The Future State of Race/Ethnicity in Urology: Urology Workforce Projection From 2021-2061.

OBJECTIVE: To project the proportion of the urology workforce that is from under-represented in medicine (URiM) groups between 2021-2061. METHODS: Demographic data were obtained from AUA Census and ACGME Data Resource Books. The number of graduating urology residents and proportion of URiM graduating residents were characterized with linear models. Stock and Flow models were used to project future population numbers and proportions of URiM practicing urologists, contingent on assumptions regarding trainee demographics, retirement trends, and growth in the field. RESULTS: Currently, there is an increase in the percentage of URiM graduates by 0.145% per year. If historical trends continue, URiM urologists will likely comprise 16.2% of urology residency graduates and 13.3% of the practicing urological workforce in 2061. These percentages would constitute an underrepresentation of URiM urologists relative to the projected 44.2% of the U.S. population who would identify as American Indian/Alaskan Native, Black/African American, Latinx/Hispanic and Native Hawaiian/Pacific Islander by 2060.1 An increase in the percentage of URiM graduates by 0.845% per year would result in 44.2% URiM urology residency graduates and 26.1% URiM practicing urologists by 2061. An interactive app was designed to allow for a range of assumptions to be explored and for future data to be incorporated. CONCLUSION: URiM physician representation within urology over the next 40years will remain disproportionately low compared to that of the projected share of people of color in the general U.S. POPULATION: In order to achieve the AUA's Diversity, Equity and Inclusion goals, a concerted effort to implement interventions to recruit, train, and retain a generation of racially diverse urologists appears necessary.

Is song processing distinct and special in the auditory cortex?

Is the singing voice processed distinctively in the human brain? In this Perspective, we discuss what might distinguish song processing from speech processing in light of recent work suggesting that some cortical neuronal populations respond selectively to song and we outline the implications for our understanding of auditory processing. We review the literature regarding the neural and physiological mechanisms of song production and perception and show that this provides evidence for key differences between song and speech processing. We conclude by discussing the significance of the notion that song processing is special in terms of how this might contribute to theories of the neurobiological origins of vocal communication and to our understanding of the neural circuitry underlying sound processing in the human cortex.

US Postgraduate Trainee Racial, Ethnic, and Gender Representation and Faculty Compensation By Specialty.

This study compares postgraduate trainee racial, ethnic, and gender representation and faculty compensation for 21 clinical specialties using 2015-2022 data.

Racial and Ethnic Differences in Medical Student Timing and Perceived Quality of Exposure to Urology.

OBJECTIVE: To contextualize the low representation of Under-Represented in Medicine (URiM) in urology, we examine differences in timing and perceived quality of urology clinical and research exposures for medical students across race/ethnicity. METHODS: A cross-sectional survey was distributed to all medical students at University of California, Los Angeles. Dependent variables were timing of urology exposure and perceived quality of urology exposure. Descriptive statistics and multivariate analyses were used to compare variables across race/ethnicity. Logistic regression was used to determine odds of early exposure to urology across race/ethnicity. RESULTS: Black and Latinx students were significantly less likely to discover urology before MS3 (P <.001). Although URiM students were more likely to recall receiving a urology interest group invitation (Asian 46%, Black 53%, Latinx 67%, White 48%, P = .03), they were less likely to attend an event (Asian 23%, Black 4%, Latinx 3% and White 15%, P <.001) despite being more likely to be interested in urology (Asian 32%, Black 38%, Latinx 50%, White 28%, P = .01). Black students were more likely to gain exposure via family/friend with a urological diagnosis. Black and Latinx students were twice as dissatisfied with timing and method of medical school exposure to urology versus their peers. There were differences across race/ethnicity for whether or not a student had engaged in urology research (Asian 10%, Black 5%, Latinx 2%, White 2%, P = .01). CONCLUSION: Racial/ethnic disparities exist in early exposure to urology, involvement in urology interest group, access to research, and satisfaction with exposure to urology. Interventions addressing the timing and quality of urology exposures may optimize recruitment of URiM students into urology.

Diversifying Graduate Medical Education & the Urology Workforce: Re-imagining our Structures, Policies, Practices, Norms, & Values.

This article offers a framework for critically examining the structures, policies, norms, practices, and values that shape the Urology Match as a foundation for interventions to improve diversity, equity, inclusion, and justice in the workforce. Points of leverage for transformational change in the urology workforce diversification include modifying the structure of the urology application process, optimizing reviewer factors, addressing Under-Represented in Medicine applicant experience, providing resources to applicants, and evaluating selection criteria. To achieve an inclusive diverse urology workforce, we must change policy and practice, expand what we include in the norm, which will translate into increased value ascribed to a more varied cohort of applicants, leading to the establishment of structures that accommodate true diversity.

Careful whispers: when sounds feel like a touch.

There are anatomical and functional links between auditory and somatosensory processing. We suggest that these links form the basis for the popular internet phenomenon where people enjoy a sense of touch from auditory (and often audiovisual) stimuli.

KCa3.1 Channels Confer Radioresistance to Breast Cancer Cells.

KCa3.1 K+ channels reportedly contribute to the proliferation of breast tumor cells and may serve pro-tumor functions in the microenvironment. The putative interaction of KCa3.1 with major anti-cancer treatment strategies, which are based on cytotoxic drugs or radiotherapy, remains largely unexplored. We employed KCa3.1-proficient and -deficient breast cancer cells derived from breast cancer-prone MMTV-PyMT mice, pharmacological KCa3.1 inhibition, and a syngeneic orthotopic mouse model to study the relevance of functional KCa3.1 for therapy response. The KCa3.1 status of MMTV-PyMT cells did not determine tumor cell proliferation after treatment with different concentrations of docetaxel, doxorubicin, 5-fluorouracil, or cyclophosphamide. KCa3.1 activation by ionizing radiation (IR) in breast tumor cells in vitro, however, enhanced radioresistance, probably via an involvement of the channel in IR-stimulated Ca2+ signals and DNA repair pathways. Consistently, KCa3.1 knockout increased survival time of wildtype mice upon syngeneic orthotopic transplantation of MMTV-PyMT tumors followed by fractionated radiotherapy. Combined, our results imply that KCa3.1 confers resistance to radio- but not to chemotherapy in the MMTV-PyMT breast cancer model. Since KCa3.1 is druggable, KCa3.1 targeting concomitant to radiotherapy seems to be a promising strategy to radiosensitize breast tumors.

Foreign peptide triggers boost in pneumococcal metabolism and growth.

BACKGROUND: Nonencapsulated Streptococcus pneumoniae bacteria are successful colonizers of the human nasopharynx and often possess genes aliB-like ORF 1 and 2 in place of capsule genes. AliB-like ORF 2 binds peptide FPPQSV, found in Prevotella species, resulting in enhanced colonization. How this response is mediated is so far unknown. RESULTS: Here we show that the peptide increases expression of genes involved in release of host carbohydrates, carbohydrate uptake and carbohydrate metabolism. In particular, the peptide increased expression of 1,5-anhydro-D-fructose reductase, a metabolic enzyme of an alternative starch and glycogen degrading pathway found in many organisms, in both transcriptomic and proteomic data. The peptide enhanced pneumococcal growth giving a competitive advantage to a strain with aliB-like ORF 2, over its mutant lacking the gene. Possession of aliB-like ORF 2 did not affect release of inflammatory cytokine CXCL8 from epithelial cells in culture and the nonencapsulated wild type strain was not able to establish disease or inflammation in an infant rat model of meningitis. CONCLUSIONS: We propose that AliB-like ORF 2 confers an advantage in colonization by enhancing carbohydrate metabolism resulting in a boost in growth. This may explain the widespread presence of aliB-like ORF 2 in the nonencapsulated pneumococcal population in the human nasopharynx.

KCa3.1 Channels and Glioblastoma: In Vitro Studies.

BACKGROUND: Several tumor entities including brain tumors aberrantly overexpress intermediate conductance Ca2+ activated KCa3.1 K+ channels. These channels contribute significantly to the transformed phenotype of the tumor cells. METHOD: PubMed was searched in order to summarize our current knowledge on the molecular signaling upstream and downstream and the effector functions of KCa3.1 channel activity in tumor cells in general and in glioblastoma cells in particular. In addition, KCa3.1 expression and function for repair of DNA double strand breaks was determined experimentally in primary glioblastoma cultures in dependence on the abundance of proneural and mesenchymal stem cell markers. RESULTS: By modulating membrane potential, cell volume, Ca2+ signals and the respiratory chain, KCa3.1 channels in both, plasma and inner mitochondrial membrane, have been demonstrated to regulate many cellular processes such as migration and tissue invasion, metastasis, cell cycle progression, oxygen consumption and metabolism, DNA damage response and cell death of cancer cells. Moreover, KCa3.1 channels have been shown to crucially contribute to resistance against radiotherapy. Futhermore, the original in vitro data on KCa3.1 channel expression in subtypes of glioblastoma stem(-like) cells propose KCa3.1 as marker for the mesenchymal subgroup of cancer stem cells and suggest that KCa3.1 contributes to the therapy resistance of mesenchymal glioblastoma stem cells. CONCLUSION: The data suggest KCa3.1 channel targeting in combination with radiotherapy as promising new tool to eradicate therapy-resistant mesenchymal glioblastoma stem cells.

TRPM8 is required for survival and radioresistance of glioblastoma cells.

TRPM8 is a Ca2+-permeable nonselective cation channel belonging to the melastatin sub-group of the transient receptor potential (TRP) family. TRPM8 is aberrantly overexpressed in a variety of tumor entities including glioblastoma multiforme where it reportedly contributes to tumor invasion. The present study aimed to disclose further functions of TRPM8 in glioma biology in particular upon cell injury by ionizing radiation. To this end, TCGA data base was queried to expose the TRPM8 mRNA abundance in human glioblastoma specimens and immunoblotting was performed to analyze the TRPM8 protein abundance in primary cultures of human glioblastoma. Moreover, human glioblastoma cell lines were irradiated with 6 MV photons and TRPM8 channels were targeted pharmacologically or by RNA interference. TRPM8 abundance, Ca2+ signaling and resulting K+ channel activity, chemotaxis, cell migration, clonogenic survival, DNA repair, apoptotic cell death, and cell cycle control were determined by qRT-PCR, fura-2 Ca2+ imaging, patch-clamp recording, transfilter migration assay, wound healing assay, colony formation assay, immunohistology, flow cytometry, and immunoblotting. As a result, human glioblastoma upregulates TRPM8 channels to variable extent. TRPM8 inhibition or knockdown slowed down cell migration and chemotaxis, attenuated DNA repair and clonogenic survival, triggered apoptotic cell death, impaired cell cycle and radiosensitized glioblastoma cells. Mechanistically, ionizing radiation activated and upregulated TRPM8-mediated Ca2+ signaling that interfered with cell cycle control probably via CaMKII, cdc25C and cdc2. Combined, our data suggest that TRPM8 channels contribute to spreading, survival and radioresistance of human glioblastoma and, therefore, might represent a promising target in future anti-glioblastoma therapy.

Renal cell carcinoma with inferior vena cava thrombus extending to the right atrium diagnosed during pregnancy.

Only one case of renal cell carcinoma (RCC) with inferior vena cava (IVC) tumor thrombus diagnosed and treated during pregnancy has been reported in the literature. In that report, the tumor thrombus extended to the infrahepatic IVC (level II tumor thrombus). In the present case, a 37-year-old woman with lupus anticoagulant antibodies was diagnosed with RCC and IVC tumor thrombus extending to the right atrium (level IV tumor thrombus) at 24 weeks of pregnancy. The fetus was safely delivered by cesarean section at 30 weeks of gestation. At 4 days later, an open right radical nephrectomy and IVC and right atrial thrombectomy were performed on cardiopulmonary bypass (CPB) once the patient's hemodynamic status had been optimized. Fetal and maternal concerns included the risk of a thromboembolic event (due to increased hypercoagulability from pregnancy, active malignancy, and lupus anticoagulant), intraoperative hemorrhage risk (due to extensive venous collaterals and anticoagulation), and fetal morbidity and mortality (due to fetal lung immaturity). Standardized guidelines for treatment of RCC with or without IVC tumor thrombus during pregnancy are unavailable due to the infrequency of such cases. Treatment decisions are therefore individualized and this case report may inform the management of future patients diagnosed with RCC with level IV tumor thrombus during pregnancy.

Ion Channels in Brain Metastasis.

Breast cancer, lung cancer and melanoma exhibit a high metastatic tropism to the brain. Development of brain metastases severely worsens the prognosis of cancer patients and constrains curative treatment options. Metastasizing to the brain by cancer cells can be dissected in consecutive processes including epithelial-mesenchymal transition, evasion from the primary tumor, intravasation and circulation in the blood, extravasation across the blood-brain barrier, formation of metastatic niches, and colonization in the brain. Ion channels have been demonstrated to be aberrantly expressed in tumor cells where they regulate neoplastic transformation, malignant progression or therapy resistance. Moreover, many ion channel modulators are FDA-approved drugs and in clinical use proposing ion channels as druggable targets for future anti-cancer therapy. The present review article aims to summarize the current knowledge on the function of ion channels in the different processes of brain metastasis. The data suggest that certain channel types involving voltage-gated sodium channels, ATP-release channels, ionotropic neurotransmitter receptors and gap junction-generating connexins interfere with distinct processes of brain metastazation.