Graduating resident and fellow readiness for general urologic practice during the COVID-19 pandemic: A survey-based assessment of trainees and program directors.

INTRODUCTION: Our goal was to compare the perceived readiness of graduating urologic residents and fellows to program directors (PDs) in U.S.-based postgraduate training programs. Additionally, we set out to assess the impact of COVID-19 on postgraduation plans to pursue fellowship training. METHODS: Graduating residents, fellows, and PDs of accredited residency/fellowship programs in the U.S. were surveyed. The ranked preparedness of trainees to perform common urologic procedures was measured using a Likert scale from 1 (not comfortable) to 5 (fully proficient). The impact of COVID-19 was measured using a three-point Likert scale. Chi-squared and Kruskal-Wallis analyses were used to compare the groups. RESULTS: From 93 responders, 21 were residents, 19 were fellows, 24 were residency PDs, and 29 were fellowship PDs. The median levels of comfort for transurethral resection of the prostate, hydrocelectomy, vasectomy, and urethral sling were at or above (≥3) moderate for both PDs and trainees. PDs were more likely to report underperformance for hypospadias repair (60% vs. 39%), penile prosthesis implantation (39% vs. 26%), and orthotopic neobladder formation (57% vs. 18%) than the trainees. Fifty-three (57.0%) of the surveyors felt that COVID-19 did not impact the trainees' comfort in performing general urologic procedures. COVID-19 influenced trainees' decision to pursue a fellowship or opt to practice as general urologists (p=0.002). CONCLUSIONS: Our study suggests there may be a self-reported discrepancy between graduating trainees and their PDs regarding trainees' comfort levels performing general urologic procedures.

Evaluation of Educational Feedback in Urology Training: A Survey-Based Assessment of Trainees and Program Directors.

OBJECTIVE: Our objective was to evaluate current satisfaction with the feedback provided during post-graduate urological training, including the quality and frequency of feedback, with participants consisting of both trainees and program directors. Additionally, we aimed to identify areas for future improvement in resident and fellow-level urological training. METHODS: Graduating residents, fellows, and program directors from accredited residency/fellowship programs in the United States were surveyed. A total of 575 surveys were sent out. Information on feedback frequency, quality, form, and satisfaction was collected using applicable multiple-choice responses and a five-point Likert scale. An open-ended question gathered suggestions for improving current feedback processes. A chi-square test of independence was used to compare the responses to individual questions. RESULTS: Ninety-two respondents answered our survey: 22 residents, 18 fellows, 25 residency program directors (PDs), and 27 fellowship PDs. The distribution of age, race, and gender categories was not significantly different between PDs and trainees. However, there was a significant difference in their subspecialties and American Urological Association (AUA) sections. The majority of fellowship PDs, residency PDs, fellows, and residents (88 total) reported verbal feedback as the predominant method within their practice. This was followed by written (68 total), electronic (54 total), and app-based feedback (19 total). CONCLUSION: Our study suggests that there may be a need for ongoing improvement or standardization of feedback mechanisms in the field of urological training and highlights the perceived discrepancies between learners and educators.

Gasdermin D restricts Burkholderia cenocepacia infection in vitro and in vivo.

Burkholderia cenocepacia (B. cenocepacia) is an opportunistic bacterium; causing severe life threatening systemic infections in immunocompromised individuals including cystic fibrosis patients. The lack of gasdermin D (GSDMD) protects mice against endotoxin lipopolysaccharide (LPS) shock. On the other hand, GSDMD promotes mice survival in response to certain bacterial infections. However, the role of GSDMD during B. cenocepacia infection is not yet determined. Our in vitro study shows that GSDMD restricts B. cenocepacia replication within macrophages independent of its role in cell death through promoting mitochondrial reactive oxygen species (mROS) production. mROS is known to stimulate autophagy, hence, the inhibition of mROS or the absence of GSDMD during B. cenocepacia infections reduces autophagy which plays a critical role in the restriction of the pathogen. GSDMD promotes inflammation in response to B. cenocepacia through mediating the release of inflammasome dependent cytokine (IL-1ß) and an independent one (CXCL1) (KC). Additionally, different B. cenocepacia secretory systems (T3SS, T4SS, and T6SS) contribute to inflammasome activation together with bacterial survival within macrophages. In vivo study confirmed the in vitro findings and showed that GSDMD restricts B. cenocepacia infection and dissemination and stimulates autophagy in response to B. cenocepacia. Nevertheless, GSDMD promotes lung inflammation and necrosis in response to B. cenocepacia without altering mice survival. This study describes the double-edged functions of GSDMD in response to B. cenocepacia infection and shows the importance of GSDMD-mediated mROS in restriction of B. cenocepacia.

Defective immunometabolism pathways in cystic fibrosis macrophages.

BACKGROUND: Mitochondria play a key role in immune defense pathways, particularly for macrophages. We and others have previously demonstrated that cystic fibrosis (CF) macrophages exhibit weak autophagy activity and exacerbated inflammatory responses. Previous studies have revealed that mitochondria are defective in CF epithelial cells, but to date, the connection between defective mitochondrial function and CF macrophage immune dysregulation has not been fully elucidated. Here, we present a characterization of mitochondrial dysfunction in CF macrophages. METHODS: Mitochondrial function in wild-type (WT) and CF F508del/F508del murine macrophages was measured using the Seahorse Extracellular Flux analyzer. Mitochondrial morphology was investigated using transmission electron and confocal microscopy. Mitochondrial membrane potential (MMP) as well as mitochondrial reactive oxygen species (mROS) were measured using TMRM and MitoSOX Red fluorescent dyes, respectively. All assays were performed at baseline and following infection by Burkholderia cenocepacia, a multi-drug resistant bacterium that causes detrimental infections in CF patients. RESULTS: We have identified impaired oxygen consumption in CF macrophages without and with B. cenocepacia infection. We also observed increased mitochondrial fragmentation in CF macrophages following infection. Lastly, we observed increased MMP and impaired mROS production in CF macrophages following infection with B. cenocepacia. CONCLUSIONS: The mitochondrial defects identified are key components of the macrophage response to infection. Their presence suggests that mitochondrial dysfunction contributes to impaired bacterial killing in CF macrophages. Our current study will enhance our understanding of the pathobiology of CF and lead to the identification of novel mitochondrial therapeutic targets for CF.