International Physiology

Background: Vitamin D deficiency is increasingly recognized as a modifiable factor influencing respiratory physiology. Adults with dietary imbalance are particularly vulnerable to low serum 25(OH)D levels, which may contribute to subtle impairments in pulmonary function even in the absence of established lung disease. Limited evidence exists on whether correcting vitamin D deficiency alone can improve pulmonary performance in such individuals. Objective: To evaluate the impact of vitamin D supplementation on pulmonary function test (PFT) parameters in adults with dietary imbalance and low baseline vitamin D levels. Methods: A prospective observational pre–post study was conducted among adults aged 18–60 years with confirmed vitamin D deficiency or insufficiency and documented dietary imbalance. Fifty participants underwent baseline assessment including serum 25(OH)D levels and spirometry (FEV1, FVC, FEV1/FVC ratio, PEF). All participants received standardized cholecalciferol supplementation (60,000 IU weekly for 8 weeks). Serum vitamin D levels and PFTs were repeated after supplementation. Paired t-tests assessed pre–post differences, and Pearson correlation evaluated associations between changes in vitamin D and PFT parameters. Results: Mean serum 25(OH)D increased from 17.3 ± 4.2 ng/mL to 34.6 ± 5.1 ng/ mL post-supplementation (p < 0.001). Significant improvements were observed in FEV 1 (2.45 ± 0.48 L to 2.62 ± 0.50 L; p < 0.001), FVC (3.12 ± 0.52 L to 3.25 ± 0.54 L; p = 0.004), FEV1/FVC ratio (78.5 ± 5.6% to 80.4 ± 5.8%; p = 0.002), and PEF (5.82 ± 1.05 L/s to 6.12 ± 1.08 L/s; p = 0.001). Approximately 80% of participants showed improvement in at least one PFT parameter. Changes in 25(OH)D were positively correlated with improvements in FEV1 (r = 0.36, p = 0.010) and PEF (r = 0.31, p = 0.028). Conclusion: Vitamin D supplementation significantly improved pulmonary function in adults with dietary imbalance and low baseline vitamin D levels. The findings support the role of vitamin D repletion as a simple, low-cost intervention to enhance respiratory performance in nutritionally vulnerable adults. Larger controlled trials are needed to confirm these results and elucidate underlying mechanisms.

Background and objectives: Stress is a huge problem in today’s society. Although stress has a psychological origin, it affects several physiological processes in the human body causing changes in the heart rate variability, hypothalamic pituitary adrenal axis and concentration of several hormones in the body.1 Stress induces increased levels of cortisol. Studies reveal that salivary cortisol level measurement is the most accepted sample for cortisol analysis inmental stress conditions.2 Heart rate variability can be used as an indicator to assess the autonomic nervous system’s role.3 Heart rate variability biofeedback (HRVBF) is a method that showed improvements in cognitive performance resulting from the slowed respiratory rate and increased heart rate variability. Objectives were to study the effect of a brief heart rate variability biofeedback session on salivary cortisol reactivity to mental stress, and to devise an effective and practical tool to assess and to devise an interventional tool that might act as a coping strategy that can be used as a treatment in stress and anxiety management program.4 Methods: Thirty healthy male subjects of 20 to 45 years age were included in study. On Day 1 the subject was introduced to HRVBF, including its benefits and techniques, and their resonance frequency was determined. On Day 2, subject came without taking tea or breakfast, baseline physiological parameters were recorded (R1) and salivary sample for cortisol was collected, followed by a mental arithmetic test7 (MAT-I). Post-test, the same parameters were (T1) recorded again. The subject was then asked to relax for 10 minutes and physiological parameters (R2) were taken before undergoinga 10-minute HRV biofeedback session, breathing at their resonance frequency. Then, they were subjected to another mental arithmetic test (MAT-II), and the physiological parameters (T2) were measured and saliva sample was collected again. The reactivity was assessed by comparing pre (T1-R1) and post-HRV Biofeedback (T2-R2) data. Salivary cortisol reactivity is measured as the difference between cortisol levels before and after mental arithmetic test. Results: The Mean salivary cortisol reactivity after 10 minutes of HRV biofeedback intervention was less than that of salivary cortisol reactivity before intervention. Conclusion: The Heart rate variability biofeedback intervention causes decrease in stress levels which was measured by comparing the salivary cortisol reactivity. In our study, 30 subjects who are in the age between 20 and 45 years. We found adecrease in the salivary cortisol reactivity to mental stressafter 10 minutes of HRVBF intervention.

Sleep is an essential biological process required for the maintenance of physiological homeostasis, cognitive performance, and metabolic balance. In modern societies, chronic sleep deprivation has become increasingly prevalent due to lifestyle changes, occupational demands, and technological influences. Insufficient sleep affects multiple physiological systems including the nervous, endocrine, cardiovascular, metabolic, immune, and gastrointestinal systems. Experimental and epidemiological studies demonstrate that sleep deprivation impairs cognitive functions, alters hormonal balance, increases sympathetic nervous system activity, promotes systemic inflammation, and disrupts metabolic regulation. Furthermore, chronic sleep loss is associated with increased risks of obesity, diabetes mellitus, cardiovascular diseases, and mental health disorders. The mechanisms underlying these physiological alterations involve dysregulation of circadian rhythms, increased oxidative stress, neuroendocrine disturbances, and inflammatory responses. This review summarizes the current understanding of the physiological consequences of sleep deprivation in humans, focusing on its effects on major organ systems and underlying biological mechanisms. Understanding these effects is essential for developing preventive strategies and public health policies aimed at reducing the burden of sleep-related health disorders.

Myocardial ischaemia reperfusion (I/R) injury remains a critical challenge in cardiovascular therapy, particularly in patients receiving anthracycline chemotherapy. Doxorubicin, though highly effective as an anticancer agent, is limited by its cardiotoxic effects that are exacerbated during I/R events. Nuclear factor-kappa B (NF-KB), a key transcription factor regulating inflammation and apoptosis, is strongly implicated in this dual-insult mechanism. In this in-silico study, molecular docking and structural analyses were performed to evaluate the interaction between doxorubicin and NF-KB, and to assess the resulting conformational and physicochemical changes. Docking simulations revealed nine binding modes, with Mode-1 showing the strongest affinity (-8.5 kcal/ mol), stabilized by hydrogen bonds, van der Waals forces, and hydrophobic interactions. Hydrophobicity and isotropic displacement analyses demonstrated that doxorubicin binding introduced marked fluctuations and enhanced protein flexibility, leading to structural destabilization. Ramachandran plot evaluation further confirmed significant loss of residues in favorable conformational regions, suggesting impaired folding. Visualization of NF-KB under drug exposure revealed increased intensity and altered spatial distribution, indicative of enhanced activation. Collectively, these findings suggest that doxorubicin modulates NF-KB through strong binding and structural perturbation, thereby amplifying myocardial injury mechanisms. The study provides molecular insights into cardiotoxicity and identifies NF-KB as a potential target for cardioprotective interventions.