[Adequate nutritional indices and intake are the corner stone of long term success of renal replecement therapies (hemo- and peritoneal dialysis, transplantation) characterized by favourable survial rates and a good quality of life. There has been no major change in basic principles of nutritional prescription (protein, energy, fluid intake, restriction of sodium, potassium and phosphorous), increasing emphasis has been placed on the reduction of calcium load and ”native” vitamin-D therapy in these patients. Less avareness has been put however in the past ten years (according to recent metaanalyses) on the role and replacement of the full scale of vitamins, in spite of their occasionally altered metabolism and replacement-requirements in ESRD patients. Usually there is a need for their replacement, but some of them are represented in abundant, sometimes toxic amounts in commercially available multivitamin preparates. With in the scope of general aspects of nutrition in ESRD patients, the article gives a detalied overview of their multivitamin recommendations and alternatives of a specified substition.]

[Angiotensin II (Ang II) by activating angiotensin type 1 receptors (AT1R) is one of the most potent vasoconstrictors in the regulation of vasomotor tone and thus systemic blood pressure. In this study, we hypothesized that aging alters Ang II - induced vasomotor responses and expression of vascular mRNA and protein angiotensin type 1 receptor (AT1R). Thus, carotid arteries were isolated from newborn, young, middle age, old and senescent rats and their vasomotor responses were measured in a myograph (DMT-600) to repeated administrations of Ang II. Vascular relative AT1R mRNA level was determined by qRT-PCR and the AT1R protein density was measured by Western blot. Contractions of vessels to the first administration of Ang II increased from newborn to young and middle age rats then they decreased to senescent rats. In general, second administration of Ang II elicited reduced contractions, but they also first increased and then they decreased to old age. Similarly, the AT1R mRNA level and the AT1R protein density increased from newborn to young and middle age rats then they decreased to senescent rats. The pattern of these changes correlated with functional vasomotor data. We conclude that aging (newborn to senescence) has substantial effects on Ang II-induced vasomotor responses and AT1R signaling suggesting that it is - and thus regulation of systemic blood pressure is - determined primarily by genetic programs.]

[During the COVID-19 pandemic caused by the SARS-CoV-2 virus, elderly people in long-term nursing homes were espe­cially risks exposed. In this study, the au­thors analyse the causes of local outbreak at the Olajág Elderly Home Vezér street facility in Budapest and the means and ways to curb the spreading of infection. They summarise the measures, which proved to be effective in isolation and treat­ing the patients. The number of infected residents as well as the course of the disease are demonstrated by statistical data. The authors consider as pre-eminently important to identify asymptomatic but in­fec­ted residents, further the rapid introduc­tion of screening tests, strict compliance with protocols, patient path regulation and the use of enhanced, supportive communication.]

[The world population in both industrialized and developing countries is aging. The clinical and economic implications of this demographic shift are staggering because age is the most powerful risk factor for cardiovascular diseases. The incidence and prevalence of hypertension, coronary artery disease, congestive heart failure, and stroke increase steeply with advancing age. Although epidemiologic studies have discovered that some aspects of lifestyle and genetics are risk factors for these diseases, age, per se, confers the major risk. There is a continuum of age-related alterations of cardiovascular structure and function in healthy humans, however these alterations are not synonymous with diseases processes. Old age is not a disease. Although cardiovascular aging changes are considered “normative”, they lower the threshold for development of cardiovascular disease, and appear to influence the steep increases in hypertension, atherosclerosis, stroke, left ventricular hypertrophy, chronic heart failure, and atrial fibrillation with increasing age. Specific pathophysiologic mechanisms that underlie these diseases become superimposed on cardiac and vascular substrates that have been modified by an “aging process”, and the latter modulates disease occurrence and severity. Age-associated changes in cardiovascular structure and function become “partners” with pathophysiologic disease mechanisms, lifestyle, genetics, and other presently unknown factors in determining the threshold, severity, prognosis, and therapeutic response of cardiovascular disease in older persons. However, the role of specific age-associated changes in cardiovascular structure and function in such age-disease interactions has not been considered in most epidemiologic and clinical studies of cardiovascular disease. Quantitative information on age-associated alterations in cardiovascular structure and function in health is essential to unravel age-disease interactions and to target the specific characteristics of cardiovascular aging that render it such a major risk factor for cardiovascular diseases. Such information is also of practical value to differentiate between the limitations of an older person that relate to disease and those that might be expected, within limits, to accompany advancing age or a sedentary lifestyle.]