Challenges to the Choice Discourse: Women’s Views of Their Family and Academic-Science Career Options and Constraints

Women are underrepresented as tenure-stream faculty in U.S. academia, particularly in science fields, despite the growth of women among doctorate holders. The decision to pursue an academic career matures during the graduate-school years. What are female science graduate students’ views of an academic career, and what values and priorities influence their career intentions and choices? Twenty-five women in a U.S. science graduate program were interviewed about these matters. A dominant theme in these interviews was that an academic career would best fulfill their science interests and aspirations. However, an academic career was viewed as requiring, of them as women, giving up family life—mainly due to the belief that household and family work are women’s responsibilities as well as the expectation that science requires relentless focus. Frustration about the lack of options, for women, to pursue their dream of being a scientist while having a family was another recurrent theme. These findings, together with those of other studies, suggest that it is not by choice, but because of gender ideologies and practices about work and family at the disadvantage of women, that women give up on academic-science careers

Building an “old girls’ network” in academic science, technology, engineering, and mathematics

Over the last decade the University of Wisconsin (UW) System has repeatedly faced budget shortfalls. Reductions in state funding led to increased course loads, class sizes, and turnover of administrators and faculty, producing chronic low morale (e.g., Read 2016). Amidst this turmoil, senior women scientists from campuses across the UW System met annually to offer support, promote retention and achievement of individual members, and build a network of women who could enact systemic change on their individual campuses. The chapter describes the history and components of the 11-campus program, provides examples of the participants’ resiliency and resourcefulness, and identifies ways in which the women’s senior status and disciplinary skills led to effective change

Angiopoietin-1 deficiency increases renal capillary rarefaction and tubulointerstitial fibrosis in mice

Presence of tubulointerstitial fibrosis is predictive of progressive decline in kidney function, independent of its underlying cause. Injury to the renal microvasculature is a major factor in the progression of fibrosis and identification of factors that regulate endothelium in fibrosis is desirable as they might be candidate targets for treatment of kidney diseases. The current study investigates how loss of Angipoietin-1 (Angpt1), a ligand for endothelial tyrosine-kinase receptor Tek (also called Tie2), affects tubulointerstitial fibrosis and renal microvasculature. Inducible Angpt1 knockout mice were subjected to unilateral ureteral obstruction (UUO) to induce fibrosis, and kidneys were collected at different time points up to 10 days after obstruction. Staining for aSMA showed that Angpt1 deficient kidneys had significantly more fibrosis compared to wildtype mice 3, 6, and 10 days after UUO. Further investigation 3 days after UUO showed a significant increase of Col1a1 and vimentin in Angpt1 deficient mice, as well as increased gene expression of Tgfb1, Col1a1, Fn1, and CD44. Kidney injury molecule 1 (Kim1/Havcr1) was significantly more increased in Angpt1 deficient mice 1 and 3 days after UUO, suggesting a more severe injury early in the fibrotic process in Angpt1 deficient mice. Staining for endomucin showed that capillary rarefaction was evident 3 days after UUO and Angpt1 deficient mice had significantly less capillaries 6 and 10 days after UUO compared to UUO kidneys in wildtype mice. RNA sequencing revealed downregulation of several markers for endothelial cells 3 days after UUO, and that Angpt1 deficient mice had a further downregulation of Emcn, Plvap, Pecam1, Erg, and Tek. Our results suggest that loss of Angpt1 is central in capillary rarefaction and fibrogenesis and propose that manipulations to maintain Angpt1 levels may slow down fibrosis progression

Angpt1 deficiency resulted in increased aSMA area at several time points.

<p>(A) UUO in WT and Angpt1KO mice induced tubulointerstitial fibrosis starting 1 day post UUO as seen from aSMA staining of renal cortex. (B) Quantifications of aSMA-positive areas showed a significant increase in fibrotic area in Angpt1KO mice 3 days after UUO and onward. A minimum of 10 images from renal cortex were used from each mouse (n = 3 for day 1, n = 13 for day 3, n = 3–6 for day 6, and n = 3–4 for day 10 post UUO). Scale bar, 50 μm. Data expressed as mean ± SEM. ### p<0.001 compared to WT CL3.5h, *p<0.05, **p<0.01, ***p0.001 compared to WT at the corresponding time point.</p