Books on 'apoptosis'
Total books: 357 Page 8 of 36
publisher: Worldwide Videotex, published: 2001-04-01
Product Description
This digital document is an article from Biotech Business, published by Worldwide Videotex on April 1, 2001. The length of the article is 536 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available in your Amazon.com Digital Locker immediately after purchase. You can view it with any web browser.Citation DetailsTitle: MAXIM CASPASE INHIBITOR PROTECTS AGAINST LIVER APOPTOSIS.Publication: Biotech Business (Newsletter)Date: April 1, 2001Publisher: Worldwide VideotexVolume: 14 Issue: 4 Page: NADistributed by Thomson Gale
Review
by: Zs. Varga, L. Ujhelyi, A. Kiss, J. Balla, A. Czompa, S. Antus
publisher: Thomson Gale, published: 2004-02-01
Product Description
This digital document is an article from Phytomedicine: International Journal of Phytotherapy & Phytopharmacology, published by Thomson Gale on February 1, 2004. The length of the article is 4293 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available in your Amazon.com Digital Locker immediately after purchase. You can view it with any web browser.Citation DetailsTitle: Effect of silybin on phorbol myristate acetate-induced protein kinase C translocation, NADPH oxidase activity and apoptosis in human neutrophils.Author: Zs. VargaPublication: Phytomedicine: International Journal of Phytotherapy & Phytopharmacology (Magazine/Journal)Date: February 1, 2004Publisher: Thomson GaleVolume: 11 Issue: 2-3 Page: 206(7)Distributed by Thomson Gale
Review
by: C. Fimognari, F. Berti, R. Iori, G Cantelli-Forti
publisher: Elsevier, published: 2005-04-04
Product Description
This digital document is a journal article from Mut.Res.-Genetic Toxicology and Environmental Mutagenesis, published by Elsevier in 2005. The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.Description: Isothiocyanates (ITCs) are the main sulfur-containing metabolites found in cruciferous vegetables. There is evidence that some ITCs may act as chemopreventive agents against different tumor types and induce apoptosis and modulate cell-cycle progression of highly proliferative cancer cells. However, there are also studies reporting genotoxic or co-carcinogenic effects for some ITCs, such as benzyl ITC and phenyl ITC. Since selectivity for transformed cells and absence of genotoxicity for healthy cells are important pre-requisites for new chemopreventive agents, we investigated micronucleus formation and induction of apoptosis by 4-(methylthio)butylisothiocyanate (MTBITC), sulforaphane and a mixture of ITCs in human T-lymphocyte cultures. We demonstrate that MTBITC, sulforaphane and the mixture of ITCs did not induce micronuclei. Moreover, sulforaphane induced a dose-dependent increase in the number of apoptotic cells, which was significant at the highest concentration tested (30@mM) (41% versus 18% in the untreated samples, P
Review
publisher: Springer, published: 2004-08-03
ISBN: 1402022166
sales rank: 4651585
Product Description
The series Cell Engineering is the first and only major reference work on the development of cellular systems for the production of recombinant glycoproteins, gene and cell therapies, drug screening and tissue engineering. This volume on "Apoptosis" is intended to review the state-of-the-art with in-depth assessments of this type of programmed cell death. The aim of the volume is to make the recent developments in apoptotic research readily accessible to biologists, biotechnologists and cellular engineers. The implication of apoptosis in the suppression of diseases and prolonging survival of cells in culture is presented to indicate the great potential of apoptotic research for drug production and the development of human therapies. All chapters are written as self-contained treatments of the important topics in apoptosis that are presented on an essential information basis. Topics covered range from understanding the role of signalling and effector molecules, mathematical modelling of cell death, RNAi tools in apoptosis research, to monitoring and imaging of apoptosis. This volume will be an invaluable resource for biotechnologists and researchers in apoptosis, cell biology, cell culture and molecular medicine.
Review
by: B. Burmeister, T. Schwerdtle, I. Poser, Hoffmann
publisher: Elsevier, published: 2004-03-14
Product Description
This digital document is a journal article from Mut.Res.-Genetic Toxicology and Environmental Mutagenesis, published by Elsevier in 2004. The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.Description: Human mesothelial cells (HMC), the progenitor cells of asbestos-induced mesothelioma, are particularly sensitive to the genotoxic effects of asbestos, although the molecular mechanisms by which asbestos induces injury in HMC are not well known. The high susceptibility of HMC to simian virus 40 (SV40)-mediated transformation is assumed to play a causative role in the pathogenesis of mesothelioma. The aim of this study was to investigate the asbestos-induced DNA damage in cultured HMC and SV40-transformed HMC (MeT-5A) compared with their malignant counterparts, i.e. human mesothelioma cells (MSTO). The time-dependent initiation of DNA-strand breaks as well as the induction of oxidative DNA base modifications were key factors for investigation. HMC, MeT-5A and MSTO cells were exposed to chrysotile and crocidolite asbestos (3@mg/cm^2) during different time periods (1-72h). DNA damage was investigated by use of the Comet assay and alkaline unwinding, the latter in combination with the Fpg protein. The P53 level was analyzed by immunofluorescence, and measurement of apoptosis was conducted by flow cytometry. We found a significant induction of DNA damage in asbestos-treated HMC already after an exposure time of 1.5h. This effect could not be observed in treated MeT-5A and MSTO cells. Also, a time-dependent significant increase in DNA-strand breaks was observed by alkaline unwinding in asbestos-treated HMC, but not in treated MeT-5A and MSTO cells. In none of the three cell lines we could detect oxidative DNA damage recognized by the Fpg protein (e.g. 8-oxo-guanine), up to 24 h after exposure to asbestos. In contrast to what was found in HMC, P53 was over-expressed in untreated MeT-5A and MSTO. The induction of apoptosis by asbestos fibers was suppressed in MeT-5A and MSTO cells. Crocidolite fibers induced the higher genotoxic effects and chrysotile the more pronounced apoptotic effects. We conclude that asbestos induces DNA damage in HMC already after a very short exposure time in the absence of 8-oxo-guanine formation. The presence of SV40-Tag in MeT-5A and MSTO cells results in an increased expression of P53, but not in additive genotoxic effects after exposure to asbestos. The deregulation of the apoptotic pathway may lead to proliferation of genomically damaged cells and finally to the development of mesothelioma.
Review
by: S.J. DeWitte-Orr, N.C. Bols
publisher: Elsevier, published: 2005-06-01
Product Description
This digital document is a journal article from Comparative Biochemistry and Physiology, Part C, published by Elsevier in 2005. The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.Description: Epithelial (CHSE-214), fibroblast (RTG-2) and macrophage (RTS11) cell lines from Chinook salmon and rainbow trout were tested for their sensitivity to gliotoxin, a fungal metabolite. Gliotoxin treatment for 6 or 24 h caused cell viability to decrease in a dose-dependent manner, with effective concentrations (EC"5"0s) being similar for the three cell lines but varying with exposure time. Under some exposure conditions, hallmarks of apoptosis were detected. Apoptosis was evaluated by the appearance of fragmented nuclei upon H33258 staining and of genomic DNA laddering into 180 bp oligomers. Gliotoxin induced cell detachment in RTG-2 and CHSE-214 cultures, under some conditions. These were the only cultures of these two cell lines in which apoptosis was detected, and apoptotic cells appeared more frequent in the detached population. At the highest concentration, 15 @mM, the cells died by an alternative mode, likely necrosis. By contrast, in RTS11 cultures cell detachment was not observed, and apoptosis occurred over a wider concentration range, even 15 @mM, reaching levels of over 90%. The preferential death by necrosis for epithelial cells (CHSE-214) and by apoptosis for macrophages (RTS11) could be a beneficial host response to gliotoxin-producing fungi, leading respectively to the development and then resolution of inflammation.
Review
by: R.T. Bree, C. Neary, A. Samali, N.F. Lowndes
publisher: Elsevier
Product Description
This digital document is a journal article from DNA Repair, published by Elsevier in 2004. The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.Description: Eukaryotic cells have evolved highly sophisticated cellular responses to DNA double strand breaks (DSBs) that increase the likelihood of survival. However, cells can also respond to DSBs by undergoing programmed cell death. The mechanisms underlying the cellular decision on whether to repair and survive or to die are not well understood but may be related to the efficiency of repair or the extent of the damage. Presumably, a few easily reparable DSBs will not result in cell death in most cell types. However, abundant complex DSBs will present a severe challenge to the repair machineries with repeated attempts at repair likely to result in genome instability. For multicellular eukaryotes at least, struggling to complete repair is folly, whereas removal of severely damaged cells is a more sensible strategy. Here we discuss recent evidence linking DSBs to a highly regulated form of cell death termed, apoptosis. In particular, we focus on the roles of the tumour suppressor, p53 and a recently discovered role for an isotype of the linker histone H1. We present a hypothesis that the elevated levels of ssDNA produced during ongoing attempts at DSB repair may be involved in the switch from repair to apoptosis.
Review
by: S. Datta, D.R. Saha, D. Ghosh, T. Majumdar, Bhatta
publisher: Elsevier, published: 2007-04-01
Product Description
This digital document is a journal article from Comparative Biochemistry and Physiology, Part C, published by Elsevier in 2007. The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.Description: We studied the hepatocellular alterations induced by sub-lethal concentrations (0.50 @mM) of arsenic in Indian catfish Clarias batrachus L. Sub-lethal arsenic exposure altered serum aspartate aminotransferase and alkaline phosphatase levels and brought about significant changes in different serum biochemical parameters. Arsenic exposure reduced total hepatocyte protein content and suppressed the proliferation of hepatocytes in a time-dependent manner. Routine histological studies on liver documented arsenic-induced changes characterized by dilated sinusoids, formation of intracellular edema, megalocytosis, vacuolation and appearance of hepatic cells with distorted nuclei. Transmission electron microscopy of hepatocytes further revealed hyperplasia and hypertrophy of mitochondria, development of dilated rough endoplasmic reticulum and changes in peroxisome size with duration of arsenic exposure. Degeneration of mitochondrial cristae and condensation of chromatin was also evident in arsenic-exposed hepatocytes. A significant number of hepatocytes isolated from arsenic-exposed fish stained with annexin V and demonstrated DNA ladder characteristic of apoptosis. Single-cell gel electrophoresis of exposed hepatocytes also revealed the development of comets usually seen in apoptotic cells. Using specific inhibitors it was determined that the arsenic-induced apoptosis of hepatocytes was caspase-mediated, involving the caspase 3 pathway.
Review
by: Devalraju Sreekanth, M.K. Arunasree, Karnati R. Roy, T. Chandramohan Reddy, Gorla V. Reddy, Pallu Reddanna
publisher: Thomson Gale, published: 2007-11-01
Product Description
This digital document is an article from Phytomedicine: International Journal of Phytotherapy & Phytopharmacology, published by Thomson Gale on November 1, 2007. The length of the article is 4746 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available in your Amazon.com Digital Locker immediately after purchase. You can view it with any web browser.Citation DetailsTitle: Betanin a betacyanin pigment purified from fruits of Opuntia ficus-indica induces apoptosis in human chronic myeloid leukemia Cell line-K562.Author: Devalraju SreekanthPublication: Phytomedicine: International Journal of Phytotherapy & Phytopharmacology (Magazine/Journal)Date: November 1, 2007Publisher: Thomson GaleVolume: 14 Issue: 11 Page: 739(8)Distributed by Thomson Gale
Review
by: Elliott Richelson
publisher: Thomson Gale, published: 2005-11-01
Product Description
This digital document is an article from Psychopharmacology Educational Updates (PsychEd Up), published by Thomson Gale on November 1, 2005. The length of the article is 1143 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available in your Amazon.com Digital Locker immediately after purchase. You can view it with any web browser.Citation DetailsTitle: The Prostate Apoptosis Response 4 (PAR-4): a new role for an old protein in depression.(Second Messenger)Author: Elliott RichelsonPublication: Psychopharmacology Educational Updates (PsychEd Up) (Magazine/Journal)Date: November 1, 2005Publisher: Thomson GaleVolume: 1 Issue: 11 Page: 2Distributed by Thomson Gale
Review
cell culture, methods in cell biology, apoptosis, cell cycle, mitosis, signal transduction, receptor, mitochondria, ribosome, stem cell, flow cytometry
Total 357 books of 36 pages