The slow advancement of women in scientific fields remains a persistent problem, especially in academia. Highly trained doctoral women in the sciences drop out of the academic pipeline for a variety of reasons that are poorly documented. This paper reports on a qualitative exploratory study based on structured interviews with 15 women who have taken career breaks after receiving their science, technology, engineering or mathematics (STEM) PhD, but wish to re-enter the academic career track. The study aims to understand the pressures that contribute to taking such breaks, how women remain connected (or not) to their field during breaks and how re-entering the field after a career break could be facilitated. Suggestions based on the interviews include career development workshops and networking opportunities for women in breaks, as well as systemic changes such as reduced fees for society membership and conferences, changes in the way resumés are reviewed by faculty search committees, and in the design and implementation of maternity and child care leave policies.
The ubiquitous free radical, nitric oxide (NO), plays an important role in many biological processes including the regulation of the inflammatory response. Alterations in NO synthesis by endogenous systems likely influence inflammatory processes occurring in a wide range of diseases including many in the cardiovascular system (e.g. atherosclerosis). Progression of inflammatory conditions depends not only upon the recruitment and activation of inflammatory cells but also upon their subsequent removal from the inflammatory milieu. Apoptosis, or programmed cell death, is a fundamental process regulating inflammatory cell survival and is critically involved in ensuring the successful resolution of an inflammatory response. Apoptosis results in shutdown of secretory pathways and renders effete, but potentially highly histotoxic, cells instantly recognisable for non-inflammatory clearance by phagocytes (e.g., macrophages). However, dysregulation of apoptosis and phagocytic clearance mechanisms can have drastic consequences for development and resolution of inflammatory processes. In this review we highlight the complexities of NO-mediated regulation of inflammatory cell apoptosis and clearance by phagocytes and discuss the molecular mechanisms controlling these NO mediated effects. We believe that manipulation of pathways involving NO may have previously unrecognised therapeutic potential for limiting or resolving inflammatory and cardiovascular disease.