Books on 'apoptosis'
Total books: 378 Page 10 of 38
publisher: W. B. Saunders, published: 2001
Review
by: Philip J. Barr, Michael C. Kiefer
publisher: Chemical Institute of Canada, published: 1995-11-01
Product Description
This digital document is an article from Canadian Chemical News, published by Chemical Institute of Canada on November 1, 1995. The length of the article is 785 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: Bak, the Bcl-2-homologous antagonist/killer, a critical modulator of apoptosis in human disease.Author: Philip J. BarrPublication: Canadian Chemical News (Magazine/Journal)Date: November 1, 1995Publisher: Chemical Institute of CanadaVolume: v47 Issue: n10 Page: p22(2)Distributed by Thomson Gale
Review
by: I. D. Bowen
publisher: Springer, published: 1998-01-15
ISBN: 0412710706
sales rank: 3427330
Product Description
This work addresses the homeostatic balance between the birth and death of cells in tissues, organs and organisms and emphasizes the molecular processes involved in cellular cycles. Aimed at undergraduates, this book is illustrated, using line drawings and cartoons to explain the concepts involved. It should be of use to those studying biology, biomedicine and medicine, and to those involved in laboratory-based cancer studies.
Review
publisher: Springer, published: 2004-08-03
ISBN: 1402022166
sales rank: 4813380
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: Gale Reference Team
publisher: Worldwide Videotex, published: 2007-09-01
Product Description
This digital document is an article from Worldwide Biotech, published by Worldwide Videotex on September 1, 2007. The length of the article is 697 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available immediately after purchase. You can view it with any web browser.Citation DetailsTitle: BIOLINERX/UNIVERSITY OF ILLINOIS TO DEVELOP APOPTOSIS AGENT.Author: Gale Reference TeamPublication: Worldwide Biotech (Newsletter)Date: September 1, 2007Publisher: Worldwide VideotexVolume: 19 Issue: 9 Page: NADistributed by Gale, a part of Cengage Learning
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: T. Gichner, A. Mukherjee, E.D. Wagner, M.J. Plewa
publisher: Elsevier
Product Description
This digital document is a journal article from Mut.Res.-Genetic Toxicology and Environmental Mutagenesis, published by Elsevier in . 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 applied the nuclear DNA Diffusion Assay, described as an accurate tool to estimate apoptotic and necrotic cells [N.P. Singh, A simple method for accurate estimation of apoptotic cells, Exp. Cell Res. 256 (2000) 328-337] to tobacco root and leaf cells. In this assay, isolated nuclei are embedded in an agarose microgel on a microscope slide and low molecular-weight DNA fragments diffuse into the microgel. Exposure of the roots to hydrogen peroxide significantly increased the average nuclear area of isolated nuclei. After 4 and 24h of recovery, all DNA damage was repaired. The data clearly demonstrate that the manifestation of diffused nuclei upon exposure to hydrogen peroxide is not the result of non-repairable apoptotic or necrotic DNA fragmentation, but represents repairable genotoxin-induced DNA damage. In contrast, treatment with the alkylating agent ethyl methanesulphonate (EMS) followed by 24h of recovery produced a significant increase in the average nuclear area. The contribution of apoptosis to this increase cannot be excluded. Heat treatment of leaves at 50^oC for 1-15min leading to necrosis, and treatment of isolated nuclei with DNase-I, which digests DNA to nucleosome-sized fragments as during apoptosis, also led to a dose-dependent increase in the nuclear area. The use of different fluorochromes (ethidium bromide, DAPI or YOYO-1) for DNA staining yielded similar results in the DNA Diffusion Assay. As all types and sizes of diffused nuclei were observed after EMS and hydrogen peroxide treatments, we were unable to differentiate, on the basis of the structure of the nuclei, between apoptotic or necrotic DNA fragmentation and other types of genotoxin-induced DNA damage in plants.
Review
publisher: Nova Biomedical Books, published: 2006-10-25
ISBN: 1600215068
sales rank: 8749100
Review
publisher: Springer, published: 1998-09-18
ISBN: 354064153X
sales rank: 8372286
Product Description
The aim of this volume is to provide an in-depth overview of the state-of-the-art research on apoptosis with contributions from key groups working in the field. This type of programme cell death has received wide and rapid attention and now is considered as one of the hottest areas of science. The volume covers various aspects of the apoptotic death process from the morphological and biochemical features, mechanisms and genetic regulation to its role in pathological process and potential implications for biomedical research and biopharmaceutical production.
Review
cell culture, methods in cell biology, apoptosis, cell cycle, mitosis, signal transduction, receptor, mitochondria, ribosome, stem cell, flow cytometry
Total 378 books of 38 pages