Characterization of a Novel Implant Intended to Expand and Reshape the Prostatic Urethra for the Treatment of Benign Prostatic Hyperplasia: A Pre-Clinical Feasibility Study in the Canine Model.

Objective: To evaluate the safety, feasibility, and tissue response of a novel device for the treatment of lower urinary tract symptoms secondary to benign prostatic hyperplasia, using the first-generation Urocross Expander System (Mercury Expander System).

Methods: The implant was deployed and retrieved using flexible cystoscope in 8 adult male canines, separated into three study arms by retrieval date (1-, 6-, and 12- months post-deployment). Cystoscopy and urethrograms verified implant position/diameter; bladder neck and external sphincter function/changes; prostatic tissue response; and implant condition.

Impact of bioresorbable versus permanent polymer on longterm vessel wall inflammation and healing: a comparative drug-eluting stent experimental study.

Aims: Drug-eluting stents (DES) have evolved to using bioresorbable polymers as a method of drug delivery. The impact of bioresorbable polymer on long-term neointimal formation, inflammation, and healing has not been fully characterised. This study aimed to evaluate the biological effect of polymer resorption on vascular healing and inflammation.

Historical Incidence of Spontaneous Lesions in Kidneys from Naïve Swine Utilized In Interventional Renal Denervation Studies.

The use of preclinical animal models is integral to the safety assessment, pathogenesis research, and testing of diagnostic technologies and therapeutic interventions. With inherent similarity to human anatomy and physiology, various porcine models have been the preferred preclinical model in some research areas such as medical devices, wound healing, and skin therapies. The porcine model has been the cornerstone for interventional cardiology for the evaluation and development of this catheter-based renal denervation (RDN) therapy.

Safety of direct administration of AAV2(CU)hCLN2, a candidate treatment for the central nervous system manifestations of late infantile neuronal ceroid lipofuscinosis, to the brain of rats and nonhuman primates.

Late infantile neuronal ceroid lipofuscinosis (LINCL), a pediatric autosomal recessive neurodegenerative lysosomal storage disorder, results from mutations in the CLN2 gene and consequent deficiency in tripeptidyl-peptidase I (TPP-I) and progressive destruction of neurons. We have previously demonstrated that CNS gene transfer of AAV2(CU)hCLN2 (an AAV2-based vector expressing the human CLN2 cDNA) in rats and nonhuman primates mediates long-term TPP-I expression in the CNS neurons [Sondhi, D., Peterson, D.