A High Elevation Record of the Star-nosed Mole (Condylura cristata) in Northeastern Vermont

A single male Star-nosed Mole, Condylura cristata, was captured in a rock pile at the top of East Mountain (elevation 1042 m; 3240 ft) in northeastern Vermont. Although known from high elevations (up to 1676 m; 5500 ft) in southern U.S. states, this species was not known to occur above 573 m (1880 ft) in the northern part of its range. This record is also important in confirming that C. cristata has some climbing ability when travelling above ground

What Can We Learn About Effective Mathematics Teaching?:A Framework for Estimating Causal Effects using Longitudinal Survey Data.

This study investigates the impact of teacher characteristics and instructional strategies on the mathematics achievement of students in kindergarten and first grade and tackles the question of how best to use longitudinal survey data to elicit causal inference in the face of potential threats to validity due to nonrandom assignment to treatment. We develop a step-by-step approach to selecting a modeling and estimation strategy and find that teacher certification and courses in methods of teaching mathematics have a slightly negative effect on student achievement in kindergarten, whereas postgraduate education has a positive effect in first grade. Various teaching modalities, such as working with counting manipulatives, using math worksheets, and completing problems on the chalkboard, have positive effects on achievement in kindergarten, and pedagogical practices relating to explaining problem solving and working on problems from textbooks have positive effects on achievement in first grade. We show that the conclusions drawn depend on the estimation and modeling choices made and that several prior studies of teacher effects using longitudinal survey data likely neglected important features needed to establish causal inference

Surface Phenotype and Functionality of WNV Specific T Cells Differ with Age and Disease Severity

West Nile virus (WNV) infection can result in severe neuroinvasive disease, particularly in persons with advanced age. As rodent models demonstrate that T cells play an important role in limiting WNV infection, and strong T cell responses to WNV have been observed in humans, we postulated that inadequate antiviral T cell immunity was involved in neurologic sequelae and the more severe outcomes associated with age. We previously reported the discovery of six HLA-A*0201 restricted WNV peptide epitopes, with the dominant T cell targets in naturally infected individuals being SVG9 (Env) and SLF9 (NS4b). Here, memory phenotype and polyfunctional CD8+ T cell responses to these dominant epitopes were assessed in 40 WNV seropositive patients displaying diverse clinical symptoms. The patients' PBMC were stained with HLA-I multimers loaded with the SVG9 and SLF9 epitopes and analyzed by multicolor flow cytometry. WNV-specific CD8+ T cells were found in peripheral blood several months post infection. The number of WNV-specific T cells in older individuals was the same, if not greater, than in younger members of the cohort. WNV-specific T cells were predominantly monofunctional for CD107a, MIP-1β, TNFα, IL-2, or IFNγ. When CD8+ T cell responses were stratified by disease severity, an increased number of terminally differentiated, memory phenotype (CD45RA+ CD27− CCR7− CD57+) T cells were detected in patients suffering from viral neuroinvasion. In conclusion, T cells of a terminally differentiated/cytolytic profile are associated with neuroinvasion and, regardless of age, monofunctional T cells persist following infection. These data provide the first indication that particular CD8+ T cell phenotypes are associated with disease outcome following WNV infection

Financial impact of reducing door-to-balloon time in ST-elevation myocardial infarction: a single hospital experience

<p>Abstract</p> <p>Background</p> <p>The impact of reducing door-to-balloon time on hospital revenues, costs, and net income is unknown.</p> <p>Methods</p> <p>We prospectively determined the impact on hospital finances of (1) emergency department physician activation of the catheterization lab and (2) immediate transfer of the patient to an immediately available catheterization lab by an in-house transfer team consisting of an emergency department nurse, a critical care unit nurse, and a chest pain unit nurse. We collected financial data for 52 consecutive ST-elevation myocardial infarction patients undergoing emergency percutaneous intervention from October 1, 2004–August 31, 2005 and compared this group to 80 consecutive ST-elevation myocardial infarction patients from September 1, 2005–June 26, 2006 after protocol implementation.</p> <p>Results</p> <p>Per hospital admission, insurance payments (hospital revenue) decreased ($35,043 ±$36,670 vs. $25,329 ±$16,185, P = 0.039) along with total hospital costs ($28,082 ±$31,453 vs. $18,195 ±$9,242, P = 0.009). Hospital net income per admission was unchanged ($6962 vs.$7134, P = 0.95) as the drop in hospital revenue equaled the drop in costs. For every $1000 reduction in total hospital costs, insurance payments (hospital revenue) dropped$1077 for private payers and $1199 for Medicare/Medicaid. A decrease in hospital charges ($70,430 ± $74,033 vs.$53,514 ± $23,378, P = 0.059), diagnosis related group relative weight (3.7479 ± 2.6731 vs. 2.9729 ± 0.8545, P = 0.017) and outlier payments with hospital revenue>$100,000 (7.7% vs. 0%, P = 0.022) all contributed to decreasing ST-elevation myocardial infarction hospitalization revenue. One-year post-discharge financial follow-up revealed similar results: Insurance payments: $49,959 ±$53,741 vs. $35,937 ±$23,125, P = 0.044; Total hospital costs: $39,974 ±$37,434 vs. $26,778 ±$15,561, P = 0.007; Net Income: $9984 vs.$9159, P = 0.855.</p> <p>Conclusion</p> <p>All of the financial benefits of reducing door-to-balloon time in ST-elevation myocardial infarction go to payers both during initial hospitalization and after one-year follow-up.</p> <p>Trial Registration</p> <p><b>ClinicalTrials.gov ID</b>: NCT00800163</p

Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis.

Multiple sclerosis is a common disease of the central nervous system in which the interplay between inflammatory and neurodegenerative processes typically results in intermittent neurological disturbance followed by progressive accumulation of disability. Epidemiological studies have shown that genetic factors are primarily responsible for the substantially increased frequency of the disease seen in the relatives of affected individuals, and systematic attempts to identify linkage in multiplex families have confirmed that variation within the major histocompatibility complex (MHC) exerts the greatest individual effect on risk. Modestly powered genome-wide association studies (GWAS) have enabled more than 20 additional risk loci to be identified and have shown that multiple variants exerting modest individual effects have a key role in disease susceptibility. Most of the genetic architecture underlying susceptibility to the disease remains to be defined and is anticipated to require the analysis of sample sizes that are beyond the numbers currently available to individual research groups. In a collaborative GWAS involving 9,772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the HLA-DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the class I region. Immunologically relevant genes are significantly overrepresented among those mapping close to the identified loci and particularly implicate T-helper-cell differentiation in the pathogenesis of multiple sclerosis

Stress sensitization and adolescent depressive severity as a function of childhood adversity: A link to anxiety disorders

The goal of the present study was to determine whether exposure to adversity in childhood contributes to a differential threshold at which stressful life events provoke depressive reactions in adolescence. In addition, to address empirical and conceptual questions about stress effects, the moderating effect of anxiety disorder history was also explored. This examination was conducted in a sample of 816 children of depressed and nondepressed mothers, who were followed from birth to age 15. Information on adversities experienced in childhood was collected both from mothers during the first five years of their youth's life and from the youths themselves at age 15, and included information on the mother's relationship with her partner, maternal psychopathology, as well as youth-reported abuse. Results indicated that youths with both greater exposure to adversity in childhood and a history of an anxiety disorder displayed increased depressive severity following low levels of episodic stress compared to youths with only one or neither of these risk factors. The results are speculated to reflect the possibility that early anxiety disorders associated with exposure to adversity in childhood may be a marker of dysregulated stress responses, and may help to account for the comorbidity of depression and anxiety in some individuals

A Transcription Factor Map as Revealed by a Genome-Wide Gene Expression Analysis of Whole-Blood mRNA Transcriptome in Multiple Sclerosis

Background: Several lines of evidence suggest that transcription factors are involved in the pathogenesis of Multiple Sclerosis (MS) but complete mapping of the whole network has been elusive. One of the reasons is that there are several clinical subtypes of MS and transcription factors that may be involved in one subtype may not be in others. We investigate the possibility that this network could be mapped using microarray technologies and contemporary bioinformatics methods on a dataset derived from whole blood in 99 untreated MS patients (36 Relapse Remitting MS, 43 Primary Progressive MS, and 20 Secondary Progressive MS) and 45 age-matched healthy controls. Methodology/Principal Findings: We have used two different analytical methodologies: a non-standard differential expression analysis and a differential co-expression analysis, which have converged on a significant number of regulatory motifs that are statistically overrepresented in genes that are either differentially expressed (or differentially co-expressed) in cases and controls (e.g., V$KROX_Q6, p-value ,3.31E-6; V$CREBP1_Q2, p-value ,9.93E-6, V$YY1_02, p-value ,1.65E-5). Conclusions/Significance: Our analysis uncovered a network of transcription factors that potentially dysregulate several genes in MS or one or more of its disease subtypes. The most significant transcription factor motifs were for the Early Growth Response EGR/KROX family, ATF2, YY1 (Yin and Yang 1), E2F-1/DP-1 and E2F-4/DP-2 heterodimers, SOX5, and CREB and ATF families. These transcription factors are involved in early T-lymphocyte specification and commitment as well as in oligodendrocyte dedifferentiation and development, both pathways that have significant biological plausibility in MS causation