Books on 'apoptosis'
Total books: 357 Page 5 of 36
by: Christian Oberdanner
publisher: VDM Verlag Dr. Mueller e.K., published: 2008-03-25
ISBN: 3836482118
sales rank: 6190247
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: Not Avail, published: 2003-11
ISBN: 3805577001
Product Description
Since the first description of apoptosis by Kerr, Wyllie and Currie three decades ago, the field has expanded immensely, and recent research findings have revealed a role for dysregulated apoptosis in many hematological disorders. This series of review articles serves to apprise the hematologist of the basic mechanisms of apoptosis as well as to point out its relevance in clinical conditions. The collection begins with a discussion of the mitochondria and their central role in apoptosis. Leading experts describe how Granzyme B triggers cell death and how Bcl-2 family proteins regulate apoptosis in the lymphoid system. The unique features of apoptosis in PMN and in platelet biogenesis are explained in detail, while subsequent papers cover its role in pathological processes such as myelodysplastic syndrome and myeloid leukemia. Finally, new therapeutic approaches based on the knowledge of apoptotic mechanisms are outlined.
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
by: A. Poersch, F.V.d. Santos, M.A.M. Maciel, Camara
publisher: Elsevier, published: 2007-04-20
Product Description
This digital document is a journal article from Mut.Res.-Genetic Toxicology and Environmental Mutagenesis, 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: The use of medicinal plants to combat diseases has increased in the last years despite the little information available with regard to the possible health risks they represent. The aim of the present study was to determine in vitro the possible clastogenic, apoptotic and cytotoxic effects of the active principle of Croton cajucara, trans-dehydrocrotonin (DCTN), and determine its protective effect against three mutagenic agents using the micronucleus test (MN) and apoptosis index in CHO-K1 cells. Three DNA damage inducing agents were utilized in the clastogenicity and anticlastogenicity tests (methylmethane sulfonate (MMS), mitomycin C (MMC) and doxorubicin (DXR); a negative control (PBS) and solvent control were also included. DCTN at concentrations of 400, 320, 240, 160 and 80@mM did not show clastogenic activity in cultured CHO-K1 cells in the micronucleus test, did not induce apoptosis and showed negligible cytotoxicity in all cases. DCTN at concentrations of 240 and 400@mM was tested for protective activity using three treatment protocols in relation to positive controls: pre-treatment, simultaneous treatment and post-treatment. The micronucleus test showed a protective effect for DCTN which varied among the different treatment protocols and with regard to the different DNA damage inducing agents. In the apoptosis test, DCTN was seen to have a protective effect under the following conditions: (I) at both concentrations in relation to MMS, in all three treatment protocols; (II) at both concentrations against damage caused by MMC with pre-treatment and at the higher concentration with simultaneous treatment; (III) at both concentrations against DXR with simultaneous treatment. Therefore, DCTN itself is not a clastogenic or cytotoxic substance, and does not induce apoptosis the in vitro system used. These results together with findings reported for DCTN in vivo, support the indication of this active principle at these concentrations for therapeutic use.
Review
by: Bérengère Luthringer
publisher: VDM Verlag, published: 2009-11-17
ISBN: 3639214935
Product Description
Survivin, a unique member of the family of inhibitors of apoptosis (IAP) proteins, orchestrates intracellular pathways during cell division and apoptosis. Its central regulatory function has inspired several approaches that target survivin for cancer therapy. Analyses in early-branching Metazoa so far propose an exclusive role of survivin as a chromosomal passenger protein, whereas only later during evolution the second, complementary antiapoptotic function might have arisen, concurrent with increased organismal complexity. To lift the veil on the ancestral function(s) of this key regulatory molecule, a survivin homologue of the phylogenetically oldest extant metazoan taxon (phylum Porifera) was identified and functionally characterized. Additionally, new components of the innate defense sentinel in sponges were also identified. This new prototypes could represent a very efficient defense mechanism and may correspond to a new family of intracellular sensing protein, forming a subclass of pattern recognition receptors (PRR).
Review
by: M. Gajewska, T. Motyl
publisher: Elsevier, published: 2004-10-01
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: TGF-@b1 is an antiproliferative and apoptogenic factor for mammary epithelial cells (MEC) acting in an auto/paracrine manner and thus considered an important local regulator of mammary tissue involution. However, the apoptogenic signaling pathway induced by this cytokine in bovine MEC remains obscure. The present study was focused on identification of molecules involved in apoptogenic signaling of transforming growth factor-beta 1 (TGF-@b1) in the model of bovine mammary epithelial cell line (BME-UV1). Laser scanning cytometry (LSC), Western blot and electrophoretic mobility shift assay (EMSA) were used for analysis of expression and activity of TGF-@b1-related signaling molecules. The earliest response occurring within 1-2 h after TGF-@b1 administration was an induction and activation of R-Smads (Smad2 and Smad3) and Co-Smad (Smad4). An evident formation of Smad-DNA complexes began from 2nd hour after MEC exposure to TGF-@b1. Similarly to Smads, proteins of AP1 complex: phosphorylated c-Jun and JunD appeared to be early reactive molecules; however, an increase in their expression was detected only in cytosolic fraction. In the next step, an increase of IGF binding protein-3 (IGFBP-3) and IGFBP-4 expression was observed from 6th hour followed by a decrease in the activity of protein kinase B (PKB/Akt), which occurred after 24 h of MEC exposure to TGF-@b1. The decrease in PKB/Akt activity coincided in time with the decline of phosphorylated Bad expression (inactive form). Present study supported additional evidence that stimulation of insulin-like growth factor I (IGF-I) was associated with complete abrogation of TGF-@b1-induced activation of Bad and Bax and in the consequence protection against apoptosis. In conclusion, apoptotic effect of TGF-@b1 in bovine MEC is mediated by IGFBPs and occurs through IGF-I sequestration, resulting in inhibition of PKB/Akt-dependent survival pathway.
Review
by: N. Puebla-Osorio, K.S. Ramos, M.H. Falahatpisheh
publisher: Elsevier, published: 2004-08-01
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: The halogenated aromatic hydrocarbon 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is known to induce immunotoxicity, but relatively little is known regarding its effects on B-lymphocytes, and on avian B-cells in particular. In this study, the avian bursal pre-B-cell line DT40 was exposed to TCDD ranging from 1 to 500 nM for 1 and 6 h. At 100 nM, TCDD caused a significant increase in the number of apoptotic cells, as assessed by terminal deoxynucleotidyl transferase-mediated dUTP nick-end-labeling (TUNEL) assay, and induced the expression of the chicken cytochrome P450 1A4 (CYP1A4) mRNA, a hallmark of TCDD exposure. TCDD induced transient upregulation of aryl hydrocarbon receptor (AhR) mRNA. At 100 nM, both caspase 3 and caspase 9 were transiently upregulated after 1 h, but returned to normal levels after 6 h of exposure. Challenge with TCDD after AhR blockade with resveratrol, a competitive AhR antagonist, prevented changes in caspases 3 and 9 and in the AhR message itself, suggesting that the effects of TCDD were mediated via the AhR. TCDD did not cause significant changes in the relative gene expression of caspase 8, Bcl-2 and Bcl-xL. We conclude that avian DT40 pre-B-cells exposed to TCDD are susceptible to apoptosis, likely through activation of executioner caspase 3.
Review
by: N. Shaun B. Thomas
publisher: Garland Science, published: 1995-06-15
ISBN: 1872748899
sales rank: 6716759
Product Description
Over the past few years, there have been major breakthroughs in our understanding of the molecular mechanisms which control cell division and apoptosis (programmed cell death). This book adopts a multi-disciplinary approach to explore how the deregulation of basic molecular controls can lead to malignancy in a variety of cell types. The authors are leading international experts whose chapters span the state of the art in cell and molecular biology, clinical treatment of cancer and new drug design.
Review
by: F. Mattioli, C. Garbero, M. Gosmar, V. Manfredi, C
publisher: Elsevier, published: 2004-11-14
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: Four steroids that share the 17-hydroxy-3-oxopregna-4,6-diene structure - cyproterone acetate, chlormadinone acetate, megestrol acetate, and potassium canrenoate - have been shown previously to behave with different potency as liver-specific genotoxic agents, the response being markedly higher in female than in male rats, but similar in humans of both genders. In this study, performed to better define the relationship between chemical structure and genotoxicity, dydrogesterone (DGT) with double bonds C4?C5 and C6?C7, dienogest (DNG) with double bonds C4?C5 and C9?C10, and 1,4,6-androstatriene-17@b-ol-3-one acetate (ADT) with double bonds C1?C2, C4?C5 and C6?C7, were compared with cyproterone acetate (CPA) for their ability to induce DNA fragmentation and DNA repair synthesis in primary cultures of hepatocytes from three rats of each sex. At subtoxic concentrations, ranging from 10 to 90@mM, all four steroids consistently induced a dose-dependent increase of DNA fragmentation, which in all cases was higher in females than in males; their DNA damaging potency decreased in the order CPA > DNG > ADT > DGT. Under the same experimental conditions, the responses provided by the DNA repair-synthesis assay were positive or inconclusive in hepatocytes from female rats and consistently negative in hepatocytes from male rats. In the induction of apoptotic cells, examined in primary hepatocytes from female rats, CPA was more active than ADT and DGT, and DNG was inactive. Considered as a whole these findings suggest that a liver-specific genotoxic effect more marked in female than in male rats might be a common property of steroids with two or three double bonds.
Review
by: Rama Malaviya, Yvonne Sun, Jennifer K. Tan, Melissa Magliocco, Alice B. Gottlieb
publisher: Thomson Gale, published: 2006-10-01
Product Description
This digital document is an article from Journal of Drugs in Dermatology, published by Thomson Gale on October 1, 2006. The length of the article is 1776 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: Induction of lesional and circulating leukocyte apoptosis by infliximab in a patient with moderate to severe psoriasis.(CASE REPORTS)Author: Rama MalaviyaPublication: Journal of Drugs in Dermatology (Magazine/Journal)Date: October 1, 2006Publisher: Thomson GaleVolume: 5 Issue: 9 Page: 890(4)Distributed 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