Background and objectives: Boxing is a popular combat sport that requires high intensity and cooperation. However, there are limited data about the influence of boxing matches on blood parameters. The purpose of the present study was to investigate the match-induced changes in the metabolic, hormonal, and inflammatory status in male elite boxers. Materials and methods: High-level 20 male boxers with more than 5 years experience in boxing voluntarily participated in this study. Venous blood samples of the boxers, before and after combat, were taken for determination of the plasma parameters. Results: Our results indicated that a 9-min boxing match caused significant increases in plasma energy fuels (glucose and lactate), metabolic hormones (insulin, adrenocorticotropic hormone (ACTH), cortisol, and growth hormone), inflammatory markers (interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α)), muscle damage indicators (alanine aminotransferase (ALT) and aspartate aminotransferase (AST)), and oxidative stress marker (SOD). A decrease in total oxidant status (TOS) was also considered. However, there were no significant alterations in the plasma levels of androgenic hormone (free and total testosterone), anabolic hormone (IGF-1), lipids (total cholesterol, triglyceride, high-density lipoprotein (HDL), and low-density lipoprotein (LDL)), kidney function markers (creatinine and urea), and minerals (iron (Fe) and magnesium (Mg)). Conclusion: Elevations in the level of energy fuels and metabolic hormones of the boxers could be taken as a reflection of high-energy turnover during combat performance. The increases in inflammatory and tissue damage indicators may possibly be an indication of traumatic injury. Understanding the biochemical changes that occur during boxing match could be valuable to optimize the performance improvement of the athletes.

Background and Objectives: The excess consumption of fructose in the diet may cause metabolic syndrome, which is associated with an increased risk of kidney disease. There is limited data on probiotic treatment in high-fructose-induced metabolic syndrome. The present study aims to investigate whether the supplementation of Lactobacillus plantarum (L. plantarum) and Lactobacillus helveticus (L. helveticus) could provide an improving effect on the renal insulin signaling effectors, inflammatory parameters, and glucose transporters in fructose-fed rats. Materials and Methods: The model of metabolic syndrome in male Wistar rats was produced by fructose, which was given as 20% solution in drinking water for 15 weeks. L. plantarum and L. helveticus supplementations were given by gastric gavage from 10 to 15 weeks of age. Results: High-fructose consumption in rats reduced renal protein expressions of insulin receptor substrate (IRS)-1, protein kinase B (AKT), and endothelial nitric oxide synthase (eNOS), which were improved by L. plantarum and partially by L. helveticus supplementations. Dietary fructose-induced elevations in renal tissue levels of tumor necrosis factor α (TNF-α), interleukin (IL)-1β, IL-6, and IL-10, as well as expression of IL-6 mRNA, were attenuated, especially in L. plantarum treated rats. The increased renal expression of sodium-glucose cotransporter-2 (SGLT2), but not that of glucose transporter type-5 (GLUT5), was suppressed by the treatment with L. plantarum. Conclusion: Suppression in insulin signaling pathway together with the induction of inflammatory markers and upregulation of SGLT2 in fructose-fed rats were improved by L. plantarum supplementation. These findings may offer a new approach to the management of renal dysregulation induced by dietary high-fructose.

Background/Objectives: Understanding the pathogenesis of chronic lymphocytic leukemia (CLL) has led to the development of new prognostic and diagnostic tools, and efforts are underway to extend survival with new prognostic markers and treatment agents. This study aims to evaluate the factors affecting the prognosis and survival of patients with CLL via a retrospective study. Methods: Accordingly, the demographic features of, clinical and laboratory findings for, and hematological parameters and treatment responses of 178 CLL patients who were followed between 1 January 2015 and 31 December 2024 were analyzed before and after treatment protocols were carried out. Results: During the follow-up period, 40.8% of the patients received medical therapy, with 42.5% achieving complete remission, 49.3% experiencing partial remission, and 8.2% demonstrating no response to the treatments. The results demonstrated that an advanced Binet stage, the presence of splenomegaly, a positive direct Coombs test, the presence of a 17p deletion, thrombocytopenia, and elevated creatinine, leukocyte, and lymphocyte counts were associated with increased mortality. Elevated Binet and Rai stages, the existence of 17p deletion, and reduced hemoglobin levels were identified as statistically significant factors. Conclusions: Given the unfavorable prognosis of CLL patients exhibiting a positive direct Coombs test and compromised renal function, further investigations are required to validate the necessity of more rigorous monitoring and, possibly, early intervention. These findings underscore the importance of identifying high-risk factors in CLL to optimize patient management and improve long-term outcomes.

Objectives: Phosphodiesterases (PDEs) mediate several physiological activities, and alterations in PDE expressions might cause conflicts between functional and clinical effects. This study clarifies the eventual relationship between the hepatic insulin resistance-associated signaling elements and PDEs together with inflammatory markers and investigates the role of kefir in the treatment. Methods: Male Wistar rats were grouped as Control, Kefir, HFCS (high-fructose corn syrup), and HFCS + Kefir. Daily HFCS (20% w/v) and kefir (1 mL/100 g weight) were given for 8-weeks. Hepatic expressions of PDE isoforms and insulin signaling elements were determined with qPCR and Western blot. The changes in hepatic phospholipase A2 (cPLA2) and insulin-like growth factor 1 receptor-α (IGF-1Rα) were investigated histologically. Results: HFCS upregulated hepatic PDEs while repressed primary insulin signaling elements at gene and protein levels. It also augmented cPLA2 and IGF-1Rα expression. Kefir suppressed the PDEs and normalized the insulin signaling, and down-regulated cPLA2 and IGF-1Rα in the liver of HFCS-fed rats. Conclusions: The disruption of the insulin signaling pathway and activation of PDEs were negatively correlated in liver tissues of the HFCS-fed rats. Kefir treatment achieved a remarkable improvement in HFCS-dependent modifications, and it could be an excellent functional food against HFCS-induced insulin resistance, PDE hyperactivity, and inflammation.