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The present study aimed to evaluate association between plasma vitamin B12 and heart rate variability in clusters of population of various ages across life cycle.47 healthy children from an ongoing pregnancy and birth cohort, 32 young adults and 47 healthy elderly subjects were recruited following inclusion and exclusion criteria. All subjects underwent plasma vitamin B12, anthropometry and heart rate variability (HRV).The prevalence of vitamin B12 deficiency (lt;148 pmol/l) across age groups were 51.1 % for children, 56.2 % for young adults and 61.7 % for the elderly group respectively. There was large variability in vitamin B12 status across the age groups. Frequency distribution of low frequency (LF) absolute units HRV in the elderly was skewed, whereas in children and young adult group there was wide distribution of LF HRV. Association between Log LF absolute units HRV and plasma vitamin B12 across groups were tested using curve fit models. In children a linear curve estimation best fitted and explained 9.3 % of the association (n=47, .=0.003, P=0.03, R2=0.09). There was no association between log LF absolute units HRV and plasma vitamin B12 in the young adult group. In the elderly group a power curve fit model best fitted and explained 8.9 % of the association. Inspection of the power curve fit model demonstrated a curvilinear pattern; there was a linear association in the elderly with vitamin B12 levels less than 200 pmol/l. However, elderly with vitamin B12 valuesgt;200 pmol/l demonstrated saturation (plateauing) of log LF HRV.The study demonstrated varied pattern of responses between vitamin B12 status and LF power of HRV across age groups. Thus, it is important to consider these associations before planning supplementation of vitamin B12.

Prevalence of vitamin B12 deficiency in the Indian population is not known, however; it is considered to be higher than in the Western population. Vitamin B12 deficiency is generally diagnosed by the plasma vitamin B12 level. Metabolites of vitamin B12 such as homocysteine (Hcy) and methylmalonic acid (MMA) are considered to be better markers to diagnose vitamin B12 deficiency at the tissue level. Autonomic neuropathy in vitamin B12 deficiency appears to precede other neurological signs. One of the recent techniques to evaluate autonomic neuropathy is heart rate variability (HRV). We evaluated 14 healthy young adults to explore the association of plasma vitamin B12, MMA, and Hcy levels with HRV. Resting lead II ECG was recorded and power spectral analyses were performed. Plasma MMA level was significantly and negatively correlated with the log-transformed low frequency (r = - 0.74, p = 0.002) and total power spectra (r = - 0.55, p = 0.03) of HRV in absolute units. Low frequency (LF) (r = - 0.56, p = 0.03) and high frequency (HF) (r = 0.57, p = 0.03), when represented in normalized units, were also correlated significantly with plasma MMA. In summary, plasma MMA but not vitamin B12 was significantly associated with HRV indices in a young adult population, suggesting that a tissue-level marker of vitamin B12 deficiency is more closely correlated with functional changes.

Background.One third of Indian population is said to be suffering from chronic energy deficiency (CED), with increased risk of developing chronic diseases. A new anthropometric measure called A Body Shape Index (ABSI) is said to be a better index in predicting risks for premature mortality. ABSI is also in part said to be a surrogate of visceral fat.Objective. The present study aimed to explore the association between indices of HRV (heart rate variability), BMI, WC, and ABSI in healthy Indian males with low BMI (BMI < 18.5 kg/m2) and to compare with normal BMI group (BMI 18.5 to 24.9 kg/m2).Methodology. ABSI and BMI were derived from anthropometric parameters, namely, height, weight, and waist circumference in 178 males aged 18 to 78 years. Subjects were categorized into two groups based on their BMI.Results and Conclusions. Power spectral analysis of HRV demonstrated a significant negative correlation between Log HF (high frequency) and ABSI in both low BMI [−24.2 (9.4),P<0.05] and normal BMI group [−23.41 (10.1),P<0.05] even after controlling for age. Thus even with slight increase in BMI among low BMI individuals, there could be a greater risk of cardiovascular morbidity and mortality.

Background αB-Crystallin is a heat shock chaperone protein which binds to misfolded proteins to prevent their aggregation. It is overexpressed in a wide-variety of cancers. Previous studies using human cancer cell lines and human xenograft models have suggested potential tumor promoter (oncogene) roles for αB-Crystallin in a wide-spectrum of cancers. Methods To determine the causal relationship between CRYAB overexpression and cancer, we generated a Cryab overexpression knock-in mouse model and monitor them for development of spontaneous and carcinogen (DMBA)-induced tumorigenesis. In order to investigate the mechanism of malignancies observed in this model multiple techniques were used such as immunohistochemical characterizations of tumors, bioinformatics analysis of publically available human tumor datasets, and generation of mouse embryonic fibroblasts (MEFs) for in vitro assays (clonogenic survival and migration assays and proteome analysis by mass-spectrometry). Results This model revealed that constitutive overexpression of Cryab results in the formation of a variety of lethal spontaneous primary and metastatic tumors in mice. In vivo, the overexpression of Cryab correlated with the upregulation of epithelial-to-mesenchymal (EMT) markers, angiogenesis and some oncogenic proteins including Basigin. In vitro, using E1A/Ras transformed MEFs, we observed that the overexpression of Cryab led to the promotion of cell survival via upregulation of Akt signaling and downregulation of pro-apoptotic pathway mediator JNK, with subsequent attenuation of apoptosis as assessed by cleaved caspase-3 and Annexin V staining. Conclusions Overall, through the generation and characterization of Cryab overexpression model, we provide evidence supporting the role of αB-Crystallin as an oncogene, where its upregulation is sufficient to induce tumors, promote cell survival and inhibit apoptosis.