BackgroundThe physiopathology of sepsis continues to be poorly understood, and despite recent advances in its management, sepsis is still a life-threatening condition with a poor outcome. If new diagnostic markers related to sepsis pathogenesis will be identified, new specific therapies might be developed and mortality reduced. Small regulatory non-coding RNAs, microRNAs (miRNAs), were recently linked to various diseases; the aim of our prospective study was to identify miRNAs that can differentiate patients with early-stage sepsis from healthy controls and to determine if miRNA levels correlate with the severity assessed by the Sequential Organ Failure Assessment (SOFA) score.Methodology/Principal FindingsBy using genome-wide miRNA profiling by microarray in peripheral blood leukocytes, we found that miR-150, miR-182, miR-342-5p, and miR-486 expression profiles differentiated sepsis patients from healthy controls. We also proved by quantitative reverse transcription-polymerase chain reaction that miR-150 levels were significantly reduced in plasma samples of sepsis patients and correlated with the level of disease severity measured by the SOFA score, but were independent of the white blood counts (WBC). We found that plasma levels of tumor necrosis factor alpha, interleukin-10, and interleukin-18, all genes with sequence complementarity to miR-150, were negatively correlated with the plasma levels of this miRNA. Furthermore, we identified that the plasma levels ratio for miR-150/interleukin-18 can be used for assessing the severity of the sepsis.Conclusions/SignificanceWe propose that miR-150 levels in both leukocytes and plasma correlate with the aggressiveness of sepsis and can be used as a marker of early sepsis. Furthermore, we envision miR-150 restoration as a future therapeutic option in sepsis patients.

Partial robotic splenectomy seems to offer safety and all benefits of minimally invasive surgery, preserves the immune function of the spleen and allows the surgeon to conserve as much of the splenic parenchyma as possible.

Health education programmes and regulatory interventions addressing e-cigarettes are needed in Romania. More research is necessary on how to develop effective public health messages.

Background and objectives: The primary oral disease during adolescence is dental caries. Less is known about the caries prevalence, oral health behavior, and sweets nutritional habits in Romanian adolescents. The objective of this study was to assess the actual caries prevalence among Romanian adolescents in a representative area of Romania, Cluj, and to correlate with oral hygiene behaviors and dietary sugary foods intake. Materials and methods: We have done a cross-sectional study of 650 adolescents aged 10 to 19-years-old (average age 15.3 ± 2.8). We performed the oral dental examination according to the WHO methodology, calculated the number of decayed, missing (due to caries), and filled teeth (DMFT index), assessed the oral hygiene and dietary behaviors using a two-section valid questionnaire and statistically analyzed the interrelation between DMFT, oral hygiene and eating behaviors by multivariate statistical analysis. Results: (a) The caries prevalence in the adolescent population enrolled in the study was 95.5%; (b) the mean DMFT was 3.13 ± 2.0, without significant differences between the urban and rural adolescents (p = 0.253); lower in females than males (p < 0.050), (c) more than one third (33.7%, n = 219) of teenagers are seldom or never brush their teeth in the evening; (c) 40.6% of adolescents are missing the regular annual dental check-ups leading to an increased DMFT as shown in the multivariate analysis (p = 0.038); and (d) there is an increased prevalence of caries with age (p = 0.020), and with sugary sweetened beverages consumption (p = 0.028). Conclusions: Our study evidenced a persistent high caries prevalence in Romanian teenagers. Their dietary habits and irregular dental check-up were associated with the occurrence of dental conditions.

Nonalcoholic fatty liver disease (NAFLD) is a new challenge in modern medicine, due to its high prevalence in the world. The pathogenesis of NAFLD is a complex dysmetabolic process, following the “multiple-hit” hypothesis that involves hepatocytes excessive accumulation of triglycerides, insulin resistance (IR), increased oxidative stress, chronic low-grade inflammatory response and lipotoxicity. In this review, we provide an overview of the interrelation of these processes, the link between systemic and local inflammation and the role of dysfunctional adipose tissue (AT) in the NAFLD development. Multiple extrahepatic triggers of the pathophysiological mechanisms of NAFLD are described: nutritional deficiency or malnutrition, unhealthy food intake, the dysfunction of the liver–gut axis, the involvement of the mesenteric adipose tissue, the role of adipokines such as adiponectin, of food intake hormone, the leptin and leptin resistance (LR) and adipose tissue’s hormone, the resistin. In addition, a wide range of intrahepatic players are involved: oxidative stress, fatty acid oxidation, endoplasmic reticulum stress, mitochondrial dysfunction, resident macrophages (Kupffer cells), neutrophils, dendritic cells (DCs), B and T lymphocytes contributing to the potential evolution of NAFLD to nonalcoholic steatohepatitis (NASH). This interdependent approach to complex dysmetabolic imbalance in NAFLD, integrating relevant studies, could contribute to a better clarification of pathogenesis and consequently the development of new personalized treatments, targeting de novo lipogenesis, chronic inflammation and fibrosis. Further studies are needed to focus not only on treatment, but also on prevention strategy in NAFLD.