Measles is an extremely contagious viral disease. Even though a safe vaccine exists for this disease, it remains one of the leading causes of mortality and morbidity in infants and young children. We aimed to create a retrospective descriptive study in which to analyze the evolution of the measles epidemic at the European level. The documentation was carried out using European Centre for Disease Prevention and Control (ECDC) and World Health Organization (WHO) statistics. At the same time, we present the epidemic's evolution in Romania, using data provided by the Romanian National Institute of Public Health and Ministry of Health. European statistical data indicate a high number of patients diagnosed with measles both among children and adults. All European countries benefit from the measles vaccination in the form of the measles-mumps-rubella (MMR) trivaccine included in their National Vaccination Programme. Palazestrant in vivo The vaccination schedule varies from country to country. In the vaccination scheme, most European coual contact in the context of the social distancing imposed by the Sars-CoV-2 virus pandemic are discussed. We consider necessary a detailed documentation of the percentage of new disease cases that will appear in the pediatric population in the near future, in the context of the resumption of daily activity after the reopening of nurseries, kindergartens and schools.Numerous previous studies have found that C-reactive protein (CRP) is associated with cardiac arrhythmia and cardiac remodeling. However, the underlying mechanisms of this association remain unclear. Sodium-calcium exchanger 1 (NCX1) serves an important role in the regulation of intracellular calcium concentration, which is closely related with cardiac arrhythmia and cardiac remodeling. The present study aimed to evaluate the effects of CRP on NCX1 and intracellular calcium concentration in cardiomyocytes. Primary neonatal mouse ventricular cardiomyocytes were cultured and treated with varying concentrations of CRP (0, 5, 10, 20 and 40 µg/ml). The cardiomyocytes were also treated with NF-κB-specific inhibitor PTDC and a specific inhibitor of the reverse NCX1 KB-R7943 before their intracellular calcium concentrations were measured. mRNA and protein expression levels of NCX1 were detected by reverse transcription-quantitative PCR and western blotting, respectively and intracellular calcium concentration was evaluated by flow cytometry. CRP treatment significantly increased mRNA and protein expression levels of NCX1 in myocytes (P=0.024), as well as intracellular calcium concentration (P=0.01). These results were significantly attenuated by the NF-κB-specific inhibitor PDTC and a specific inhibitor of the reverse NCX1, KB-R7943. CRP significantly upregulated NCX1 expression and increased intracellular calcium concentration in cardiomyocytes via the NF-κB pathway, suggesting that CRP may serve a pro-arrhythmia role via direct influence on the calcium homeostasis of cardiomyocytes.Renal tubular interstitial injury plays a key role in the progression of diabetic nephropathy (DN) and, thus, the study of renal tubular injury in DN is important. The aim of the present study was to elucidate the role of the NLR family CARD domain containing 4 (NLRC4) inflammasome in renal tubular epithelial cell (RTEC) injury in DN. Human kidney biopsy tissues were obtained from patients with DN, and normal kidney tissues were obtained from nephrectomies performed for renal hamartoma. Human RTECs (HK2 cells) were divided into normal glucose (D-glucose 5.6 mmol/l), high glucose (HG; 30 mmol/l), high osmotic (D-glucose 5.6 mmol/l + D-mannitol 24.4 mmol/l), HG + NLRC4 small interfering (si)RNA or HG + siRNA control groups. Then, the expression levels of NLRC4, PTEN-induced kinase 1 (PINK1) and parkin, as well as the levels of mitochondrial reactive oxygen species, which are associated with mitophagy, were observed. The expression levels of NLRC4, PINK1, parkin and phosphorylated parkin in the RTECs of patients with DN were higher compared with those in normal controls. In HK2 cells, HG stimulated the expression of NLRC4, the secretion of IL-1β and IL-18 and cell death. Moreover, knockdown of NLRC4 expression in HK2 cells treated with HG reduced the secretion of the inflammatory cytokines, IL-1β and IL-18. The findings of the present study may provide a rationale for the development of treatments for patients with DN by preventing inflammasome activation.Inflammatory bowel diseases (IBDs) are chronic immune disorders that occur in the intestinal tract. Previous studies have revealed that intestinal epithelial cells (IECs) play critical roles in the development of IBDs, and therapies targeting IECs hold great potential for the treatment of IBDs. However, the roles of microRNAs (miRs) in the regulation of IEC properties and whether they can be used as targets for IEC regulation and IBD treatment are largely unknown. The aim of the present study was to investigate the role of the miR-452-5p/Mcl-1 axis in the regulation of the properties of IECs during the pathology of IBD. A dextran sulfate sodium-induced mouse model of ulcerative colitis (UC) and an in vitro lipopolysaccharide-stimulated IEC-6 cell model were investigated. The results revealed that miR-452-5p expression in the IECs of the mice increased significantly upon UC induction, and the knockdown of miR-452-5p alleviated the IBD symptoms. Furthermore, the suppression of miR-452-5p downregulated the expression of the inflammatory cytokines IL-6, IL-8 and TNFα, and upregulated the expression of intestinal barrier-associated molecules, namely occludin, zona occludens 1 and mucin-2 in IECs in vitro and in vivo. Notably, the results indicated that miR-452-5p modulated the responses of IECs by negatively regulating the expression of Mcl-1, as the knockdown of Mcl-1 abrogated the effects of miR-452-5p suppression on IECs. The present study suggested that miR-452-5p regulated the responsiveness of IECs to influence the development of UC in an Mcl-1-dependent manner. These observations provide important information to improve the understanding of IBD pathogenesis and indicate that targeting the miR-452-5p-Mcl-1 signaling axis in IECs holds potential for IBD treatment.