Sexuality and gender: change through reflection and action

Gender and sexuality inequalities lie at the root of poor sexual and reproductive health (SRH). An India-based non-governmental organization (NGO) implemented a field-based methodology to integrate gender and sexuality into existing SRH projects in two states. Personal and organizational change occurred through critical analysis and experiential exercises which normalized topics on sexuality for program staff and communities. Staff learned how biases prevented them from engaging with communities. Community women came to understand sexual pleasure as an important aspect of strengthening the family and community. Mapping women's mobility revealed the link between sexuality, mobility and family honour. Gender myths, portraying men as oppressors, made explicit the narrow and biased picture of men that perpetuates through social norms maintained by staff and not only by communities in which they work. Methods improved social relations and prompted both behaviour and social changes at the community level.     

Societal awareness on neonatal hyperbilirubinemia: A systematic review and meta-analysis

Early recognition of neonatal hyperbilirubinemia is essential for prevention of bilirubin neurotoxicity and its long-term sequelae. High rates of home delivery in low- and middle-income countries (LMICs) as well as early discharge post-delivery (within 24hours) make community surveillance for neonatal hyperbilirubinemia highly important. Here, we performed a literature review to estimate the level of societal awareness of neonatal hyperbilirubinemia. We searched several databases for studies assessing the knowledge and awareness of neonatal hyperbilirubinemia. We retrieved 211 citations from 206 databases with five being in the grey literature. 52 selected articles were further reviewed. Data from these studies were then analyzed using Stata software (Statacorp® LLC Texas USA). We found that the pooled estimate of societal awareness of neonatal hyperbilirubinemia was 67% (95% confidence interval [CI]: 60, 74). There however was a publication bias (Begg test: P ≤ 0.01; Egger P = 0.06). Studies that scored or graded knowledge reported lower estimates [adjusted odds ratio (aOR) = -0.17; 95% CI: -0.32–0.02; P = 0.03]. Hospital location was an important determinant of awareness of complications [aOR = 0.30; 95% CI: 0.30–0.57; P = 0.03]. We therefore concluded that there is a significant need to improve societal awareness of neonatal hyperbilirubinemia.     

How Picky Eating Becomes an Illness—Marketing Nutrient-Enriched Formula Milk in a Chinese Society

The essential adaptive food selection behavior of young children has become increasingly medicalized as a kind of disease—the “picky-eating” syndrome in Hong Kong. The researcher used the multiple case studies approach with data collected from in-depth interviews and advertisements to examine the process of the medicalization of picky-eating disorder, which demonstrates how an essential adaptive human behavior can be redefined by the market and medical system as a deviant, abnormal behavior that needs to be eliminated and how the resulting health risks can be resolved by modern medicine produced by this pharmaceutical nexus.     

Targeting Janus tyrosine kinase 3 (JAK3) with an inhibitor induces secretion of TGF-β by CD4+ T cells

Regulatory T cells (Tregs) are critical for the peripheral maintenance of the autoreactive T cells in autoimmune disorders such as type 1 diabetes (T1D). Pharmacological inhibition of Janus tyrosine kinase 3 (JAK3) has been proposed as a basis for new treatment modalities against autoimmunity and allogeneic responses. Targeting JAK3 with an inhibitor has previously been shown to exhibit protective action against the development of T1D in non-obese diabetic (NOD) mice. As the mechanism of such preventative action has been unknown, we hypothesized that JAK3 inhibition induces generation of Tregs. Here, we show that the JAK3 inhibitor 4-(4′-hydroxyphenyl)-amino-6,7-dimethoxyquinazoline (WHI-P131) suppresses proliferation of short-term cultured NOD CD4⁺ T cells through induction of apoptosis, while promoting survival of a particular population of long-term cultured cells. It was found that the surviving cells were not of the CD4⁺CD25⁺FoxP3⁺ phenotype. They secreted decreased amounts of IL-10, IL-4 and interferon (IFN)-γ compared to the cells not exposed to the optimal concentrations of JAK3 inhibitor. However, an elevated transforming growth factor (TGF)-β secretion was detected in their supernatants. In vivo treatment of prediabetic NOD mice with WHI-P131 did not affect the frequency and number of splenic and pancreatic lymph node CD4⁺FoxP3⁺ Tregs, while generating an elevated numbers of CD4⁺FoxP3⁻ TGF-β-secreting T cells. In conclusion, our data suggest an induction of TGF-β-secreting CD4⁺ T cells as the underlying mechanism for antidiabetogenic effects obtained by the treatment with a JAK3 inhibitor. To our knowledge, this is the first report of the JAK3 inhibitor activity in the context of the murine Tregs.