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2 programmed cell death

The main types of cellular injury induced by chemical compounds are necrotic and apoptotic (programmed) cell death. Necrosis implies chaotic ending... [Pg.284]

Orrenius, S., McCabe, M. J., and Nicotera, P. (1992). Ca- -dependenr mechanisms of cytotoxicity and programmed cell death. Toxicol. Lett. 64/64, 357-364. [Pg.340]

HBV, hepatitis B HCV, hepatitis C IAP, inhibitor of apoptosis protein DBM, IAP binding motifs INCA, inhibitory CARD NASH, non-alcoholic steatohepatitis PCD, programmed cell death PCI, pan-caspase inhibitor OA, osteoarthritis RA, rheumatoid arthritis Smac, second mitochondria-derived activator of caspases TRAIL, tumor necrosis factor-related apoptosis-inducing ligand. [Pg.334]

Apoptosis is known as programmed cell death and represents also a control mechanism within the cell that reacts to the changes in its environment. This active cellular death process is characterized by distinctive morphological changes... [Pg.357]

HiBASAMi H, ACHiwA Y, FUJIKAWA T and KOMIYA T (1996) Induction of programmed cell death (apoptosis) in human lymphoid leukemia cells by catechin compounds . Anticancer Res, 16, 1943-46. [Pg.152]

Numerous cellular changes occur in the genetic material of the cancer cell so that programmed cell death, or apoptosis, does not occur. Proliferation of cancer cells goes unregulated. [Pg.1277]

Apoptosis Programmed cell death, a normal process in which cells perish in an orderly, highly controlled manner to control an organism s development. [Pg.1560]

Raff This also works in the other direction. If one stimulates hepatocytes to go through a round of division in the adult, programmed cell death will bring the fiver back to its normal size within a week. Thus, survival control seems to contribute to size control in the adult fiver. But the big question remains how does an organ know what size it should be ... [Pg.162]

Signals from neighbouring cells or tissues will instruct a particular cell to proliferate, differentiate into another cell type or to commit suicide by programmed cell death. Figure 10.4 shows that NFKB can play a major role in countering programmed cell death and hence survival of the cell after stimulation of the TNFa pathway. Such a pathway depends upon the activation of NFKB which will activate a variety of anti-apoptopic genes. [Pg.286]

Luo L et al. Gene expression profiles of laser-captured adjacent neuronal sub-types. Nature Med 1999 5 117-122. Chiang LW et al. An orchestrated gene expression component of neuronal programmed cell death revealed by cDNA array analysis. Proc Nat Acad Sci USA 2001 98 2814-2819. [Pg.116]

They have been shown to initiate apoptosis (programmed cell death). [Pg.362]


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