Perinatal HIV infection is characterized by faster HIV disease progression and higher initial rate of HIV replication compared to adults. While antiretroviral therapy (ART) has greatly reduced HIV replication to undetectable levels, there is persistent elevated inflammation associated with HIV disease progression. Alteration of gut microbiota is associated with increased inflammation in chronic adult HIV infection. Here, we aim to study the gut microbiome and its role in inflammation in treated and untreated HIV-infected children. Examination of fecal microbiota revealed that perinatally infected children living with HIV had significantly higher levels of genus Prevotella that persisted despite ART. These children also had higher levels of soluble CD14 (sCD14), a marker of microbial translocation, and IP-10 despite therapy. The Prevotella positively correlated with IP-10 levels in both treated and untreated HIV-infected children, while genus Prevotella and species Prevotella copri was inversely associated with CD4 count. Relative abundance of genus Prevotella and species Prevotella copri showed positive correlation with sCD14 in ART-suppressed perinatally HIV-infected children. Our study suggests that gut microbiota may serve as one of the driving forces behind the persistent inflammation in children despite ART. Reshaping of microbiota using probiotics may be recommended as an adjunctive therapy along with ART.

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BACKGROUND Poisoning is a global public health problem causing significant morbidity and mortality. It is important to know the pattern and outcome of acute poisoning cases for proper planning, prevention and management of these cases. The aim of the study is to determine the mode (suicidal, accidental, homicidal) and type of poisoning in North Indian population; relation to age, sex, occupation, marital status; outcome of different type of poisons and requirement of ventilatory support in different type of poisonings. MATERIALS AND METHODS This observational study was conducted in Department of Medicine of a tertiary care hospital in North India. A total of 379 patients were enrolled in the study after obtaining informed consent. RESULTS Poisoning was more common among males (59.89%). Maximum number of patients were in the age group 21-30 years (40.63%) and consumption was found to be more prevalent in rural population (75.99%). Most of the patients were farmers and students. Most common types of poisoning were organophosphate (n=95, 25.07%), snake bite (n=77, 20.32%) followed by aluminium phosphide (n=71, 18.73%). Out of 379 patients, 318 (83.91%) improved while 61 (16.09%) expired. Mortality was highest in aluminium phosphide poisoning. Requirement of ventilatory support was most commonly associated with aluminium phosphide poisoning (37.89%) followed by organophosphate poisoning (28.42%). CONCLUSION Poisoning was more common in young males. Pesticides and snake bite were major causes of poisoning. Of the total, 318 improved while rest of the 61 expired. Mortality was higher with use of aluminium phosphide poisoning (57.38%), snake bite (21.31%) and organophosphate consumption (9.84%). Requirement of ventilator was most commonly associated with aluminium phosphide poisoning. We suggest strict statutory measures covering import, manufacture, sale, transport, distribution and use of pesticides. Training of peripheral health center personnel to manage cases of poisoning, to provide ventilatory support and escalation in public awareness about the importance of problem should be done.

Type 2 diabetes mellitus (T2DM) is a heterogeneous condition that is related to both defective insulin secretion and peripheral insulin resistance. Beta cells are the major organ for secreting insulin hence, it is important to maintain an adequate beta-cell mass in response to various changes. Insulin resistance is a major cause of T2DM leads to elevated free fatty acid (FFA) levels which increases beta-cell mass and insulin secretion to compensate for insulin insensitivity. Chronic increase of plasma FFA levels results in disturbances in lipid metabolism, which contributes to decreased beta-cell function and lipotoxicity thus promoting T2DM. In the present review, we have discussed the process of beta-cell destruction, the role of genes in contributing to the fast increase in the progression of T2DM in detail. More than 130 variants in various T2DM susceptibility and candidate genes have been discovered to be associated with T2DM. Still, these variants elucidate only a small amount of total heritability of T2DM. Further, there is also an inventory of presently used therapeutic tools and a review of novel therapeutic approaches like incretinbased therapies or sodium-glucose transporter-2 inhibitors. Additionally, providing a concise but comprehensive update, this review will be essential to every clinician involved in the treatment of diabetes mellitus.

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