Does the Stigma of Hooking Up Predict Sexual Assault at College?

This study examines the relationship between the stigma of hooking up and reported sexual assault. Guided by Goffman’s (1963) social stigma theory and Gagnon and Simon’s (1973) sexual script theory, I propose that 1) the more strongly the respondent agrees he or she would disrespect women who hook up frequently, the fewer times he or she reports nonconsensual sex; 2) the more strongly the respondent agrees he or she would disrespect for men who hook up frequently, the fewer times he or she reports nonconsensual sex; and 3) the more strongly the respondent agrees he or she would be less interested in someone who hooks up frequently as a boyfriend/girlfriend, the fewer times he or she reports nonconsensual sex. Using the Online College Social Life Survey data collected between 2005 and 2011, I analyze the attitudes about and reports of sexual behaviors in a non-probability sample of 16,914 students at 21 U.S. colleges and universities. Controlling for sex, age, current religion preference, and Greek affiliation, disrespect towards women who hook up frequently is positively and significantly related to fewer reports of nonconsensual sex. However, the results do not support the second and third hypotheses as there is no statistically significant relationship between disrespect towards men who hook up frequently as well as the lack of interest in people who hook up frequently and the incidents of reported nonconsensual sex. The findings suggest that the efforts to reduce the stigma of hooking up should be taken into consideration in rape prevention programming

Structure fusion based on graph convolutional networks for semi-supervised classification

Suffering from the multi-view data diversity and complexity for semi-supervised classification, most of existing graph convolutional networks focus on the networks architecture construction or the salient graph structure preservation, and ignore the the complete graph structure for semi-supervised classification contribution. To mine the more complete distribution structure from multi-view data with the consideration of the specificity and the commonality, we propose structure fusion based on graph convolutional networks (SF-GCN) for improving the performance of semi-supervised classification. SF-GCN can not only retain the special characteristic of each view data by spectral embedding, but also capture the common style of multi-view data by distance metric between multi-graph structures. Suppose the linear relationship between multi-graph structures, we can construct the optimization function of structure fusion model by balancing the specificity loss and the commonality loss. By solving this function, we can simultaneously obtain the fusion spectral embedding from the multi-view data and the fusion structure as adjacent matrix to input graph convolutional networks for semi-supervised classification. Experiments demonstrate that the performance of SF-GCN outperforms that of the state of the arts on three challenging datasets, which are Cora,Citeseer and Pubmed in citation networks

Apoptotic cell-mediated suppression of streptococcal cell wall-induced arthritis is associated with alteration of macrophage function and local regulatory T-cell increase: a potential cell-based therapy?

International audienceINTRODUCTION: Experimental streptococcal cell wall (SCW)-induced arthritis is characterized by two successive phases of the disease. The acute phase occurs early and is associated with an inflammatory process and neutrophil infiltration into the synovium. The second chronic phase is related to effector T-cell activation and the dysregulation of macrophage function. Creation of an immunomodulatory environment has been attributed to apoptotic cells themselves, apoptotic cell uptake by phagocytes as well as a less sensibility of phagocytes capturing apoptotic bodies to activation. Therefore we evaluated the potential of apoptotic cell injection to influence the course of inflammation in SCW-induced arthritis in rats. METHODS: Rat apoptotic thymocytes were injected intraperitoneally (2 x 108) in addition to an arthritogenic dose of systemic SCW in LEW female rats. Control rats received SCW immunization and PBS. Rats were then followed for arthritis occurrence and circulating cytokine detection. At sacrifice, regulatory T cells (Tregs) and macrophages were analyzed. RESULTS: Apoptotic cell injection profoundly suppressed joint swelling and destruction typically observed during the acute and chronic phases of SCW-induced arthritis. Synovial inflammatory cell infiltration and bone destruction were also markedly suppressed. Ex vivo experiments revealed reduced levels of TNF in cultures of macrophages from rats challenged with SCW in the presence of apoptotic thymocytes as well as reduced macrophage response to lipopolysaccharide. Moreover, apoptotic cell injection induced higher Foxp3+ Tregs in the lymphoid organs, especially in the draining lymph nodes. CONCLUSIONS: Our data indicate that apoptotic cells modulate macrophage function and result in Treg generation/increase. This may be involved in inhibition of inflammation and amelioration of arthritis. This highlights and confirms previous studies showing that in vivo generation of Tregs using apoptotic cell injection may be a useful tool to prevent and treat inflammatory autoimmune responses

Multiple origins of a frameshift insertion in a mitochondrial gene in birds and turtles

BACKGROUND: During evolutionary history, molecular mechanisms have emerged to cope with deleterious mutations. Frameshift insertions in protein-coding sequences are extremely rare because they disrupt the reading frame. There are a few known examples of their correction through translational frameshifting, a process that enables ribosomes to skip nucleotides during translation to regain proper reading frame. Corrective frameshifting has been proposed to act on the single base pair insertion at position 174 of the mitochondrial NADH dehydrogenase subunit 3 gene (ND3) that has been observed in several turtles and birds. However, the relatively sparse taxonomic representation has hampered our understanding of the evolution of this insertion in vertebrates. RESULTS: Here, we analyzed 87,707 ND3 sequences from 10,309 vertebrate taxa to reveal the evolutionary history of this insertion and its common genomic characteristics. We confirmed that the insertion only appears in turtles and birds and reconstructed that it evolved independently in both groups with complex patterns of gains and losses. The insertion was observed in almost all bird orders but was absent in all members of the diverse Passeriformes. We found strong conservation in the nucleotides surrounding the insertion in both turtles and birds, which implies that the insertion enforces structural constraints that could be involved in its correction. CONCLUSIONS: Our study demonstrates that frameshifts can be widespread and can be retained for millions of years if they are embedded in a conserved sequence theme

Endogenous TGF-β activation by reactive oxygen species is key to Foxp3 induction in TCR-stimulated and HIV-1-infected human CD4+CD25- T cells

<p>Abstract</p> <p>Background</p> <p>CD4⁺CD25⁺T regulatory cells (Tregs) play an important role in regulating immune responses, and in influencing human immune diseases such as HIV infection. It has been shown that human CD4⁺CD25⁺Tregs can be induced in vitro by TCR stimulation of CD4⁺CD25^-T cells. However, the mechanism remains elusive, and intriguingly, similar treatment of murine CD4⁺CD25^-cells did not induce CD4⁺CD25⁺Foxp3⁺Tregs unless exogenous TGF-β was added during stimulation. Thus, we investigated the possible role of TGF-β in the induction of human Tregs by TCR engagement. We also explored the effects of TGF-β on HIV-1 infection mediated induction of human Tregs since recent evidence has suggested that HIV-1 infection may also impact the generation of Tregs in infected patients.</p> <p>Results</p> <p>We show here that endogenous TGF-β is key to TCR induction of Foxp3 in human CD4⁺CD25^-T cells. These events involve, first, the production of TGF-β by TCR and CD28 stimulation and the activation of latent TGF-β by reactive oxygen species generated from the activated T cells. Biologically active TGF-β then engages in the induction of Foxp3. Neutralization of active TGF-β with anti-TGF-β antibody or elimination of ROS with MnTBAP abrogated Foxp3 expression. HIV-1 infection enhanced Foxp3 expression in activated CD4⁺CD25^-T cells; which was also abrogated by blockade of endogenous TGF-β.</p> <p>Conclusion</p> <p>Several conclusions can be drawn from this work: (1) TCR and CD28-induced Foxp3 expression is a late event following TCR stimulation; (2) TGF-β serves as a link in Foxp3 induction in human CD4⁺CD25^-T cells following TCR stimulation, which induces not only latent, but also active TGF-β; (3) the activation of TGF-β requires reactive oxygen species; (4) HIV infection results in an increase in Foxp3 expression in TCR-activated CD25^-T cells, which is also associated with TGF-β. Taken together, our findings reinforce a definitive role of TGF-β not only in the generation of Tregs with respect to normal immune responses, but also is critical in immune diseases such as HIV-1 infection.</p