Books on 'apoptosis'
Total books: 383 Page 8 of 39
publisher: Informa HealthCare, published: 2010-12-15
ISBN: 0824729765
Product Description
Keeping pace with current discoveries in the study of apoptosis as a key biological regulatory mechanism, this guide analyzes the possible role of apoptosis in the pathogenesis of various disorders including cancer, diabetes, rheumatoid arthritis, and Parkinson's and Alzheimer's diseases. The only monograph to provide an all-encompassing approach to the topic, this guide explores in-vivo and in-vito mechanisms of apoptosis, in-vivo model systems, the genetic regulation of apopotosis, and information spanning key target organs.
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: 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
by: Nafiseh Nafissi
publisher: VDM Verlag, published: 2009-07-05
ISBN: 3639162463
Product Description
Apoptosis is a genetically regulated form of cell death that occurs when the cell is exposed to physiological, pathogenic, or cytotoxic stimuli. Unregulated apoptosis at any time from embryogenesis to adulthood can result in a variety of disease states, such as neurodegenerative disorders, autoimmunity, cardiovascular disease, liver and kidney problems, and cancer. A reasonable estimation is that either too little or too much cell death contributes to half of the main medical illnesses for which adequate therapy or prevention is lacking. The apoptotic pathways can be initiated by reactive oxygen species (ROS) and inflammatory molecules, both of which are believed to be up-regulated in a state of obesity. In addition, multiple studies have shown that the risk of developing cardiovascular disease, type 2 diabetes mellitus, nonalcoholic fatty liver disease, and certain types of cancers increase with increasing degree of obesity in both men and women. Despite the well characterized association of obesity and disease incidence, the mechanisms by which obesity contributes to disease pathology are poorly understood.
Review
by: Edited by Benjamin Bonavida
publisher: Transworld Research Network, published: 2006-01-01
ISBN: 8178952424
Product Description
This volume has been conceived to provide different approaches used to overcome resistance through the use of chemo or immunosensitizing agents, used in combination with cytotoxic drugs. This volume has been divided arbitrarily into two sections, namely, chemosensitization and immunosensitization. Chemosensitization refers to the use of sensitizing agents that can reverse resistance to chemotherapeutic drugs. Immunosensitization refers to agents that can sensitize tumor cells through cytotoxic mechanisms mediated by host immune cells and/or corresponding cytotoxic factors. The authors in this volume are well established investigators in the field of sensitization and represent expertise in novel approaches used for sensitization. This volume is by no means all inclusive and primarily represents some examples that have been selected for reference.
Review
by: E.A. Stokes, W. Lonergan, L.P. Weber, D.M. Janz, P
publisher: Elsevier, published: 2004-06-01
Product Description
This digital document is a journal article from Comparative Biochemistry and Physiology, Part C, 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: Endocrine disrupting compounds (EDCs), especially those that are estrogenic, are an issue of growing concern because they may ultimately adversely affect wildlife survival. 17-@b-Estradiol and its synthetic counterpart, 17-@a-ethinylestradiol, two common EDCs, are associated with intersex conditions and impaired male reproductive behavior in fish. Male and female Japanese medaka (Oryzias latipes) were exposed to 10 ng/l ethinylestradiol for 6 months. Using terminal dideoxynucleotidyl-mediated dUTP nick end-labeling (TUNEL) to quantitate cell death, we found that ethinylestradiol-exposed males had significantly fewer apoptotic cells in the forebrain compared to untreated males and exposed females. Our results show that the effects of ethinylestradiol exposure are highly variable among individuals of the same species and even within tissues of the same individual. Thus, when examining the effects of EDCs on natural populations, data from a variety of tissues should be examined and the interpretation of any effects should include consideration of tissue-specific processes.
Review
publisher: Betascript Publishing, published: 2010-02-18
ISBN: 6130414374
Product Description
High Quality Content by WIKIPEDIA articles! A restriction digest is a procedure used in molecular biology to prepare DNA for analysis or other processing. It is also known as DNA fragmentation (not to be mistaken with Apoptosis DNA Fragmentation).This enzymatic technique can be used for cleaving DNA molecules at specific sites, ensuring that all DNA fragments that contain a particular sequence have the same size; furthermore, each fragment that contains the desired sequence has the sequence located at exactly the same position within the fragment. The cleavage method makes use of an important class of DNA-cleaving enzymes isolated primarily from bacteria. These enzymes are called restriction endonucleases or restriction enzymes, and they are able to cleave DNA molecules at the positions at which particular short sequences of bases are present .
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: davide cattano
publisher: VDM Verlag, published: 2009-05-28
ISBN: 3639145798
Product Description
Worldwide every year, anesthetics are used in millions of neonates and infants during surgical procedures and imaging studies, moreover hundreds of pregnant women receive surgery for no-pregnancy related problems. Advances in this field have resulted in an increased complexity, duration, and number of anesthesia procedures. A deep difference however exists between developing and adult neurons. During normal CNS development, an excess of neurons is produced and most of them have to die for the correct synaptic network formation. In this case, death is the default; immature neurons are competent to die and, in the absence of life-signals (trophic supports), they achieve this target by apoptosis, the active programmed-cell-death pathway. Adult neurons indeed, need to survive for the lifetime of the organism, and their premature death can cause irreversible functional deficits.Recent findings demonstrate that the transient exposure to several classes of drugs, including the intravenous anesthetic propofol, during the brain growth spurt period, triggers widespread and dose-dependent apoptosis in the developing brain.
Review
publisher: Springer, published: 1998-09-18
ISBN: 354064153X
sales rank: 8398523
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 383 books of 39 pages