Skin, as the outermost organ of the body, is constantly exposed to both intrinsic and extrinsic causative factors of aging. Intrinsic aging is related to compromised cellular proliferative capacity, and may be accelerated by harmful environmental influences with the greatest significance of ultraviolet radiation exposure, contributing not only to premature aging, but also to skin carcinogenesis. The overall skin cancer burden and steadily increasing global antiaging market provide an incentive for searching novel targets to improve skin resistance against external injury. Sirtuin 1, initially linked to extension of yeast and rodent lifespan, plays a key role in epigenetic modification of proteins, histones, and chromatin by which regulates the expression of genes implicated in the oxidative stress response and apoptosis. The spectrum of cellular pathways regulated by sirtuin 1 suggests its beneficial impact on skin aging. However, the data on its role in carcinogenesis remains controversial. The aim of this review was to discuss the relevance of sirtuin 1 in skin aging, in the context of intrinsic factors, related to genetic premature aging syndromes, as well as extrinsic modifiable ones, with the assessment of its future application. PubMed were searched from inception to 4 January 2021 for relevant papers with further search carried out on ClinicalTrials.gov. The systematic review included 46 eligible original articles. The evidence from numerous studies proves sirtuin 1 significance in both chronological and premature aging as well as its dual role in cancer development. Several botanical compounds hold the potential to improve skin aging symptoms.

The microbiota, as a complex of microorganisms in a particular ecosystem, is part of the wider term—microbiome, which is defined as the set of all genetic content in the microbial community. Imbalanced gut microbiota has a great impact on the homeostasis of the organism. Dysbiosis, as a disturbance in bacterial balance, might trigger or exacerbate the course of different pathologies. Small intestinal bacterial overgrowth (SIBO) is a disorder characterized by differences in quantity, quality, and location of the small intestine microbiota. SIBO underlies symptoms associated with functional gastrointestinal disorders (FGD) as well as may alter the presentation of chronic diseases such as heart failure, diabetes, etc. In recent years there has been growing interest in the influence of SIBO and its impact on the whole human body as well as individual systems. Therefore, we aimed to investigate the co-existence of SIBO with different medical conditions. The PubMed database was searched up to July 2022 and we found 580 original studies; inclusion and exclusion criteria let us identify 112 eligible articles, which are quoted in this paper. The present SIBO diagnostic methods could be divided into two groups—invasive, the gold standard—small intestine aspirate culture, and non-invasive, breath tests (BT). Over the years scientists have explored SIBO and its associations with other diseases. Its role has been confirmed not only in gastroenterology but also in cardiology, endocrinology, neurology, rheumatology, and nephrology. Antibiotic therapy could reduce SIBO occurrence resulting not only in the relief of FGD symptoms but also manifestations of comorbid diseases. Although more research is needed, the link between SIBO and other diseases is an important pathway for scientists to follow.

Background: Hepcidin synthesis in hepatocytes is modulated in response to anemia, hypoxia or inflammation. A cross-sectional study was performed to assess hepcidin correlations with markers of iron status, erythropoietin therapy and markers of inflammation in hemodialyzed patients and in the healthy volunteers. Methods: Iron status, complete blood count, creatinine, albumin, lipids were assessed using standard laboratory methods. Hepcidin and high-sensitivity CRP were measured using commercially available kits. Results: Serum iron, TIBC, TSAT, erythrocyte count, Hb, Ht, platelet count, albumin, and cholesterol were lower, whereas ferritin and hepcidin were higher in hemodialyzed patients over controls. Hepcidin correlated positively with triglycerides, albumin, aspartate aminotransferase, lymphocyte count, ferritin and erythropoietin dose and negatively with erythrocyte count, Hb, and Ht in hemodialyzed patients. In multiple regression analysis, triglycerides (β value was 0.28, p = 0.02) and albumin (β value was –0.31, p = 0.006) were correlates of hepcidin in hemodialyzed patients. Conclusions: Elevated hepcidin levels in hemodialyzed patients may be due to functional iron deficiency and anemia. Liver plays an important role in the synthesis of hepcidin. Low-grade inflammation, frequently found in hemodialyzed patients, might also contribute to elevated hepcidin concentration. Hypothesis that hepcidin might link anemia, inflammation and liver function in kidney disease should be further evaluated.

Background: The use of noncuffed nontunneled central venous catheters is a widely accepted method of gaining temporary vascular access for hemodialysis. Malfunction and bacteremia are the main factors limiting catheter survival. Methods: We followed up prospectively 73 hemodialysis catheters (HC) (40 internal jugular, 33 femoral) in order to establish factors influencing HC malfunction. HC malfunction was defined as a catheter that was unable to attain and maintain blood flows of at least 150 ml/min. 73 HC were used for a total 1,100 days. Results: HC malfunction occurred in 23 cases (31.51%) during the study period, giving an overall rate of 21 episodes per 1,000 catheter days at risk. An analysis revealed a higher risk of HC malfunction with the catheterization of the femoral vein compared to the internal jugular vein (hazard ratio (HR) 6.3; 95% confidence interval (CI) 5.3–7.3). After correction for confounding factors in multivariate Cox analysis, the site of the catheterization remained a statistically significant predictor of HC malfunction (HR 5.03, 95% CI 3.83–6.23). After the first week malfunction rate was 42 and 8% for femoral and internal jugular site, respectively (relative risk (RR) for malfunction 5.3 (95% CI, 2.5–8). After the second and third week, the incidence of malfunction was 51 and 14% for femoral and internal jugular vein, respectively (RR 3.6, 95% CI 2.2–5.1). Conclusions: Catheterization of the internal jugular vein is associated with longer catheter survival when compared to the femoral vein. Hemodialysis catheters should be placed, if possible, in internal jugular vein to prevent their premature malfunction.

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a pro-apoptotic protein showing broad biological functions. Data from animal studies indicate that TRAIL may possibly contribute to the pathophysiology of cardiomyopathy, atherosclerosis, ischemic stroke and abdominal aortic aneurysm. It has been also suggested that TRAIL might be useful in cardiovascular risk stratification. This systematic review aimed to evaluate whether TRAIL is a risk factor or risk marker in cardiovascular diseases (CVDs) focusing on major adverse cardiovascular events. Two databases (PubMed and Cochrane Library) were searched until December 2020 without a year limit in accordance to the PRISMA guidelines. A total of 63 eligible original studies were identified and included in our systematic review. Studies suggest an important role of TRAIL in disorders such as heart failure, myocardial infarction, atrial fibrillation, ischemic stroke, peripheral artery disease, and pulmonary and gestational hypertension. Most evidence associates reduced TRAIL levels and increased TRAIL-R2 concentration with all-cause mortality in patients with CVDs. It is, however, unclear whether low TRAIL levels should be considered as a risk factor rather than a risk marker of CVDs. Further studies are needed to better define the association of TRAIL with cardiovascular diseases.