Not Available

Not AvailableAn attempt was made to estimate the geomorphological degradation due to sedimentation ofSarda Sagar reservoir, located in Pilibhit and Udhamsingh Nagar, district of Uttar Pradash and Uttarakhand respectively. The study was conducted using multidated IRS LIISS III remote sensing data for the year 2006¬2007. Using satellite images of different seasons during 2006¬2007, a total of 45.23 million m3 volume of sedimentation was computed in ¬between the 183.704 m and 190.504m elevation. The reservoir has lost 11.72 % of the total capacity of water storage and an average rate of sedimentation was calculated as 0.26 % per year. Due to this sedimentation the new feeder channel of Sarda Sagar is choked with silt and the water flow from this channel has almost stopped. The morphology of the reservoir has been changed due to sedimentation during the period 1962 to2007. This has altered breeding ground of fishes since important indigenous fish species which need flowing water condition to perform the breeding. This study would be helpful for the planners to manage the reservoir and to assess the biological productivity.ICA

Not Available

Not AvailableAn attempt was made to estimate the geomorphological degradation due to sedimentation of Sarda Sagar reservoir, located in Pilibhit and Udhamsingh Nagar, district of Uttar Pradash and Uttarakhand respectively. The study was conducted using multidated IRS LIISS III remote sensing data for the year 2006­2007. Using satellite images of different seasons during 2006­2007, a total of 45.23 million m3 volume of sedimentation was computed in­between the 183.704 m and 190.504 m elevation. The reservoir has lost 11.72 % of the total capacity of water storage and an average rate of sedimentation was calculated as 0.26 % per year. Due to this sedimentation the new feeder channel of Sarda Sagar is choked with silt and the water flow from this channel has almost stopped. The morphology of the reservoir has been changed due to sedimentation during the period 1962 to 2007. This has altered breeding ground of fishes since important indigenous fish species which need flowing water condition to perform the breeding. This study would be helpful for the planners to manage the reservoir and to assess the biological productivityNot Availabl

DNA-damage response network at the crossroads of cell-cycle checkpoints, cellular senescence and apoptosis*

Tissue homeostasis requires a carefully-orchestrated balance between cell proliferation, cellular senescence and cell death. Cells proliferate through a cell cycle that is tightly regulated by cyclin-dependent kinase activities. Cellular senescence is a safeguard program limiting the proliferative competence of cells in living organisms. Apoptosis eliminates unwanted cells by the coordinated activity of gene products that regulate and effect cell death. The intimate link between the cell cycle, cellular senescence, apoptosis regulation, cancer development and tumor responses to cancer treatment has become eminently apparent. Extensive research on tumor suppressor genes, oncogenes, the cell cycle and apoptosis regulatory genes has revealed how the DNA damage-sensing and -signaling pathways, referred to as the DNA-damage response network, are tied to cell proliferation, cell-cycle arrest, cellular senescence and apoptosis. DNA-damage responses are complex, involving “sensor” proteins that sense the damage, and transmit signals to “transducer” proteins, which, in turn, convey the signals to numerous “effector” proteins implicated in specific cellular pathways, including DNA repair mechanisms, cell-cycle checkpoints, cellular senescence and apoptosis. The Bcl-2 family of proteins stands among the most crucial regulators of apoptosis and performs vital functions in deciding whether a cell will live or die after cancer chemotherapy and irradiation. In addition, several studies have now revealed that members of the Bcl-2 family also interface with the cell cycle, DNA repair/recombination and cellular senescence, effects that are generally distinct from their function in apoptosis. In this review, we report progress in understanding the molecular networks that regulate cell-cycle checkpoints, cellular senescence and apoptosis after DNA damage, and discuss the influence of some Bcl-2 family members on cell-cycle checkpoint regulation