Intrasexual competition among males of different species, including humans, is well documented. Among females, far less is known. Recent nonexperimental studies suggest that women are intolerant of attractive females and use indirect aggression to derogate potential rivals. In Study 1, an experimental design was used to test the evolutionary-based hypothesis that women would be intolerant of sexy women and would censure those who seem to make sex too readily available. Results provide strong empirical support for intrasexual competition among women. Using independent raters, blind to condition, we found that almost all women were rated as reacting negatively ("bitchy") to an attractive female confederate when she was dressed in a sexually provocative manner. In contrast, when she was dressed conservatively, the same confederate was barely noticed by the participants. In Study 2, an experimental design was used to assess whether the sexy female confederate from Study 1 was viewed as a sexual rival by women. Results indicated that as hypothesized, women did not want to introduce her to their boyfriend, allow him to spend time alone with her, or be friends with her. Findings from both studies are discussed in terms of evolutionary theory.

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Background:The mechanism by which the p75 neurotrophin receptor (p75 NTR ) and TrkA interact to enhance neurotrophin signaling is unknown. Results: The p75NTR intracellular domain fragment, p75 ICD , but not full-length p75 NTR enhanced NGF binding to TrkA and neurite outgrowth. Conclusion:The results suggest that p75 ICD causes a conformational change within the extracellular domain of TrkA. Significance: The findings challenge our current understanding of how p75 NTR enhances neurotrophic activity.

Hepatocellular carcinoma (HCC) is a primary malignancy of the liver and is a major cause of cancer related deaths worldwide. Only 10 to 20% of HCC can be surgically excised. Therefore, chemotherapeutic intervention and treatment is essential for achieving favorable prognosis. However, therapeutic outcome of chemotherapy is generally poor owing to inherent resistance of cancer cells to the treatment or due to development of acquired resistance. To differentiate and delineate the molecular events, we developed drug resistant Hep3B cells (DRC) by treating cells with the increasing concentration of paclitaxel. We also developed a unique single cell clone of Hep3B cells (SCC) by selecting single cell colonies and screening them for resistant phenotype. Interestingly, both DRC and SCC were resistant to paclitaxel in comparison to parental Hep3B cells. We analyzed the contributory factors that may be involved in the development of resistance. As expected, level of P-glycoprotein (P-gp) was elevated in DRC. In addition, Caveolin-1 (Cav-1), Fatty acid synthase (FASN) and Cytochrome P450 (CYP450) protein levels were elevated in DRC whereas in SCC, FASN and CYP450 levels were elevated. Downregulation of these molecules by respective siRNAs and/or by specific pharmacological inhibitors resensitized cells to paclitaxel. Interestingly, these drug resistant cells were also less sensitive to vinblastine, doxorubicin and methotrexate with the exception of cisplatin. Our results suggested that differential levels of P-gp, Cav-1 and FASN play a major role in acquired resistant phenotype whereas FASN level was associated with the presentation of inherent resistant phenotype in HCC.

Heat shock proteins (Hsps) modulate several cellular functions and are ubiquitously present in cell. Here, we investigated alterations in the expression of Hsps and explored functional consequences of the same. Moreover, effect of quercetin (Qctn), an inhibitor of Hsps, on chemotherapeutic drugs treatment in hepatoma cells Hep3B and HepG2 was investigated. We for the first time report that 5-fluorouracil (5-FU) and carboplatin specifically induce expression of Hsp40 in addition to Hsp27 in Hep3B and HepG2 cells. Induction of Hsps following exposure to sub lethal dose of drugs is a cellular challenge to survival. However, under lethal environmental conditions with reduced cell viability, cells fail to sustain the induction of survival proteins, Hsp27 and Hsp40. Though Qctn itself, to certain extent is cytotoxic to cells, it potentiates the pro-apoptotic action of 5-FU and carboplatin, by inhibiting expression of Hsps. The increased cell killing correlates with decreased levels of procaspase-3. Furthermore, siRNA mediated knockdown of Hsp27 and Hsp40 diminishes survival of drugs exposed cells. Altogether, our data provides clear evidence that Hsp27 and 40 promote cell survival and inhibition of their expression does not allow cells to adapt to drug exposure and survive. Collectively, our novel findings on compelling action of 5-FU or carboplatin following knockdown of Hsp40 and that of Hsp27 highlights their strategic implications towards an effective therapy against HCC.