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    <title>Recent ulab_phhs_2026 items</title>
    <link>https://escholarship.org/uc/ulab_phhs_2026/rss</link>
    <description>Recent eScholarship items from Research Publications, 2025-2026</description>
    <pubDate>Thu, 3 Sep 2026 00:41:13 +0000</pubDate>
    <item>
      <title>Environmental Pesticide Exposure, Structural Exclusion, and Epilepsy Care Utilization Disparities in Agricultural California</title>
      <link>https://escholarship.org/uc/item/9107t2gn</link>
      <description>California’s agriculture sector relies heavily on pesticides, with an estimated use of 176million pounds per year. While these pesticides do increase crop yield, long-term exposure toboth organophosphate and organochlorine pesticides has been found to result in variousneurological effects, such as epilepsy. We seek to explore the relationship between exposure to pesticides in agricultural areas of California and epilepsy, and to evaluate the role of structural determinants such as insurance coverage, lack of transportation, unstable housing, and distance from epilepsy specialists in terms of health care utilization. We seek to demonstrate the link between chronic pesticide exposure and increased susceptibility to epilepsy by analyzing studiesand public health surveillance data and by conducting a systematic review and meta-analysis of 14 studies. We found that uninsured patients have 86% lower access to specialty care, transportation barriers reduce access by 58%, and housing...</description>
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      <pubDate>Thu, 6 Aug 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Mahmud, Zarin</name>
      </author>
      <author>
        <name>Lam, Olivia</name>
      </author>
      <author>
        <name>Pham, Tianna</name>
      </author>
      <author>
        <name>Zhu, Elissa</name>
      </author>
      <author>
        <name>Bravo, Jazmin Luna</name>
      </author>
    </item>
    <item>
      <title>Non-Motor Consequences of Dopaminergic Therapy in Parkinson's Disease: A Systematic Review of Effects on Mood, Sleep, and Cognition</title>
      <link>https://escholarship.org/uc/item/6830j53b</link>
      <description>Parkinson's disease (PD) is commonly treated with dopaminergic therapies that effectivelyaddress motor symptoms; however, their effects on the non-motor aspects of one’s life remain underexplored. By systematically synthesizing data across mood, sleep, and cognition, this study intends to evaluate how levodopa, dopamine agonists, and monoamine oxidase B (MAO-B) inhibitors influence non-motor symptoms and overall quality of life in patients with PD. Data were collected from nine studies published between 1999 and 2025, spanning longitudinal observational, cross-sectional, within-subject ON/OFF, randomized crossover, systematic review, and case series designs to ensure that both the breadth and depth of current research are considered. Dopamine agonists are associated with reduced motivational and apathy symptoms, while MAO-B inhibitors are associated with reduced depressive symptoms; anxiety scores were higher in the ON medication state. Moreover, higher dopaminergic exposure was...</description>
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      <pubDate>Thu, 6 Aug 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Farhadian, Melina</name>
      </author>
      <author>
        <name>Park, Sarah</name>
      </author>
      <author>
        <name>Lee, Hannah</name>
      </author>
      <author>
        <name>Rana, Faria</name>
      </author>
      <author>
        <name>Sahoo, Fiona</name>
      </author>
      <author>
        <name>Kumar, Harini Suresh</name>
      </author>
      <author>
        <name>Yongho, Adrianne</name>
      </author>
    </item>
    <item>
      <title>Impact of Traumatic Brain Injury on Hippocampal Synaptic Plasticity and Memory Consolidation</title>
      <link>https://escholarship.org/uc/item/3904q12x</link>
      <description>Traumatic brain injury (TBI) causes a disturbance in hippocampal synaptic plasticity leading to deficits in episodic memory and spatial memory. In this review, we explore alterations in long-term potentiation (LTP) and long-term depression (LTD) that contribute to memory consolidation deficits. These alterations are associated with glutamate excitotoxicity, neuroinflammation, and network imbalance. Ultimately, the review provides evidence that these deficits are due to alterations in signaling rather than complete loss of these pathways.</description>
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      <pubDate>Thu, 6 Aug 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Kaur, Piyusha</name>
      </author>
      <author>
        <name>Hartman, Benjamin</name>
      </author>
      <author>
        <name>Vázquez, Montserrat</name>
      </author>
      <author>
        <name>Wong, Victoria</name>
      </author>
      <author>
        <name>Correa, Isabel</name>
      </author>
    </item>
    <item>
      <title>How does environmental quality during childhood and adolescence influence mental healthoutcomes in young adulthood?</title>
      <link>https://escholarship.org/uc/item/8vv483tv</link>
      <description>Climate change poses growing threats to public health, with mounting evidence linkingenvironmental exposures to various mental health outcomes. While climate change isincreasingly recognized as a threat to mental health with well-established research on acuteclimate disasters, less is understood about the psychological effects of environmental stressors experienced during upbringing. This study examined whether perceived environmental quality during childhood and adolescence, such as air quality, water quality, and access to green space, is associated with mental health outcomes in adulthood. Participants (n = 33) completed ananonymous online survey assessing self-reported environmental exposures alongside a modified Mental Health Inventory (MHI) measuring anxiety, depression, tension, and hopelessness. Statistics utilizing regression analysis revealed that participants reported moderate environmental quality and moderate levels of psychological distress. Results include significant...</description>
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      <pubDate>Fri, 17 Jul 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Krishnan, Ajay</name>
      </author>
      <author>
        <name>Cheng, Sophia</name>
      </author>
      <author>
        <name>Kwon, April</name>
      </author>
      <author>
        <name>Mirza, Safiyyah</name>
      </author>
    </item>
    <item>
      <title>Targeting KRAS-Mediated Pathways: Challenges of Feedback and Resistance</title>
      <link>https://escholarship.org/uc/item/7dx0t140</link>
      <description>KRAS mutations are among the most common oncogenic drivers in human cancer,affecting switch control pathways that regulate cell growth, survival, and metabolism. Mutations in KRAS interfere with this regulation by keeping the protein in an active state, which causes constant signaling and is linked to cancers like pancreatic, lung, and colorectal cancer. Although significant progress has been made in developing KRAS-target therapies, many approaches focus on static protein structures and may not fully capture its dynamic behavior within living cells. This paper investigates how KRAS mutations affect signaling pathways, with a particular focuson the MAPK pathway and its role in tumor progression and therapeutic resistance. Aliterature-based methodology was used, focusing on recent peer-reviewed studies with strong mechanistic and experimental evidence, while excluding outdated or non-translational models.The analysis shows that different intervention points in the MAPK signal transduction...</description>
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      <pubDate>Fri, 17 Jul 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Darbinian, Isabella</name>
      </author>
      <author>
        <name>Hsia, Harry</name>
      </author>
      <author>
        <name>Kasbari, Fedora</name>
      </author>
      <author>
        <name>Wu, Amy</name>
      </author>
    </item>
    <item>
      <title>Investigating Nucleotide Editing of Phosphorylated Tau Pathology as a Therapeutic Strategy for Alzheimer’s Disease</title>
      <link>https://escholarship.org/uc/item/4v84v965</link>
      <description>Alzheimer’s disease (AD) is an irreversible, progressive neurodegenerative disorder andthe leading cause of dementia worldwide, affecting nearly 55 million individuals. Hallmarkpathological features include extracellular amyloid-β plaques and intracellular neurofibrillary tangles composed of hyperphosphorylated tau protein. Despite decades of research, conventional therapeutic approaches targeting tau pathology, including kinase inhibitors, phosphatase activators, and tau aggregation modulators, have demonstrated limited clinical success and primarily address symptoms rather than underlying disease mechanisms. Recent advances in programmable nucleotide editing technologies, including CRISPR-Cas9, base editing, and prime editing, offer promising strategies for both investigating and therapeutically targeting tau-related pathology at the genomic level. This literature review examines the application of CRISPR-based technologies in neuronal cell models, animal models, and induced...</description>
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      <pubDate>Fri, 17 Jul 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Phan, Natalie W.</name>
      </author>
      <author>
        <name>Fukushima, Yasmin</name>
      </author>
      <author>
        <name>Pesala, Dheeraj</name>
      </author>
      <author>
        <name>Sarathy, Meghna</name>
      </author>
      <author>
        <name>Shadab, Nesarulhaq</name>
      </author>
      <author>
        <name>Jiminez-Uribe, Lilian</name>
      </author>
    </item>
    <item>
      <title>Impacts of a High-Fat Diet on Juveniles</title>
      <link>https://escholarship.org/uc/item/3fh3f21b</link>
      <description>Childhood obesity and metabolic disorders have risen sharply as the consumption ofhigh-fat diets (HFDs) increases, yet the neurocognitive consequences - specifically during the juvenile development window - remain under-researched. This paper synthesizes current literature to examine how HFD-induced metabolic shifts suppress brain-derived neurotrophic factor (BDNF) in the hippocampus, leading to impaired learning and memory independent of body weight. Our analysis identifies dual-pathway mechanism of suppression: first, HFD-driven gut dysbiosis reduces the production of microbial short-chain fatty acids (SCFAs), particularly butyrate, hence limiting the histone deacetylase (HDAC) inhibition required for BDNF gene expression. Second, HFD consumption chronically elevates corticosterone levels, which directly downregulates BDNF mRNA and increases neuroinflammation. Synthesis of rodent modelsreveals that these molecular changes manifest as structural hippocampal shrinkage andbehavioral...</description>
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      <pubDate>Fri, 17 Jul 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Kith, Natalie</name>
      </author>
      <author>
        <name>Dinh, Amy</name>
      </author>
      <author>
        <name>Franco, Jarely</name>
      </author>
      <author>
        <name>Ma, Jade</name>
      </author>
      <author>
        <name>Wang, Audrey</name>
      </author>
    </item>
    <item>
      <title>Beyond Intraocular Pressure: A Multifactorial Analysis of Primary Open-Angle Glaucoma (POAG) Risk and Progression</title>
      <link>https://escholarship.org/uc/item/38j239z2</link>
      <description>In this paper, we will focus on the demographic and clinical factors that cause open-angleglaucoma. Open-angle glaucoma is a progressive eye disease that increases intraocular pressure (IOP), eventually leading to optic nerve damage and vision loss. Currently, researchers have focused on IOP,depression, sleep apnea, and decreased outer nasal macular perfusion density as strong clinical indicators of glaucoma. Conditions like depression can lead to chronic stress physiology changes, leading to IOP. Sleep apnea is associated with intermittent hypoxia and vascular dysregulation, and decreased nasal macular perfusion density is associated with reduced retinal microvascular circulation, leading to degeneration of the optic nerve. Demographic factors like age and access to medical education also play a significant role, especially since glaucoma remains underdiagnosed in underdeveloped regions due to limited ophthalmologic resources and medical education. Aging is also associated with...</description>
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      <pubDate>Fri, 17 Jul 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Ramasamy, Prisha Selvamani</name>
      </author>
      <author>
        <name>Wang, Fantasy</name>
      </author>
      <author>
        <name>Lucero, Isaac</name>
      </author>
    </item>
    <item>
      <title>Mechanistic Links Between Chronic Stress and Alzheimer’s Disease:HPA Axis Activation and Neuroinflammation</title>
      <link>https://escholarship.org/uc/item/10b972pt</link>
      <description>Alzheimer’s Disease (AD) pathology has been shown to begin decades before theappearance of cognitive symptoms. This is backed by imaging and biomarker studies showing amyloid and tau abnormalities followed by neurodegeneration (Ottoy et al., 2025). Hence, current research being done to understand the cause of Alzheimer’s focuses on the “plaques and tangles” theory, in which amyloid beta (Aβ) deposits build up, blocking cell communication and tau proteins tangle inside neurons, disrupting nutrient transport (P, Vellapandian, 2024). After surveying existing literature, we seek to better understand the risk factors that influence these biomarkers and the mechanistic pathways that drive AD progression. With age serving as theprimary risk factor, with those over 65 most affected, looking at earlier adulthood allows us to assess the potential role that chronic stress plays in AD pathology throughhypothalamic-pituitary-adrenal (HPA) axis dysregulation and neuroinflammation.</description>
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      <pubDate>Fri, 17 Jul 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Chandler, Alessandra C.</name>
      </author>
      <author>
        <name>Gutierrez, Annmarie Mae</name>
      </author>
    </item>
    <item>
      <title>RNA Modifications Regulating Early Cancer Development</title>
      <link>https://escholarship.org/uc/item/0wn96936</link>
      <description>RNA modifications including adenosine-to-inosine (A-to-I) editing and N6-methyladenosine (m6A) play important roles in post-transcriptional gene regulation and havebeen identified as major factors in the initiation and spread of cancer. The most prevalent internal alteration in eukaryotic mRNA, m6A, is dynamically controlled by "writers"(METTL3/METTL14), "erasers" (FTO/ALKBH5), and "readers" (YTH domain proteins), whichcollectively affect RNA stability, splicing, translation, and destruction. Studies have shown that dysregulation of m6A plays a role in cancers such leukemia, breast cancer, and clear cell renal cell carcinoma through pathways involving METTL3 and SETD2 mutations. This dysregulation has been closely linked to tumor growth, metastasis, and therapeutic resistance. Similar to this,A-to-I RNA editing, which is mostly mediated by ADAR1, modifies RNA transcripts withoutaltering DNA sequences and promotes protein variety and immune control. By modifyingendogenous double-stranded...</description>
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      <pubDate>Fri, 17 Jul 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Cho, Rachel</name>
      </author>
      <author>
        <name>Islam, Nazia</name>
      </author>
      <author>
        <name>Lee, Andrew</name>
      </author>
      <author>
        <name>Kim, Matthew</name>
      </author>
      <author>
        <name>Gengiti, Rishitha</name>
      </author>
      <author>
        <name>Wafadar, Medina</name>
      </author>
    </item>
    <item>
      <title>The Psychological Cost of Survival: Balancing Clinical Efficacy and Mental Health in Evolving Endocrine Therapies</title>
      <link>https://escholarship.org/uc/item/0mp1s853</link>
      <description>Estrogen receptors drive cancer cell proliferation in hormone receptor-positive cancer, which constitutes 70% of breast cancers. These require long-term endocrine therapy to suppress estrogen signaling and prevent recurrence. While these treatments significantly prolong progression-free and overall survival, the systemic depletion of estrogen and dysregulation of the HPA axis leads to severe, frequently underreported psychiatric toxicities, primarily depression and anxiety. This review evaluates the currentstandard of care and developing therapies, specifically Selective Estrogen Receptor Modulators (SERMs), Aromatase Inhibitors (AIs), Ovarian Function Suppression (OFS), and Selective Estrogen Receptor Degraders (SERDs), and how they balance clinical efficacy against their respective neurobiological andpsychological costs. A comprehensive synthesis of primary literature, clinical trials, and case evaluations was conducted to analyze survival endpoints alongside neuropsychiatric...</description>
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      <pubDate>Fri, 17 Jul 2026 00:00:00 +0000</pubDate>
      <author>
        <name>Ho, Evan</name>
      </author>
      <author>
        <name>Hallaji, Doenia</name>
      </author>
      <author>
        <name>Kim, Seojin</name>
      </author>
      <author>
        <name>Opeyany, Abbas</name>
      </author>
      <author>
        <name>Tsang, Charlotte</name>
      </author>
      <author>
        <name>Xu, Carolyn</name>
      </author>
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