Are delay ages at marriage increasing? Pre-marital sexual relation among youth people in the place of residence in India.

BACKGROUND: Adolescent sexual and reproductive health is a major public health issue throughout the world. At the same time shifting of marriage are undergoing discernible changes in country like India. This paper attempts to examine the effect of delay age at marriage on the risks of pre-marital sexual intercourse for the youth people in the place of residence. METHODS: Data used in the present study is from various annual publications of Sample Registration System (SRS) and four round of National Family Health Survey, which was conducted in 2015-2016. The Kaplan-Meier life table technique and multivariate regression models are used to examine the premarital sex by the place of residence and marriage cohort. RESULTS: Findings of the study indicate that the reasons underlying delayed marriage differs between blow 21 years age group and 22-30 years age group. Multinomial analysis clearly shows education, wealth quintile and mass media are major controlling factors of delayed age at marriage. Residing in urban adolescent women who belonged to better economic family background and exposed to mass media had a higher probability to experience premarital sexual intercourse than the rural adolescent in delay age group. CONCLUSION: The study concludes that the restorative the empowerment of youth especially for women and health care provider should consider a multidimensional approach for higher education among youth people and safe sexual behaviour in pre-marital sexual intercourse.

Reprogramming of profibrotic macrophages for treatment of bleomycin-induced pulmonary fibrosis.

Fibrotic diseases cause organ failure that lead to ~45% of all deaths in the United States. Activated macrophages stimulate fibrosis by secreting cytokines that induce fibroblasts to synthesize collagen and extracellular matrix proteins. Although suppression of macrophage-derived cytokine production can halt progression of fibrosis, therapeutic agents that prevent release of these cytokines (e.g., TLR7 agonists) have proven too toxic to administer systemically. Based on the expression of folate receptor ß solely on activated myeloid cells, we have created a folate-targeted TLR7 agonist (FA-TLR7-54) that selectively accumulates in profibrotic macrophages and suppresses fibrosis-inducing cytokine production. We demonstrate that FA-TLR7-54 reprograms M2-like fibrosis-inducing macrophages into fibrosis-suppressing macrophages, resulting in dramatic declines in profibrotic cytokine release, hydroxyproline biosynthesis, and collagen deposition, with concomitant increases in alveolar airspaces. Although nontargeted TLR7-54 is lethal at fibrosis-suppressing doses, FA-TLR7-54 halts fibrosis without evidence of toxicity. Taken together, FA-TLR7-54 is shown to constitute a novel and potent approach for treating fibrosis without causing dose-limiting systemic toxicities.