1,817 research outputs found
Anti-Discrimination in a Contemporary American Fraternity: A Case Study
This doctoral dissertation is an empirical study employing the case study research design and aims at gathering the perspectives of fraternity men concerning the utility of anti-discrimination clauses in protecting minority membersâ interests and contributing to a sense of belonging. The case includes a mixed methodology of a survey, focus group interviews, document review, and one on one interviews in terms of data collection. The participants in this study are active and alumni fraternity men affiliated with a social fraternity in the North American Interfraternity Conference. The active member sample comes from a single chapter of the organization at a large, research, public institution in the northeastern region of the United States. The alumni were selected based in consultation with the leadership of the organization. The data indicates that the sampled chapter of the organization has a generally welcoming environment to men of different races, religions, and sexual orientations, but that fraternity bylaws and anti-discrimination clauses are not credited by members for this. Instead, a welcoming organizational climate as promoted within the given chapter allows for this appreciation of diversity to continue
Robust Allocation of Funds for Nonstructural Flood Risk Mitigation in Coastal Louisiana
Coastal Louisiana is a critical economic, ecological and cultural asset, acting as a major hub for waterborne commerce, fisheries, and the petrochemical industry, and also as one of the worldâs unique wetlands. Unfortunately, this rich environment is in great danger from the threat of hurricanes and storm surge flooding. Direct economic losses are estimated to average 12 billion a year, or more, within 50 years if nothing is done. To prevent this catastrophe, Louisiana has developed a Comprehensive Master Plan for a Sustainable Coast, which plans to spend 6 billion budget for nonstructural risk mitigation that will improve upon the current strategy recommended in the coastal Master Plan
Evaluating the role of a galanin enhancer genotype on a range of metabolic, depressive and addictive phenotypes
Funded by âąERC. Grant Number: 284167 âąNIH. Grant Number: 1RO1DK0921127-01 âąNWO. Grant Numbers: 463-06-001, 451-04-034Peer reviewedPublisher PD
Angiopoietin-like protein 2 regulates endothelial colony forming cell vasculogenesis
Angiopoietin-like 2 (ANGPTL2) has been reported to induce sprouting angiogenesis; however, its role in vasculogenesis, the de novo lumenization of endothelial cells (EC), remains unexplored. We sought to investigate the potential role of ANGPTL2 in regulating human cord blood derived endothelial colony forming cell (ECFC) vasculogenesis through siRNA mediated inhibition of ANGPTL2 gene expression. We found that ECFCs in which ANGPTL2 was diminished displayed a threefold decrease in in vitro lumenal area whereas addition of exogenous ANGPTL2 protein domains to ECFCs lead to increased lumen formation within a 3 dimensional (3D) collagen assay of vasculogenesis. ECFC migration was attenuated by 36 % via ANGPTL2 knockdown (KD) although proliferation and apoptosis were not affected. We subsequently found that c-Jun NH2-terminal kinase (JNK), but not ERK1/2, phosphorylation was decreased upon ANGPTL2 KD, and expression of membrane type 1 matrix metalloproteinase (MT1-MMP), known to be regulated by JNK and a critical regulator of EC migration and 3D lumen formation, was decreased in lumenized structures in vitro derived from ANGPTL2 silenced ECFCs. Treatment of ECFCs in 3D collagen matrices with either a JNK inhibitor or exogenous rhTIMP-3 (an inhibitor of MT1-MMP activity) resulted in a similar phenotype of decreased vascular lumen formation as observed with ANGPTL2 KD, whereas stimulation of JNK activity increased vasculogenesis. Based on gene silencing, pharmacologic, cellular, and biochemical approaches, we conclude that ANGPTL2 positively regulates ECFC vascular lumen formation likely through its effects on migration and in part by activating JNK and increasing MT1-MMP expression
Acute high-intensity exercise and skeletal muscle mitochondrial respiratory function: role of metabolic perturbation
Recently it was documented that fatiguing, high-intensity exercise resulted in a significant attenuation in maximal skeletal muscle mitochondrial respiratory capacity, potentially due to the intramuscular metabolic perturbation elicited by such intense exercise. With the utilization of intrathecal fentanyl to attenuate afferent feedback from group III/IV muscle afferents, permitting increased muscle activation and greater intramuscular metabolic disturbance, this study aimed to better elucidate the role of metabolic perturbation on mitochondrial respiratory function. Eight young, healthy males performed high-intensity cycle exercise in control (CTRL) and fentanyl-treated (FENT) conditions. Liquid chromatography-mass spectrometry and high-resolution respirometry were used to assess metabolites and mitochondrial respiratory function, respectively, pre- and postexercise in muscle biopsies from the vastus lateralis. Compared with CTRL, FENT yielded a significantly greater exercise-induced metabolic perturbation (PCr: â67% vs. â82%, Pi: 353% vs. 534%, pH: â0.22 vs. â0.31, lactate: 820% vs. 1,160%). Somewhat surprisingly, despite this greater metabolic perturbation in FENT compared with CTRL, with the only exception of respiratory control ratio (RCR) (â3% and â36%) for which the impact of FENT was significantly greater, the degree of attenuated mitochondrial respiratory capacity postexercise was not different between CTRL and FENT, respectively, as assessed by maximal respiratory flux through complex I (â15% and â33%), complex II (â36% and â23%), complex I + II (â31% and â20%), and state 3CI+CII control ratio (â24% and â39%). Although a basement effect cannot be ruled out, this failure of an augmented metabolic perturbation to extensively further attenuate mitochondrial function questions the direct role of high-intensity exercise-induced metabolite accumulation in this postexercise response
Lengthened Predelivery Stay and Antepartum Complications in Women with Depressive Symptoms During Pregnancy
Background: It is crucial to understand the timing and mechanisms behind depression's effect on peripartum stay because attempts to intervene will vary based on the time period involved. We designed this study to compare predelivery and postdelivery length of stay in women with and without elevated depressive symptoms during pregnancy. Methods: This study involved secondary data analysis of a larger study exploring antepartum depression. Each subject completed the Center for Epidemiological Studies Depression Scale (CES-D) during pregnancy at a mean of 25.8 weeks' gestation. We used time-stamped data to compare total peripartum, predelivery, and postdelivery lengths of stay in women with and without elevated depressive symptoms during pregnancy. In addition, we used a Cox proportional hazards regression model to evaluate potential mechanisms for depression's effect on length of stay. Results: The study sample included 802 pregnant women. Overall, 18% of study subjects scored >=16 on the CES-D. Bivariate analyses demonstrated a significant association between elevated depressive symptoms and longer predelivery stays (time from admission to delivery). Interaction analyses demonstrated a significant interaction effect between depressive symptoms and parity, such that depressive symptoms were significantly associated with predelivery length of stay in multiparas but not so in primiparous subjects. In a multivariate model of multiparous subjects, depression's effect on length of stay was partially influenced by sociodemographic confounders but remained significant until antepartum complications were added to the model. Conclusions: Depressive symptoms during pregnancy are significantly associated with a subsequent increase in predelivery length of stay, and this association is mediated in part by antepartum complications, even after controlling for sociodemographic factors. These longer hospital stays can present significant burdens to the patient, her family, and the healthcare system. Future studies should evaluate whether interventions for depression during pregnancy can impact this relationship among depressive symptoms during pregnancy, antepartum complications, and extensive predelivery hospitalizations.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/90486/1/jwh-2E2010-2E2380.pd
Quadriceps exercise intolerance in patients with chronic obstructive pulmonary disease: the potential role of altered skeletal muscle mitochondrial respiration
This study sought to determine if qualitative alterations in skeletal muscle mitochondrial respiration, associated with decreased mitochondrial efficiency, contribute to exercise intolerance in patients with chronic obstructive pulmonary disease (COPD). Using permeabilized muscle fibers from the vastus lateralis of 13 patients with COPD and 12 healthy controls, complex I (CI) and complex II (CII)-driven State 3 mitochondrial respiration were measured separately (State 3:CI and State 3:CII) and in combination (State 3:CI+CII). State 2 respiration was also measured. Exercise tolerance was assessed by knee extensor exercise (KE) time to fatigue. Per milligram of muscle, State 3:CI+CII and State 3:CI were reduced in COPD (P \u3c 0.05), while State 3:CII and State 2 were not different between groups. To determine if this altered pattern of respiration represented qualitative changes in mitochondrial function, respiration states were examined as percentages of peak respiration (State 3:CI+CII), which revealed altered contributions from State 3:CI (Con 83.7 ± 3.4, COPD 72.1 ± 2.4%Peak, P \u3c 0.05) and State 3:CII (Con 64.9 ± 3.2, COPD 79.5 ± 3.0%Peak, P \u3c 0.05) respiration, but not State 2 respiration in COPD. Importantly, a diminished contribution of CI-driven respiration relative to the metabolically less-efficient CII-driven respiration (CI/CII) was also observed in COPD (Con 1.28 ± 0.09, COPD 0.81 ± 0.05, P \u3c 0.05), which was related to exercise tolerance of the patients (r = 0.64, P \u3c 0.05). Overall, this study indicates that COPD is associated with qualitative alterations in skeletal muscle mitochondria that affect the contribution of CI and CII-driven respiration, which potentially contributes to the exercise intolerance associated with this disease
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