The liver is a central metabolic organ that regulates numerous physiological processes, including glucose and lipid metabolism, detoxification, and the synthesis of essential proteins and bile. Bile acids (BAs), synthesized from cholesterol in hepatocytes, not only facilitate the emulsification and absorption of dietary fats but also act as potent signaling molecules through receptors such as the farnesoid X receptor (FXR) and Takeda G-protein-coupled receptor 5. Metabolic dysfunction-associated steatotic liver disease (MASLD) is a leading cause of chronic liver disease globally, closely linked with obesity, insulin resistance, and other components of metabolic syndrome. In MASLD, the metabolism of BAs is markedly disrupted, resulting in alterations in their synthesis, composition, and signaling activity. These changes contribute to hepatic steatosis, inflammation, and fibrosis, thereby exacerbating metabolic dysfunction and liver damage. The altered profiles and signaling activity of BAs in MASLD patients suggest that BAs act not only as biomarkers of disease severity, but also as active mediators of its pathogenesis. Modulators of BA signaling pathways, especially FXR agonists, are the focus of intense research for their potential to beneficially influence liver steatosis and inflammation in MASLD. Recent research has yielded promising results, indicating potential therapeutic application and the introduction of novel agents aimed at modulating BA homeostasis and function. This minireview outlines the physiological roles of BAs, seeks to advance the elucidation of the mechanisms by which their dysregulation contributes to MASLD progression, and highlights current and emerging therapeutic approaches. A deeper understanding of these complex interactions is essential for improving the diagnosis, prognosis and treatment of MASLD.

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Insertion/deletion polymorphism of the angiotensin converting enzyme (ACE) gene is a key component of the Renin-Angiotensin-Aldosterone System (RAAS). It has been proposed as an independent factor for hypertension and other cardiovascular diseases. Consequently, it has been extensively studied in various populations. The aim of this study is to investigate I/D polymorphism of ACE gene and its connection to hypertension in population of Tuzla Canton (Bosnia & Herzegovina). The study included 60 hypertensive subjects and 60 healthy control subjects with no risk factors for hypertension. I/D polymorphism was genotyped by polymerase chain reaction followed by gel electrophoresis and data obtained were statistically analysed using Chi square test. Odd’s ratios were calculated with a 95% confidence interval. P-value < 0.05 was considered significant. Odd’s ratios were calculated with a 95% confidence interval. P-value <0.05 was considered significant. Higher frequency of genotype D/D and allele D was determined in subjects with hypertension compared to control subjects but there is no statistical significance (p>0.05). However, statistically significant association was found in compared groups of subjects with genotypes DD + ID, in regards to genotype I/I (p<0.05). The results indicate the conclusion that ACE I/D polymorphism cannot be considered the main risk factor for development of hypertension, but its influence should be investigated together with other genetic and acquired risk factors that are associated with hypertension. This research contributes to the on-going exploration of molecular-genetic associations with hypertension.

Portal vein aneurysm (PVA) is a rare vascular abnormality, representing 3% of all venous aneurysms in the human body, and is not well understood. It can be congenital or acquired, located mainly at the level of confluence, main trunk, branches and bifurcation. A PVA as an abnormality of the portal venous system was first reported in 1956 by Barzilai and Kleckner. A review from 2015 entitled “Portal vein aneurysm: What to know” considered fewer than 200 cases. In the last seven years, there has been an increase in the number of PVAs diagnosed thanks to routine abdominal imaging. The aim of this review is to provide a comprehensive update of PVA, including aetiology, epidemiology, and clinical assessment, along with an evaluation of advanced multimodal imaging features of aneurysm and management approaches.

Molecular-genetic diagnostics of polygenic diseases is a new and interesting area in laboratory diagnostics, especially in the area of cardiovascular diseases, as one of the leading causes of mortality in the world population. Aims: The aim of the paper was to analyse variants of the endothelial nitric oxide synthase gene (NOS3) (Glu298Asp/G894T) in the human population of Tuzla Canton in relation to cardiovascular diseases. Study Design: The study included 112 respondents of both sexes over 18 years old. The experimental group for the analysis of the polymorphism (Glu298Asp) of the endothelial nitric oxide synthase gene included 56 respondents of both sexes with cardiovascular disease (hypertension), while the control group comprised 56 healthy respondents of both sexes without a prior history of cardiovascular disease (sample/control). Place and Duration of Study: Blood sampling was performed at Medical Center "Plava Poliklinika", “Plava Medical Group”, Department of Biochemistry, Microbiology and Genetics, Tuzla. DNA isolation and molecular-genetic analysis of the samples were performed in Laboratory for scientific research at the Department of Biology, Faculty of Natural Sciences and Mathematics in Tuzla. Methodology: The genotyping of eNOS Glu298Asp polymorphism for all respondents was determined by an optimized method based on PCR-RFLP reaction. Results: In the total sample of respondents, the highest genotype frequencies of the eNOS gene were recorded for the GG genotype (53.5%) and the GT genotype (35.7%). The lowest frequency was recorded for the TT genotype, which was 10.8%. Conclusion: The results obtained in the study provide good guidelines for further study of a molecular-genetic association between a high number of gene candidates and cardiovascular diseases, which will contribute to the incorporation of these results into the existing regional and European genetic database.

Aims: To evaluate the efficacy of metronidazole monotherapy and modified therapy with metronidazole + nifuroxazidefor the for treatment of a mild form of Clostridium difficile infection (CDI). Study Design: A prospective, randomized, controlled clinical trial. Place and Duration of Study: University of Applied Sciences Tuzla in the period from June 2018 to June 2019. Methodology: Sixty patients were included in the study, divided into two groups. One group received standard therapy (metronidazole) for the treatment of a mild form of CDI, while the other group was treated with modified therapy (metronidazole + nifuroxazide). Subjects with a developed clinical picture and a positive toxin test for Clostridium difficile were surveyed on the day of admission, then on the 4th, 10th, 14th and 30th days from the start of therapy. The goal of the research was to determine the impact of the modified therapy protocol on the number of stools and the presence of pain compared to standard therapy. Results: The modified therapy with metronidazole + nifuroxazide showed better pharmacological efficacy in the treatment of CDI compared to the standard therapy with metronidazole alone. The group of subjects who were treated with modified therapy reported a significantly lower number of stools (P=.001) and the absence of pain at the first and second check-ups. Conclusion: Nifuroxazide and metronidazole represent a combination of drugs that reduce the number of stools in the shortest possible time and result in the absence of abdominal pain in patients diagnosed with a mild form of CDI.