31 research outputs found
Chilly Climates, Balancing Acts, and Shifting Pathways: What Happens to Women in STEM Doctoral Programs
Women in doctoral programs in Science, Technology, Engineering and Math (STEM) leave without finishing at higher rates than men and, as with men, turn away from academic and research careers. This qualitative study examines the day-to-day influences on female doctoral students during their third or fourth year in physical science and engineering programs. Ethnographic cognitive interviewing and online incident reports document the specific experiences and reactions of 28 participants over a six-month period. The data were analyzed to identify key incidents, categories and recurring themes. Some incidents contributed to women’s growing sense of competence, recognition and identification of oneself as a scientist. Others fit a model of microaggressions and gender barriers in a predominantly masculine culture. Problems of work-life balance were demonstrated for some women. Incidents generated responses by some participants that they would disengage from a research-intensive career trajectory toward alternate career interests outside of academic research. The findings provide information about the lived experiences of women in doctoral programs and suggest that the metaphor of career pathways may be more useful than pipelines in explaining the direction of women who are advanced doctoral students in research-intensive fields
Effects of iron deficiency on physical aptitude
peer reviewe
Adiponectin Deficiency Protects Mice From Chemically Induced Colonic Inflammation
Background & Aims: Adiponectin (APN) is an adipokine that regulates insulin sensitivity and is anti-inflammatory in atherosclerosis. The goal of this study was to investigate the role of APN in intestinal inflammation. Methods: APN knockout (KO) mice and their wild-type (WT) littermates received dextran sulfate sodium (DSS) or trinitrobenzene sulfonic acid (TNBS) to induce intestinal inflammation. Clinical and histologic scores and proliferation of epithelial cells were assessed. Cytokines and APN levels were measured. Expression of APN and heparin binding epidermal growth factor (HB-EGF) was analyzed by immunohistochemistry. Expression of APN and its receptors, HB-EGF, and basic fibroblast growth factor (bFGF) messenger RNA was assessed by reverse-transcription polymerase chain reaction. Association of serum APN with HB-EGF and bFGF was studied by coimmunoprecipitation. Results: APN KO mice are protected from chemically induced colitis; administration of APN restores inflammation. APN is expressed in the colon, luminal APN associates with colonic epithelial cells. In vitro, APN increases production of proinflammatory cytokines from colonic tissue. Expression of colonic APN overlaps with that of bFGF and HB-EGF, which play a protective role in colitis. Circulating APN binds to bFGF and HB-EGF, likely inhibiting their protective activity. Inhibition of EGF receptor signaling, which is required for biologic activity of HB-EGF, restores inflammation in APN KO mice. Conclusions: APN deficiency is associated with protection from chemically induced colitis. APN exerts proinflammatory activities in the colon by inducing production of proinflammatory cytokines and inhibiting bioactivity of protective growth factors. Thus, in colitis, APN exerts an opposite role compared with atherosclerosis. © 2007 AGA Institute.link_to_subscribed_fulltex
CXCR4 expression in vitreoretinal membranes
Background/aim: Proliferative vitreoretinopathy (PVR) and macular pucker (MP) vitreoretinal membranes are caused by abnormal cell migration. By their role in chemotactism, chemokine receptors represent good candidates to sustain this process. The authors thus investigated the expression of one of them, CXCR4, in these pathologies. Methods: Three PVR and four MP membranes were surgically removed and processed for immunochemical studies with antibodies for CXCR4, cytokeratins or smooth muscle actin. Results: CXCR4 expression was found in all membranes. There was no relation between severity of PVR or MP and presence of CXCR4. In addition, there was no difference in CXCR4 expression between MP and PVR. Conclusion: CXCR4 is expressed in PVR and MP. Further experiments are needed to test if CXCR4 and other chemokine receptors are implicated in vitreoretinal membrane formation