Chronic renal failure (CRF) is the most prevalent, worldwide public health problem of the elderly population. The main cause of CRF is a damaged kidney. There are five stages of CRF based on the glomerular filtration rate (GFR), and stage 5 (GFR < 15 ml/min/1.73m2) is often called an end-stage renal disease (ESRD). In CRF, there is an accumulation of toxins and excess water due to compromised renal function. Dialysis is the preferred way to treat ESRD and remove accumulated toxins from the body. The cardiovascular risk associated with dialysis is 10 to 20 times higher in patients undergoing dialysis than in normal people. The inflamed kidneys and the process of dialysis also affect endothelial function, aggravating the risk of hypertension and cardiac problems. Therefore, both physicians and patients should be aware of the consequences of undergoing dialysis. There is an urgent need to educate CRF patients regarding facts about the disease, medications, dietary habits, and various measures required to manage the condition and lead a normal life. This paper attempts to delineate the mechanisms that could result in cardiovascular and other complications among CRF patients undergoing dialysis.

DNA methylation, a process of adding a methyl group to DNA done by a DNA methyltransferase is a heritable (epigenetic) alteration leading to cancer, atherosclerosis, nervous disorders (Imprinting disorders), and cardiovascular diseases. The role of nutrition in DNA methylation is revealed by identification of methyl variable positions (MVP) on DNA. These regions are more susceptible to DNA methylations. Nutritional supplementation of folic acid and methionine in utero and in adults decreased epigenetic modifications due to its role in DNA metabolism (one carbon metabolism). Thus, in utero and adult supplementation of folic acid and methionine may reduce DNA methylation. This review attempts to highlight the process of DNA methylation, its effect on various diseases, and the probable protective role of nutrition.

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Background The significance of the global prevalence and incidence of coronavirusdisease 2019 (COVID-19) is a measure of its severity. However, without statistical data, one cannot understand the novel severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) pandemic. This study, based on good data, enables us to know how the disease is spreading, what impact the pandemic has on the lives of people around the world, and whether the countermeasures that countries have been taking are successful for controlling and preventing the disease. Therefore, this study is undertaken to estimate the infection fatality rates (IFRs) and case-fatality rates (CFRs) in various countries and regions of the world. Methods COVID-19-related data were collected from various countries belonging to different World Bank categories based on economies (low-income, low-middle income, upper-middle income, and high-income countries) and the World Health Organization's (WHO's) regional classification of countries (the Americas, European, African, South-East Asia, Eastern Mediterranean, and Western Pacific regions). The data were collected from the WHO’s dedicated website on COVID-19, and statistical methods like mean, standard deviation, p-value, and percentages were used to calculate the IFR and CFR. Results Mexico (8.94%) reported the highest IFR among all the countries. The low-income countries reported increased IFR (2.46±1.91) as compared to the other groups. The European region (7.3%) and the American region (5.3%) recorded the highest CFRs. The South-East Asian region reported the lowest CFR (1.1%). Conclusions The low-income group countries showed higher rates of IFR and lower CFRs. Lower IFRs and increased CFRs were noted among the high-income group countries and the American and European regions respectively. The varied IFRs and CFRs could be attributed to multiple factors that include climatic conditions, living environments, age, sex, comorbidities, among others.

Metabolic disorders are a group of interrelated conditions which increases the risk of developing heart diseases, stroke, and diabetes. These usually occur as a consequence of deficiency of enzymes involved in biochemical reactions in the body. The dietary habits, lack of physical exercise, stress, and genetic susceptibility leads to an increased risk of developing metabolic disorders. A diet rich in processed food items containing high calories aggravates the production of a purine metabolite, the uric acid (UA). UA functions as an antioxidant, protects against inflammation, aging, and cancer. It exists as urate ions in the circulation and blood level of UA is maintained by a balance between its production in the liver and its excretion by the renal tubules. The regular excretion of UA through the kidneys is necessary to maintain optimum blood levels of UA (3-7 mg/dl). There are various transporters of uric acid present around the renal tubules, which help in reabsorption of UA into the blood. These urate transporters (UT) are proteins coded in the genes. Mutations in these genes may prompt disturbances in UA reabsorption, and could lead to the development of hyperuricaemia, insulin resistance, endothelial dysfunction, diabetes and other metabolic diseases. This paper reviews eight such genes coding for UTs and attempts to unravel the link between the activities of UA, UTs, and the consequences during mutations in the genes coding for the UTs in the development of metabolic disorders. The genes reviewed included SLC2A9, SLC17A1, SLC22A12, SLC16A9, GCKR, LRRC16A, PDZK1, and ABCG2.

Introduction Aging brings about several changes in humans that include both physiological and anatomical changes. As individuals' age, the activity of the thyroid gland and its hormones decline, causing significant metabolic disorders. Most thyroid gland disorders have been noted among young and middle-aged women. Very little is known regarding the activities of thyroid hormones among older aged women. Methods The study included 350 young to middle-aged pre-menopausal women between 25 and 49 years and 350 older post-menopausal women above 50 years of age. The study was conducted in the department of biochemistry, Prathima Institute of Medical Sciences (PIMS), Nagunur, Karimnagar, Telangana, India. The subjects included in the study were euthyroid (not having any signs and symptoms of thyroid disorder) and were not on any medication. The thyroid profile, including thyroid stimulating hormone (TSH), triiodothyronine (T 3), and tetra-iodothyronine (T 4), was analyzed in all the study subjects using the chemiluminescence immunoassay (CLIA) technique on a completely automated Abbott i1000SR Architect Plus instrument (Abbott Core Laboratory, Illinois, US). Results There was no statistically significant difference in thyroid hormone activities in the two age groups compared, as noted by the unpaired student's 't' test. The mean serum TSH levels in the older postmenopausal women (3.39+2.45) were found to be higher than those noted in pre-menopausal women (2.60+1.31). The activities of T 3 and T 4 showed no difference in both groups (p=0.8397). Conclusion The study results clearly indicate an increase in the activities of TSH among the older-aged post-menopausal women.

The human immune system is not adequately equipped to eliminate new microbes and could result in serious damage on first exposure. This is primarily attributed to the exaggerated immune response (inflammatory disease), which may prove detrimental to the host, as evidenced by SARS‐CoV‐2 infection. From the experiences of Novel Coronavirus Disease‐19 to date, male patients are likely to suffer from high‐intensity inflammation and disease severity than the female population. Hormones are considered the significant pillars of sex differences responsible for the discrepancy in immune response exhibited by males and females. Females appear to be better equipped to counter invading respiratory viral pathogens, including the novel SARS‐CoV‐2, than males. It can be hypothesized that females are more shielded from disease severity, probably owing to the diverse action/influence of estrogen and other sex hormones on both cellular (thymus‐derived T lymphocytes) and humoral immunity (antibodies).

Krabbe disease is a rare (one in 100,000 births) autosomal recessive condition, usually noticed among children. It causes sphingolipidosis (dysfunctional metabolism of sphingolipids) and leads to fatal degenerative changes affecting the myelin sheath of the nervous system. We report a case of a six-year-old male child who presented with symptoms of muscle spasticity and irritability. Diagnosis of this disease can only be made with clinical suspicion. Laboratory diagnosis includes brain magnetic resonance imaging (MRI), magnetic resonance (MR) spectroscopy, biochemical analysis of cerebrospinal fluid, and genetic analysis for detecting mutation in genes coding for galactosyl cerebroside (GALC). We report a case of late infantile Krabbe disease.