Explore the vast range of titles available.

Background/Objectives: Benign prostatic hyperplasia (BPH) is a common condition in older men and represents a major contributor to lower urinary tract symptoms, prostate enlargement, and features of metabolic syndrome (MetS). Androgen receptor (AR) signaling and extracellular matrix (ECM) remodeling play central roles in BPH pathology, yet the clinical relevance of AR coactivators and structural genes remains incompletely understood. Methods: Prostate tissues from 76 BPH patients and five non-hyperplastic controls were analyzed by quantitative PCR to assess AR coactivators (SRC-1, SRC-2, SRC-3, PCAF, p300) and ECM-related genes (COL1A1, COL3A1). Results: BPH tissues showed marked overexpression of AR coactivators and collagen genes compared to controls (fold changes ≥ 7.8). Higher prostate-specific antigen (PSA) levels (≥10 ng/mL) and enlarged prostate volumes (≥100 mL) were associated with increased expression of PCAF, p300, SRC-1, and COL1A1. PSA and prostate volume correlated positively with triglycerides and VLDL, and inversely with HDL. Strong associations between collagen genes and p160 coactivators suggest coordinated androgenic and stromal remodeling activity. COL1A1 expression was reduced in patients under pharmacological treatment, particularly with alpha-blockers or combination therapies. PCAF and p300 were elevated in patients with MetS, hyperlipidemia, or hyperglycemia. Conclusions: These findings define a molecular signature in BPH linking androgenic, metabolic, and stromal pathology. SRC-1, PCAF, p300, and COL1A1 emerge as potential biomarkers and therapeutic targets, providing new insights into the molecular mechanisms of BPH progression.

Background Financial toxicity (FT), first reported in oncologic patients and generally defined as harm to patients caused by the cost of treatment, is less well described in non-malignant urology. In chronic conditions related to lower urinary tract symptoms (LUTS), such as BPH, treatment costs may result in a significant substantial burden. The goal of this study was to characterize the association between FT and LUTS. Methods A cross-sectional web-based survey was administered to a random sample of adult men through a national registry of volunteers (ResearchMatch). Disease-specific information, validated symptom scores, and an 11-item measure of LUTS-related financial toxicity were used to characterize participants. Multivariable logistic regression was performed to identify predictors of financial toxicity. Results A total of 294 respondents with a self-reported history of BPH-associated LUTS were included, 41% of whom met the criteria for financial toxicity. Men with FT had worse LUTS symptom scores across all measures ( p  < 0.001). The presence of stress, urge, or mixed incontinence was significantly higher in men with FT (52% vs. 8%, 46% vs. 15%, and 36% vs. 5% respectively; p  < 0.001). Men with FT spent more out-of-pocket on incontinence products than those without FT ( p  < 0.001). On multivariable analysis, mixed incontinence was a predictor of FT (OR 3.233, 95% CI 1.15–9.084). Conclusion Two of five men with LUTS met the criteria for financial toxicity. These men had worse urinary symptom scores, higher rates of all types of incontinence, and higher out-of-pocket costs for incontinence products.

Severe life-threatening thromboembolism may be caused exclusively by the presence of an acute CMV infection or due to the association of this agent and other thrombogenic factors. We report a case of an immunocompetent young female patient who presented a pulmonary embolism associated with acute CMV infection. The patient did not have any other apparent cause of thrombosis. She was successfully treated with rivaroxaban for 6 months without further episodes. To the best of our knowledge, this is the first report of a pulmonary embolism associated with CMV treated with a direct oral anticoagulant. The current case report calls attention to the importance of signs and symptoms of thromboembolism among patients with CMV. Direct oral anticoagulants can potentially bring the same benefits to treat pulmonary embolism associated with CMV as those observed in patients not infected.

Bladder carcinoma (BC) is the tenth most frequent malignancy worldwide, with high morbidity and mortality rates. Despite recent treatment advances, high-grade BC and muscle-invasive BC present with significant progression and recurrence rates, urging the need for alternative treatments. The microRNA-21 (miR-21) has superexpression in many malignancies and is associated with cellular invasion and progression. One of its mechanisms of action is the regulation of RECK, a tumor suppressor gene responsible for inhibiting metalloproteinases, including MMP9. In a high-grade urothelial cancer cell line, we aimed to assess if miR-21 downregulation would promote RECK expression and decrease MMP9 expression. We also evaluated cellular migration and proliferation potential by inhibition of this pathway. In a T24 cell line, we inhibited miR-21 expression by transfection of a specific microRNA inhibitor (anti-miR-21). There were also control and scramble groups, the last with a negative microRNA transfected. After the procedure, we performed a genetic expression analysis of miR-21, RECK, and MMP9 through qPCR. Migration, proliferation, and protein expression were evaluated via wound healing assay, colony formation assay, flow cytometry, and immunofluorescence.After anti-miR-21 transfection, miR-21 expression decreased with RECK upregulation and MMP9 downregulation. The immunofluorescence assay showed a significant increase in RECK protein expression ( p  < 0.0001) and a decrease in MMP9 protein expression ( p  = 0.0101). The anti-miR-21 transfection significantly reduced cellular migration in the wound healing assay ( p  < 0.0001). Furthermore, in the colony formation assay, the anti-miR-21 group demonstrated reduced cellular proliferation ( p  = 0.0008), also revealed in the cell cycle analysis by flow cytometry ( p  = 0.0038). Our results corroborate the hypothesis that miR-21 is associated with BC cellular migration and proliferation, revealing its potential as a new effective treatment for this pathology.

Normothermic organ perfusion (NEVOP) promises to catalyze organ preservation, therapeutic discovery, and organ-specific disease modeling. Existing technology platforms remain inaccessible for research due to restricted access to commercial organ perfusion devices, high costs of both devices and proprietary consumables, and steep technical learning curves. Additionally, the available technology is not optimized to perfuse smaller organs such as the kidney. To overcome these barriers, a custom NEVOP circuit was developed using recycled, repurposed, and low-cost components. Porcine kidneys and autologous blood were used to iteratively optimize circuit design. A porcine kidney autotransplantation protocol was adapted to evaluate kidney function after perfusion. To pilot the flexibility of this system as a multi-organ platform for human biology, non-transplantable human donor kidney, spleen, and pancreas specimens were stably perfused using human blood products and analyzed. An ultra low-cost NEVOP system engineered to perfuse porcine kidneys and diverse human organs (kidney, pancreas, and spleen) sustained viable organs for up to 24 hours with evidence of both function and viability. Key innovations included a parallel flow resistor to facilitate low-flow perfusion in non-heparinized organs and a containment bag with adjustable magnets to provide vascular stability and recycling of venous overflow. The circuit costs less than 1,500USD to construct, and porcine kidneys perfused for 24 hours on this platform demonstrated healthy function upon autotransplantation. Custom NEVOP platforms constitute novel and potentially transformative research platforms which use low-cost and readily available materials. Paired with access to non-transplantable research organs from altruistic donors, this model provides a road map for investigators to advance biomedical discovery and human biology.