Background and Objectives: Given the fact that galectin-3 has a predictive significance on the development of myocardial dysfunction after acute myocardial infarction, the aim of our study was to examine potential factors that could be important for the dynamics of the concentration of this biomarker in the early postinfarction period. Materials and Methods: This study included 89 patients with a diagnosis of stable angina pectoris (SAP) or the first non-ST elevation (NSTEMI) or ST-elevation (STEMI) myocardial infarction, who underwent percutaneous coronary intervention (PCI). The study group included 23 patients with the first NSTEMI and 42 patients with STEMI, while the control group consisted of 24 patients with SAP hospitalized for elective PCI without a previous MI. All patients had preserved left ventricular ejection fraction. Galectin-3 levels were determined on days 1, 5, and 30 after PCI. The significance of various independent variables as predictors of galectin-3 concentration was analyzed after a series of univariate linear regression modeling in a multivariate linear regression model. Results: The average patients’ age was 63.99 ± 9.13 years. Statistically significantly higher values of C-reactive protein were established in STEMI compared to SAP (p < 0.01) or NSTEMI (p < 0.001), whereas WBC count was significantly lower in SAP than in STEMI (p < 0.001) and NSTEMI (p < 0.01) group. Although there were no statistically significant differences in measured galectin-3 concentrations between the examined groups on days 1, 5, and 30 after PCI, HTA, triglyceride level, LA size, treatment with trimetazidine and long-acting nitrates, as well as percentage of LM stenosis and E/A ratio were identified as independent predictors of galectin-3 concentration. Conclusions: In the post-MI period, very early values of galectin-3 correlate mostly with atherosclerosis factors, while on day 30 this biomarker correlates with diastolic dysfunction and “announces” left ventricular remodeling.

Galectins represent a family of widely expressed lectins that have the ability to bind β-galactoside in modulating “cell-to-cell” and “cell-to-matrix” interactions in all organisms. These proteins are expressed in many inflammatory cells, such as macrophages, and depending on the inflammatory environment, they promote pro-inflammatory or anti-inflammatory responses. Galectin-3 (Gal-3) is predominantly located in the cytoplasm, but, as noted, it has also been detected in the nucleus, on the cell surface and in the extracellular environment, which indicates the multifunctionality of this molecule. It has been shown in many studies that Gal-3 is involved in immune regulation, fibrosis, and tissue remodeling, making it an important player in disorders such as inflammatory bowel disease (IBD), non-alcoholic steatohepatitis (NASH), and liver fibrosis. In IBD, this protein is associated with activation of the NLRP3 inflammasome, contributing to chronic intestinal inflammation. Also, in primary biliary cholangitis and autoimmune hepatitis, Gal-3 potentiate development of fibrosis through fibroblast-to-myofibroblast transition and extracellular matrix deposition, while in liver fibrosis, it is upregulated in hepatic stellate cells and macrophages, promoting fibrosis and inflammation. Studies show that Gal-3 inhibition reduces fibrosis and inflammation, making it a promising therapeutic target.

Background and objectives: Metabolic syndrome (MetS) is a cluster of risk factors, such as abdominal obesity, insulin resistance, dyslipidemia and hypertension, that together increase the risk of cardiovascular disease. Chronic hemodialysis (HD) patients have multiple comorbidities and many metabolic disorders, causing the frequent occurrence of metabolic syndrome. The goal of this study was to assess the prevalence of MetS in HD patients, and its association with all-cause and cardiovascular (CV) mortality. Patients and methods: A total of 138 HD patients were included in this prospective study. We analyzed demographic, anthropometric and biochemical data. Outcome measures were all-cause and CV mortality during the three-year follow-up. Results: MetS was diagnosed in 57.24% of enrolled patients. During the 36 months of follow-up, 33 patients died. MetS patients showed a significantly higher mortality rate than non-MetS (30.4% versus 16.36%, p < 0.001). The association of different MetS components with cardiovascular mortality reached significance when a minimum of three components were present (1.81 (95% confidence interval CI = 1.21–2.33)), with a grouped increase in effect size for subjects with four or five MetS components. Subjects with MetS exhibited nearly twice as high risk for all-cause (hazard ratio HR = 1.99 (95%CI) = 1.42–2.97) and 2.5 times for CV (HR = 2.51 (95%CI) = 1.25–3.83) mortality compared with those without MetS, after adjustment for age, gender, and cardiovascular disease. Conclusions: The study demonstrates that MetS is widespread in HD patients. In future, the focus must be on an active screening approach, and treatment of cardiometabolic risk factors, aiming to reduce mortality.

Background: Patients with end-stage renal disease (ESRD) receiving hemodialysis (HD) often experience bleeding. However, mechanisms behind this bleeding tendency are incompletely understood but may involve platelet dysfunction. We, therefore, studied platelet-dependent thrombus formation in flowing whole blood inside a microchip coated with collagen, and its association with circulating von Willebrand factor (VWF). Methods: Blood samples were obtained in 22 patients before and after HD. The area under the 10 min flow pressure curve in a microchip (AUC10) reflecting total platelet thrombogenicity was measured, using the Total Thrombus-formation Analysis System (T-TAS01). AUC10 < 260 indicates platelet dysfunction. VWF activity and antigen in plasma were also assayed. Results: VWF levels were moderately elevated and increased further after HD (P < 0.01 or lower). In contrast, AUC10 before and after HD was < 260 in 17/22 patients and < 130 in 15/22 patients, with no statistically significant difference in pre- vs post-HD measurements, indicating reduced platelet thrombogenicity, but with some variability as 5/22 patients showed normal platelet responsiveness. AUC10 and VWF activity or antigen levels in plasma were not correlated, either before or after HD. Conclusions: Most ESRD patients display moderate-to-severe platelet dysfunction as assessed by shear-induced platelet-dependent thrombus formation with T-TAS01. HD does not influence platelet function despite HD-induced elevations in VWF. T-TAS01 should be further evaluated as a tool in the assessment of bleeding risk in patients on HD. Graphical

Brain fingerprinting is a scientific technology that detects hidden information stored in the brain noninvasively measuring brainwave responses. The suspect is tested by looking for three types of information that display different-colored lines: red - information which is expected to be known by the suspect ('target'); green - information which is unknown to the suspect ('irrelevant'); blue - information relating to the crime that only the perpetrator knows ('probes'). Effective application of brain fingerprinting in the laboratory and in the field requires an understanding of relevant scientific principles and the proper role of brain fingerprinting in forensic science and legal proceedings. Detection of hidden information that is found in the brain of suspects, witnesses and intelligence sources is of great interest for all phases of law enforcement, for the Government, private investigations and intelligence operations. Scientific evidence in criminal proceedings will be only part of the totality of the evidence to be considered by a judge or a jury in order to make the final decision, preferably the most appropriate and just one. The court will take into account all other evidence submitted to it for review, together with the opinion of scientific experts that is only part of the evidence to be taken into account and appreciated as probative.