How gender- and violence-related norms affect self-esteem among adolescent refugee girls living in Ethiopia.

BACKGROUND: Evidence suggests adolescent self-esteem is influenced by beliefs of how individuals in their reference group perceive them. However, few studies examine how gender- and violence-related social norms affect self-esteem among refugee populations. This paper explores relationships between gender inequitable and victim-blaming social norms, personal attitudes, and self-esteem among adolescent girls participating in a life skills program in three Ethiopian refugee camps. METHODS: Ordinary least squares multivariable regression analysis was used to assess the associations between attitudes and social norms, and self-esteem. Key independent variables of interest included a scale measuring personal attitudes toward gender inequitable norms, a measure of perceived injunctive norms capturing how a girl believed her family and community would react if she was raped, and a peer-group measure of collective descriptive norms surrounding gender inequity. The key outcome variable, self-esteem, was measured using the Rosenberg self-esteem scale. RESULTS: Girl's personal attitudes toward gender inequitable norms were not significantly predictive of self-esteem at endline, when adjusting for other covariates. Collective peer norms surrounding the same gender inequitable statements were significantly predictive of self-esteem at endline (ß = -0.130; p  =  0.024). Additionally, perceived injunctive norms surrounding family and community-based sanctions for victims of forced sex were associated with a decline in self-esteem at endline (ß = -0.103; p  =  0.014). Significant findings for collective descriptive norms and injunctive norms remained when controlling for all three constructs simultaneously. CONCLUSIONS: Findings suggest shifting collective norms around gender inequity, particularly at the community and peer levels, may sustainably support the safety and well-being of adolescent girls in refugee settings

Corneal recovery in a rabbit limbal stem cell deficiency model by autologous grafts of tertiary outgrowths from cultivated limbal biopsy explants

PubMed ID: 26937166Purpose: To determine the corneal regenerative capacity of sequentially generated primary, secondary, and tertiary limbal explant outgrowths in a limbal stem cell deficiency (LSCD) surgical model. Methods: Two-millimeter-long limbal shallow biopsies were surgically excised from the upper quadrant of the right eye of rabbits and set on preserved amniotic membrane for explant culture. After the generation of primary outgrowth, the biopsies were sequentially transferred to new amniotic membrane to generate secondary and then tertiary outgrowths. Eighteen rabbits were subjected to a 360° limbal peritomy extending into the scleral zone and combined with superficial keratectomy of the corneal periphery and thorough mechanical debridement of the central cornea in their left eye. Right eye outgrowths, six of each generation, were engrafted on the ocular surface. Clinical outcomes (neovascularization, corneal clarity, and corneal fluorescein staining) were graded after 6 months. Post-mortem corneas were compared with histology, immunochemistry for p63 and Krt3, ABCG2-dependent dye exclusion, and capacity for outgrowths in explant culture. Results: Immunohistology and western blot of the outgrowths for p63 and Krt3 indicated no differences in expression between the primary and tertiary outgrowths for these two markers of growth and differentiation. Clinically, all rabbits treated with amniotic membrane alone developed severe LSCD. Most rabbits grafted with cell outgrowths from all three outgrowth generations achieved stable (>6 months) recovery of the ocular surface. There were partial failures of grafts performed with two secondary and tertiary outgrowths. However, Kruskal-Wallis statistical analysis of the clinical scores yielded no significant difference between the three groups (p=0.524). Histology showed full anatomic recovery of grafts made with primary and tertiary outgrowths. Krt3 and p63 expression throughout the whole limbal corneal epithelium with primary or tertiary outgrowths was not distinguishable from each other. The percentage of dye-excluding cells present within this zone and the capacity of the explant epithelial outgrowth of the regenerated peripheral corneal zone were also on par with those of the donor corneas. The Krt3-negative cells that characterize the basal epithelial layer of the normal limbus could not be found in any regenerated cornea from the primary to tertiary outgrowths. Conclusions: Our results demonstrate that in rabbits post-primary explant outgrowths retain the capacity for LSCD recovery found in primary explants. © 2016, Molecular Vision.National Institutes of Health, NIH: K08EY02399

The cellular prion protein counteracts cardiac oxidative stress

Aims. The cellular prion protein, PrPC, whose aberrant isoforms are related to prion diseases of humans and animals, has a still obscure physiologic function. Having observed an increased expression of PrPC in two in vivo paradigms of heart remodelling, we focused on isolated mouse hearts to ascertain the capacity of PrPC to antagonize oxidative damage induced by ischemic and non-ischemic protocols. Methods and results. Hearts isolated from mice expressing PrPC in variable amounts were subjected to different and complementary oxidative perfusion protocols. Accumulation of reactive oxygen species, oxidation of myofibrillar proteins and cell death were evaluated. We found that overexpressed PrPC reduced oxidative stress and cell death caused by post-ischemic reperfusion. Conversely, deletion of PrPC increased oxidative stress during both ischemic preconditioning and perfusion (15 min) with H2O2. Supporting its relation with intracellular systems involved in oxidative stress, PrPC was found to influence the activity of catalase and, for the first time, the expression of p66Shc, a protein implicated in oxidative stress-mediated cell death. Conclusions. Our data demonstrate that PrPC contributes to the cardiac mechanisms antagonizing oxidative insults

Toll-like receptor 9 signaling after myocardial infarction: Role of p66ShcA adaptor protein

: During myocardial infarction, cellular debris is released, causing a sterile inflammation via pattern recognition receptors. These reactions amplify damage and promotes secondary heart failure. The pattern recognition receptor, Toll-like receptor 9 (TLR9) detects immunogenic fragments of endogenous DNA, inducing inflammation by NFκB. The p66ShcA adaptor protein plays an important role in both ischemic myocardial damage and immune responses. We hypothesized that p66ShcA adaptor protein promotes DNA-sensing signaling via the TLR9 pathway after myocardial infarction. TLR9 protein expression increased in cardiac tissue from patients with end-stage heart failure due to ischemic heart disease. Myocardial ischemia in mice in vivo induced gene expression of key TLR9 pathway proteins (MyD88 and Unc93b1). In this model, a functional link between TLR9 and p66ShcA was revealed as; (i) ischemia-induced upregulation of TLR9 protein was abrogated in myocardium of p66ShcA knockout mice; (ii) when p66ShcA was overexpressed in NFkB reporter cells stably expressing TLR9, NFkB-activation increased during stimulation with the TLR9 agonist CpG B; (iii) in cardiac fibroblasts, p66ShcA overexpression caused TLR9 upregulation. Co-immunoprecipitation showed that ShcA proteins and TLR9 may be found in the same protein complex, which was dissipated upon TLR9 stimulation in vivo. A proximity assay confirmed the co-localization of TLR9 and ShcA proteins. The systemic immune response after myocardial ischemia was dampened in p66ShcA knockout mice as interleukin-4, -17 and -22 expression in mononuclear cells isolated from spleens was reduced. In conclusion, p66ShcA adaptor may be an interaction partner and a regulator of the TLR9 pathway post-infarction