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Mahatma Gandhi National Rural Employment Guarantee Scheme (MGNREGS) played a very vital role by providing wage employment for one hundred days in a year to each rural household whose adult member volunteer to do unskilled manual work. It acts as a fall back measures during these lean seasons by becoming an alternative source of income for these poor household, acting as a social safety net for them. This study analyses the impact of the program on the rural development . Rural development is the overall development of rural areas with respect to food security, economic security, habitat security, health security, nutritional security etc. So, respective index are being constructed to find the impact on rural development. Randomized selection of beneficiary and non-beneficiary communities has been done. A randomisation impact evaluation design was used with households eligible and the rural development index (RDI) is constructed. It has been found that there is significant impact of the program on the rural development.

Solid malignancies contain sphere-forming stem-like cells that are particularly efficient in propagating tumors. Identifying agents that target these cells will advance the development of more effective therapies. Recent converging evidence shows that c-Met expression marks tumor-initiating stem-like cells and that c-Met signaling drives human glioblastoma multiforme (GBM) cell stemness in vitro. However, the degree to which tumor-propagating stem-like cells depend on c-Met signaling in histologically complex cancers remains unknown. We examined the effects of in vivo c-Met pathway inhibitor therapy on tumor-propagating stem-like cells in human GBM xenografts. Animals bearing pre-established tumor xenografts expressing activated c-Met were treated with either neutralizing anti- hepatocyte growth factor (HGF) monoclonal antibody L2G7 or with the c-Met kinase inhibitor PF2341066 (Crizotinib). c-Met pathway inhibition inhibited tumor growth, depleted tumors of sphere-forming cells, and inhibited tumor expression of stem cell markers CD133, Sox2, Nanog, and Musashi. Withdrawing c-Met pathway inhibitor therapy resulted in a substantial rebound in stem cell marker expression concurrent with tumor recurrence. Cells derived from xenografts treated with anti-HGF in vivo were depleted of tumor-propagating potential as determined by in vivo serial dilution tumor-propagating assay. Furthermore, daughter xenografts that did form were 12-fold smaller than controls. These findings show that stem-like tumor-initiating cells are dynamically regulated by c-Met signaling in vivo and that c-Met pathway inhibitors can deplete tumors of their tumor-propagating stem-like cells.