Residency Surgical BPH Training Paradigms from MIST to HOLEP.

PURPOSE OF REVIEW: Benign prostatic hyperplasia (BPH) is a common medical condition of older men that often requires medical or surgical therapy. Surgical options for BPH have grown exponentially over the last two decades. The numerous options and/or lack of access to them can make it challenging for new trainees to gain proficiency. We examine the literature for available BPH surgical simulators, learning curves, and training pathways. RECENT FINDINGS: Each BPH surgical therapy has a learning curve which must be overcome. There is an abundance of TURP simulators which have shown face, content, and construct validity in the literature. Similarly, laser therapies have validated simulators. Newer technologies do have available simulators, but they have not been validated. There are strategies to improve learning and outcomes, such as having a structured training program. Simulators are available for BPH surgical procedures and some have been implemented in urology residencies. It is likely that such simulation may make urologists more facile on their learning curves for newer technologies. Further studies are needed. Future directions may include integration of simulator technology into training pathways that include surgical observation and proctorship.

Priming of myelin-specific T cells in the absence of dendritic cells results in accelerated development of Experimental Autoimmune Encephalomyelitis.

Experimental autoimmune encephalomyelitis (EAE) is an established animal model of multiple sclerosis (MS). Inflammatory CD4+ T cell responses directed against CNS antigens, including myelin proteolipid protein (PLP), are key mediators of EAE. Dendritic cells (DCs) are critical for the induction of T cell responses against infectious agents. However, the importance of DCs in priming self-reactive CD4+ T cells in autoimmune disease such as MS has been unclear. To determine the requirement of DCs in PLP-specific CD4+ T cell responses and EAE, we genetically deleted CD11c+ DCs in PLP T cell receptor (TCR) transgenic SJL mice constitutively. DC deficiency did not impair the development, selection or the pathogenic function of PLP-specific CD4+ T cells in these mice, and resulted in accelerated spontaneous EAE compared to DC sufficient controls. In addition, using a genetic approach to ablate DCs conditionally in SJL mice, we show that CD11c+ DCs were dispensable for presenting exogenous or endogenous myelin antigen to PLP-specific T cells and for promoting pro-inflammatory T cell responses and severe EAE. Our findings demonstrate that constitutive or conditional ablation of CD11c+ DCs diminished self-tolerance to PLP autoantigen. They further show that in the absence of DCs, non-DCs can efficiently present CNS myelin antigens such as PLP to self-reactive T cells, resulting in accelerated onset of spontaneous or induced EAE.

Pretreatment screening and counseling on prolonged erections for patients prescribed trazodone.

PURPOSE: We examined whether patients are appropriately screened for previous prolonged erections or priapism and counseled about trazodone complications, specifically prolonged erections and priapism, prior to trazodone treatment. MATERIALS AND METHODS: We identified patients under the age of 50 on trazodone as of February 27, 2019 at the VA New Jersey Health Care System. Patients were asked about information provided to them prior to medication initiation, occurrence of prolonged erections/priapism, and reporting rate of side effects. RESULTS: Two hundred and twenty nine out of five hundred and twenty four male patients agreed to participate in the study. Forty three out of two hundred and twenty nine of patients were informed about the side effects of prolonged erections and 37/229 of patients were informed of risk of priapism prior to treatment. Only 17/229 of patients were asked if they had had any episodes of prolonged erection or priapism in the past. Eighteen patients developed prolonged erection while taking trazodone. Only 5/18 patients who had developed prolonged erections informed their physicians. CONCLUSIONS: Only a fraction of patients were properly screened for previous prolonged erections or priapism and properly informed about the side effects of trazodone. Urologist should better educate trazodone prescribers, such as family medicine and psychiatric colleagues, regarding the side effects of trazodone. It is imperative that prescribing physicians appropriately screen and educate patients prior to trazodone initiation and instruct patients to report any treatment side effects to avoid potential long-term adverse outcomes.

Postoperative Complications After Robotic Partial Nephrectomy.

Objectives: To assess the incidence of postoperative arterial malformation (AM) and urine leak/urinoma (UL) after robotic partial nephrectomy (RPN) in a contemporary series and to evaluate risk factors for these complications. Materials and Methods: All RPNs were queried from Institutional Review Board-approved retrospective and prospective nephrectomy databases. Demographics, perioperative variables, and postoperative complications were collected. Differences between cohorts were analyzed using univariate analysis. Postoperative complications were graded using the Clavien-Dindo system. UL was defined in the context of signs and symptoms of a collection with supporting evidence of urine collection through drainage or aspiration. AM was identified based on postoperative imaging indicative of arteriovenous fistula or pseudoaneurysm and/or requirement for selective embolization. Predictors of AM and UL were assessed by univariate analysis. Results: A total of 395 RPNs were performed by four urologists between January 2014 and October 2018. Tumor complexity, defined by nephrometry score, was significantly greater in the prospective cohort (p = 0.01). Overall incidence of postoperative complications was 5.6% with cohort-specific incidences of 5.3% and 5.8%. The retrospective cohort had a greater percentage of complications classified as ≥IIIa: 8/13 (61.5%) vs 2/8 (25%). Overall incidence of AM was 2.3% with cohort-specific incidence of 3.1% (7/225) vs 1.1% (2/170). Overall incidence of UL was 0.25% with cohort-specific incidence of 0.55% (1/225) and 0.0% (0/170). The difference in incidence of both complications between cohorts was significant (p < 0.05). No significant predictors for AM were identified. Conclusions: The incidence of postoperative complications after RPN remains low (5.3% vs 5.8%, overall: 5.6%). UL and AM are becoming rarer with experience, despite increasing surgical complexity (0.55% vs 0%, 3.1% vs 1.1%).

Genome-wide transcriptional analyses of islet-specific CD4+ T cells identify Idd9 genes controlling diabetogenic T cell function.

Type 1 diabetes (T1D) is a polygenic disease with multiple insulin-dependent diabetes (Idd) loci predisposing humans and NOD mice to disease. NOD.B10 Idd9 congenic mice, in which the NOD Idd9 chromosomal region is replaced by the Idd9 from T1D-resistant C57BL/10 mice, are significantly protected from T1D development. However, the genes and pathways conferring T1D development or protection by Idd9 remain to be fully elucidated. We have developed novel NOD.B10-Idd9 (line 905) congenic mice that predominantly harbor islet-reactive CD4(+) T cells expressing the BDC2.5 TCR (BDC-Idd9.905 mice). To establish functional links between the Idd9 genotype and its phenotype, we used microarray analyses to investigate the gene expression profiles of ex vivo and Ag-activated CD4(+) T cells from these mice and BDC2.5 (BDC) NOD controls. Among the differentially expressed genes, those located within the Idd9 region were greatly enriched in islet-specific CD4(+) T cells. Bioinformatics analyses of differentially expressed genes between BDC-Idd9.905 and BDC CD4(+) T cells identified Eno1, Rbbp4, and Mtor, all of which are encoded by Idd9 and part of gene networks involved in cellular growth and development. As predicted, proliferation and Th1/Th17 responses of islet-specific CD4(+) T cells from BDC-Idd9.905 mice following Ag stimulation in vitro were reduced compared with BDC mice. Furthermore, proliferative responses to endogenous autoantigen and diabetogenic function were impaired in BDC-Idd9.905 CD4(+) T cells. These findings suggest that differential expression of the identified Idd9 genes contributed to Idd9-dependent T1D susceptibility by controlling the diabetogenic function of islet-specific CD4(+) T cells.