Objective To describe the publication productivity of academic urologists in the United States by gender. Materials and Methods Gender inequality is prevalent in most surgical subspecialties, including urology. Despite small numbers of women in academic positions, differences in scholarly impact by gender are relatively unknown. We assembled a list of 1922 academic urologists (1686 male (87.7%), 236 female (12.3%)) at 124 academic institutions throughout the United States as of February 2016. Scopus and Google Scholar were queried for bibliometric data on each individual, including h-index and m-quotient. We analyzed these metrics for both genders by educational background, subspecialty, NIH funding, and academic rank. Results Men had higher median h-indices than women overall (p<0.05), and by successive academic ranks (p<0.05). Proportionally fewer women attained senior academic ranking (professor/chair), (p<0.05). There was no difference in research productivity by successive rank after controlling for career duration (m-quotient). Women were more likely to choose a practice that specialized in pediatric urology or female urology/pelvic reconstructive surgery than their male counterparts (p<0.05). Conclusions and Relevance Women represent a growing proportion of academic urology faculty, but despite the recent increase in number entering the field, relatively few women occupy senior leadership positions. Improving psychosocial barriers to advancement such as lack of mentorship or discriminatory policies may help pioneering female urologists as they progress in their careers.

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Background: Inactivation of the human type Ia regulatory subunit (RIa) of cyclic AMP dependent protein kinase (PKA) (PRKAR1A) leads to altered kinase activity, primary pigmented nodular adrenocortical disease (PPNAD), and sporadic adrenal and other tumours. Methods and results: A transgenic mouse carrying an antisense transgene for Prkar1a exon 2 (X2AS) under the control of a tetracycline responsive promoter (the Tg(Prkar1a*x2as)1Stra, Tg(tTAhCMV)3Uh or tTA/X2AS line) developed thyroid follicular hyperplasia and adenomas, adrenocortical hyperplasia and other features reminiscent of PPNAD, including late onset weight gain, visceral adiposity, and nondexamethasone suppressible hypercorticosteronaemia, with histiocytic, epithelial hyperplasias, lymphomas, and other mesenchymal tumours. These lesions were associated with allelic losses of the mouse chromosome 11 Prkar1a locus, an increase in total type II PKA activity, and higher RIIb protein levels; the latter biochemical and protein changes were also documented in Carney complex tumours associated with PRKAR1A inactivating mutations and chromosome 17 PRKAR1A locus changes. Conclusion: We conclude that the tTA/X2AS mouse line with a downregulated Prkar1a gene replicates several of the findings in Carney complex patients and their affected tissues, supporting the role of RIa as a candidate tumour suppressor gene.

Mutations of the human type I␣ regulatory subunit (RI␣) of cyclic AMP-dependent protein kinase (PKA; PRKAR1A) lead to altered kinase activity, primary pigmented nodular adrenocortical disease, and tumors of the thyroid and other tissues. To bypass the early embryonic lethality of Prkar1a ؊/؊ mice, we established transgenic mice carrying an antisense transgene for Prkar1a exon 2 (X2AS) under the control of a tetracyclineresponsive promoter. Down-regulation of Prkar1a by up to 70% was achieved in transgenic mouse tissues and embryonic fibroblasts, with concomitant changes in kinase activity and increased cell proliferation, respectively. Mice developed thyroid follicular hyperplasia and adenomas, adrenocortical hyperplasia, and other features reminiscent of primary pigmented nodular adrenocortical disease, histiocytic and epithelial hyperplasias, lymphomas, and other mesenchymal tumors. These were associated with allelic losses of the mouse chromosome 11 Prkar1a locus, an increase in total type II PKA activity, and higher RII␤ protein levels. This mouse provides a novel, useful tool for the investigation of cyclic AMP, RI␣, and PKA functions and confirms the critical role of Prkar1a in tumorigenesis in endocrine and other tissues.