20 research outputs found

    Contextualizing students' alcohol use perceptions and practices within French culture: an analysis of gender and drinking among sport-science college students

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    Although research has examined alcohol consumption and sport in a variety of contexts, there is a paucity of research on gender and gender dynamics among French college students. The present study addresses this gap in the literature by examining alcohol use practices by men and women among a non-probability sample of French sport science students from five different universities in Northern France. We utilized both survey data (N = 534) and in-depth qualitative interviews (n = 16) to provide empirical and theoretical insight into a relatively ubiquitous health concern: the culture of intoxication. Qualitative data were based on students’ perceptions of their own alcohol use; analysis were framed by theoretical conceptions of gender. Survey results indicate gender differences in alcohol consumption wherein men reported a substantially higher frequency and quantity of alcohol use compared to their female peers. Qualitative findings confirm that male privilege and women’s concern for safety, masculine embodiment via alcohol use, gendering of alcohol type, and gender conformity pressures shape gender disparities in alcohol use behavior. Our findings also suggest that health education policy and educational programs focused on alcohol-related health risks need to be designed to take into account gender category and gender orientation

    A Path To 2030: Targeting Women And Girls To End The Hiv/Aids Epidemic In Sub-Saharan Africa

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    HIV/AIDS remains a significant problem in sub-Saharan Africa, even though international efforts have been working in the region for the last fifteen years. This paper examines HIV/AIDS data from four international health organization, the ONE Campaign, PEPFAR, the WHO, and the UN. Findings suggest UN’s Fast Track goals will not be met by 2020, which will jeopardize eradicating HIV/AIDS by 2030, unless changes to programing are made. First, women and girls who are HIV positive in the sub-Saharan Africa should follow the WHO’s Treat All Approach to prevent HIV transmission and those who are HIV negative should be placed on pre-exposure prophylaxis to prevent infection. Second, pregnant women should follow the WHO’s Treat All Approach in order to prevent mother to child transmission. Third, non-medical interventions such as reducing gender based violence and increasing access to education should be increased. Fourth, men’s health should be changed to help reach the Fast Track goals. These changes would include discrete testing services for men to encourage them to know their HIV status and get treated and an increase in voluntary make circumcisions to reduce infection rates. Funding is a major barrier to these recommendations. In order to close the funding gap, the US must keep its funding at current levels and G7 countries and middle and low income nations must increase their funding levels

    A novel SERPINA1 mutation causing serum alpha(1)-antitrypsin deficiency.

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    Mutations in the SERPINA1 gene can cause deficiency in the circulating serine protease inhibitor α(1)-Antitrypsin (α(1)AT). α(1)AT deficiency is the major contributor to pulmonary emphysema and liver disease in persons of European ancestry, with a prevalence of 1 in 2500 in the USA. We present the discovery and characterization of a novel SERPINA1 mutant from an asymptomatic Middle Eastern male with circulating α(1)AT deficiency. This 49 base pair deletion mutation (T379Δ), originally mistyped by IEF, causes a frame-shift replacement of the last sixteen α(1)AT residues and adds an extra twenty-four residues. Functional analysis showed that the mutant protein is not secreted and prone to intracellular aggregation

    Functional Characterisation of α<sub>1</sub>AT

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    <p><sup>Δ<b>379</b></sup><b> Mutant.</b> (A) Immunoblot (anti-GFP) detection of α<sub>1</sub>AT-GFP fusion protein (C-terminal tag) in whole-cell lysate and concentrated conditioned media (ie secreted) from HEK293T cells transfected with plasmids expressing either wild-type or Δ379 mutant α<sub>1</sub>AT-GFP. Red arrow denotes position of ∼75 kDa α<sub>1</sub>AT-GFP band, note the absence of this band in conditioned media from cells transfected with Δ379 mutant, indicating impaired secretion of mutant protein; (B) Immunoblot (anti-α<sub>1</sub>AT) detection of α<sub>1</sub>AT-GFP fusion protein (C-terminal tag) in whole-cell lysate, or following immunprecipitation from conditioned media (i.e. secreted) from HEK293T cells transfected with plasmids expressing either wild-type or Δ379 mutant α<sub>1</sub>AT-GFP; (C) Transfection of either wild-type or Δ379 mutant α<sub>1</sub>AT with an N-terminal EGFP fusion into HEK293T cells clearly indicated normal proteolytic processing of the secretion signal peptide. Both ∼75 kDA and ∼27 kDA bands are visible, representing full-length and processed (i.e. signal peptide cleaved) α<sub>1</sub>AT-GFP fusion protein respectively; (D) At higher expression levels, accumulation of insoluble Δ379 mutant α<sub>1</sub>AT was observed in HEK293T cells, clearly denoted by the presence of a darker band in the insoluble fraction from cells transfected with Δ379 mutant; (E) Detection of soluble (whole-cell lysate), insoluble and secreted (concentrated conditioned media) α<sub>1</sub>AT in HeLa cells transfected with either wild-type or Δ379 mutant α<sub>1</sub>AT-GFP. Red arrow denotes position of ∼75 kDa α<sub>1</sub>AT-GFP band. Note the absence of this band in conditioned media from cells transfected with Δ379 mutant, indicating impaired secretion of mutant protein; (E) Fluorescent micrographs of HEK293T cells following transfection with either wild-type or Δ379 mutant α<sub>1</sub>AT-GFP expression plasmids. Increased intracellular aggregation of mutant protein is clearly visible. NB: Loading controls represent α-tubulin immunoblot or PonceauS staining in lysate or secreted (conditioned media) samples, respectively.</p

    Identification of a novel SerpinA1 Mutant. A.

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    <p>DGGE banding patterns representing four controls (lanes 2–5) heterozygous for the M3 mutation (E376D), while our patient (lane 1), although also heterozygous for the M3 variant also presents with a shifted (faster migrating) banding depicting the novel deletion mutation (T379Δ). <b>B.</b> Sanger sequencing defines the deleted base pairs. The predicted amino acid sequence resulting from the novel 49 bp deletion (denoted by * on lower chromatogram) observed in our patient, results in the replacement of 16 amino acids and the addition of 24 amino acids through partial translation of the 3′ UTR.</p
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