The nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome in the kidney and the heart is increasingly being suggested to play a key role in mediating inflammation. In the kidney, NLRP3 activation was associated with the progression of diabetic kidney disease. In the heart, activation of the NLRP3 inflammasome was related to the enhanced release of interleukin-1β (IL-1β) and the subsequent induction of atherosclerosis and heart failure. Apart from their glucose-lowering effects, SGLT-2 inhibitors were documented to attenuate activation of the NLRP3, thus resulting in the constellation of an anti-inflammatory milieu. In this review, we focus on the interplay between SGLT-2 inhibitors and the inflammasome in the kidney, the heart and the neurons in the context of diabetes mellitus and its complications.

Cancer persists as a significant global health challenge, claiming millions of lives annually despite remarkable strides in therapeutic innovation. Challenges such as drug resistance, toxicity, and suboptimal efficacy underscore the need for novel treatment paradigms. In this context, the repurposing of antibiotics as anti-cancer agents has emerged as an attractive prospect for investigation. Diverse classes of antibiotics have exhibited promising anti-cancer properties in both in vitro and in vivo studies. These mechanisms include the induction of apoptosis and cell cycle arrest, generation of reactive oxygen species, and inhibition of key regulators of cell proliferation and migration. Additional effects involve the disruption of angiogenesis and modulation of pivotal processes such as inflammation, immune response, mitochondrial dynamics, ferroptosis, and autophagy. Furthermore, antibiotics have demonstrated the potential to enhance the efficacy of conventional modalities like chemotherapy and radiotherapy, while alleviating treatment-induced toxicities. Nevertheless, the integration of antibiotics into oncological applications remains contentious, with concerns centered on their disruption of gut microbiota, interference with immunotherapeutic strategies, contribution to microbial resistance, and potential association with tumorigenesis. This narrative review explores the mechanisms of antibiotics’ anti-cancer activity, addresses controversies about their dual role in cancer biology, and envisions future perspectives that include the development of novel derivatives and innovative frameworks for their incorporation into cancer treatment paradigms.

Purposeof Review: Ultra-processed foods (UPFs) are becoming more and more important in daily diets around the world; in some cases, they can account for as much as 60% of daily energy intake. Epidemiological evidence suggests that this shift toward high levels of food processing may be partially responsible for the global obesity epidemic and the rise in the prevalence of chronic diseases. Recent Findings: Few prospective studies have examined the relationship between UPF consumption and cancer outcomes. According to currently available information, UPFs may increase the risk of cancer due to their obesogenic properties and exposure to substances that can cause cancer, such as certain food additives and pollution from product processing. The complex relationship between obesity and cancer involves factors such as immune dysregulation, altered adipokine and sex hormone levels, abnormal fatty acid metabolism, extracellular matrix remodeling, and chronic inflammation. Addressing cancer risk associated with UPF consumption could involve a multifaceted approach, including consumer behavior modification programs and robust public health regulations aimed at enhancing food environments. Improved knowledge of the potential dual negative impacts of UPFs on the environment and cancer risk is one of the priority areas we identify for future research and policy implications. Various approaches could be used to prevent cancers associated with UPF consumption, such as consumer behavior change programs and stricter public health regulations needed to improve the food environment. Summary: This review examines for the first time the potential role of UPFs in cancer risk associated with obesity, exploring underlying biological mechanisms and identifying key areas for future research and policy action, including the dual environmental and health impact of UPFs.

Renal vein thrombosis (RVT) is a relatively uncommon condition that is most frequently observed in individuals with nephrotic syndrome. While rare, pyelonephritis (PN) may serve as a predisposing factor for secondary RVT. In such cases, one should consider the possibility of RVT when patients fail to respond to appropriate antibiotic treatment. Typically, these patients require additional anticoagulation therapy for a duration of 3 to 6 months, with a generally favorable prognosis. In this report, we present the case of a 74-year-old female who developed RVT due to Klebsiella pneumoniae PN. Additionally, we reviewed 11 cases of PN complicated by RVT, which were documented in the PubMed database over a span of 40 years, emphasizing key elements in diagnostic and therapeutic approaches. Lastly, we elaborated upon the role of thrombo-inflammation, especially in the context of sepsis.

Intravenous methylprednisolone (IVMP) pulses, widely used for managing multiple sclerosis (MS) exacerbations, can lead to acute liver injury, presenting a diagnostic challenge in distinguishing between drug-induced autoimmune-like hepatitis (DI-ALH) and idiopathic autoimmune hepatitis (AIH). This study aimed to delineate the clinical and biochemical features of IVMP-induced liver injury, discern its etiology, and evaluate the efficacy of glucocorticoid (GC) therapy in treatment. A retrospective analysis of 13 relapsing MS patients with IVMP-induced liver injury was conducted. Liver injury was classified as hepatocellular, cholestatic, or mixed, with severity assessment guiding liver biopsy in selected cases. Causality was assessed using the Roussel Uclaf Causality Assessment Method (RUCAM) and the Simplified Diagnostic Criteria for AIH. All patients were initially monitored for a minimum of six months, with a mean follow-up period of 4.30 years. The median onset of liver injury was 37.46 days post-IVMP, with a mean peak alanine transaminase (ALT) level of 618.46 U/L. antinuclear antibody (ANA) positivity was observed in 61.53% of cases, with elevated serum immunoglobulin G (IgG) at 15.38%. Hepatocellular injury was universal among patients, and causality assessment predominantly supported DI-ALH. GC therapy was administered in six cases, achieving favorable outcomes in all but one, which necessitated rituximab. Biochemical normalization occurred within a mean of 55.41 days, with GC-treated patients recovering faster (48 days). These findings support the hypothesis that IVMP can induce hepatocellular injury, likely DI-ALH, during MS exacerbations. A tapering GC regimen proved effective in promoting recovery, particularly in severe cases. Additionally, this study introduced a diagnostic and therapeutic algorithm for managing IVMP-induced liver injury, offering a practical framework for clinical application.