Books on 'apoptosis'
Total books: 383 Page 5 of 39
by: Kerri Wachter
publisher: Thomson Gale, published: 2006-12-01
Product Description
This digital document is an article from Skin & Allergy News, published by Thomson Gale on December 1, 2006. The length of the article is 446 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: Nitric oxide cream stems UVB-induced apoptosis.(Dermatologic Therapy)Author: Kerri WachterPublication: Skin & Allergy News (Magazine/Journal)Date: December 1, 2006Publisher: Thomson GaleVolume: 37 Issue: 12 Page: 51(1)Distributed by Thomson Gale
Review
by: Christian Oberdanner
publisher: VDM Verlag Dr. Mueller e.K., published: 2008-03-25
ISBN: 3836482118
sales rank: 6376596
Product Description
Increased intracellular levels of reactive oxygen species (ROS) may result in tissue damage and are therefore associated with various diseases, especially with cancer. Apart from their potentially harmful functions, ROS have been identified as important mediators of essential cellular processes like apoptosis. Antioxidants are the cellular antagonists of ROS and act to neutralize the cytotoxic impact of oxyradicals. In healthy individuals, antioxidant systems serve to maintain intracellular ROS levels below a certain threshold, permitting the functionality of essential ROS-mediated signaling processes but preventing ROS overproduction and potential tissue damage. Even small shifts of the ROS-antioxidant balance may entail serious biological consequences. In the context of ROS-based anti-cancer applications inducing apoptosis, the action of antioxidants may critically influence the outcome of the therapy. Decreased antioxidant capacity that is induced purposefully as a therapeutic strategy may result in an improved anti-cancer action, whereas the external addition of antioxidants may reduce the cytotoxic potential of the therapy.
Review
publisher: Betascript Publishing, published: 2010-03-14
ISBN: 6130535120
Product Description
High Quality Content by WIKIPEDIA articles! Tumor necrosis factor (TNF, cachexin or cachectin and formally known as tumor necrosis factor-alpha) is a cytokine involved in systemic inflammation and is a member of a group of cytokines that stimulate the acute phase reaction.The primary role of TNF is in the regulation of immune cells. TNF is also able to induce apoptotic cell death, to induce inflammation, and to inhibit tumorigenesis and viral replication. Dysregulation of TNF production has been implicated in a variety of human diseases, as well as cancer. Recombinant TNF is used as an immunostimulant under the INN tasonermin.
Review
by: Dana Perkins
publisher: CreateSpace, published: 2009-12-30
ISBN: 1449991319
Product Description
PhD Thesis (2002). Apoptosis is an etiologic component of neurodegenerative disorders [e.g. Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS)] and acute brain injury ischemia/hypoxia and trauma). Previous studies have shown that a Herpes Simplex Virus Type 2 (HSV-2) gene, ICP10 PK, activates the Ras/MEK/ERK pathway in non-neuronal cells. Because this pathway was implicated in neuronal cell survival, the present studies tested whether ICP10 PK blocks apoptosis in various experimental paradigms of neuronal apoptosis. The broad anti-apoptotic activity of ICP10 PK suggests that it may be used in gene therapy of neurological disorders that involve apoptosis. In addition, the gene can be delivered non-invasively to the central nervous system using a replication-deficient HSV-2 mutant (ICP10deltaRR).
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publisher: Betascript Publishing, published: 2010-03-14
ISBN: 6130535384
Product Description
High Quality Content by WIKIPEDIA articles! TNF receptor-associated factor 2 is a protein that in humans is encoded by the TRAF2 gene.The protein encoded by this gene is a member of the TNF receptor associated factor (TRAF) protein family. TRAF proteins associate with, and mediate the signal transduction from members of the TNF receptor superfamily. This protein directly interacts with TNF receptors, and forms complexes with other TRAF proteins. TRAF2 is required for TNF-alpha-mediated activation of MAPK8/JNK and NF-kappaB. The protein complex formed by TRAF2 and TRAF1 interacts with the IAP family members cIAP1 and cIAP2, and functions as a mediator of the anti-apoptotic signals from TNF receptors. The interaction of this protein with TRADD, a TNF receptor associated apoptotic signal transducer, ensures the recruitment of IAPs for the direct inhibition of caspase activation. cIAP1 can unbiquitinate and induce the degradation of this protein, and thus potentiate TNF-induced apoptosis. Multiple alternatively spliced transcript variants have been found for this gene, but the biological validity of only one transcript has been determined.
Review
publisher: Springer, published: 2001-04-27
ISBN: 3540411070
sales rank: 8300489
Product Description
Louisiana State Univ., New Orleans. Proceedings of the 4th International Symposium held in New Orleans in October/November 1999. Outlines the present status of investigations and provides further stimulation for research in this field. Softcover.
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by: David S. Pisestsky
publisher: Saunders, published: 2004
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publisher: Nova Science Publishers, published: 2006-10-29
ISBN: 1600214533
sales rank: 7447175
Product Description
Apoptosis is the regulated form of cell death. It is a complex process defined by a set of characteristic morphological and biochemical features that involves the active participation of affected cells in a self-destruction cascade. This programmed cell death plays a critical role in physiological functions such as cell deletion during embryonic development, balancing cell number in continuously renewing tissues and immune system development. Additionally, a dysregulation of apoptosis is underlying in numerous pathological situations such as Parkinson, Alzheimer s disease and cancer. A number of studies have pointed out an association between consumption of fruits and vegetables, and certain beverages such as tea and wine, which are rich in polyphenols, with reduced risk of chronic diseases, including cancer. Apoptosis is also the regulatory mechanism involved in the removal of unnecessary cells during development and in tissue homeostasis in a wide range of organisms from insects to mammals. The aim of this book is to provide new studies in the field of apoptosis research.
Review
by: R.R. Miller, C.M. Hay, T.R. Striegnitz, L. Honsey
publisher: Elsevier, published: 2006-09-01
Product Description
This digital document is a journal article from Comparative Biochemistry and Physiology, Part C, published by Elsevier in 2006. 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: The effects of exogenous glycine on homocysteine (HoCys)-induced reductions in chick (Gallus gallus) embryo viability, HoCys-induced increases in brain and hepatic membrane lipid peroxidation, HoCys-induced apoptosis (caspase-3 activities) in brain and hepatic tissues, and HoCys-induced reductions in brain and hepatic S-adenosylemethionine (SAM)/S-adenosylhomocysteine (SAH) levels were studied. Exogenous HoCys caused reductions in percent living embryos and reductions in embryo masses. Exogenous glycine attenuated these HoCys-induced reductions in embryo viability. Brain and liver tissues of HoCys-treated embryos exhibited increased caspase-3 activities, increased lipid hydroperoxide (LPO) levels, and reduced levels of long-chain polyunsaturated membrane fatty acids. While exogenous glycine attenuated HoCys-induced changes in brain caspase-3 activities, brain LPO levels, and brain membrane PUFA levels, exogenous glycine was less effective in attenuating HoCys-induced changes in hepatic caspase-3 activities and hepatic membrane PUFA levels. HoCys-induced reductions in SAM/SAH ratios were observed in brains and livers. Exogenous glycine attenuated HoCys-induced reductions in brain SAM/SAH. However, glycine was unable to attenuate HoCys-induced reductions in hepatic SAM/SAH levels.
Review
by: Maria Florian
publisher: VDM Verlag, published: 2009-05-21
ISBN: 3639152999
Product Description
The place of estrogen in women's health remains controversial. Premenopausal women have a lower prevalence of cardiovascular disease (CVD) than men and hormone replacement therapy (HRT) decreases CVD in postmenopausal women. However, clinical trials failed to substantiate a protective effect of HRT and even showed some harm. Estrogen rapidly mediates the activation of endothelial nitric oxide synthase (eNOS) and increases production of nitric oxide (NO), an important factor for endothelial health. Distinctive results for eNOS, NO and superoxide levels are highlighted by studies on acute and long term effects of estrogen. In human endothelial cells, apoptosis induced by oxidized low-density lipoprotein and the cytokine TNF?, associated with atherosclerosis, is reduced by estrogen. Estrogen's angiogenic properties help healthy endothelium respond to injury, but they also potentiate TNF?- induced angiogenesis, which revascularizes plaques of women with advanced atherosclerosis and exacerbates cardiovascular events. Researchers and clinicians could appreciate this contribution to the undestanding of the paradoxical effects of estrogen on the vascular wall.
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