Andrew J. Paik

Genicular artery embolization (GAE) has emerged as a minimally invasive treatment for symptomatic knee osteoarthritis, but the evolution of its clinical evidence base remains incompletely characterized. This study evaluated the development of GAE research, emphasizing the composition and distribution of clinical evidence, collaboration patterns, embolic strategies, and conceptual themes. Scopus and Web of Science Core Collection were searched for peer-reviewed human studies of GAE published through 17 December 2025. Publication characteristics, study design, geographic origin, collaboration networks, embolic strategy, funding, and keyword trends were analyzed using Microsoft Excel, VOSviewer, and Bibliometrix in R. Among 128 included publications, 116 (90.6%) were published after 2020, and 48.4% (62/128) were original clinical investigations. Prospective cohorts and RCTs reporting clinical outcomes accounted for 24.2% (31/128) of publications, including only four RCTs (3.1%). Prospective cohort studies involved authors from 18 countries and RCTs from four countries. Permanent microspheres were the predominant embolic strategy in 24 of 62 (38.7%) original clinical studies, with differences in study-design composition across embolic strategies. GAE research has expanded rapidly across research groups and settings, although prospective and randomized evidence remains a minority of the literature. Continued prospective, randomized, and comparative investigation may further strengthen the clinical evidence base.

Catheter-associated urinary tract infections (CAUTIs) are amongst the most common nosocomial infections worldwide and are difficult to treat partly due to development of multidrug-resistance from CAUTI-related pathogens. Importantly, CAUTI often leads to secondary bloodstream infections and death. A major challenge is to predict when patients will develop CAUTIs and which populations are at-risk for bloodstream infections. Catheter-induced inflammation promotes fibrinogen (Fg) and fibrin accumulation in the bladder which are exploited as a biofilm formation platform by CAUTI pathogens. Using our established mouse model of CAUTI, here we identified that host populations exhibiting either genetic or acquired fibrinolytic-deficiencies, inducing fibrin deposition in the catheterized bladder, are predisposed to severe CAUTI and septicemia by diverse uropathogens in mono- and poly-microbial infections. Furthermore, here we found that Enterococcus faecalis, a prevalent CAUTI pathogen, uses the secreted protease, SprE, to induce fibrin accumulation and create a niche ideal for growth, biofilm formation, and persistence during CAUTI.

Catheter-associated urinary tract infections (CAUTIs) are amongst the most common nosocomial infections worldwide and are difficult to treat due to multi-drug resistance development among the CAUTI-related pathogens. Importantly, CAUTI often leads to secondary bloodstream infections and death. A major challenge is to predict when patients will develop CAUTIs and which populations are at-risk for bloodstream infections. Catheter-induced inflammation promotes fibrinogen (Fg) and fibrin accumulation in the bladder which are exploited as a biofilm formation platform by CAUTI pathogens. Using our established mouse model of CAUTI, we identified that host populations exhibiting either genetic or acquired fibrinolytic-deficiencies, inducing fibrin deposition in the catheterized bladder, are predisposed to severe CAUTI and septicemia by diverse uropathogens in mono- and poly-microbial infections. Furthermore, we found that E. faecalis, a prevalent CAUTI pathogen, uses the secreted protease, SprE, to induce fibrin accumulation and create a niche ideal for growth, biofilm formation, and persistence during CAUTI.