District-level HIV estimates using the spectrum model in five states of India, 2017

Decentralized response has been the hallmark of the National AIDS Control Programme in India. District-level HIV burden estimates quantifying the distribution of the epidemics are needed to enhance this decentralized response further to monitor the progress on prevention, testing, and treatment interventions. In this paper, we describe the methodology and results of district-level estimates using the Spectrum model piloted in 5 states of India under National AIDS Control Programme.Using state spectrum model for HIV estimations 2017, we disaggregated state results by the district in pilot states. Each district was considered a subepidemic and HIV epidemic configuration was carried out in its general population as well as in key population. We used HIV surveillance data from antenatal clinics and routine pregnant women testing to model the general population''s epidemic curve. We used HIV prevalence data available from HIV sentinel surveillance and integrated biological and behavioral surveys to inform the epidemic curve for key population. Estimation and projection packgage classic platform was used for the curve fitting. District-wide estimates extracted from subpopulation summary in Spectrum results section were used to calculate relative burden for each district and applied to approved State HIV Estimations 2017 estimates.No district in Tamil Nadu had an adult HIV prevalence of higher than 0.5% except for one, and the epidemic seems to be declining. In Maharashtra, the epidemic has shown a decline, with all except 5 districts showing an adult prevalence of less than 0.50%. In Gujarat and Uttar Pradesh, few districts showed rising HIV prevalence. However, none had an adult prevalence of higher than 0.50%. In Mizoram, 6 of 8 districts showed a rising HIV trend with an adult prevalence of 1% or more in 5 districts.Disaggregation of state-level estimates by districts provided insights on epidemic diversity within the analyzed states. It also provided baseline evidence to measure the progress toward the goal of end of AIDS by 2030.     

Dose-response efficacy of caraway (Carum carvi L.) on tissue lipid peroxidation and antioxidant profile in rat colon carcinogenesis

Colon cancer is a leading cause of cancer death and its prevention is of great interest throughout the world. This study was conducted to examine the efficacy of different doses of dietary caraway (Carum carvi L.) on tissue lipid peroxidation (LPO) and antioxidant profile in rat colon carcinogenesis. Wistar male rats were divided into 6 groups and were fed a modified pellet diet for the whole of 30 weeks. To induce colon cancer, rats were given a weekly subcutaneous injection of 1,2-dimethylhydrazine (DMH) at a dose of 20 mg kg(-1) (based on body weight) for the first 15 weeks. Caraway was supplemented every day orally at doses of 30, 60 and 90 mg kg(-1) for different groups of rats for the total period of 30 weeks. All rats were sacrificed at the end of 30 weeks, the colons were examined visually for masses and were subsequently evaluated histologically. The results showed diminished levels of intestinal, colonic and caecal LPO products, such as conjugated dienes (CD), lipid hydroperoxides (LOOH) and thiobarbituric acid reactive substances (TBARS) and also the antioxidants superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH) and glutathione reductase (GR) in DMH treated rats, which were significantly reversed (P<0.05) on caraway supplementation. Moreover, enhanced activity of intestinal, colonic and caecal glutathione peroxidase (GPx), glutathione S-transferase (GST) and colonic ascorbic acid and alpha-tocopherol levels were observed in carcinogen-treated rats, which were significantly (P<0.05) reduced on caraway supplementation. Thus, our study showed that caraway supplementation at a dose of 60 mg kg(-1) had a modulatory role on tissue LPO, antioxidant profile and prevented DMH-induced histopathological lesions in colon cancer rats.     

Dose response effect of rutin a dietary antioxidant on alcohol‐induced prooxidant and antioxidant imbalance – a histopathologic study

The present study was designed to investigate the effect of rutin on ethanol‐induced hepatotoxicity in a dose‐dependent manner in rats. Male albino rats were divided into six groups. Group 1 rats served as control and group 2 rats received rutin 100 mg/kg body weight. Hepatotoxicity was induced in groups 3–6 rats (20% ethanol) for 60 days. In addition, groups 4–6 rats received rutin at doses of 25, 50, 100 mg/kg body weight, respectively for the last 30 days of the experiment. We observed a significant increase in the activities of liver marker enzymes, serum amino transferases, alkaline phosphatase, γ‐glutamyl transpeptidase the levels of thiobarbituric acid reactive substances, conjugated dienes, lipid hydroperoxides, and a decrease in the activities of superoxide dismutase (SOD), catalase (CAT), glutathione and its related enzymes, vitamins C and E when compared to ethanol‐fed rats. Rutin supplementation along with ethanol significantly decreased the levels of liver marker enzymes, lipid peroxidation and significantly elevated the activities of liver SOD, CAT, GSH, glutathione peroxidase, vitamins C and E when compared to untreated ethanol supplemented rats. Among the three doses, 100 mg/kg body weight of rutin was found to exert a more pronounced hepatoprotective effect against ethanol‐induced toxicity. Our results were also confirmed by the histopathologic observations.