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We adapted the Sexual Experiences Survey (SES) to be more inclusive of transgender, nonbinary, and gender-expansive people and undertook preliminary validation of the measure. We added gender-neutral language, assault types thought to be more common and more emotionally impactful among these individuals, and coercion tactics specific to transgender, nonbinary, and gender-expensive people. We piloted this Gender-Inclusive SES (GI-SES) with an online survey of transgender and gender-expansive undergraduates who experienced campus sexual assault. We assessed acceptability via rapid qualitative analysis of feedback. We gathered preliminary evidence of validity by calculating the agreement in assault type and coercion tactic between open-ended descriptions of the assault and the GI-SES response, as well as by testing four hypotheses about the relative frequency and severity of different types of assaults within the sample. Three hundred eighty-eight transgender, nonbinary, and gender-expensive students completed the survey. Qualitative responses indicated that participants felt the GI-SES was inclusive and respectful. Results were partially consistent with hypotheses supporting validity, and there was 90.9% agreement in assault type and 85.9% agreement in coercion tactics between GI-SES responses and written narratives. The GI-SES provides researchers, clinicians, and service providers with a tool, preliminarily validated with a trans and gender-diverse college sample, to capture the unique experiences of transgender, nonbinary, and gender-expensive sexual assault survivors. [ABSTRACT FROM AUTHOR]

Background and Aims: Brivanib is a selective inhibitor of vascular endothelial growth factor receptor (VEGFR) and fibroblast growth factor receptor (FGFR) tyrosine kinases, which are both involved in mechanisms of liver fibrosis. We hypothesized that inhibition of VEGFR and FGFR by brivanib would inhibit liver fibrosis. We therefore examined the effect of brivanib on liver fibrosis in three mouse models of fibrosis. Methods: In vivo, we induced liver fibrosis by bile duct ligation (BDL), chronic carbon tetrachloride (CCl4), and chronic thioacetamide (TAA) administration. Liver fibrosis was examined by immunohistochemistry and Western immunoblotting. In vitro, we used LX-2 human hepatic stellate cells (HSCs) to assess the effect of brivanib on stellate cell proliferation and activation. Results: After in vivo induction with BDL, CCl4, and TAA, mice treated with brivanib showed reduced liver fibrosis and decreased expression of collagen Iα1 and α-smooth muscle actin in the liver. In vitro, brivanib decreased proliferation of HSCs induced by platelet-derived growth factor (PDGF), VEGF, and FGF. Brivanib also decreased stellate cell viability and inhibited PDGFBB-induced phosphorylation of its cognate receptor. Conclusion: Brivanib reduces liver fibrosis in three different animal models and decreases human hepatic stellate cell activation. Brivanib may represent a novel therapeutic approach to treatment of liver fibrosis and prevention of liver cancer. [ABSTRACT FROM AUTHOR]