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Introduction: The worldwide higher prevalence of obesity is currently one of the most important reasons for the occurrence of several health disorders, along with an increased risk of mortality and morbidity. However, the magnitude of the effect of sub-maximal aerobic exercise on cardiac autonomic and electrical function among Indian obese individuals has yet to be established. Aim: To evaluate the effect of exercise on ECG components and their correlation with Body Mass Index (BMI) among young asymptomatic obese and non-obese individuals, in order to assess the risk for developing Cardiovascular Diseases (CVD) in the future. Materials and Methods: An observational cross-sectional study was conducted at the Autonomic Research Laboratory of the Physiology Department at RG Kar Medical College and Hospital, Kolkata, between January 2017 to December 2017. Two hundred healthy medicos were divided into two groups: Obese (BMI =25 kg/m²; n=88) and non-obese (BMI =18.5 to =23 kg/m²; n=112). Resting Blood Pressure (BP) was manually recorded, followed by the recording of long lead-II ECG in the supine posture both at rest and ten minutes after submaximal (50% VO2max) aerobic exercise on a treadmill using the modified Bruce protocol and following the Astrand-Rhyming nomogram. The HR, QT interval, and RR interval were recorded from the lead-II ECG. The measured QT interval was corrected using Bazett's formula (QTC=QT/vRR). The results were analysed using both unpaired and paired t-tests and the Pearson correlation coefficient in Graphpad-Quickcalc software. Results: Significant prolongation of the QTc interval both at rest (p-value: 0.019) and after exercise (p-value: 0.044), along with delayed Heart Rate Recovery (HRR) (p-value: 0.001), were observed among the obese compared to the non-obese population. Additionally, a significantly positive linear correlation was observed between BMI and ECG components at rest (BMIRHR: r:+0.293; p: 0.005 and BMI-QTc Interval: r:+0.226; p-value: 0.034) and during the recovery state (BMI-HRR: r:+0.42; p-value: 0.00004 and BMI-QTc Interval: r:+0.365; p-value: 0.0004), only among the obese. Conclusion: At rest, obese individuals had an elevated QTc, which could be due to alterations in cardiac autonomic function, along with a significant positive correlation between BMI and RHR, indicating lower aerobic fitness in this population. Prolongation of the QTc interval, delayed decrease in HR, and a significant positive correlation with BMI after exercise in obese individuals indicated myocardial repolarisation instability, autonomic dysfunction, and an increased risk of out-of-hospital sudden cardiac events in these individuals. [ABSTRACT FROM AUTHOR]

Multiple mechanisms have been proposed by which tumors induce T cell apoptosis to circumvent tumor immunesurveillance. Although sarco/endoplasmic reticulum Ca2+- ATPase (SERCA) have long been known to regulate intracellular Ca2+ homeostasis, few studies have examined the role of SERCA in processes of T lymphocyte survival and activation. In this context it remains largely unexplored as to how tumors jeopardize SERCA function to disable T cell-mediated anti-tumor immunity. Here, we show that human CD4+ T cells in the presence of tumor conditions manifested an up-regulation of SERCA3 expression that resulted in development of endoplasmic reticulum stress leading to CD4+ T cell apoptosis. Prostaglandin E2 produced by the tumor cell plays a critical role in up-regulating SERCA3 by enhancing the binding of its transcription factor Sp1. Gene manipulation and pharmacological approaches further established that an increase in SERCA expression also resulted in subsequent inhibition of PKCα and -θ and retention of NFκB in the cytosol; however, down-modulation of SERCA3 expression by a dihydropyrimidone derivative, ethyl-4-(3-nitro)-phenyl- 6-methyl-2-oxo-1,2,3,4-tetrahydropyrimidine-5 carboxylate (nifetepimine), protected the CD4+ T cells from tumor-induced apoptosis. In fact, nifetepimine-mediated restoration of PKC activity resulted in nuclear translocation of p65NFκB, thereby ensuring its survival. Studies further undertaken in a tumor-bearing mice model revalidated the immunoprotective role of nifetepimine. Our present study thus strongly suggests that imbalance in cellular calcium homeostasis is an important factor leading to CD4+ T cell death during cancer and holds promise that nifetepimine may have the potential to be used as an immunorestoring agent in cancer bearers. [ABSTRACT FROM AUTHOR]