Artificial Intelligence (AI) is revolutionizing prostate cancer (PCa) care, addressing the major clinical challenges of subjectivity and overtreatment. Our traditional tools - like PSA, DRE, mpMRI, and Gleason scoring - often lack the precision needed to distinguish truly aggressive tumors from indolent disease, leading to unnecessary morbidity in up to 50% of low-risk men. This review explains how AI, specifically machine learning (ML) and deep learning (DL), is poised to solve this. We cover AI's role from initial diagnosis, where radiomics and digital pathology boost grading accuracy and reduce inter-reader variability, to treatment selection and surgical precision through predictive models and Augmented Reality (AR) guidance. We also detail its utility in predicting biochemical recurrence (BCR) and managing long-term side effects. Finally, we address the critical barriers to adoption, including the need for large, diverse datasets (to combat algorithmic bias), the "black box" problem (solved by Explainable AI, XAI), and navigating FDA regulation. The future of PCa care hinges on this precise, data-driven approach.

Renal aging contributes to declining kidney function and heightened susceptibility to chronic kidney disease (CKD). A key factor in this process is the diminished number and functionality of renal stem/progenitor cells, though the underlying mechanisms remain incompletely understood. Human urine-derived stem/progenitor cells (USCs) represent a promising, non-invasive source with notable regenerative potential. In this study, we examined cellular proliferation, reactive oxygen species (ROS) production, and senescence-associated protein expression as indicators of age-related degeneration in renal progenitor cells. USCs obtained from older healthy and diabetic individuals were compared to those from young, healthy donors. Our results demonstrate that USCs from aged and diabetic donors exhibit significantly reduced proliferation, elevated ROS levels, and increased β-galactosidase expression. Moreover, these cells showed impaired capacity to form 3D renal spheroids with tubular-like structures over a two-week culture period, relative to young controls. Together, these findings suggest that USCs from older or diabetic individuals - when cultured in both 2D and 3D systems - serve as a valuable model for studying renal aging and progenitor cell dysfunction. This model may facilitate the identification of biomarkers for renal aging and CKD risk and inform future regenerative and therapeutic strategies.

Radical prostatectomy (RP) is a highly effective treatment for localized prostate cancer; unfortunately, post-prostatectomy urinary incontinence (UI) remains a prevalent and distressing complication, significantly diminishing patients’ quality of life. Current therapeutic options often provide incomplete continence restoration and may lead to substantial morbidity. This review examines the rapidly advancing field of regenerative medicine, specifically focusing on stem cell and exosome-based therapies as innovative approaches to address post-RP UI. We go deeper into the unique pathophysiology of male post-prostatectomy UI, distinguishing it from other forms of UI, and present the compelling biological rationale for these regenerative interventions. Highlighting advancements from 2014 to 2025, we explore recent preclinical and clinical progress in this domain. Furthermore, we critically assess the persistent challenges crucial for widespread clinical application, including optimizing cell dose and source, ensuring long-term efficacy and safety, and interpreting complex regulatory environments. By bridging the understanding of sex-related differences between females and males in UI and tackling the specific challenges of male post-RP incontinence, this review emphasizes that while promising, the journey from laboratory bench to bedside for these innovative therapies demands rigorous scientific inquiry and collaborative efforts.

Age-related macular degeneration (AMD), particularly its dry form, is a leading cause of irreversible vision loss due to retinal pigment epithelium (RPE) dysfunction and loss. Addressing this unmet therapeutic need requires non-invasive strategies for generating patient-specific RPE cells. This study reports the successful generation and initial characterization of RPE cells derived from urine-derived induced pluripotent stem cells (u-iPSC-RPE). Urine-derived stem cells (USCs) were isolated from healthy individuals and comprehensively characterized, confirming strong expression of renal progenitor makers and mesenchymal stem cell markers, while lacking standard hematopoietic markers. USCs were reprogrammed into iPSCs using the integration-free Sendai virus expressing the Yamanaka factors. The reprogrammed u-iPSC clones displayed characteristic pluripotency marker expression and demonstrated clearance of the Sendai virus by later passages. Subsequently, these u-iPSCs were efficiently differentiated into RPE cells, exhibiting characteristic hexagonal morphology and pigmentation which was confirmed by the expression of key RPE-specific proteins. Our findings demonstrated the feasibility of generating patient-specific RPE cells from readily accessible USCs. This reliable method for producing u-iPSC-RPE from urine-derived progenitor cells provides a promising foundation for future studies investigating their functional potential in vitro and their use in in vivo models for retinal disease modeling and therapeutic applications for AMD.

Introduction: Acute-on-chronic liver failure (ACLF) is a highly lethal clinical syndrome with limited effective therapeutic options. Urine-derived stem cells (USCs) represent a non-invasive and readily accessible cell source, but whether USCs obtained from patients with severe liver dysfunction retain therapeutic and immunomodulatory potential remains unclear. Methods: To address this question, USCs derived from ACLF patients (LF-USCs) were evaluated in a Concanavalin A (Con A)-induced immune-mediated acute liver injury mouse model. Hydrogel-encapsulated LF-USCs were transplanted, and therapeutic efficacy was assessed by survival analysis, serum biochemical parameters, histological examination, and inflammatory cytokine profiling. Results: Transplantation of hydrogel-encapsulated LF-USCs significantly improved mouse survival, reduced serum transaminase levels, and alleviated hepatocellular necrosis (p < 0.05). At the mechanistic level, LF-USC treatment was associated with decreased systemic inflammatory cytokine levels, attenuation of intrahepatic inflammatory injury, and dynamic modulation of macrophage-associated inflammatory signatures. Discussion: These findings demonstrate that functionally competent USCs can be successfully obtained from ACLF patients and highlight their potential as a readily accessible autologous cell source for immune modulation and liver tissue repair in immune-mediated acute liver injury.