The purpose of this bibliometric analysis was to identify and assess the 100 most-cited articles (T100 articles) on urological surgery. The Web of Science (WoS) Core Collection database was used to investigate the T100 articles in the field of urological surgery. Different aspects of the T100 articles, including the countries, journals, authors, and topics, were analyzed. The number of citations of T100 articles published between 1989 and 2016 ranged from 334 to 2189. The T100 articles originated from 28 countries, with more than half originating from the USA (n = 80). Professor Bill-Axelson A from Uppsala University Hospital published the largest number of T100 articles as the first author (4) and as a coauthor (1). The Memorial Sloan Kettering Cancer Center from the USA is the top institution with the most T100 articles in the field of urological surgery. The special journal Journal of Urology published 41 of the T100 articles, which had a total of 19780 citations. Our study analyzed the 100 most-cited articles in the field of urological surgery. The USA is the dominant country in terms of the number of T100 articles, scientists and institutions. Surgery related to urological cancer has garnered the most academic attention, especially prostate cancer and renal cancer.

To highlight the scientific progress in immunotherapy of urological cancer by identifying and analyzing the 100 top-cited (T100) articles from the last 15 years.Papers in immunotherapy of urologica...

Journal of Men's Health (JOMH) is the official journal of the International Society of Men's Health (ISMH). JOMH is a peer-reviewed, open-access journal that covers all aspects of men's health

Heme oxygenase (HO-1) affords protection against ischaemia/reperfusion (I/R) injury; however, its effects on testicular I/R injury remain poorly explored. Herein, we aimed to examine the effects of HO-1 on testicular I/R injury and elucidate the underlying mechanism. Using the TALEN technique, we knocked out the HO-1 gene from rats. In vivo: Thirty hmox+/+ and 30 hmox−/− rats were randomly assigned to six groups: sham-operated (sham), I/R (the left testicle torsion/detorsion) 0 d,I/R 1d, I/R 3d, I/R 7d and I/R 28d. In vitro: GC-1 were suffered from: control,H/R (oxygen-deprivation/reoxygenation),H/R + HO-1 siRNA,H/R + c-Jun siRNA or H/R + HO-1 siRNA + c-jun.We performed immunofluorescence and immunohistochemistry experiments to detect HO-1 nuclear translocation. Flow cytometry was used to detect cell apoptosis and analyse the cell cycle. High-resolution miRNA, mRNA sequencing, reverse transcription-quantitative PCR, and western blotting were performed to identify testicular I/R injury-related genes strongly conserved in HO-1 knockout rats. A double luciferase reporter assay was performed to verify the relationship between C-jun and miR-221/222. In vivo, HO-1 improved the pathological damage induced by testicular I/R. In GC-1 cells, we confirmed the nuclear translocation of HO-1 and its protective effect against hypoxia/reoxygenation (H/R) damage. Accordingly, HO-1 protein itself, rather than heme metabolites, might play a key role in testicular I/R. Gene sequencing was performed to screen for miR221/222 and its downstream gene, thymocyte selection-associated high mobility group box (TOX). HO-1 increased c-Jun phosphorylation in the H/R group, knocked down c-Jun in GC-1 cells, and decreased miR-221/222 expression. Inhibition of HO-1 expression decreased the expression of c-Jun and miR-221/222, which was rescued by adding c-Jun. Dual-luciferase reporter assay confirmed the interaction between c-Jun and miR-221/222. HO-1 could exert a protective effect against testicular I/R via the phosphorylated c-Jun-miR-221/222-TOX pathway.

Refractory bladder neck contracture (BNC) poses significant challenges after transurethral resection of the prostate. This study compares laparoscopic bladder neck wedge resection with posterior urethral bed preservation (LCBNRE) versus transurethral resection of the bladder neck (TURBN) in managing refractory BNC. A retrospective analysis was conducted of 103 patients (2018–2023) divided into the LCBNRE (n = 58) and TURBN (n = 45) groups. Outcomes included operative parameters, urodynamics, International Prostate Symptom Score, and recurrence rates. LCBNRE showed longer operative time (100 vs 43 min, p < 0.01) but lower 30-d reoperation (1.7% vs 31.1%, p < 0.01) and recurrence (5.2% vs 28.9%, p = 0.01) rates. Urodynamic improvements favored LCBNRE (p < 0.01). Limitations include single-center design and short follow-up. LCBNRE is more effective for refractory BNC, with durable outcomes. Multicenter randomized trials are needed for validation. This study compared two surgical methods for bladder neck scarring. The laparoscopic approach resulted in better urine flow, fewer repeat surgeries, and lower recurrence rates than traditional methods.

Programmed degradation of maternal proteins is essential for the oocyte-to-embryo transition (OET). While pharmacological inhibition studies have established the importance of proteasomes in ovarian reserve maintenance, oocyte maturation and fertilization, the physiological impact of intrinsic proteasome insufficiency and underlying molecular mechanisms remain poorly understood. In mice, endolysosomal vesicular assemblies (ELVAs), specialized membraneless compartments composed of proteasomes, endolysosomes and autophagosomes, facilitate protein degradation during oocyte maturation and early embryogenesis. In this study, we generated mice with oocyte-specific deletion of the proteasomal core subunit Psma7 , to investigate the physiological function of the 20S proteasome and its roles in ELVAs-mediated protein degradation. PSMA7-deficiency destabilized 20S proteasomes and disrupted translocation of ELVAs, leading to pronounced accumulation of ubiquitinated proteins in oocytes and zygotes. Consequently, maternal Psma7 deletion resulted in female infertility, manifested by impaired oocyte maturation and developmental arrest at one- to two-cell stage. Furthermore, we observed reduced proteasome abundance and dysfunction of ELVAs in aged oocytes, providing a mechanistic explanation for the decline in developmental competence associated with oocyte aging. Taken together, our findings elucidate the critical function of proteasome-regulated proteostasis within ELVAs in maintaining oocyte quality during OET and reproductive aging.