Widow Discrimination and Family Care-Giving in India

The purpose of this research is to address the lack of a region-wide view of widow discrimination in India, the home of 42 million widows. This study analyzed the household data collected in face-to-face interviews from January to March of 2011 in six major Indian cities including Delhi, Mumbai, Bangalore, Chennai, Kolkata, and Hyderabad. It was revealed that widow discrimination does not prevail across the nation. That is, this research did not deny the existence of traditional widow discrimination in some areas, but demonstrated that this phenomenon does not represent the whole nation if we focus on the widow's old age and the treatment by their family. Certainly, this research has some limitations, including the fact that the observations came only from cities. However, this is pioneering research, and more significantly, it addresses the lack of a region-wide view analysis of widow discrimination in India with an aging population

NFV, an HIV-1 protease inhibitor, induces growth arrest, reduced Akt signalling, apoptosis and docetaxel sensitisation in NSCLC cell lines

HIV-1 protease inhibitor (PI), nelfinavir (NFV) induced growth arrest and apoptosis of NCI-H460 and -H520, A549, EBC-1 and ABC-1 non-small-cell lung cancer (NSCLC) cells in association with upregulation of p21waf1, p27 kip1 and p53, and downregulation of Bcl-2 and matrix metalloproteinase (MMP)-2 proteins. We found that NFV blocked Akt signalling in these cells as measured by Akt kinase assay with glycogen synthase kinase-3α/β (GSK-3α/β) as a substrate. To explore the role of Akt signalling in NFV-mediated growth inhibition of NSCLC cells, we blocked this signal pathway by transfection of Akt small interfering RNA (siRNA) in these cells; transient transfection of Akt siRNA in NCI-H460 cells decreased the level of Bcl-2 protein and slowed their proliferation compared to the nonspecific siRNA-transfected cells. Conversely, forced-expression of Akt partially reversed NFV-mediated growth inhibition of these cells, suggesting that Akt may be a molecular target of NFV in NSCLC cells. Also, we found that inhibition of Akt signalling by NFV enhanced the ability of docetaxel to inhibit the growth of NCI-H460 and -H520 cells, as measured by MTT assay. Importantly, NFV slowed the proliferation and induced apoptosis of NCI-H460 cells present as tumour xenografts in nude mice without adverse systemic effects. Taken together, this family of compounds might be useful for the treatment of individuals with NSCLC