How Do Student and Secondary School Characteristics Explain College English I Completion in a Rural Arkansas Community College?

Community colleges serve diverse populations that may not be as academically prepared as at four-year institutions. Accountability of higher education institutions is ever-increasing in importance, so understanding the contributing factors to student success is critical. Students bring a unique set of characteristics to the community college, including individual traits and secondary school experiences. Many studies have examined these characteristics at large urban or mid-western institutions, but few in rural settings. Rural areas of the United States have lower rates of educational attainment than other areas, which often translates to lower incomes. It is the mission of community colleges to train the future workforce which should result in a highly skilled workforce with wages to make a comfortable living. To graduate from any higher education institution in Arkansas, students must complete college-level gateway courses. These courses are the first indicators of success. There are many established predictors of college success. These factors could fall in any level of Bronfenbrenner’s Theory of Ecological Development which is the foundation of this study. Two levels of characteristics, student and high school, that may influence the likelihood of gateway course success, College English I, at a rural Arkansas community college are examined. The study included 409 students from 13 secondary schools. Individual characteristics examined include high school grade point average, ACT composite of reading and English only, gender, race/ethnicity, socio-economic status, and parent education level. School characteristics examined were high school rating, racial make-up, school socio-economic status, average years of teaching experience, and school ACT average. The study used a quantitative, two-staged nested, between-subjects design using multi-level modeling with logistic regression. Despite other studies, this analysis determined that high school attended and student characteristics of gender, race/ethnicity, SES, and parent ed level does not influence College English I course success. However, in alignment with most studies, past academic performance measured by HS GPA and ACT score has a strong influence on the success rate. These findings should not be generalized beyond the institution in the study but may be used as a baseline for an institution examining its student population

Investigations of the AhR-induced Treg : transcriptional regulation and suppressive mechanisms

The aryl hydrocarbon receptor (AhR) has recently been described as a novel therapeutic target, given the potent suppression of multiple immune-mediated diseases following activation by the prototypic ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). In the parent-into-F1 graft-versus-host (GVH) model, suppression of the cytotoxic T-lymphocyte (CTL) response is associated with the presence of CD25⁺CTLA-4⁺IL-10⁺Foxp3[superscript neg] regulatory donor CD4⁺ T-cells (AhR-Tregs). These AhR-Treg have a suppressive capacity greater than thymus-derived natural Treg. Therefore it is hypothesized that suppression of the CTL response is mediated by the AhR-Treg. The purpose of these studies was two-fold: 1) to identify mechanisms by which TCDD-activated AhR induces AhR-Tregs and 2) to determine the mechanism by which AhR-Tregs suppress the CTL response. To address the first aim, we hypothesized that the AhR, a transcription factor, may directly influence gene expression during CD4⁺ T-cell activation and differentiation, thereby driving their differentiation into AhR-Treg. T-cell differentiation is dependent upon expression of certain transcription factors and lineage-specific genes for proteins and cytokines. Therefore, gene expression associated with CD4⁺ T-cell activation and/or differentiation was evaluated in CD4⁺ T-cells cultured under different polarizing conditions. Unexpectedly, treatment with TCDD did not alter lineage-specific genes that drive CD4⁺ T-cell differentiation. Apart from the known AhR-regulated genes Cyp1a1, Cyp1b1 and Ahrr, only expression of Il22 was inappropriately up- regulated across all conditions tested. The increase in Il22 expression translated to increased IL-22 protein n. Of the 49 genes evaluated there were no other changes in gene expression consistent across polarizing conditions. This suggests that the role of AhR is superimposed upon the cytokine milieu, and therefore may have been obscured by the use of strongly polarizing cytokines. Ultimately, the results cast doubt on the use of in vitro conditions to recapitulate in vivo events, although the role of IL-22 in AhR biology remains of interest. To address the second part of my hypotheses, the suppressive mechanism(s) of the AhR-Treg were examined, focusing primarily on the increased expression of CTLA-4, CD25 and IL-10 seen on day 2 of the GVH response in previous studies. Expression of CTLA-4 induces the IFNγ - IDO tolerogenic pathway. Expression of CD25, the high-affinity subunit for the IL-2R is associated with regulatory function, through induction of tolerogenic cytokines and sequestration of IL-2. The immunosuppressive cytokine IL-10 is known to inhibit T-cell activation and expansion. Independent blockade of CTLA-4 and IDO function revealed that the AhR-Treg do not appear to use the IDO tolerogenic pathway to mediate suppression. Furthermore, antibody-mediated blockade of neither CD25 nor IL-10 were able to alleviate TCDD-mediated immunosuppression. During these studies we discovered that treatment with TCDD induced Foxp3, the transcription factor for Treg, in donor CD4⁺ and CD8⁺ T-cells 15 days after adoptive transfer. Interestingly, the up-regulation of Foxp3 was also seen in un-activated host cells, indicating non-specific regulation of Foxp3 by TCDD-activated AhR. Furthermore, concurrent blockade of CD25 and Foxp3 had no effect on TCDD's ability to suppress the GVH response. In sum, these studies suggest that the AhR-Treg is a novel regulatory cell, with characteristics of a Treg and increased IL-22 production. Regulatory T-cells have a wide repertoire of suppressive mechanisms, including production of TGFβ1 and TGFβ3, sequestration of IL-2 and granzyme B. Understanding the mechanism of suppression utilized by the AhR-Treg is crucial to develop the AhR as a novel therapeutic target. Future studies will continue to evaluate the potential for the AhR-Treg to use alternative mechanisms to suppress T-dependent immune diseases

Attribution to Deviant and Nondeviant Social Roles

A questionnaire was used to study causal attribution to social roles as influenced by perceived deviance of the role, instructions to identify with the role, and participant gender. The perceived deviance or nondeviance of the roles was determined by a pilot study. The roles were varied randomly through 12 hypothetical events, and identification or nonidentification instructions randomly assigned. The participants were 194 male and female university students. Participants gave the cause of each event and rated the cause on five dimensions: internality, externality, stability, globality, and controllability. Causal attribution to deviant social roles was found to result in a significantly higher across-scales score and to be more internal, less external, and more global than attribution to nondeviant roles. Participant gender showed an interaction with deviance overall and on the dimensions of stability and globality due to significantly higher ratings by women participants than those by men. Identification instructions did not produce a significant effect

Magnitude of behavioral deficits varies with job-related chlorpyrifos exposure levels among Egyptian pesticide workers.

Chronic occupational exposure to organophosphorus pesticides (OPs) is consistently associated with deficits on behavioral tests when compared to unexposed comparison groups. However, a dose-response relationship has yet to be established, leading some to doubt an association between occupational OP exposure and behavioral deficits. Pesticide application teams in Egypt who are primarily exposed to one OP, chlorpyrifos (CPF), were recruited into a field assessment. Trail Making A and the more challenging Trail Making B tests were administered to 54 engineers (who supervise the pesticide application process, usually from the side of the field), 59 technicians (who guide the pesticide applicators in the field), 31 applicators (who mix and apply pesticides using knapsack sprayers), and 150 controls (who did not work in the fields) at two different times during the OP application season as well as immediately after applications had ended and 1.5 months later. All participants were males since only males work on pesticide application teams in Egypt. Urinary levels of 3,5,6-trichloro-2-pyridinol (TCPy), a specific metabolite of CPF, confirmed the pattern of lower to higher CPF exposures from engineers to technicians to applicators, and these were all greater than urinary metabolite levels in controls. A consistent relationship between job title and performance speed on the behavioral task was observed: Controls had the best (fastest) performance on Trail Making A and B tests throughout the application season, and applicators had significantly slower performance than engineers on Trail Making A (p = 0.015) and B (p = 0.003). However, individual urinary TCPy, blood acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) levels did not predict individual performance. This study identifies a dose-related effect based on job title, which serves as a surrogate for chronic exposure in that differing job titles exhibit varying group exposure levels. The results establish that chronic occupational exposure to chlorpyrifos is neurotoxic and suggest that the classic biomarkers of recent CPF exposure are not predictive of chronic exposure effects

Work organization factors associated with health and work outcomes among apprentice construction workers: Comparison between the residential and commercial sectors

There are substantial differences in work organization between residential and commercial construction sectors. This paper examined differences in work factors between construction sectors and examined the association between sector and health behaviors, health outcomes, and work outcomes. We surveyed 929 male construction apprentices (44% residential and 56% commercial) and found that residential apprentices reported fewer workplace safety policies, higher frequency of heavy lifting, and greater likelihood of reporting musculoskeletal pain compared to apprentices in commercial work. Residential apprentices reported higher job strain, lower supervisor support, more lost workdays due to pain or injury, and lower productivity related to health than commercial apprentices. Multivariate Poisson regression models controlling for multiple work factors showed that residential construction work, high job strain, heavy lifting, low coworker support, and low supervisor support were each independently associated with one or more work or health outcomes. These findings suggest that interventions should seek to improve coworker and supervisory supportive behaviors, decrease job strain, and reduce organizational stressors, such as mandatory overtime work. Our study shows disparities in health and safety between construction sectors and highlights the need for interventions tailored to the residential sector

A global perspective on the influence of environmental exposures on the nervous system

Economic transitions in the era of globalization warrant a fresh look at the neurological risks associated with environmental change. These are driven by industrial expansion, transfer and mobility of goods, climate change and population growth. In these contexts, risk of infectious and non-infectious diseases are shared across geographical boundaries. In low- and middle-income countries, the risk of environmentally mediated brain disease is augmented several fold by lack of infrastructure, poor health and safety regulations, and limited measures for environmental protection. Neurological disorders may occur as a result of direct exposure to chemical and/or non-chemical stressors, including but not limited to, ultrafine particulate matters. Individual susceptibilities to exposure-related diseases are modified by genetic, epigenetic and metagenomic factors. The existence of several uniquely exposed populations, including those in the areas surrounding the Niger Delta or north western Amazon oil operations; those working in poorly regulated environments, such as artisanal mining industries; or those, mostly in sub-Saharan Africa, relying on cassava as a staple food, offers invaluable opportunities to advance the current understanding of brain responses to environmental challenges. Increased awareness of the brain disorders that are prevalent in low- and middle-income countries and investments in capacity for further environmental health-related research are positive steps towards improving human health

Organophosphate Pesticide Exposure and Neurobehavioral Performance in Agricultural and Nonagricultural Hispanic Workers

Our understanding of the health risks of farmworkers exposed to pesticides in their work and home environments is rapidly increasing, although studies designed to examine the possible neurobehavioral effects of low-level chronic pesticide exposure are limited. We measured dialkyl phosphate urinary metabolite levels, collected environmental dust samples from a subset of homes, obtained information on work practices, and conducted neurobehavioral tests on a sample of farmworkers in Oregon. Significant correlations between urinary methyl metabolite levels and total methyl organophosphate (azinphos-methyl, phosmet, malathion) house dust levels were observed. We found the neurobehavioral performance of Hispanic immigrant farmworkers to be lower than that observed in a nonagricultural Hispanic immigrant population, and within the sample of agricultural workers there was a positive correlation between urinary organophosphate metabolite levels and poorer performance on some neurobehavioral tests. These findings add to an increasing body of evidence of the association between low levels of pesticide exposure and deficits in neurobehavioral performance

Ethanol Induces Secretion of Proinflammatory Extracellular Vesicles That Inhibit Adult Hippocampal Neurogenesis Through G9a/GLP-Epigenetic Signaling

Adult hippocampal neurogenesis (AHN) is involved in learning and memory as well as regulation of mood. Binge ethanol reduces AHN, though the mechanism is unknown. Microglia in the neurogenic niche are important regulators of AHN, and ethanol promotes proinflammatory microglia activation. We recently reported that extracellular vesicles (EVs) mediate ethanol-induced inflammatory signaling in microglia. Therefore, we investigated the role of EVs in ethanol-induced loss of adult hippocampal neurogenesis. At rest, microglia promoted neurogenesis through the secretion of pro-neurogenic extracellular vesicles (pn-EVs). Depletion of microglia using colony-stimulating factor 1 receptor (CSFR1) inhibition in vivo or using ex vivo organotypic brain slice cultures (OBSCs) caused a 30% and 56% loss of neurogenesis in the dentate, respectively, as measured by immunohistochemistry for doublecortin (DCX). Likewise, chemogenetic inhibition of microglia using a CD68.hM4di construct caused a 77% loss in OBSC, indicating a pro-neurogenic resting microglial phenotype. EVs from control OBSC were pro-neurogenic (pn-EVs), enhancing neurogenesis when transferred to other naive OBSC and restoring neurogenesis in microglia-depleted cultures. Ethanol inhibited neurogenesis and caused secretion of proinflammatory EVs (EtOH-EVs). EtOH-EVs reduced hippocampal neurogenesis in naïve OBSC by levels similar to ethanol. Neurogenesis involves complex regulation of chromatin structure that could involve EV signaling. Accordingly, EtOH-EVs were found to be enriched with mRNA for the euchromatin histone lysine methyltransferase (Ehm2t/G9a), an enzyme that reduces chromatin accessibility through histone-3 lysine-9 di-methylation (H3K9me2). EtOH-EVs induced G9a and H3K9me2 by 2-fold relative to pn-EVs in naïve OBSCs. Pharmacological inhibition of G9a with either BIX-01294 or UNC0642 prevented loss of neurogenesis caused by both EtOH and EtOH-EVs. Thus, this work finds that proinflammatory EtOH-EVs promote the loss of adult hippocampal neurogenesis through G9a-mediated epigenetic modification of chromatin structure