Search

Research Summary: Career paths depend not only on individuals' own competitiveness but also on the competitiveness of others in a position to advocate for them. In this article, we study competitiveness when rewards accrue to another individual. In particular, we ask how female and male managers' competitiveness changes when rewards from competition accrue to their female or male protégés, relative to when they accrue to themselves. Using an experimental approach, we find that when rewards accrue to protégés, male and female managers are equally competitive because female managers increase their competitiveness. However, male managers compete more for male rather than female protégés. This gap disappears when male managers know their protégés' risk preferences, suggesting a novel intervention to ensure equity in the sponsorship process. Managerial Summary: Sponsorship is key to individuals' career development and firms' human capital strategy. In this experimental study simulating an organizational setting, we investigate one aspect of sponsorship and ask whether managers' and protégés' genders affect managers' willingness to compete on behalf of their protégés. We find that when the rewards from competition accrue to protégés, female managers increase their competitiveness and eliminate the gender competitiveness gap present when rewards accrue to managers themselves. This suggests that, from a competitiveness standpoint, female and male managers are equally strong sponsors. However, male managers compete more for male, relative to female, protégés. This gap disappears when male managers have information about protégés' risks preferences, suggesting a novel approach that organizations can implement to reduce discrimination in sponsorship. [ABSTRACT FROM AUTHOR]

Detection of circulating tumor cells (CTCs) from patient blood samples offers a desirable alternative to invasive tissue biopsies for screening of malignant carcinomas. A rigorous CTC detection method must identify CTCs from millions of other formed elements in blood and distinguish them from healthy tissue cells also present in the blood. CTCs are known to overexpress certain surface receptors, many of which aid them in invading other tissue, and these provide an avenue for their detection. We have developed carbon nanotube (CNT) thin film devices to specifically detect these receptors in intact cells. The CNT sidewalls are functionalized with antibodies specific to Epithelial Cell Adhesion Molecule (EpCAM), a marker overexpressed by breast and other carcinomas. Specific binding of EpCAM to anti-EpCAM causes a change in the local charge environment of the CNT surface which produces a characteristic electrical signal. Two cell lines are tested in the device: MCF7, a mammary adenocarcinoma line which overexpresses EpCAM, and MCF10A, a non-tumorigenic mammary epithelial line which does not. Introduction of MCF7s causes significant changes in the electrical conductance of the devices due to specific binding and associated charge environment change near the CNT sidewalls. Introduction of MCF10A displays a different profile due to purely nonspecific interactions. The profile of specific vs. nonspecific interaction signatures using carbon based devices will guide development of this diagnostic tool towards clinical sample volumes.

Previously we described the release of hr44 from the ciliary epithelium to coincide with the loss of the late endosomal/lysosomal marker protein CD63 in mildly inflamed rat eyes. We showed that both proteins are released with microvesicles into the supernatant of cultured retinal pigmented epithelial cells (ARPE-19). Here we wish to determine whether there is a concomitant loss of fas-ligand (FasL) in vivo and whether ocular epithelial cells have secretory lysosomes similar to T cells, from where FasL and hr44 could derive. FasL plays an important role in immunity, immune cell homeostasis and in the maintenance of immune privilege in the eye. However the mode of release of FasL from ocular epithelial cells or its activity in the eye is not fully understood. In normal rat eyes, FasL was detected in the epithelia of the iris and ciliary body and in the anterior region of the retinal pigmented epithelium. FasL is expressed constitutively and is associated with vesicular structures in the normal ciliary epithelium but is not detectable in the ciliary epithelium of inflamed eyes. In contrast, the posterior RPE, which under normal conditions is negative for FasL and hr44 showed strong staining for both molecules in areas adjacent to sub-retinal inflammatory infiltrates. Immunofluorescence and Western blot analysis indicated that cultured ARPE-19 cells express both the soluble and membrane form of FasL. The intracellular concentration of FasL was significantly increased in cells grown in presence of interferon (INF)-gamma. The microvesicles released by cultured ARPE-19 cells and previously shown to be positive for hr44 and CD63 are also positive for membrane FasL. Expression of a recombinant fluorescent construct of FasL together with immuno-staining for CD63 demonstrated that FasL localises to the endocytic compartment of ARPE-19 cells and of melanoma cells (positive control). In cells with lysosomes devoid of specialised secretory functions (e g. HeLa cells) recombinant FasL localised to the cell membrane, demonstrating that RPE cells have secretory lysosomes. We suggest that ocular epithelial cells release soluble FasL and the membrane form of FasL with vesicles. Both forms may contribute in different ways to the effectiveness of the ocular immune response and immune privilege.