This data article includes information on institutional data at a large public research university in Southern California. In particular, data on undergraduate student enrollments in online and face-to-face courses during summer terms from 2014 to 2017 cumulating in 72,441 course enrollments from 23,610 undergraduate students in 433 courses is provided. This data includes additional information on the statistical models examining factors influencing student enrollment by course modality and the associations of course modality with course grades. This includes descriptive data and data derived from multi-level logistic regression analyses and multi-way fixed effects linear regression analyses. This data article is associated with the article "Effects of course modality in summer session: Enrollment patterns and student performance in face-to-face and online classes" [1].

This quantitative study examined student participation in an introductory project-based engineering course offered in fully face-to-face and hybrid course modes (N = 160). This course attempted to counteract trends of decreased student motivation and high attrition rates among engineering majors. Mixed-design analysis of variance examined differences in motivational constructs including student self-efficacy, effort regulation, and interest in engineering, as well as engineering skills throughout the course and across instructional modes. None of the motivational constructs were associated with significant decreases throughout the course nor with differences across instructional modes. However, students' engineering skills increased throughout the course with no significant differences across course modalities. Furthermore, interest in engineering and effort regulation were positively associated with course performance. The instructional modality was not significantly associated with course performance. Overall, this study provides an example of a project-based introductory engineering course which may help maintain student motivation and foster student success in engineering.

With the nationwide emphasis on improving outcomes for STEM undergraduates, it is important that we not only focus on modifying classroom instruction, but also provide students with the tools to maximize their independent learning time. There has been considerable work in laboratory settings examining two beneficial practices for enhancing learning: spacing and self-testing. In the current study, we examine biology students' study practices, particularly in the context of these two behaviors. We specifically investigate whether a light-touch study skills intervention focused on encouraging spacing and self-testing practices impacted their utilization. Based on pre- and post-course surveys, we found that students report utilizing both beneficial and ineffective study practices and confirm that usage of spacing and self-testing correlates with a higher course grade. We also found that students in the section of the course which received the study skills intervention were more likely to report continued use or adoption of spacing and self-testing compared to students in control sections without the intervention. Surprisingly, we found that underrepresented minorities (URMs) under-utilize self-testing, and that our intervention helped to partially ameliorate this gap. Additionally, we found that URMs who reported self-testing earned similar course grades compared to non-URMs who also self-tested, but that there was a much larger drop in performance for URMs who did not self-test relative to non-URMs who also did not self-test. Overall, we would encourage instructors to dedicate class time towards discussing the merits of beneficial study practices, especially for students that have historically underperformed in STEM disciplines.

Long-term monitoring of microbial communities in the rhizosphere of post-fire forests is currently one of the key knowledge gaps. Knowing the time scale of the effects is indispensable to aiding post-fire recovery in vulnerable woodlands, including holm oak forests, that are subjected to a Mediterranean climate, as is the case with forests that are found in protected areas such as the Sierra Nevada National and Natural Park in southeastern Spain. We took rhizosphere soil samples from burned and unburned holm oak trees approximately 3, 6, and 9 years after the 2005 fire that devastated almost 3500 ha in southeastern Spain. We observed that the prokaryotic communities are recovering but have not yet reached the conditions observed in the unburned forest. A common denominator between this fire and other fires is the long-term persistence of three ecosystem recovery biomarkers—specifically, higher proportions of the genera Arthrobacter, Blastococcus, and Massilia in soil microbial communities after a forest fire. These pyrophilous microbes possess remarkable resilience against adverse conditions, exhibiting traits such as xerotolerance, nitrogen mineralization, degradation of aromatic compounds, and copiotrophy in favorable conditions. Furthermore, these biomarkers thrive in alkaline environments, which persist over the long term following forest fires. The relative abundance of these biomarkers showed a decreasing trend over time, but they were still far from the values of the control condition. In conclusion, a decade does not seem to be enough for the complete recovery of the prokaryotic communities in this Mediterranean ecosystem.

Fusarium wilt, caused by Fusarium oxysporum f. sp. lycopersici (Fol), causes losses in tomato production worldwide, with major impacts on Californian tomato processing. Single-gene resistance is the primary management tool, but its efficacy has been compromised following the emergence of two successive resistance-breaking races, which, in California, emerged within 12 years of resistance deployment. Fol race 3-resistant (F3) processing tomato cultivars (containing the I3 resistance gene) were deployed in the state starting in approximately 2009. The emergence of a new resistance-breaking race (which would be called race 4) is imminent, and early detection will be critical to delay the spread while new resistance is sought. The detection of Fol race 4 is challenged by the lack of validated, rapid, and accurate diagnostic tools. In evaluating in planta phenotyping methods, this study found that rapid seedling phenotyping is not reliable and generates false positives for nonpathogens. Longer (10 weeks) mature plant assays are the most reliable, but may not be sufficiently timely. As an additional challenge, based on field and greenhouse studies, Fol race 3 can cause symptoms in resistant F3 cultivars at frequencies greater (30%) than expected for off-types (<2%). We developed a three-F3 cultivar in planta assay to overcome the challenges this posed to differentiating Fol race 3 and Fol race 4. Using the assay, we determined that all putative resistance-breaking cases were Fol race 3; Fol race 4 was not detected in these early survey efforts. These results highlight the need for developing rapid Fol race 4 detection tools and a better understanding of the factors underlying inconsistent I3 gene expression in Fol race 3.

Background

This study identified early immune gene responses in peripheral blood associated with 90-day ischemic stroke (IS) outcomes.

Methods

Peripheral blood samples from the CLEAR trial IS patients at ≤ 3 h, 5 h, and 24 h after stroke were compared to vascular risk factor matched controls. Whole-transcriptome analyses identified genes and networks associated with 90-day IS outcome assessed using the modified Rankin Scale (mRS) and the NIH Stroke Scale (NIHSS).

Results

The expression of 467, 526, and 571 genes measured at ≤ 3, 5 and 24 h after IS, respectively, were associated with poor 90-day mRS outcome (mRS ≥ 3), while 49, 100 and 35 genes at ≤ 3, 5 and 24 h after IS were associated with good mRS 90-day outcome (mRS ≤ 2). Poor outcomes were associated with up-regulated genes or pathways such as IL-6, IL-7, IL-1, STAT3, S100A12, acute phase response, P38/MAPK, FGF, TGFA, MMP9, NF-kB, Toll-like receptor, iNOS, and PI3K/AKT. There were 94 probe sets shared for poor outcomes vs. controls at all three time-points that correlated with 90-day mRS; 13 probe sets were shared for good outcomes vs. controls at all three time-points; and 46 probe sets were shared for poor vs. good outcomes at all three time-points that correlated with 90-day mRS. Weighted Gene Co-Expression Network Analysis (WGCNA) revealed modules significantly associated with 90-day outcome for mRS and NIHSS. Poor outcome modules were enriched with up-regulated neutrophil genes and with down-regulated T cell, B cell and monocyte-specific genes; and good outcome modules were associated with erythroblasts and megakaryocytes. Finally, genes identified by genome-wide association studies (GWAS) to contain significant stroke risk loci or loci associated with stroke outcome including ATP2B, GRK5, SH3PXD2A, CENPQ, HOXC4, HDAC9, BNC2, PTPN11, PIK3CG, CDK6, and PDE4DIP were significantly differentially expressed as a function of stroke outcome in the current study.

Conclusions

This study suggests the immune response after stroke may impact functional outcomes and that some of the early post-stroke gene expression markers associated with outcome could be useful for predicting outcomes and could be targets for improving outcomes.

Intracerebral hemorrhage (ICH) and perihematomal edema (PHE) volumes are major determinants of ICH outcomes as is the immune system which plays a significant role in damage and repair. Thus, we performed whole-transcriptome analyses of 18 ICH patients to delineate peripheral blood genes and networks associated with ICH volume, absolute perihematomal edema (aPHE) volume, and relative PHE (aPHE/ICH; rPHE). We found 440, 266, and 391 genes correlated with ICH and aPHE volumes and rPHE, respectively (p < 0.005, partial-correlation > |0.6|). These mainly represented inflammatory pathways including NF-κB, TREM1, and Neuroinflammation Signaling-most activated with larger volumes. Weighted Gene Co-Expression Network Analysis identified seven modules significantly correlated with these measures (p < 0.05). Most modules were enriched in neutrophil, monocyte, erythroblast, and/or T cell-specific genes. Autophagy, apoptosis, HIF-1α, inflammatory and neuroinflammatory response (including Toll-like receptors), cell adhesion (including MMP9), platelet activation, T cell receptor signaling, and mRNA splicing were represented in these modules (FDR p < 0.05). Module hub genes, potential master regulators, were enriched in neutrophil-specific genes in three modules. Hub genes included NCF2, NCF4, STX3, and CSF3R, and involved immune response, autophagy, and neutrophil chemotaxis. One module that correlated negatively with ICH volume correlated positively with rPHE. Its genes and hubs were enriched in T cell-specific genes including hubs LCK and ITK, Src family tyrosine kinases whose modulation improved outcomes and reduced BBB dysfunction following experimental ICH. This study uncovers molecular underpinnings associated with ICH and PHE volumes and pathophysiology in human ICH, where knowledge is scarce. The identified pathways and hub genes may represent novel therapeutic targets.

The peripheral immune system response to Intracerebral Hemorrhage (ICH) may differ with ICH in different brain locations. Thus, we investigated peripheral blood mRNA expression of Deep ICH, Lobar ICH, and vascular risk factor-matched control subjects (n = 59). Deep ICH subjects usually had hypertension. Some Lobar ICH subjects had cerebral amyloid angiopathy (CAA). Genes and gene networks in Deep ICH and Lobar ICH were compared to controls. We found 774 differentially expressed genes (DEGs) and 2 co-expressed gene modules associated with Deep ICH, and 441 DEGs and 5 modules associated with Lobar ICH. Pathway enrichment showed some common immune/inflammatory responses between locations including Autophagy, T Cell Receptor, Inflammasome, and Neuroinflammation Signaling. Th2, Interferon, GP6, and BEX2 Signaling were unique to Deep ICH. Necroptosis Signaling, Protein Ubiquitination, Amyloid Processing, and various RNA Processing terms were unique to Lobar ICH. Finding amyloid processing pathways in blood of Lobar ICH patients suggests peripheral immune cells may participate in processes leading to perivascular/vascular amyloid in CAA vessels and/or are involved in its removal. This study identifies distinct peripheral blood transcriptome architectures in Deep and Lobar ICH, emphasizes the need for considering location in ICH studies/clinical trials, and presents potential location-specific treatment targets.