54 research outputs found

    Founder effects and species introductions: A host versus parasite perspective

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    Species colonizations (both natural and anthropogenic) can be associated with genetic founder effects, where founding populations demonstrate significant genetic bottlenecks compared to native populations. Yet, many successfully established free�living species exhibit little reduction in genetic diversity—possibly due to multiple founding events and/or high propagule pressure during introductions. Less clear, however, is whether parasites may show differential signatures to their free�living hosts. Parasites with indirect life cycles may particularly be more prone to founder effects (i.e., more genetically depauperate) because of inherently smaller founding populations and complex life cycles. We investigated this question in native (east coast) and introduced (west coast) North American populations of a host snail Tritia obsoleta (formerly Ilyanassa obsoleta, the eastern mudsnail) and four trematode parasite species that obligately infect it. We examined genetic diversity, gene flow, and population structure using two molecular markers (mitochondrial and nuclear) for the host and the parasites. In the host snail, we found little to no evidence of genetic founder effects, while the trematode parasites showed significantly lower genetic diversity in the introduced versus native ranges. Moreover, the parasite's final host influenced infection prevalence and genetic diversity: Trematode species that utilized fish as final hosts demonstrated lower parasite diversity and heightened founder effects in the introduced range than those trematodes using birds as final hosts. In addition, inter�regional gene flow was strongest for comparisons that included the putative historical source region (mid�Atlantic populations of the US east coast). Overall, our results broaden understanding of the role that colonization events (including recent anthropogenic introductions) have on genetic diversity in non�native organisms by also evaluating less studied groups like parasites

    Response To The Pandemic: Housing For Health In The Va Tent Community

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    In response to the COVID-19 pandemic, an innovative approach to providing integrated primary care services was initiated in the Veterans Administration Greater Los Angeles Healthcare System (Figure 1). The Care, Treatment and Rehabilitation Services, a unique street medicine program, was placed within an encampment that is supported by the West Los Angeles VA health care services including onsite provision of 24/7 security, stability of tent sites, 3 meals a day, unlimited water, hygiene stations, face masks, showers and housing placement services.http://deepblue.lib.umich.edu/bitstream/2027.42/170780/1/AFM-348-21_PP.pdfDescription of AFM-348-21_PP.pdf : Main ArticleSEL

    word~river literary review (2009)

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    wordriver is a literary journal dedicated to the poetry, short fiction and creative nonfiction of adjuncts and part-time instructors teaching in our universities, colleges, and community colleges. Our premier issue was published in Spring 2009. We are always looking for work that demonstrates the creativity and craft of adjunct/part-time instructors in English and other disciplines. We reserve first publication rights and onetime anthology publication rights for all work published. We define adjunct instructors as anyone teaching part-time or full-time under a semester or yearly contract, nationwide and in any discipline. Graduate students teaching under part-time contracts during the summer or who have used up their teaching assistant time and are teaching with adjunct contracts for the remainder of their graduate program also are eligible.https://digitalscholarship.unlv.edu/word_river/1002/thumbnail.jp

    General practitioners' opinions on how to improve treatment of mental disorders in primary health care. Interviews with one hundred Norwegian general practitioners

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    <p>Abstract</p> <p>Background</p> <p>Improvements in treatment of mental disorders are repeatedly called for. General practitioners (GPs) are responsible for the majority of treatment of mental disorders. Consequently, we interviewed GPs about their opinions on how treatment of mental disorders in primary health care contexts could be improved.</p> <p>Methods</p> <p>Among GPs affiliated within the Norwegian reimbursement system, we approached 353, and made contact with 246 GP's. One-hundred of these agreed to participate in our study, and 95 of them expressed opinions on how to improve treatment of mental disorders. The telephone interviews were based on open-ended questions, responses were transcribed continuously, and content analysis was applied. Results are presented both as frequency tables of common responses, and as qualitative descriptions and quotations of opinions.</p> <p>Results</p> <p>Nearly all (95%) of the GPs had suggestions on how to improve treatment of mental disorders in primary health care. Increased capacity in secondary health care was suggested by 59% of GPs. Suggestions of improved collaboration with secondary health care were also common (57%), as were improvements of GPs' skills and knowledge relevant for diagnosing and treating mental disorders (40%) and more time for patients with mental disorders in GP contexts (40%).</p> <p>Conclusions</p> <p>The GPs' suggestions are in line with international research and debate. It is thought-provoking that the majority of GPs call for increased capacity in secondary care, and also better collaboration with secondary care. Some GPs made comparisons to the health care system for physical disorders, which is described as better-functioning. Our study identified no simple short-term cost-effective interventions likely to improve treatment for mental disorders within primary health care. Under-treatment of mental disorders is, however, also associated with significant financial burdens.</p

    Serum levels of osteoprotegerin and receptor activator of nuclear factor -κB ligand in children with early juvenile idiopathic arthritis: a 2-year prospective controlled study

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    <p>Abstract</p> <p>Background</p> <p>The clinical relevance of observations of serum levels of osteoprotegerin (OPG) and receptor activator of nuclear factor -κB ligand (RANKL) in juvenile idiopathic arthritis (JIA) is not clear. To elucidate the potential role of OPG and RANKL in JIA we determined serum levels of OPG and RANKL in patients with early JIA compared to healthy children, and prospectively explored changes in relation to radiographic score, bone and lean mass, severity of the disease, and treatment.</p> <p>Methods</p> <p>Ninety children with early oligoarticular or polyarticular JIA (ages 6-18 years; mean disease duration 19.4 months) and 90 healthy children individually matched for age, sex, race, and county of residence, were examined at baseline and 2-year follow-up. OPG and RANKL were quantified by enzyme-immunoassay. Data were analyzed with the use of t-tests, ANOVA, and multiple regression analyses.</p> <p>Results</p> <p>Serum OPG was significantly lower in patients than controls at baseline, and there was a trend towards higher RANKL and a lower OPG/RANKL ratio. Patients with polyarthritis had significantly higher increments in RANKL from baseline to follow-up, compared to patients with oligoarthritis. RANKL was a significant negative predictor for increments in total body lean mass. Patients who were receiving corticosteroids (CS) or disease-modifying antirheumatic drugs (DMARDs) at follow-up had higher OPG/RANKL ratio compared with patients who did not receive this medication.</p> <p>Conclusions</p> <p>The data supports that levels of OPG are lower in patients with JIA compared to healthy children, and higher levels of RANKL is associated with more serious disease. RANKL was a significant negative predictor of lean mass in patients with JIA. The OPG/RANKL ratio was higher in patients on DMARDs or CS treatment.</p

    Dopaminergic Activation of Estrogen Receptors Induces Fos Expression within Restricted Regions of the Neonatal Female Rat Brain

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    Steroid receptor activation in the developing brain influences a variety of cellular processes that endure into adulthood, altering both behavior and physiology. Recent data suggests that dopamine can regulate expression of progestin receptors within restricted regions of the developing rat brain by activating estrogen receptors in a ligand-independent manner. It is unclear whether changes in neuronal activity induced by dopaminergic activation of estrogen receptors are also region specific. To investigate this question, we examined where the dopamine D1-like receptor agonist, SKF 38393, altered Fos expression via estrogen receptor activation. We report that dopamine D1-like receptor agonist treatment increased Fos protein expression within many regions of the developing female rat brain. More importantly, prior treatment with an estrogen receptor antagonist partially reduced D1-like receptor agonist-induced Fos expression only within the bed nucleus of the stria terminalis and the central amygdala. These data suggest that dopaminergic activation of estrogen receptors alters neuronal activity within restricted regions of the developing rat brain. This implies that ligand-independent activation of estrogen receptors by dopamine might organize a unique set of behaviors during brain development in contrast to the more wide spread ligand activation of estrogen receptors by estrogen

    T cell autoreactivity directed toward CD1c itself rather than toward carried self lipids

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    The hallmark function of αβ T cell antigen receptors (TCRs) involves the highly specific co-recognition of a major histocompatibility complex molecule and its carried peptide. However, the molecular basis of the interactions of TCRs with the lipid antigen–presenting molecule CD1c is unknown. We identified frequent staining of human T cells with CD1c tetramers across numerous subjects. Whereas TCRs typically show high specificity for antigen, both tetramer binding and autoreactivity occurred with CD1c in complex with numerous, chemically diverse self lipids. Such extreme polyspecificity was attributable to binding of the TCR over the closed surface of CD1c, with the TCR covering the portal where lipids normally protrude. The TCR essentially failed to contact lipids because they were fully seated within CD1c. These data demonstrate the sequestration of lipids within CD1c as a mechanism of autoreactivity and point to small lipid size as a determinant of autoreactive T cell responses
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