Somatostatin Containing δ-Cell Number Is Reduced in Type-2 Diabetes.

Recent developments suggest that increased glucagon and decreased somatostatin secretion from the pancreas contribute to hyperglycaemia in type-2 diabetes (T2D) patients. There is a huge need to understand changes in glucagon and somatostatin secretion to develop potential anti-diabetic drugs. To further describe the role of somatostatin in the pathogenesis of T2D, reliable means to detect islet δ-cells and somatostatin secretion are necessary. In this study, we first tested currently available anti-somatostatin antibodies against a mouse model that fluorescently labels δ-cells. We found that these antibodies only label 10-15% of the fluorescently labelled δ-cells in pancreatic islets. We further tested six antibodies (newly developed) that can label both somatostatin 14 (SST14) and 28 (SST28) and found that four of them were able to detect above 70% of the fluorescent cells in the transgenic islets. This is quite efficient compared to the commercially available antibodies. Using one of these antibodies (SST10G5), we compared the cytoarchitecture of mouse and human pancreatic islets and found fewer δ-cells in the periphery of human islets. Interestingly, the δ-cell number was also reduced in islets from T2D donors compared to non-diabetic donors. Finally, with the aim to measure SST secretion from pancreatic islets, one of the candidate antibodies was used to develop a direct-ELISA-based SST assay. Using this novel assay, we could detect SST secretion under low and high glucose conditions from the pancreatic islets, both in mice and humans. Overall, using antibody-based tools provided by Mercodia AB, our study indicates reduced δ-cell numbers and SST secretion in diabetic islets.

Neurocognitive Lag in School-Aged Children Living With HIV in India and Its Relevance.

Objective Objective assessment of neurocognitive lags in pediatric HIV patients and its correlation with various clinical, social and familial factors. Methods Ninety-eight school-aged children living with HIV (CLHIV) (age 7-18 years) attending regional pediatric HIV clinic were observed for neurocognitive lag using Raven's Standard Progressive Matrices by the same trained instructor. Sociodemographic data, mode of transmission, clinical staging, CD4 count, highly active antiretroviral therapy (HAART) duration were recorded and analyzed in the well-performing group and under-performing group. Results 29.6% of children had definitive neurocognitive lag. The proportion of older children (11-18 years) in the under-performing group was significantly high (P = 0.007). The mean CD4 counts were low in the under-performing group (P = 0.001). Other socioeconomic factors could not be specifically correlated with neurocognitive lag in either of the groups. Conclusion CLHIV has a significant neurocognitive lag, which is accentuated in the upper age group. Findings point toward declining intellectual gains with increasing age in CLHIV.