Background and Objectives: Endothelial dysfunction (ED) and oxidative stress play major contributions in the initiation and progression of atherosclerosis. Diabetes is a pathological state associated with endothelial damage and enhanced oxidative stress. This study evaluated endothelial dysfunction and oxidative stress in patients with severe coronary artery disease (CAD) undergoing coronary artery bypass graft (CABG) surgery, comparing those with and without type 2 diabetes mellitus (T2DM). Materials and Methods: We included 84 patients with severe coronary artery disease (33 of whom had type 2 diabetes mellitus) who underwent clinical assessments, ultrasound, and coronaryangiography. The SYNTAXI score was calculated from the coronaryangiogram. Blood samples were collected to measure plasma serotonin (5-HT; SER) levels, as well as levels of superoxide dismutase 1(SOD-1) and lectin-like oxidized low-density lipoprotein receptor-1(LOX-1) to assess oxidative stress. Brachial flow-mediated dilation (FMD) was used as a surrogate for endothelial dysfunction (ED),along with serum concentrations of 5-HT. Results: The coronary atherosclerotic burden, assessed using the SYNTAX I score, was more severe in patients with CAD and associated T2DM compared to those with CAD without T2DM (30.5 (17–54) vs. 29 (17–48); p = 0.05). The SYNTAX score was found to be positively correlated with T2DM (p = 0.029; r = 0.238).ED measured by FMD was associated with T2DM (p = 0.042; r = −0.223), with lower FMD measurements in T2DM patients when compared with individuals without this pathology (2.43% (0.95–5.67) vs. 3.46% (1.02–6.75); p = 0.079). Also, in the studied population, T2DM was correlated with serum 5-HT levels (764.78 ± 201 ng/mL vs. 561.06 ± 224 ng/mL; p < 0.001; r = 0.423), with higher plasma circulating levels of 5-HT in patients with T2DM. No statistically significant differences for oxidative stress markers (SOD-1 and LOX-1) were obtained when comparing T2DM and non-T2DM patients with severe CAD. Conclusions: ED (as assessed by brachial FMD and serum 5-HT) is more severe in in diabetic patients with severe CAD scheduled for CABG surgery, while oxidative stress (as evaluated through serum SOD-1 and LOX-1 concentrations) was not influenced by the presence of T2DM in this specific population. The most important finding of the present study is that circulating 5-HT levels are markedly influenced by T2DM. 5-HT receptor-targeted therapy might be of interest in patients undergoing CABG, but further studies are needed to confirm this hypothesis.

Background and Objectives: Renal trauma is a significant consequence of both blunt and penetrating injuries, with management strategies having continuously evolved over recent years. This management requires careful clinical evaluation to balance the need for operative or non-operative treatment. This is especially critical in the context of the increasing trend of non-operative management for stable renal injuries, largely due to advances in imaging, improved hemodynamic stabilization, and better outcomes with conservative approaches. The main objectives of this study were to evaluate the epidemiology of renal trauma, the mechanism of injury, and the outcomes of management strategies in blunt renal trauma and determine their influence on morbidity and mortality rates. Materials and Methods: A retrospective review was conducted with patients diagnosed with renal trauma in the Emergency Clinical County Hospital in Brasov, Romania from 1.01.2018 to 31.12.2023. Data were collected from medical records. Results: A total of 89 patients with blunt renal trauma were identified. The most frequent renal injuries, according to AAST classification, were grade 2 in 34.83% of the patients and grade 1 in 26.97% of the patients. Most of them, 84.27%, were managed conservatively. The overall mortality rate was 12.36%. Conclusions: This review highlights the importance of personalized management strategies for renal trauma, especially emphasizing conservative treatment for hemodynamically stable patients. Our findings contribute to understanding renal trauma outcomes and should improve future clinical practices and guidelines in renal trauma management. Further studies should explore long-term outcomes and optimize treatment protocols.

Background and Objectives: Endometriosis is associated with chronic inflammation, immune dysregulation, oestrogen-dependent growth, oxidative stress, altered steroid hormone metabolism, compromised epithelial barrier integrity, and the production of bioactive microbial metabolites. These interconnected alterations have been proposed to create, in principle, a permissive local microenvironment for malignant transformation. This narrative review examines whether endometriosis-associated dysregulation of the gut and reproductive tract microbiota may act as a hypothetical biological modulator linking these multi-axis changes to endometrial carcinogenesis, with attention to immunological, endocrine, metabolic, microbial–metabolite, oxidative, and barrier-related pathways. Material and Methods: We narratively integrated current evidence on gut and reproductive tract microbiota alterations relevant to endometrial homeostasis, with emphasis on the estrobolome, low-biomass uterine microbial communities, inflammatory and immune signaling, microbial metabolites, and pathways implicated in carcinogenesis. Results: Available data suggest that dysbiosis may influence endometrial carcinogenesis through interconnected endocrine, inflammatory, metabolic, and immune mechanisms. Attention has been given to loss of Lactobacillus dominance, enrichment of anaerobic and pro-inflammatory taxa, altered estrogen recirculation, progesterone resistance, Toll-like receptor activation, NF-κB/STAT3 signaling, COX-2/PGE2 activity, PI3K/AKT/mTOR pathway activation, oxidative stress, macrophage polarization, and impaired natural killer cell surveillance. These alterations may contribute to a permissive microenvironment characterized by persistent inflammation, defective immune control, and disrupted endometrial homeostasis. However, the current literature remains limited by small and heterogeneous cohorts, predominantly cross-sectional designs, contamination risk, and marked methodological variability, particularly in low-biomass uterine samples. Conclusions: Current evidence supports the view that microbiome dysregulation is a context-dependent biological modulator that intersects with endocrine, inflammatory, metabolic, immune, oxidative, and barrier-related pathways relevant to endometrial carcinogenesis. Microbiome dysbiosis should be regarded as a hypothetical contributory factor rather than as an established causal driver. Its near-term translational relevance appears greater for biomarker development and risk stratification than for immediate microbiome-directed therapy. Longitudinal, standardized, and functionally integrated studies are needed to clarify whether microbiome-associated signatures can be translated into clinically meaningful prevention and management strategies in endometrial cancer.