>Nienaber, Trevor</name>
      </author>
      <author>
        <name>Mishra, Tejaswini</name>
      </author>
      <author>
        <name>Khachatrian, Anna A</name>
      </author>
      <author>
        <name>Molina, Elsa</name>
      </author>
      <author>
        <name>Snyder, Michael P</name>
        <uri>https://orcid.org/0000-0003-0784-7987</uri>
      </author>
      <author>
        <name>Morris, Sheldon R</name>
      </author>
      <author>
        <name>Clements, Twyman</name>
      </author>
      <author>
        <name>Muotri, Alysson R</name>
        <uri>https://orcid.org/0000-0003-0867-2875</uri>
      </author>
      <author>
        <name>Whisenant, Thomas</name>
      </author>
      <author>
        <name>Alexandrov, Ludmil B</name>
      </author>
      <author>
        <name>Jamieson, Catriona HM</name>
      </author>
    </item>
    <item>
      <title>Meconium-related obstruction: Contemporary experience in a multi-institutional consortium</title>
      <link>https://escholarship.org/uc/item/3qp0v2f1</link>
      <description>PURPOSE: Neonatal bowel obstruction secondary to inspissated meconium has been historically associated with cystic fibrosis. Increasingly, meconium-related obstruction (MRO) has been observed in preterm infants. We conducted a multicenter mixed-methods study to better characterize the contemporary experience with MRO.
METHODS: A retrospective cohort study of infants with MRO was performed at seven children's hospitals from 2018 to 2022. Chi-squared tests, Kruskal-Wallis tests, and logistic regression were used to assess the association of cystic fibrosis, Hirschsprung disease, and prematurity with treatment strategies and clinical outcomes of MRO. Providers were surveyed regarding their management of MRO of prematurity.
RESULTS: We identified 105 infants treated for MRO, including 54 (51 %) with MRO of prematurity, 16 (15 %) with Hirschsprung disease, 6 (6 %) with cystic fibrosis, and 29 (28 %) with MRO of the term infant. Overall, 32 % (n = 34) received glycerin suppositories,...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/3qp0v2f1</guid>
      <pubDate>Wed, 24 Sep 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Rook, Jordan M</name>
      </author>
      <author>
        <name>Anderson, Jamie E</name>
        <uri>https://orcid.org/0000-0002-8259-4062</uri>
      </author>
      <author>
        <name>Kramer, Katelin P</name>
        <uri>https://orcid.org/0000-0001-7280-0558</uri>
      </author>
      <author>
        <name>Royse, Caitlin</name>
      </author>
      <author>
        <name>Evans, Michele</name>
      </author>
      <author>
        <name>West, Erin</name>
      </author>
      <author>
        <name>Ismail, Adnan</name>
      </author>
      <author>
        <name>Guner, Yigit S</name>
      </author>
      <author>
        <name>Lee, Henry C</name>
        <uri>https://orcid.org/0000-0001-8383-1720</uri>
      </author>
      <author>
        <name>Bai-Tong, Shiyu</name>
      </author>
      <author>
        <name>Lusk, Leslie</name>
      </author>
      <author>
        <name>Bautista, Geoanna M</name>
        <uri>https://orcid.org/0000-0003-0245-9272</uri>
      </author>
      <author>
        <name>Lee, Hanmin</name>
      </author>
      <author>
        <name>Uy, Cherry</name>
      </author>
      <author>
        <name>Calkins, Kara L</name>
      </author>
      <author>
        <name>Kling, Karen M</name>
      </author>
      <author>
        <name>DeUgarte, Daniel A</name>
      </author>
      <author>
        <name>Consortium, the University of California Fetal</name>
      </author>
    </item>
    <item>
      <title>Single-cell multiome and spatial profiling reveals pancreas cell type–specific gene regulatory programs of type 1 diabetes progression</title>
      <link>https://escholarship.org/uc/item/5xw8r3f6</link>
      <description>Cell type-specific regulatory programs that drive type 1 diabetes (T1D) in the pancreas are poorly understood. Here, we performed single-nucleus multiomics and spatial transcriptomics in up to 32 nondiabetic (ND), autoantibody-positive (AAB&lt;sup&gt;+&lt;/sup&gt;), and T1D pancreas donors. Genomic profiles from 853,005 cells mapped to 12 pancreatic cell types, including multiple exocrine subtypes. β, Acinar, and other cell types, and related cellular niches, had altered abundance and gene activity in T1D progression, including distinct pathways altered in AAB&lt;sup&gt;+&lt;/sup&gt; compared to T1D. We identified epigenomic drivers of gene activity in T1D and AAB&lt;sup&gt;+&lt;/sup&gt; which, combined with genetic association, revealed causal pathways of T1D risk including antigen presentation in β cells. Last, single-cell and spatial profiles together revealed widespread changes in cell-cell signaling in T1D including signals affecting β cell regulation. Overall, these results revealed drivers of T1D in the pancreas,...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/5xw8r3f6</guid>
      <pubDate>Mon, 15 Sep 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Melton, Rebecca</name>
      </author>
      <author>
        <name>Jimenez, Sara</name>
      </author>
      <author>
        <name>Elison, Weston</name>
      </author>
      <author>
        <name>Tucciarone, Luca</name>
      </author>
      <author>
        <name>Howell, Abigail</name>
      </author>
      <author>
        <name>Wang, Gaowei</name>
      </author>
      <author>
        <name>Berti, Denise</name>
      </author>
      <author>
        <name>Beebe, Elisha</name>
      </author>
      <author>
        <name>Miller, Michael</name>
      </author>
      <author>
        <name>Zeng, Chun</name>
      </author>
      <author>
        <name>McGrail, Carolyn</name>
      </author>
      <author>
        <name>VanderStel, Kennedy</name>
      </author>
      <author>
        <name>Korgaonkar, Katha</name>
      </author>
      <author>
        <name>Elgamal, Ruth</name>
      </author>
      <author>
        <name>Mummey, Hannah</name>
      </author>
      <author>
        <name>Chiou, Joshua</name>
      </author>
      <author>
        <name>Griffin, Emily</name>
      </author>
      <author>
        <name>Kusmartseva, Irina</name>
      </author>
      <author>
        <name>Atkinson, Mark</name>
      </author>
      <author>
        <name>Preissl, Sebastian</name>
      </author>
      <author>
        <name>Theis, Fabian J</name>
      </author>
      <author>
        <name>Sander, Maike</name>
        <uri>https://orcid.org/0000-0001-5308-7785</uri>
      </author>
      <author>
        <name>Gaulton, Kyle J</name>
        <uri>https://orcid.org/0000-0003-1318-7161</uri>
      </author>
    </item>
    <item>
      <title>Efficacy and Toxicity of Inotuzumab Ozogamicin for Treatment of Relapsed/Refractory B‐Cell Acute Lymphoblastic Leukemia in Pediatric and Young Adult Patients After CD19‐Chimeric Antigen Receptor T‐Cell Therapy</title>
      <link>https://escholarship.org/uc/item/8rr8m2df</link>
      <description>We retrospectively analyzed outcomes for nine children and young adults who were treated with inotuzumab ozogamicin (InO) for relapsed/refractory (R/R) B-acute lymphoblastic leukemia (ALL) after CD19-chimeric antigen receptor T-cell therapy (CART). After InO cycle 1, overall response rate was 77.8%; 66.7% achieved measurable residual disease (MRD)-negative remission. One-year event-free survival (EFS) was 37.5%; 1-year overall survival (OS) was 50%; 2-year EFS was 37.5%; 2-year OS was 37.5%. Median survivor follow-up is 2.9 years (0.5-4.7). Significant adverse events included prolonged cytopenias, hepatotoxicity, and post-transplant sinusoidal obstructive sydrome. InO showed promising efficacy as treatment for children and young adults with R/R B-ALL after CD19-CART. Extramedullary disease&amp;nbsp;prior to InO and positive MRD after InO cycle 1 were associated with poor outcomes.</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/8rr8m2df</guid>
      <pubDate>Fri, 12 Sep 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Ogrodnik, Paula</name>
      </author>
      <author>
        <name>Anderson, Eric</name>
      </author>
      <author>
        <name>Gloude, Nicholas</name>
      </author>
      <author>
        <name>Schiff, Deborah</name>
        <uri>https://orcid.org/0000-0003-3154-8987</uri>
      </author>
    </item>
    <item>
      <title>Evidence gaps among systematic reviews examining the relationship of race, ethnicity, and social determinants of health with adult inpatient quality measures</title>
      <link>https://escholarship.org/uc/item/0p7275x2</link>
      <description>Background: The field of healthcare epidemiology is increasingly focused on identifying, characterizing, and addressing social determinants of health (SDOH) to address inequities in healthcare quality. To identify evidence gaps, we examined recent systematic reviews examining the association of race, ethnicity, and SDOH with inpatient quality measures.
Methods: We searched Medline via OVID for English language systematic reviews from 2010 to 2022 addressing race, ethnicity, or SDOH domains and inpatient quality measures in adults using specific topic questions. We imported all citations to Covidence (www.covidence.org, Veritas Health Innovation) and removed duplicates. Two blinded reviewers assessed all articles for inclusion in 2 phases: title/abstract, then full-text review. Discrepancies were resolved by a third reviewer.
Results: Of 472 systematic reviews identified, 39 were included. Of these, 23 examined all-cause mortality; 6 examined 30-day readmission rates; 4 examined...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/0p7275x2</guid>
      <pubDate>Thu, 4 Sep 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Advani, Sonali D</name>
      </author>
      <author>
        <name>Smith, Alison G</name>
      </author>
      <author>
        <name>Kalu, Ibukunoluwa C</name>
      </author>
      <author>
        <name>Perez, Reinaldo</name>
      </author>
      <author>
        <name>Hendren, Stephanie</name>
      </author>
      <author>
        <name>Dantes, Raymund B</name>
      </author>
      <author>
        <name>Edwards, Jonathan R</name>
      </author>
      <author>
        <name>Soe, Minn</name>
      </author>
      <author>
        <name>Yi, Sarah H</name>
      </author>
      <author>
        <name>Young, Janine</name>
      </author>
      <author>
        <name>Anderson, Deverick J</name>
      </author>
    </item>
    <item>
      <title>Loss of USP28-mediated BRAF degradation drives resistance to RAF cancer therapies</title>
      <link>https://escholarship.org/uc/item/8xb9f980</link>
      <description>RAF kinase inhibitors are clinically active in patients with BRAF (V600E) mutant melanoma. However, rarely do tumors regress completely, with the majority of responses being short-lived. This is partially mediated through the loss of negative feedback loops after MAPK inhibition and reactivation of upstream signaling. Here, we demonstrate that the deubiquitinating enzyme USP28 functions through a feedback loop to destabilize RAF family members. Loss of USP28 stabilizes BRAF enhancing downstream MAPK activation and promotes resistance to RAF inhibitor therapy in culture and in vivo models. Importantly, we demonstrate that USP28 is deleted in a proportion of melanoma patients and may act as a biomarker for response to BRAF inhibitor therapy in patients. Furthermore, we identify Rigosertib as a possible therapeutic strategy for USP28-depleted tumors. Our results show that loss of USP28 enhances MAPK activity through the stabilization of RAF family members and is a key factor in BRAF...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/8xb9f980</guid>
      <pubDate>Thu, 28 Aug 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Saei, Azad</name>
      </author>
      <author>
        <name>Palafox, Marta</name>
      </author>
      <author>
        <name>Benoukraf, Touati</name>
      </author>
      <author>
        <name>Kumari, Nishi</name>
      </author>
      <author>
        <name>Jaynes, Patrick William</name>
      </author>
      <author>
        <name>Iyengar, Prasanna Vasudevan</name>
      </author>
      <author>
        <name>Muñoz-Couselo, Eva</name>
      </author>
      <author>
        <name>Nuciforo, Paolo</name>
      </author>
      <author>
        <name>Cortés, Javier</name>
      </author>
      <author>
        <name>Nötzel, Christopher</name>
      </author>
      <author>
        <name>Kumarakulasinghe, Nesaretnam Barr</name>
      </author>
      <author>
        <name>Richard, John Lalith Charles</name>
      </author>
      <author>
        <name>Bin Adam Isa, Zul Fazreen</name>
      </author>
      <author>
        <name>Pang, Brendan</name>
      </author>
      <author>
        <name>Guzman, Marta</name>
      </author>
      <author>
        <name>Siqin, Zhou</name>
      </author>
      <author>
        <name>Yang, Henry</name>
      </author>
      <author>
        <name>Tam, Wai Leong</name>
      </author>
      <author>
        <name>Serra, Violeta</name>
      </author>
      <author>
        <name>Eichhorn, Pieter Johan Adam</name>
      </author>
    </item>
    <item>
      <title>Identification of novel early pancreatic cancer biomarkers KIF5B and SFRP2 from “first contact” interactions in the tumor microenvironment</title>
      <link>https://escholarship.org/uc/item/4zd9n32k</link>
      <description>BackgroundPancreatic cancer is one of the most difficult cancers to detect early and most patients die from complications arising due to distant organ metastases. The lack of bona fide early biomarkers is one of the primary reasons for late diagnosis of pancreatic cancer. It is a multifactorial disease and warrants a novel approach to identify early biomarkers.MethodsIn order to characterize the proteome, Extracellular vesicles (EVs) isolated from different in vitro conditions mimicking tumor-microenvironment interactions between pancreatic cancer epithelial and stromal cells were analyzed using high throughput mass spectrometry. The biological activity of the secreted EVome was analyzed by investigating changes in distant organ metastases and associated early changes in the microbiome. Candidate biomarkers (KIF5B, SFRP2, LOXL2, and MMP3) were selected and validated on a mouse-human hybrid Tissue Microarray (TMA) that was specifically generated for this study. Additionally, a...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/4zd9n32k</guid>
      <pubDate>Thu, 28 Aug 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Charles Jacob, Harrys Kishore</name>
      </author>
      <author>
        <name>Signorelli, Rossana</name>
      </author>
      <author>
        <name>Charles Richard, John Lalith</name>
        <uri>https://orcid.org/0000-0002-1186-6390</uri>
      </author>
      <author>
        <name>Kashuv, Tyler</name>
      </author>
      <author>
        <name>Lavania, Shweta</name>
      </author>
      <author>
        <name>Middleton, Ashley</name>
      </author>
      <author>
        <name>Gomez, Beatriz Aguilar</name>
      </author>
      <author>
        <name>Ferrantella, Anthony</name>
      </author>
      <author>
        <name>Amirian, Haleh</name>
      </author>
      <author>
        <name>Tao, Junyi</name>
      </author>
      <author>
        <name>Ergonul, Ayse Burcu</name>
      </author>
      <author>
        <name>Boone, Melinda Minucci</name>
      </author>
      <author>
        <name>Hadisurya, Marco</name>
      </author>
      <author>
        <name>Tao, Weiguo Andy</name>
      </author>
      <author>
        <name>Iliuk, Anton</name>
      </author>
      <author>
        <name>Kashyap, Manoj Kumar</name>
      </author>
      <author>
        <name>Garcia-Buitrago, Monica</name>
      </author>
      <author>
        <name>Dawra, Rajinder</name>
      </author>
      <author>
        <name>Saluja, Ashok Kumar</name>
      </author>
    </item>
    <item>
      <title>Sonic hedgehog is a regulator of extracellular glutamate levels and epilepsy</title>
      <link>https://escholarship.org/uc/item/9hf9298r</link>
      <description>Sonic hedgehog (Shh), both as a mitogen and as a morphogen, plays an important role in cell proliferation and differentiation during early development. Here, we show that Shh inhibits glutamate transporter activities in neurons, rapidly enhances extracellular glutamate levels, and affects the development of epilepsy. Shh is quickly released in response to epileptic, but not physiological, stimuli. Inhibition of neuronal glutamate transporters by Shh depends on heterotrimeric G protein subunit Gαi and enhances extracellular glutamate levels. Inhibiting Shh signaling greatly reduces epileptiform activities in both cell cultures and hippocampal slices. Moreover, pharmacological or genetic inhibition of Shh signaling markedly suppresses epileptic phenotypes in kindling or pilocarpine models. Our results suggest that Shh contributes to the development of epilepsy and suppression of its signaling prevents the development of the disease. Thus, Shh can act as a modulator of neuronal activity,...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/9hf9298r</guid>
      <pubDate>Thu, 14 Aug 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Feng, Shengjie</name>
      </author>
      <author>
        <name>Ma, Shaorong</name>
        <uri>https://orcid.org/0000-0003-4643-8393</uri>
      </author>
      <author>
        <name>Jia, Caixia</name>
      </author>
      <author>
        <name>Su, Yujuan</name>
        <uri>https://orcid.org/0009-0009-9163-9996</uri>
      </author>
      <author>
        <name>Yang, Shenglian</name>
      </author>
      <author>
        <name>Zhou, Kechun</name>
      </author>
      <author>
        <name>Liu, Yani</name>
      </author>
      <author>
        <name>Cheng, Ju</name>
      </author>
      <author>
        <name>Lu, Dunguo</name>
      </author>
      <author>
        <name>Fan, Liu</name>
      </author>
      <author>
        <name>Wang, Yizheng</name>
      </author>
    </item>
    <item>
      <title>A presentation of systemic lupus erythematosus manifesting as abdominal pain: a case report</title>
      <link>https://escholarship.org/uc/item/8kb8c6rr</link>
      <description>BackgroundSystemic lupus erythematosus is a multisystem inflammatory disease with a broad range of clinical and serologic presentations. The heterogeneity of presentation poses diagnostic challenges for the clinician, and a high index of suspicion is required. Classification systems exist for both clinical and immunologic criteria; however, they may lack sensitivity in assisting with diagnosis of atypical presentations. We present a case of an initial presentation of systemic lupus erythematosus consisting of nonspecific gastrointestinal symptoms with clinical and immunologic findings that fluctuated with menstrual cycles.Case presentationA 15-year-old Hispanic female initially presented with 2 days of epigastric abdominal pain, non-bloody and non-bilious emesis, and diarrhea. There was no fever, rash, weight loss, arthralgias, or dysuria. Menses started 1 day prior to presentation. She was persistently hypertensive throughout her admission. She developed respiratory distress...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/8kb8c6rr</guid>
      <pubDate>Thu, 14 Aug 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Kupelian, Chloe</name>
      </author>
      <author>
        <name>Bowen, DeMarco</name>
      </author>
      <author>
        <name>Huang, Maria</name>
        <uri>https://orcid.org/0000-0001-6881-4754</uri>
      </author>
      <author>
        <name>Lee, Begem</name>
      </author>
      <author>
        <name>Lenzen, Christiane</name>
      </author>
      <author>
        <name>Rungvivatjarus, Tiranun</name>
      </author>
    </item>
    <item>
      <title>Sonic Hedgehog Mediates High Frequency-Dependent Deep Brain Stimulation for the Correction of Motor Deficits in a Parkinson’s Disease Model</title>
      <link>https://escholarship.org/uc/item/6f05m6r6</link>
      <description>Sonic Hedgehog Mediates High Frequency-Dependent Deep Brain Stimulation for the Correction of Motor Deficits in a Parkinson’s Disease Model</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/6f05m6r6</guid>
      <pubDate>Thu, 14 Aug 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Zhang, Hui</name>
      </author>
      <author>
        <name>Su, Yujuan</name>
        <uri>https://orcid.org/0009-0009-9163-9996</uri>
      </author>
      <author>
        <name>Qu, Zhongwei</name>
      </author>
      <author>
        <name>Zhang, Chunkui</name>
      </author>
      <author>
        <name>Ma, Shaorong</name>
      </author>
      <author>
        <name>Li, Xia</name>
      </author>
      <author>
        <name>Wang, Yizheng</name>
      </author>
    </item>
    <item>
      <title>Convergent cardiorespiratory neurons represent a significant portion of cardiac and respiratory neurons in the vagal ganglia</title>
      <link>https://escholarship.org/uc/item/6dk1p3d2</link>
      <description>Significant cardiorespiratory coordination is required to maintain physiological function in health and disease. Sensory neuronal "cross-talk" between the heart and the lungs is required for synchronous regulation of normal cardiopulmonary function and is most likely mediated by the convergence of sensory neural pathways present in the autonomic ganglia. Using neurotracer approaches with appropriate negative control experiments in a mouse model, presence of cardiorespiratory neurons in the vagal (nodose) ganglia are demonstrated. Furthermore, we found that convergent neurons represent nearly 50% of all cardiac neurons and approximately 35% of all respiratory neurons. The current findings demonstrate a pre-existing neuronal substrate linking cardiorespiratory neurotransmission in the vagal ganglia, and a potentially important link for cardiopulmonary cross-sensitization, which may play an important role in the observed manifestations of cardiopulmonary diseases.</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/6dk1p3d2</guid>
      <pubDate>Thu, 14 Aug 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Devarajan, Asokan</name>
      </author>
      <author>
        <name>Wang, Ke</name>
      </author>
      <author>
        <name>Shannon, Kassandra</name>
      </author>
      <author>
        <name>Su, Yujuan</name>
        <uri>https://orcid.org/0009-0009-9163-9996</uri>
      </author>
      <author>
        <name>Verheyden, Jamie</name>
      </author>
      <author>
        <name>Sun, Xin</name>
      </author>
      <author>
        <name>Vaseghi, Marmar</name>
      </author>
    </item>
    <item>
      <title>Alterations in lipid profiles in children with perinatally acquired HIV infection living in Ghana: A cross-sectional study</title>
      <link>https://escholarship.org/uc/item/62x6p06c</link>
      <description>Children and adolescents who acquired HIV perinatally and are on lifelong antiretroviral therapy (ART) are at increased risk of lipid abnormalities, premature atherosclerosis, and early onset cardiovascular diseases (CVD). Majority of these children reside in sub-Saharan Africa, where monitoring of lipid profiles is not routine. In this study, we assessed the age dependent prevalence of dyslipidemia among children and adolescents who acquired HIV in Ghana and explored effects of age and sex. In this cross-sectional study, we examined lipid profiles of 397 children aged 6-18 years. Dyslipidemia was defined by elevated total cholesterol (TC) (≥200 mg/dL) or triglyceride (TG) levels (&amp;gt;150 mg/dL) or low-density lipoprotein cholesterol (LDL-C) (&amp;gt;130 mg/dL) or reduced high-density lipoprotein cholesterol (HDL-C) (&amp;lt;35 mg/dL). In subgroup analyses, dyslipidemia prevalence, by at least one criterion and for each criterion separately, was compared between age groups 6-12 (pre-teen)...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/62x6p06c</guid>
      <pubDate>Thu, 14 Aug 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Ayanful-Torgby, Ruth</name>
      </author>
      <author>
        <name>Shabanova, Veronika</name>
      </author>
      <author>
        <name>Essuman, Akosua Aya</name>
      </author>
      <author>
        <name>Boafo, Emmanuel</name>
      </author>
      <author>
        <name>Amoah, Linda Eva</name>
      </author>
      <author>
        <name>Paintsil, Elijah</name>
      </author>
    </item>
    <item>
      <title>STN–ANT plasticity is crucial for the motor control in Parkinson’s disease model</title>
      <link>https://escholarship.org/uc/item/5rb1p7gm</link>
      <description>STN–ANT plasticity is crucial for the motor control in Parkinson’s disease model</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/5rb1p7gm</guid>
      <pubDate>Thu, 14 Aug 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Zhang, Hui</name>
      </author>
      <author>
        <name>Zhang, Chunkui</name>
      </author>
      <author>
        <name>Qu, Zhongwei</name>
      </author>
      <author>
        <name>Li, Bing</name>
      </author>
      <author>
        <name>Su, Yujuan</name>
        <uri>https://orcid.org/0009-0009-9163-9996</uri>
      </author>
      <author>
        <name>Li, Xia</name>
      </author>
      <author>
        <name>Gao, Yan</name>
      </author>
      <author>
        <name>Wang, Yizheng</name>
      </author>
    </item>
    <item>
      <title>Allergen induces pulmonary neuroendocrine cell hyperplasia in a model of asthma</title>
      <link>https://escholarship.org/uc/item/56j9j61x</link>
      <description>Asthma is characterized by exacerbated response to triggers such as allergen. While pulmonary neuroendocrine cells (PNECs), a rare population of airway epithelial cells, are essential for amplifying allergen-induced asthma response, how PNECs are regulated to achieve this role remains poorly understood. Here we show that in the adult mouse airway, inactivation of achaete-scute-like protein 1 gene in PNECs led to loss of these cells. Intriguingly, exposure of these mutants to house dust mites (HDM), a common allergen, led to reappearance of PNECs. Similarly, exposure of wild-type mice to HDM led to PNEC hyperplasia, a result of proliferation of existing PNECs and transdifferentiation from club cells. Single-cell RNA-Seq experiments revealed PNEC heterogeneity, including the emergence of an allergen-induced PNEC subtype. Notch signaling was downregulated in HDM-treated airway, and treatment with Notch agonist prevented PNEC hyperplasia. These findings together suggest that HDM-induced...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/56j9j61x</guid>
      <pubDate>Thu, 14 Aug 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Kim, Estelle</name>
      </author>
      <author>
        <name>Wells, Brian K</name>
      </author>
      <author>
        <name>Indralingam, Hannah</name>
      </author>
      <author>
        <name>Su, Yujuan</name>
        <uri>https://orcid.org/0009-0009-9163-9996</uri>
      </author>
      <author>
        <name>Verheyden, Jamie</name>
      </author>
      <author>
        <name>Sun, Xin</name>
      </author>
    </item>
    <item>
      <title>Adverse pregnancy outcomes across SLE subgroups: significance of cardiovascular events</title>
      <link>https://escholarship.org/uc/item/3j1093sk</link>
      <description>OBJECTIVE: SLE is associated with increased risks of maternal cardiovascular events (CVEs) as well as adverse pregnancy outcomes. The influence of maternal CVEs on pregnancy complications in lupus is not clearly known. Our primary aim was to assess the risks of adverse pregnancy outcomes in individuals with SLE, specifically examining the influence of CVEs.
METHODS: Using a California population-based birth cohort from 2005 to 2020, pregnant individuals with SLE were identified via International Classification of Diseases codes on maternal discharge records and further subdivided based on whether they had lupus nephritis (LN) or antiphospholipid syndrome (APS). We analysed adjusted relative risks (aRRs) of adverse pregnancy outcomes in SLE subgroups, comparing those with and without CVEs, to the reference group of pregnant individuals without autoimmune rheumatic diseases or APS and CVEs. CVEs were broadly defined to encompass thromboembolic and cardiovascular conditions associated...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/3j1093sk</guid>
      <pubDate>Mon, 11 Aug 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Dhital, Rashmi</name>
      </author>
      <author>
        <name>Baer, Rebecca J</name>
        <uri>https://orcid.org/0000-0001-8485-1977</uri>
      </author>
      <author>
        <name>Kalunian, Kenneth</name>
      </author>
      <author>
        <name>Chambers, Christina</name>
        <uri>https://orcid.org/0000-0003-4675-7722</uri>
      </author>
    </item>
    <item>
      <title>Lower Adherence to Breastfeeding Recommendations in Mothers Treated With Antirheumatic and Antidepressant Medications</title>
      <link>https://escholarship.org/uc/item/34z8b9cm</link>
      <description>BACKGROUND: Exclusive breastfeeding for 6 months is recommended, but breastfeeding safety data is insufficient for several medications.
AIM: To determine if mothers treated with chronic medications are less likely to breastfeed.
METHODS: For this secondary analysis, 6383 pregnant women in the MotherToBaby cohort recruited from the United States and Canada between 2010 and 2022 were included. Participants treated with antirheumatic medications (ARM), selective serotonin reuptake inhibitors (SSRIs), and asthma medications during pregnancy were divided into two groups based on their medication use: continuers and discontinuers. Breastfeeding initiation, supplementation with commercial milk formula, and discontinuation of breastfeeding before 6 months were compared between those exposed and unexposed to medication use. Adjusted risk and hazard ratios (aRR, aHR) and 95% Confidence Intervals (CI) were calculated with modified Poisson and Cox regressions adjusted for year, parity, socioeconomic...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/34z8b9cm</guid>
      <pubDate>Mon, 11 Aug 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Heinonen, Essi Whaites</name>
      </author>
      <author>
        <name>Johnson, Diana L</name>
      </author>
      <author>
        <name>Todd, Alec</name>
      </author>
      <author>
        <name>Chambers, Christina D</name>
        <uri>https://orcid.org/0000-0003-4675-7722</uri>
      </author>
    </item>
    <item>
      <title>Thromboprophylaxis for Critically Ill Adolescents: A Multicenter Case-Control Study From the Children’s Healthcare Advancements in Thrombosis Consortium</title>
      <link>https://escholarship.org/uc/item/21f5q8p1</link>
      <description>OBJECTIVES: To determine if thromboprophylaxis, including pharmacologic, mechanical, or in combination, is associated with a hospital-acquired venous thromboembolism (HA-VTE) risk reduction among critically ill adolescents.
DESIGN: Multicenter case-control study from the Children's Healthcare Advancements in Thrombosis Consortium Registry and VTE risk-model validation study from January 2012 to July 2022.
SETTING: Thirty-two North American PICUs.
PATIENTS: Critically ill adolescents 12-19 years old including cases with radiographically confirmed HA-VTE (i.e., pulmonary embolism and deep venous thrombosis) and controls without HA-VTE.
INTERVENTIONS: Pharmacologic (i.e., prophylactic anticoagulation) and mechanical (i.e., intermittent pneumatic compression) thromboprophylaxis.
MEASUREMENTS AND MAIN RESULTS: Of 163 cases and 975 controls, 7.6% received pharmacologic, 23.5% mechanical, and 9.2% pharmacologic and mechanical thromboprophylaxis. Compared with controls, cases more frequently...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/21f5q8p1</guid>
      <pubDate>Mon, 4 Aug 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Vallabhaneni, Nikhil</name>
      </author>
      <author>
        <name>Jaffray, Julie</name>
        <uri>https://orcid.org/0000-0002-1175-7266</uri>
      </author>
      <author>
        <name>Branchford, Brian R</name>
      </author>
      <author>
        <name>Betensky, Marisol</name>
      </author>
      <author>
        <name>Stillings, Amy</name>
        <uri>https://orcid.org/0000-0002-0153-0279</uri>
      </author>
      <author>
        <name>Krava, Emily</name>
      </author>
      <author>
        <name>Alleyne, Maua M</name>
      </author>
      <author>
        <name>Ashour, Dina</name>
      </author>
      <author>
        <name>Goldenberg, Neil A</name>
      </author>
      <author>
        <name>Sochet, Anthony A</name>
      </author>
    </item>
    <item>
      <title>Testing Higher Doses of Sildenafil to Repair Brain Injury Secondary to Birth Asphyxia: An Open-Label Dose-Finding Phase 1b Clinical Trial–Sildenafil Administration to Treat Neonatal Encephalopathy–Study 02</title>
      <link>https://escholarship.org/uc/item/2sh4w1b5</link>
      <description>OBJECTIVE: To evaluate the safety and tolerability of higher doses of sildenafil in neonates with hypoxic-ischemic encephalopathy (HIE) and brain injury.
STUDY DESIGN: A phase 1b open-label dose-finding clinical trial in neonates with moderate-severe HIE and confirmed brain injury on a day-2 magnetic resonance imaging during therapeutic hypothermia (TH). Enteral sildenafil was administered every 12 hours (q12 h) for 7 days. All participants received an initial dose 2.0 mg/kg, and a second dose of 2.5 mg/kg. Starting from the third dose, group 1 received 2.5 mg/kg q12 h and group 2 received 3.0 mg/kg q12 h. Primary outcome was incidence of dose-limiting toxicities. Secondary outcomes explored day-30 neuroimaging and 18-month neurodevelopment.
RESULTS: Among the 30 neonates born between October 2019 and December 2021, 20 displayed day-2 brain injury and 13 received sildenafil (8 in group 1; 5 in group 2). In group 1, 25% (2/8) experienced transient hypotension after the first dose,...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/2sh4w1b5</guid>
      <pubDate>Fri, 18 Jul 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Wintermark, Pia</name>
      </author>
      <author>
        <name>Lapointe, Anie</name>
      </author>
      <author>
        <name>Altit, Gabriel</name>
      </author>
      <author>
        <name>Steinhorn, Robin</name>
      </author>
      <author>
        <name>Rampakakis, Emmanouil</name>
      </author>
      <author>
        <name>Meid, Andreas D</name>
      </author>
      <author>
        <name>Burhenne, Jürgen</name>
      </author>
      <author>
        <name>Bajraktari-Sylejmani, Gzona</name>
      </author>
      <author>
        <name>Khairy, May</name>
      </author>
      <author>
        <name>Adamo, Marie-Therese</name>
      </author>
      <author>
        <name>Gilbert, Guillaume</name>
      </author>
      <author>
        <name>Toffoli, Daniela</name>
      </author>
      <author>
        <name>Zavalkoff, Samara</name>
      </author>
      <author>
        <name>Luu, Thuy Mai</name>
      </author>
      <author>
        <name>Hailu, Elizabeth</name>
      </author>
      <author>
        <name>Haefeli, Walter E</name>
      </author>
    </item>
    <item>
      <title>A Pediatric Cardiac Shape Atlas: Insights into the Structure of Young Healthy Hearts</title>
      <link>https://escholarship.org/uc/item/64t920s1</link>
      <description>A Pediatric Cardiac Shape Atlas: Insights into the Structure of Young Healthy Hearts</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/64t920s1</guid>
      <pubDate>Thu, 17 Jul 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Qi, Anna</name>
      </author>
      <author>
        <name>Kim, Chris</name>
      </author>
      <author>
        <name>Young, Nathan</name>
      </author>
      <author>
        <name>Yu, Xiaoyang</name>
      </author>
      <author>
        <name>Crabb, Brendan T</name>
      </author>
      <author>
        <name>Schuchardt, Eleanor L</name>
      </author>
      <author>
        <name>Hegde, Sanjeet</name>
      </author>
      <author>
        <name>Mauger, Charlène</name>
      </author>
      <author>
        <name>Young, Alistair A</name>
      </author>
      <author>
        <name>Omens, Jeffrey H</name>
        <uri>https://orcid.org/0000-0002-6851-0977</uri>
      </author>
      <author>
        <name>McCulloch, Andrew D</name>
        <uri>https://orcid.org/0000-0002-1708-5675</uri>
      </author>
      <author>
        <name>Narayan, Hari K</name>
      </author>
    </item>
    <item>
      <title>Quantifying the contribution of the rare biosphere to natural disturbances</title>
      <link>https://escholarship.org/uc/item/32m3f47r</link>
      <description>Understanding how populations respond to disturbances represents a major goal for microbial ecology. While several hypotheses have been advanced to explain microbial community compositional changes in response to disturbance, appropriate data to test these hypotheses is scarce, due to the challenges in delineating rare vs. abundant taxa and generalists vs. specialists, a prerequisite for testing the theories. Here, we operationally define these two key concepts by employing the patterns of coverage of a (target) genome by a metagenome to identify rare populations, and by borrowing the proportional similarity index from macroecology to identify generalists. We applied these concepts to time-series (field) metagenomes from the Piver's Island Coastal Observatory to establish that coastal microbial communities are resilient to major perturbations such as tropical cyclones and (uncommon) cold or warm temperature events, in part due to the response of rare populations. Therefore, these...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/32m3f47r</guid>
      <pubDate>Thu, 17 Jul 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Zhao, Jianshu</name>
        <uri>https://orcid.org/0000-0002-2586-3852</uri>
      </author>
      <author>
        <name>Brandt, Genevieve</name>
      </author>
      <author>
        <name>Gronniger, Jessica L</name>
      </author>
      <author>
        <name>Wang, Zhao</name>
      </author>
      <author>
        <name>Li, Jiaqian</name>
      </author>
      <author>
        <name>Hunt, Dana E</name>
      </author>
      <author>
        <name>Rodriguez-R, Luis M</name>
      </author>
      <author>
        <name>Hatt, Janet K</name>
      </author>
      <author>
        <name>Konstantinidis, Konstantinos T</name>
      </author>
    </item>
    <item>
      <title>Behavioral evidence of emotion dysregulation in binge eaters</title>
      <link>https://escholarship.org/uc/item/79m3q0j1</link>
      <description>Binge eating is the most common disordered eating symptom and can lead to the development of obesity. Previous self-report research has supported the hypothesis that individuals who binge eat report greater levels of general emotion dysregulation, which may facilitate binge-eating behavior. However, to date, no study has experimentally tested the relation between binge eating history and in-vivo emotion dysregulation. To do this, a sample of female college students who either endorsed binge eating (n&amp;nbsp;=&amp;nbsp;40) or denied the presence of any eating pathology (n&amp;nbsp;=&amp;nbsp;47) completed the Difficulties with Emotion Regulation Scale (DERS) and a behavioral distress tolerance task (the Paced Auditory Serial Addition Task-Computer: PASAT-C) known to induce negative affect and distress. The binge eating group was 2.96 times more likely to quit the PASAT-C early (χ&lt;sup&gt;2&lt;/sup&gt;&amp;nbsp;=&amp;nbsp;5.04, p&amp;nbsp;=&amp;nbsp;0.025) and reported greater irritability (F(1,84)&amp;nbsp;=&amp;nbsp;7.09 p&amp;nbsp;=&amp;nbsp;0.009)...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/79m3q0j1</guid>
      <pubDate>Mon, 14 Jul 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Eichen, Dawn M</name>
        <uri>https://orcid.org/0000-0001-5619-2177</uri>
      </author>
      <author>
        <name>Chen, Eunice</name>
      </author>
      <author>
        <name>Boutelle, Kerri N</name>
        <uri>https://orcid.org/0000-0002-9573-4765</uri>
      </author>
      <author>
        <name>McCloskey, Michael S</name>
      </author>
    </item>
    <item>
      <title>Design of the SHARE study: A randomized controlled trial evaluating the regulation of cues treatment for adults with overweight or obesity and high food responsiveness</title>
      <link>https://escholarship.org/uc/item/1k85m4vr</link>
      <description>Obesity is a heterogeneous disease influenced by individual behavioral factors, environment, genes, and neural processes. Behavioral weight loss (BWL), the current gold-standard treatment for overweight and obesity (OW/OB), does not produce sustained weight loss for all individuals. Appetitive traits, such as food responsiveness (FR), are risk factors that could account for differences in how individuals interact with today's food environment and increase susceptibility for overeating and weight gain. Research shows that individuals high in FR have attenuated weight loss in BWL programs. We developed the Regulation of Cues (ROC) program to reduce overeating through improving sensitivity to hunger and satiety cues and decreasing FR. In this study, we combined ROC with BWL recommendations (ROC+BWL), a treatment approach that may address the unique needs of this phenotype. The current study is a 3-arm randomized controlled trial comparing the ROC+BWL program to BWL and an active...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/1k85m4vr</guid>
      <pubDate>Fri, 11 Jul 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Boutelle, Kerri N</name>
        <uri>https://orcid.org/0000-0002-9573-4765</uri>
      </author>
      <author>
        <name>Eichen, Dawn M</name>
        <uri>https://orcid.org/0000-0001-5619-2177</uri>
      </author>
      <author>
        <name>Obayashi, Saori</name>
      </author>
      <author>
        <name>Pasquale, Ellen K</name>
      </author>
      <author>
        <name>Strong, David R</name>
        <uri>https://orcid.org/0000-0002-5383-9032</uri>
      </author>
      <author>
        <name>Tietz, Allison S</name>
      </author>
      <author>
        <name>Reed, Kristie L</name>
      </author>
      <author>
        <name>Peterson, Carol B</name>
      </author>
    </item>
    <item>
      <title>Predictors of parent self-monitoring patterns in a family-based behavioral weight loss treatment program</title>
      <link>https://escholarship.org/uc/item/0k5674km</link>
      <description>ObjectiveSelf-monitoring dietary intake is a critical component of family-based intensive health behavior and lifestyle treatment for pediatric obesity, but adherence rates are often low. This study identifies predictors of parent self-monitoring rates during treatment.MethodsA secondary analysis of parent self-monitoring data from a randomized controlled trial involving 150 parent-child dyads. Patterns of self-monitoring were identified using a latent class mixed model approach. Logistic regression analyses evaluated predictors of self-monitoring patterns.ResultsLatent class models identified two trajectory groups: a high consistent self-monitoring group and a low-decreasing self-monitoring group. When compared to parents in the low group, parents in the high group lost more weight throughout treatment. Children in the high group had a similar trajectory for weight loss; however, the groups were not statistically different. Higher levels of family chaos and poorer family problem-solving...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/0k5674km</guid>
      <pubDate>Fri, 11 Jul 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Boutelle, Kerri N</name>
        <uri>https://orcid.org/0000-0002-9573-4765</uri>
      </author>
      <author>
        <name>Kang Sim, D Eastern</name>
      </author>
      <author>
        <name>Eichen, Dawn M</name>
        <uri>https://orcid.org/0000-0001-5619-2177</uri>
      </author>
      <author>
        <name>Manzano, Michael A</name>
      </author>
      <author>
        <name>Rhee, Kyung E</name>
        <uri>https://orcid.org/0000-0001-5816-5869</uri>
      </author>
      <author>
        <name>Strong, David R</name>
        <uri>https://orcid.org/0000-0002-5383-9032</uri>
      </author>
    </item>
    <item>
      <title>Cellular heterogeneity and patterning strategies as revealed by upper respiratory epithelium single cell atlas</title>
      <link>https://escholarship.org/uc/item/32w135k3</link>
      <description>The upper respiratory tract, spanning the pharyngolaryngeal to tracheobronchial regions, enables breathing, vocalization, and frontline defense against airborne insults. We generated a cellular and molecular atlas of the mouse upper respiratory epithelium from pharynx/larynx to tracheobronchial carina by combining single-cell RNA sequencing with spatial validation. Our analysis revealed 18 epithelial cell types, organized into three spatially distinct compartments: &lt;i&gt;Tmprss11a&lt;/i&gt;+ pharyngolaryngeal, &lt;i&gt;Nkx2-1&lt;/i&gt;+ tracheobronchial, and &lt;i&gt;Dmbt1&lt;/i&gt;+ submucosal glands. Stratified squamous pharyngolaryngeal zones displayed extensive and region-specific Keratin codes. Within the pseudostratified tracheobronchial epithelium, diverse luminal cells, including multiple varieties of club cells, exhibit marker-expression gradients along the proximal-distal axes. Lastly, analysis of the submucosal gland epithelium -which contains various cell types, including distinctive myoepithelial...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/32w135k3</guid>
      <pubDate>Mon, 7 Jul 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Foote, Alexander G</name>
        <uri>https://orcid.org/0000-0002-3676-4091</uri>
      </author>
      <author>
        <name>Sun, Xin</name>
      </author>
    </item>
    <item>
      <title>Addressing population-level cancer data needs in northwestern Mexico: results from a South–South Colombian–Mexican partnership</title>
      <link>https://escholarship.org/uc/item/59g568ww</link>
      <description>"South-South" partnerships forged between institutions in resource-constrained settings, usually in low- and middle-income countries, provide innovative frameworks for resource, knowledge, and expertise exchanges to address public health challenges in regions sharing similar contexts. Population-based cancer registries (PBCRs) and surveillance systems in low- and middle-income countries are essential for cancer control, yet they are scarce. In response, the authors formed a South-South Colombian-Mexican partnership to implement the first PBCR in Tijuana, northwestern Mexico, and an integrated pediatric cancer real-time clinical outcomes monitoring system, replicated from Colombia's successful model, VIGICANCER. The newly established team assessed local needs in Mexico, adapted VIGICANCER protocols to the local context, and conducted training. In 2017, BajaREG was inaugurated in Tijuana, and, in 2018, joined the newly launched Mexican National Cancer Registry Network. In 2020,...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/59g568ww</guid>
      <pubDate>Thu, 19 Jun 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Rivera-Gómez, Rebeca</name>
      </author>
      <author>
        <name>Bolivar, Santiago</name>
      </author>
      <author>
        <name>Zazueta, Oscar E</name>
      </author>
      <author>
        <name>Piedrahita, Vivian</name>
      </author>
      <author>
        <name>Bravo, Luis</name>
      </author>
      <author>
        <name>Rangel, Gudelia</name>
      </author>
      <author>
        <name>Roberts, William</name>
      </author>
      <author>
        <name>Ramirez, Oscar</name>
      </author>
      <author>
        <name>Aristizabal, Paula</name>
      </author>
    </item>
    <item>
      <title>Identifying wastewater chemicals in coastal aerosols</title>
      <link>https://escholarship.org/uc/item/3vb185r4</link>
      <description>The Tijuana River, at the US-Mexico border, discharges millions of gallons of wastewater daily-sewage, industrial waste, and runoff-into the Pacific Ocean, making it the dominant source of coastal pollution in this region. This study examines how such wastewater influences coastal aerosols by tracking spatial gradients from near the border northward. Using benzoylecgonine (a nonvolatile cocaine metabolite) as a sewage tracer, we find that wastewater compounds-including a mixture of illicit drugs, drug metabolites, and chemicals from tires and personal care products-become aerosolized and are detectable in both water and air. Spatial analyses confirm that most measured chemicals concentrate in aerosols near the Tijuana River, potentially exposing local populations to tens of nanograms per hour (e.g., octinoxate and methamphetamine) via inhalation. This airborne pathway highlights a largely overlooked source of atmospheric pollution, emphasizing the need to reassess health risks...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/3vb185r4</guid>
      <pubDate>Thu, 19 Jun 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Cooper, Adam</name>
      </author>
      <author>
        <name>Cancelada, Lucia</name>
        <uri>https://orcid.org/0000-0002-7438-9587</uri>
      </author>
      <author>
        <name>Torres, Ralph Riley</name>
      </author>
      <author>
        <name>Belcher, Kathryn</name>
      </author>
      <author>
        <name>Small, Mallory</name>
      </author>
      <author>
        <name>Belda-Ferre, Pedro</name>
      </author>
      <author>
        <name>Morris, Clare</name>
      </author>
      <author>
        <name>Mitts, Brock</name>
      </author>
      <author>
        <name>Dinasquet, Julie</name>
      </author>
      <author>
        <name>Knight, Rob</name>
        <uri>https://orcid.org/0000-0002-0975-9019</uri>
      </author>
      <author>
        <name>Slade, Jonathan H</name>
      </author>
      <author>
        <name>Prather, Kimberly A</name>
        <uri>https://orcid.org/0000-0003-3048-9890</uri>
      </author>
    </item>
    <item>
      <title>2019 Hope Babette Tang Humanism in Healthcare Essay Contest: First Place Medical Student Essay: The Healing Yellow Raincoat.</title>
      <link>https://escholarship.org/uc/item/6mt405g2</link>
      <description>2019 Hope Babette Tang Humanism in Healthcare Essay Contest: First Place Medical Student Essay: The Healing Yellow Raincoat.</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/6mt405g2</guid>
      <pubDate>Tue, 10 Jun 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Butler, April</name>
        <uri>https://orcid.org/0000-0002-0195-4397</uri>
      </author>
    </item>
    <item>
      <title>Youth Survivors of Human Trafficking: On Improving Healthcare Access and Treatment</title>
      <link>https://escholarship.org/uc/item/9cn1q2hw</link>
      <description>Youth Survivors of Human Trafficking: On Improving Healthcare Access and Treatment</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/9cn1q2hw</guid>
      <pubDate>Sun, 8 Jun 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Titchen, Kanani</name>
      </author>
    </item>
    <item>
      <title>Labor Trafficking and Commercial Sexual Exploitation</title>
      <link>https://escholarship.org/uc/item/4tk1d71j</link>
      <description>Labor Trafficking and Commercial Sexual Exploitation</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/4tk1d71j</guid>
      <pubDate>Sun, 8 Jun 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Titchen, Kanani E</name>
      </author>
    </item>
    <item>
      <title>Severe hepatitis in pediatric patients: The Severe Hepatitis In Pediatric Patients (SHIPP) registry</title>
      <link>https://escholarship.org/uc/item/783133rx</link>
      <description>OBJECTIVES: Clusters of severe acute hepatitis in children were reported worldwide beginning in October 2021. Although most children recovered, some progressed to liver failure leading to death or liver transplantation. Herein, we characterize the clinical characteristics, and outcomes of this group of children through an international collaborative effort.
METHODS: Participation was solicited via a global listserv to pediatric gastroenterologists worldwide. Patients &amp;lt;18 years, alanine aminotransferase &amp;gt;500 U/L, without chronic liver disease or acetaminophen ingestion were eligible. Data were submitted by individual sites into a Research Electronic Data Capture registry created in July 2022.
RESULTS: Two hundred and seven cases were collected, with a peak incidence of 28 in April 2022. The median age was 40 months, 52.7% were male, 63.3% were white, and 44% were Hispanic. At presentation, 80% reported gastrointestinal symptoms followed by fever (27.7%). The median duration...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/783133rx</guid>
      <pubDate>Fri, 6 Jun 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Kehar, Mohit</name>
      </author>
      <author>
        <name>Black, Katherine</name>
      </author>
      <author>
        <name>Chu, Christopher</name>
      </author>
      <author>
        <name>Kohli, Rohit</name>
      </author>
      <author>
        <name>Mohammad, Saeed</name>
      </author>
      <author>
        <name>Alrabadi, Leina</name>
      </author>
      <author>
        <name>Amendola, Maria</name>
      </author>
      <author>
        <name>Aqul, Amal</name>
      </author>
      <author>
        <name>Husu, Anna Banc</name>
      </author>
      <author>
        <name>Beretta, Marisa R</name>
      </author>
      <author>
        <name>Chapin, Catherine</name>
      </author>
      <author>
        <name>Cheng, Katherine</name>
      </author>
      <author>
        <name>Diamond, Tamir</name>
      </author>
      <author>
        <name>Goldstein, Matthew</name>
      </author>
      <author>
        <name>Gumm, Alexis</name>
      </author>
      <author>
        <name>Guttman, Orlee</name>
      </author>
      <author>
        <name>Gupta, Nitika</name>
      </author>
      <author>
        <name>Hildreth, Amber</name>
      </author>
      <author>
        <name>Benabe, Stefany Hernandez</name>
      </author>
      <author>
        <name>Kohut, Taisa</name>
      </author>
      <author>
        <name>Mackling, Jody</name>
      </author>
      <author>
        <name>Mulder, Daniel</name>
      </author>
      <author>
        <name>Narang, Amrita</name>
      </author>
      <author>
        <name>O'Donnell, Jonathan EM</name>
      </author>
      <author>
        <name>Ovchinsky, Nadia</name>
      </author>
      <author>
        <name>Pai, Anita</name>
      </author>
      <author>
        <name>Raghu, Vikram</name>
      </author>
      <author>
        <name>Swadera, Sheetal</name>
      </author>
      <author>
        <name>Waheed, Nadia</name>
      </author>
      <author>
        <name>Watson, Jessica</name>
      </author>
      <author>
        <name>Wood, Phoebe</name>
      </author>
    </item>
    <item>
      <title>Model of metabolism and gene expression predicts proteome allocation in Pseudomonas putida</title>
      <link>https://escholarship.org/uc/item/0ph555rd</link>
      <description>The genome-scale model of metabolism and gene expression (ME-model) for Pseudomonas putida KT2440, iPpu1676-ME, provides a comprehensive representation of biosynthetic costs and proteome allocation. Compared to a metabolic-only model, iPpu1676-ME significantly expands on gene expression, macromolecular assembly, and cofactor utilization, enabling accurate growth predictions without additional constraints. Multi-omics analysis using RNA sequencing and ribosomal profiling data revealed translational prioritization in P. putida, with core pathways, such as nicotinamide biosynthesis and queuosine metabolism, exhibiting higher translational efficiency, while secondary pathways displayed lower priority. Notably, the ME-model significantly outperformed the M-model in alignment with multi-omics data, thereby validating its predictive capacity. Thus, iPpu1676-ME offers valuable insights into P. putida’s proteome allocation and presents a powerful tool for understanding resource allocation...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/0ph555rd</guid>
      <pubDate>Thu, 5 Jun 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Tibocha-Bonilla, Juan D</name>
      </author>
      <author>
        <name>Gandhi, Vishant</name>
      </author>
      <author>
        <name>Lieng, Chloe</name>
        <uri>https://orcid.org/0009-0009-9424-0016</uri>
      </author>
      <author>
        <name>Moyne, Oriane</name>
      </author>
      <author>
        <name>Santibáñez-Palominos, Rodrigo</name>
      </author>
      <author>
        <name>Zengler, Karsten</name>
      </author>
    </item>
    <item>
      <title>Phylogeographic and genetic network assessment of COVID-19 mitigation protocols on SARS-CoV-2 transmission in university campus residences</title>
      <link>https://escholarship.org/uc/item/9t12820z</link>
      <description>BACKGROUND: Congregate living provides an ideal setting for SARS-CoV-2 transmission in which many outbreaks and superspreading events occurred. To avoid large outbreaks, universities turned to remote operations during the initial COVID-19 pandemic waves in 2020 and 2021. In late-2021, the University of California San Diego (UC San Diego) facilitated the return of students to campus with comprehensive testing, vaccination, masking, wastewater surveillance, and isolation policies.
METHODS: We performed molecular epidemiological and phylogeographic analysis of 4418 SARS-CoV-2 genomes sampled from UC San Diego students during the Omicron waves between December 2021 and September 2022, representing 58% of students with confirmed SARS-CoV-2 infection. We overlaid these analyses across on-campus residential information to assess the spread and persistence of SARS-CoV-2 within university residences.
FINDINGS: Within campus residences, SARS-CoV-2 transmission was frequent among students...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/9t12820z</guid>
      <pubDate>Thu, 22 May 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Wertheim, Joel O</name>
      </author>
      <author>
        <name>Vasylyeva, Tetyana I</name>
        <uri>https://orcid.org/0000-0002-9736-7022</uri>
      </author>
      <author>
        <name>Wood, Robert J</name>
      </author>
      <author>
        <name>Cantrell, Kalen</name>
      </author>
      <author>
        <name>Contreras, Soraya Piña</name>
      </author>
      <author>
        <name>Feldheim, Aryeh</name>
      </author>
      <author>
        <name>Goyal, Ravi</name>
        <uri>https://orcid.org/0000-0002-0358-2435</uri>
      </author>
      <author>
        <name>Havens, Jennifer L</name>
      </author>
      <author>
        <name>Knight, Rob</name>
        <uri>https://orcid.org/0000-0002-0975-9019</uri>
      </author>
      <author>
        <name>Laurent, Louise C</name>
        <uri>https://orcid.org/0000-0002-2095-7534</uri>
      </author>
      <author>
        <name>Moshiri, Niema</name>
        <uri>https://orcid.org/0000-0003-2209-8128</uri>
      </author>
      <author>
        <name>Neuhard, Robert</name>
      </author>
      <author>
        <name>Sathe, Shashank</name>
      </author>
      <author>
        <name>Satterlund, Alysson</name>
      </author>
      <author>
        <name>Scioscia, Angela</name>
      </author>
      <author>
        <name>Song, Angela Y</name>
      </author>
      <author>
        <name>Alliance, SEARCH</name>
      </author>
      <author>
        <name>Aigner, Stefan</name>
        <uri>https://orcid.org/0000-0002-9511-3328</uri>
      </author>
      <author>
        <name>Andersen, Kristian G</name>
      </author>
      <author>
        <name>Baer, Nathan A</name>
      </author>
      <author>
        <name>Betty, Maryann</name>
      </author>
      <author>
        <name>Birmingham, Amanda</name>
        <uri>https://orcid.org/0000-0002-4117-3317</uri>
      </author>
      <author>
        <name>Castro-Martinez, Anelizze</name>
      </author>
      <author>
        <name>Cheung, Willi</name>
      </author>
      <author>
        <name>De Hoff, Peter</name>
      </author>
      <author>
        <name>Fisch, Kathleen M</name>
        <uri>https://orcid.org/0000-0002-0117-7444</uri>
      </author>
      <author>
        <name>King, Alison J</name>
      </author>
      <author>
        <name>Gangavarapu, Karthik</name>
      </author>
      <author>
        <name>Hakim, Abbas</name>
      </author>
      <author>
        <name>Henson, Benjamin</name>
      </author>
      <author>
        <name>Jepsen, Kristen</name>
      </author>
      <author>
        <name>Mac, Christina H</name>
      </author>
      <author>
        <name>Ngo, Toan T</name>
      </author>
      <author>
        <name>Nguyen, Kelly N</name>
      </author>
      <author>
        <name>Ostrander, Tyler R</name>
      </author>
      <author>
        <name>Perkins, Sarah</name>
      </author>
      <author>
        <name>Plascencia, Ashley</name>
      </author>
      <author>
        <name>Rivera, Andrea</name>
      </author>
      <author>
        <name>Rivera, Ariana</name>
        <uri>https://orcid.org/0009-0001-8732-8863</uri>
      </author>
      <author>
        <name>Salido, Rodolfo A</name>
      </author>
      <author>
        <name>Saucedo, Kieran C</name>
      </author>
      <author>
        <name>Schwab, Madison</name>
      </author>
      <author>
        <name>Steedman, Allison L</name>
      </author>
      <author>
        <name>Veder, Anthony</name>
        <uri>https://orcid.org/0009-0000-6708-9538</uri>
      </author>
      <author>
        <name>Weiss, Alana</name>
      </author>
      <author>
        <name>Yeo, Gene W</name>
      </author>
      <author>
        <name>Zeller, Mark</name>
      </author>
      <author>
        <name>Schooley, Robert T</name>
      </author>
      <author>
        <name>Anderson, Cheryl M</name>
      </author>
      <author>
        <name>Martin, Natasha K</name>
      </author>
    </item>
    <item>
      <title>Wastewater-integrated pathogen surveillance dashboards enable real-time, transparent, and interpretable public health risk assessment and dissemination</title>
      <link>https://escholarship.org/uc/item/8n39p0qj</link>
      <description>Timely pathogen surveillance and reporting is essential for effective public health guidance. Web dashboards have become a key tool for communicating public health information to stakeholders, health care workers, and the broader community. Over the SARS-CoV-2 pandemic, wastewater surveillance has increasingly been incorporated into public health workflows for outbreak monitoring and response, enabling community-representative and low-cost monitoring to supplement clinical surveillance. However, the methods used for visualization and dissemination of clinical and wastewater surveillance data differ across programs, and best practices are yet to be defined. In this work, we demonstrate data workflows and dashboards used to perform wastewater-based public health surveillance in tandem with clinical data across local and national scales, leveraging custom-built, reproducible, and open-source software. Using a centralized data aggregation and analysis hub approach, we establish multiple...</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/8n39p0qj</guid>
      <pubDate>Thu, 22 May 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Msomi, Nosihle S</name>
      </author>
      <author>
        <name>Levy, Joshua I</name>
      </author>
      <author>
        <name>Matteson, Nathaniel L</name>
      </author>
      <author>
        <name>Ndlovu, Nkosenhle</name>
      </author>
      <author>
        <name>Ntuli, Phindile</name>
      </author>
      <author>
        <name>Baer, Adam</name>
      </author>
      <author>
        <name>Pilz, Dylan</name>
      </author>
      <author>
        <name>Mabasa, Victor</name>
      </author>
      <author>
        <name>Gwala, Sipho</name>
      </author>
      <author>
        <name>Singh, Natasha</name>
      </author>
      <author>
        <name>Subramoney, Kathleen</name>
      </author>
      <author>
        <name>Phalane, Emmanuel</name>
      </author>
      <author>
        <name>Macheke, Mokgaetji</name>
      </author>
      <author>
        <name>Motloung, Mantshali</name>
      </author>
      <author>
        <name>Mangena, Thabo</name>
      </author>
      <author>
        <name>Monametsi, Lethabo</name>
      </author>
      <author>
        <name>Rabotapi, Lebohang</name>
      </author>
      <author>
        <name>Maposa, Sibonginkosi</name>
      </author>
      <author>
        <name>Birmingham, Amanda</name>
        <uri>https://orcid.org/0000-0002-4117-3317</uri>
      </author>
      <author>
        <name>Zeller, Mark</name>
      </author>
      <author>
        <name>Karthikeyan, Smruthi</name>
      </author>
      <author>
        <name>De Hoff, Peter</name>
      </author>
      <author>
        <name>Harris, Simon</name>
      </author>
      <author>
        <name>Knight, Rob</name>
        <uri>https://orcid.org/0000-0002-0975-9019</uri>
      </author>
      <author>
        <name>Laurent, Louise C</name>
        <uri>https://orcid.org/0000-0002-2095-7534</uri>
      </author>
      <author>
        <name>Andersen, Kristian G</name>
      </author>
      <author>
        <name>McCarthy, Kerrigan</name>
      </author>
      <author>
        <name>Yousif, Mukhlid</name>
      </author>
    </item>
    <item>
      <title>Frataxin Traps Low Abundance Quaternary Structure to Stimulate Human Fe–S Cluster Biosynthesis</title>
      <link>https://escholarship.org/uc/item/5m5672vb</link>
      <description>Iron-sulfur clusters are essential protein cofactors synthesized in human mitochondria by an NFS1-ISD11-ACP-ISCU2-FXN assembly complex. Surprisingly, researchers have discovered three distinct quaternary structures for cysteine desulfurase subcomplexes, which display similar interactions between NFS1-ISD11-ACP protomeric units but dramatically different dimeric interfaces between the protomers. Although the role of these different architectures is unclear, possible functions include regulating activity and promoting the biosynthesis of distinct sulfur-containing biomolecules. Here, crystallography, native ion-mobility mass spectrometry, and chromatography methods reveal the Fe-S assembly subcomplex exists as an equilibrium mixture of these different quaternary structures. Isotope labeling and native mass spectrometry experiments show that the NFS1-ISD11-ACP complexes disassemble into protomers, which can then undergo exchange reactions and dimerize to reform native complexes....</description>
      <guid isPermaLink="true">https://escholarship.org/uc/item/5m5672vb</guid>
      <pubDate>Thu, 22 May 2025 00:00:00 +0000</pubDate>
      <author>
        <name>Cory, Seth A</name>
      </author>
      <author>
        <name>Lin, Cheng-Wei</name>
      </author>
      <author>
        <name>Patra, Shachin</name>
      </author>
      <author>
        <name>Havens, Steven M</name>
      </author>
      <author>
        <name>Putnam, Christopher D</name>
        <uri>https://orcid.org/0000-0002-6145-1265</uri>
      </author>
      <author>
        <name>Shirzadeh, Mehdi</name>
      </author>
      <author>
        <name>Russell, David H</name>
      </author>
      <author>
        <name>Barondeau, David P</name>
      </author>
    </item>
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