Bruton tyrosine kinase (Btk), a nonreceptor-associated tyrosine kinase of the Tec family, appears to participate in many myeloid cell functions. We show that macrophages from X-linked immunodeficient (XID) mice lacking functional Btk cannot generate efficient bursts of reactive oxygen intermediates (ROIs). The induction of apoptotic cell death by inflammatory stimuli is also enhanced in XID macrophages. Phagocytosis of bacterial particles is only marginally affected in them.In vivo, XID mice show reduced severity of inflammatory diseases in models of experimental autoimmune encephalomyelitis (EAE), dextran sulfate sodium (DSS)-induced colitis, and carrageenan-induced acute edema. Also, polymorphonuclear neutrophil granulocytes (PMNs) in XID mice show poor ROI and nitric oxide (NO) induction, along with a reduction in PMN recruitment to peritoneal inflammation. XID mice show reduction in PMN numbers in peripheral blood, and their bone marrow shows a reduction in the numbers of both monocytic and granulocytic lineages, extending to the earliest progenitor populations. Thus, Btk is likely to play a significant role at multiple points during the development and functioning of the myeloid lineages, affecting the outcome of many infectious as well as noninfectious inflammatory events in vivo.

Macrophages from X-linked immunodeficient (xid) mice lacking functional Bruton’s tyrosine kinase (Btk) show poor NO induction and enhanced IL-12 induction, and contribute to delayed clearance of injected microfilaria (mf) in vivo. We now show that Btk is involved in other macrophage effector functions, such as bactericidal activity and secretion of proinflammatory cytokines (TNF-α, IL-1β), but not the T cell-directed cytokine IL-12. Induction of some transcriptional regulators of the NF-κB family, crucial for the expression of proinflammatory cytokines, is also poor in Btk-deficient macrophages. Thus, Btk appears to be involved in signaling for inducible effector functions, but not APC functions, in macrophages. Furthermore, adoptive transfer of T cells from mf-infected xid or wild-type mice did not alter the course of mf clearance in recipients, mf clearance was unaltered in IFN-γ-deficient mice, and improved mf clearance was seen only if greater inducibility of IL-12 was accompanied by greater NO secretion from macrophages, as seen in Ityr C.D2 mice as compared with congenic Itys BALB/c mice. Thus, delayed mf clearance in xid mice was correlated not with the high IL-12/Th1 phenotype but with low NO induction levels. Also, xid macrophages showed poor toxicity to mf in vitro as compared with wild-type macrophages. Inhibition of NO production blocked this mf cytotoxicity, and an NF-κB inhibitor blocked both NO induction and mf cytotoxicity. Thus, Btk is involved in inducing many macrophage effector functions, and delayed mf clearance seen in Btk-deficient xid mice is due to poor NO induction in macrophages, resulting in compromised microfilarial toxicity.

Background: Quantification of obesity/adiposity is feasible with different anthropometric characteristics along with the bioelectrical impedance analysis techniques. Recent advancements are now witnessing development of further computations derived from previously established measures to gauge obesity. Objective: Main aim of our study was to evaluate the association of anthropometric determinants of obesity with body compositional adiposity variables, and thus identifying the best marker among them emerging out as the probable predictor for compositional adiposity. Participants and Setting: 550 female participants within the age of 18 to 23 years were enrolled under this study attending graduation course at University of Delhi. Ethical clearance was received from the institutional head. Informed written consent was taken from every participant. Design: All the body measurements were recorded by trained staff using standard techniques. Derived measurements were calculated further. Analysis: Data, hence, gathered was undertaken for descriptive and inferential statistical analysis with SPSS 20.0. Variables Measured and Results: WHR overestimated the count for those at risk compared to waist circumference and WHtR. Skeletal muscle fat associated negatively with all anthropometric adiposity indicators. BMI, BAI, WHtR and waist circumference related closely with all body composition cum obesity markers compared to WHR, CI and ABSI. BAI overrated the risk for fat determining body composition parameters the most followed by BMI. ABSI revealed an underestimated risk for augmenting fat content in body, compared to other markers. Conclusion and Implications: It is difficult to establish with compliance as to which of the measures used in the study could better predict the perils of obesity but it could be ascertained that some of the newly verified anthropometric adiposity indicators could be administered for determining clinical situations after further validation.

Background: Rapid changes in global economies and industrialization have resulted in switch from traditional diets and labor intensive lifestyle to consumption of modern calorie-rich diets loaded with fat and sugar contents, accompanied with sedentary lifestyle further leading to onset of numerous non-communicable, chronic disorders; obesity being one of them. This study aims at investigating risk posed by family history of obesity over the generations for inducing extreme overweight conditions among adolescent females of Delhi. Methods: Present work is a cross-sectional study conducted in Delhi (India) with sample size of 444 females aged between 18-22 years. Socio-demographic aspect along with lifestyle-related profile of participants was assessed using a self-administered proforma. Prior history of obesity among family members, if any, was noted as well, and anthropometric and physiologic measurements were recorded using well established customary techniques. Analysis was carried out in SPSS 20.0. Results: Participants holding a history for obesity in family were comparatively more obese than their counterparts. Positive family history for the same has been found possessing a notably closer association with elevated levels of adiposity determined by various physical and physiological variables. Conclusion: Family history of excessive fatness develops high risk of pathological manifestation for the same in upcoming generations that needs to be administered effectively-at individual or population level, and addressed efficiently by one's family or by the prevailing governmental provisions.