20 research outputs found

    First Impressions of HIV Risk: It Takes Only Milliseconds to Scan a Stranger

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    Research indicates that many people do not use condoms consistently but instead rely on intuition to identify sexual partners high at risk for HIV infection. The present studies examined neural correlates for first impressions of HIV risk and determined the association of perceived HIV risk with other trait characteristics. Participants were presented with 120 self-portraits retrieved from a popular online photo-sharing community (www.flickr.com). Factor analysis of various explicit ratings of trait characteristics yielded two orthogonal factors: (1) a ‘valence-approach’ factor encompassing perceived attractiveness, healthiness, valence, and approach tendencies, and (2) a ‘safeness’ factor, entailing judgments of HIV risk, trustworthiness, and responsibility. These findings suggest that HIV risk ratings systematically relate to cardinal features of a high-risk HIV stereotype. Furthermore, event-related brain potential recordings revealed neural correlates of first impressions about HIV risk. Target persons perceived as risky elicited a differential brain response in a time window from 220–340 ms and an increased late positive potential in a time window from 350–700 ms compared to those perceived as safe. These data suggest that impressions about HIV risk can be formed in a split second and despite a lack of information about the actual risk profile. Findings of neural correlates of risk impressions and their relationship to key features of the HIV risk stereotype are discussed in the context of the ‘risk as feelings’ theory

    Ethnic–Racial Identity of Black Emerging Adults: The Role of Parenting and Ethnic–Racial Socialization

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    Ethnic–racial identity (ERI) development is important for ethnic–racial minority youth because of its association with their positive adjustment. Guided by Garcia Coll’s ecocultural framework and using survey data from 729 Black college students, we examined the associations between relationships with parents (i.e., disrespect, psychological control, nurturance, and connection), ethnic–racial socialization (ERS), and ERI in hopes of understanding ways to promote ERI formation. Findings from two multiple group models suggested that, among men, nurturance from mothers and fathers was associated with ERI and these associations were mediated by ERS. For women, connection with mothers was associated with ERI through ERS and nurturance from fathers was indirectly and positively associated with ERI through ERS. Contrary to our hypothesis, disrespect from fathers was positively associated with ERI via ERS, but only for women. Findings suggest that both ERS and the parent–child relationship are important for ERI formation among Black emerging adults. </jats:p

    Modulatory effect of interleukin-1α on expression of structural matrix proteins, MMPs and TIMPs in human cardiac myofibroblasts: Role of p38 MAP kinase

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    The proinflammatory cytokine interleukin-1 (IL-1) elicits catabolic effects on the myocardial extracellular matrix (ECM) early after myocardial infarction but there is little understanding of its direct effects on cardiac myofibroblasts (CMF), or the role of p38 mitogen-activated protein kinase (MAPK). We used a focused RT-PCR microarray to investigate the effects of IL-1α on expression of 41 ECM genes in CMF cultured from different patients, and explored regulation by p38 MAPK

    Mesenchymal–endothelial transition contributes to cardiac neovascularization

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    Endothelial cells contribute to a subset of cardiac fibroblasts by undergoing endothelial-to-mesenchymal-transition, but whether cardiac fibroblasts can adopt an endothelial cell fate and directly contribute to neovascularization after cardiac injury is not known. Here, using genetic fate map techniques, we demonstrate that cardiac fibroblasts rapidly adopt an endothelial cell like phenotype after acute ischemic cardiac injury. Fibroblast derived endothelial cells exhibit anatomical and functional characteristics of native endothelial cells. We show that the transcription factor p53 regulates such a switch in cardiac fibroblast fate. Loss of p53 in cardiac fibroblasts severely decreases the formation of fibroblast derived endothelial cells, reduces post infarct vascular density and worsens cardiac function. Conversely, stimulation of the p53 pathway in cardiac fibroblasts augments mesenchymal to endothelial transition, enhances vascularity and improves cardiac function. These observations demonstrate that mesenchymal-to-endothelial-transition contributes to neovascularization of the injured heart and represents a potential therapeutic target for enhancing cardiac repair
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