31 research outputs found

    Community Violence in Childhood

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    Experiencing violence in childhood is an all too common occurrence, especially in sexual and gender minority communities. It can be hard to dictate predictors of these such occurrences, which is the focus of our study. A survey regarding many different experiences members of these communities can have was taken by 1316 people via Reddit. Out of these participants, 309 reported experiencing some form of violence in their childhood. Among the demographic information taken for the survey, none had a significant correlation besides education. Although this factor did have statistical significance, there is no logical explanation as education can be continued after childhood, therefore it isn’t necessarily classified as a predictor. There was a larger amount of reported violence in childhood among gender minorities than sexual minorities, however. This increase can be due to many factors, the main one potentially being the difference in how a person may present their sexuality versus how they may present their gender. These findings help begin the start of the research towards why these violent experiences can be common among these communities and preventative measures that can be taken to put an end to it

    Guidelines for enhancement of visual conspicuity of trains at grade crossings. Final report.

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    Federal Railroad Administration, Office of Research and Development, Washington, D.C.Mode of access: Internet.Author corporate affiliation: Transportation Systems Center, Cambridge, Mass.Report covers the period June 1972-Nov 1974Subject code: CDJISubject code: DDBSubject code: DVGSubject code: JA*JDSubject code: NDCCSubject code: NDISubject code: NDCKSubject code: PMKHSubject code: SCESubject code: WU*NDSubject code: YE

    Community Violence in Childhood

    No full text
    Experiencing violence in childhood is an all too common occurrence, especially in sexual and gender minority communities. It can be hard to dictate predictors of these such occurrences, which is the focus of our study. A survey regarding many different experiences members of these communities can have was taken by 1316 people via Reddit. Out of these participants, 309 reported experiencing some form of violence in their childhood. Among the demographic information taken for the survey, none had a significant correlation besides education. Although this factor did have statistical significance, there is no logical explanation as education can be continued after childhood, therefore it isn’t necessarily classified as a predictor. There was a larger amount of reported violence in childhood among gender minorities than sexual minorities, however. This increase can be due to many factors, the main one potentially being the difference in how a person may present their sexuality versus how they may present their gender. These findings help begin the start of the research towards why these violent experiences can be common among these communities and preventative measures that can be taken to put an end to it

    PKCδ mediates mineralocorticoid receptor activation by angiotensin ii to modulate smooth muscle cell function

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    Angiotensin II (AngII) and the mineralocorticoid receptor (MR) ligand aldosterone both contribute to cardiovascular disorders, including hypertension and adverse vascular remodeling. We previously demonstrated that AngII activates MR-mediated gene transcription in human vascular smooth muscle cells (SMCs), yet the mechanism and the impact on SMC function are unknown. Using an MR-responsive element-driven transcriptional reporter assay, we confirm that AngII induces MR transcriptional activity in vascular SMCs and endothelial cells, but not in Cos1 or human embryonic kidney-293 cells. AngII activation of MR was blocked by the MR antagonist spironolactone or eplerenone and the protein kinase C-δ (PKCδ) inhibitor rottlerin, implicating both in the mechanism. Similarly, small interfering RNA knockdown of PKCδ in SMCs prevented AngII-mediated MR activation, whereas knocking down of MR blocked both aldosterone- and AngII-induced MR function. Coimmunoprecipitation studies reveal that endogenous MR and PKCδ form a complex in SMCs that is enhanced by AngII treatment in association with increased serine phosphorylation of the MR N terminus. AngII increased mRNA expression of the SMC-MR target gene, FKBP51, via an MR-responsive element in intron 5 of the FKBP51 gene. The impact of AngII on FKBP51 reporter activity and gene expression in SMCs was inhibited by spironolactone and rottlerin. Finally, the AngII-induced increase in SMC number was also blocked by the MR antagonist spironolactone and the PKCδ inhibitor rottlerin. These data demonstrate that AngII activates MR transcriptional regulatory activity, target gene regulation, and SMC proliferation in a PKCδ-dependent manner. This new mechanism may contribute to synergy between MR and AngII in driving SMC dysfunction and to the cardiovascular benefits of MR and AngII receptor blockade in humans160921012114FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESP2014/26192-6This work was supported by National Institutes of Health Grants HL095590 and HL119290 (to I.Z.J.), American Heart Association Grants EIA18290005 (to I.Z.J.) and 11POST5390010 (to A.P.M.), and by São Paulo Research Foundation (FAPESP) Grant 2014/26192-6 to (A.P.D.

    Functional mineralocorticoid receptors in human vascular endothelial cells regulate intercellular adhesion molecule-1 expression and promote leukocyte adhesion

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    In clinical trials, aldosterone antagonists decrease cardiovascular mortality and ischemia by unknown mechanisms. The steroid hormone aldosterone acts by binding to the mineralocorticoid receptor (MR), a ligand-activated transcription factor. In humans, aldosterone causes MR-dependent endothelial cell (EC) dysfunction and in animal models, aldosterone increases vascular macrophage infiltration and atherosclerosis. MR antagonists inhibit these effects without changing blood pressure, suggesting a direct role for vascular MR in EC function and atherosclerosis. Whether human vascular ECs express functional MR is not known. Here, we show that human coronary artery and aortic ECs express MR mRNA and protein and that EC MR mediates aldosterone-dependent gene transcription. Human ECs also express the enzyme 11-beta-hydroxysteroid dehydrogenase-2 (11betaHSD2), and inhibition of 11betaHSD2 in aortic ECs enhances gene transactivation by cortisol, supporting that EC 11betaHSD2 is functional. Furthermore, aldosterone stimulates transcription of the proatherogenic leukocyte-EC adhesion molecule intercellular adhesion molecule (ICAM)1 gene and protein expression on human coronary artery ECs, an effect inhibited by the MR antagonist spironolactone and by MR knock down with small interfering RNA. Cell adhesion assays demonstrate that aldosterone promotes leukocyte-EC adhesion, an effect that is inhibited by spironolactone and ICAM1 blocking antibody, supporting that aldosterone induction of EC ICAM1 surface expression via MR mediates leukocyte-EC adhesion. These data show that aldosterone activates endogenous EC MR and proatherogenic gene expression in clinically important human ECs. These studies describe a novel mechanism by which aldosterone may influence ischemic cardiovascular events and support a new explanation for the decrease in ischemic events in patients treated with aldosterone antagonists
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