Acute Neuronal Injury: The Role of Excitotoxic Programmed by Denson G. Fujikawa (auth.), Denson G. Fujikawa (eds.)

By Denson G. Fujikawa (auth.), Denson G. Fujikawa (eds.)

This ebook is the results of a convergence of clinical information about mechanisms that produce acute nerve phone loss of life within the mind. even though doubtless disparate, stroke, mind and spinal twine trauma, coma from a low serum glucose focus (hypoglycemia), and lengthy epileptic seizures have in universal the inciting issue of excitotoxicity, the activation of a particular subtype of glutamate receptor by means of an increased extracellular glutamate focus that ends up in an over the top inflow of calcium into nerve cells. The excessive calcium focus in nerve cells prompts numerous enzymes which are accountable for degradation of cytoplasmic proteins and cleavage of nuclear DNA, leading to nerve telephone dying. The excessive calcium focus additionally interferes with mitochondrial respiratory, with the consequent creation of loose radicals that harm mobile membranes and nuclear DNA. knowing the biochemical pathways that produce nerve cellphone demise is step one towards devising a good neuroprotective approach, the last word goal.

Acute Neuronal harm might be important to neuroscientists and normal mobile biologists drawn to phone demise. The ebook can be priceless to clinically orientated neuroscientists, together with neurologists, neurosurgeons and psychiatrists.

About the Editor:

Dr. Denson Fujikawa is an accessory Professor of Neurology on the David Geffen university of drugs at UCLA, a member of the mind study Institute at UCLA and a employees Neurologist on the division of Veterans Affairs better la Healthcare method. His curiosity in mechanisms of nerve mobilephone demise within the mind begun in the course of a two-year epilepsy learn fellowship with Dr. Claude Wasterlain, from 1981 to 1983. he's a Fellow of the yank Academy of Neurology and is a member of the yank Epilepsy Society, American Neurological organization, foreign Society for Cerebral Blood stream and Metabolism, and the Society for Neuroscience.

Show description

By Denson G. Fujikawa (auth.), Denson G. Fujikawa (eds.)

This ebook is the results of a convergence of clinical information about mechanisms that produce acute nerve phone loss of life within the mind. even though doubtless disparate, stroke, mind and spinal twine trauma, coma from a low serum glucose focus (hypoglycemia), and lengthy epileptic seizures have in universal the inciting issue of excitotoxicity, the activation of a particular subtype of glutamate receptor by means of an increased extracellular glutamate focus that ends up in an over the top inflow of calcium into nerve cells. The excessive calcium focus in nerve cells prompts numerous enzymes which are accountable for degradation of cytoplasmic proteins and cleavage of nuclear DNA, leading to nerve telephone dying. The excessive calcium focus additionally interferes with mitochondrial respiratory, with the consequent creation of loose radicals that harm mobile membranes and nuclear DNA. knowing the biochemical pathways that produce nerve cellphone demise is step one towards devising a good neuroprotective approach, the last word goal.

Acute Neuronal harm might be important to neuroscientists and normal mobile biologists drawn to phone demise. The ebook can be priceless to clinically orientated neuroscientists, together with neurologists, neurosurgeons and psychiatrists.

About the Editor:

Dr. Denson Fujikawa is an accessory Professor of Neurology on the David Geffen university of drugs at UCLA, a member of the mind study Institute at UCLA and a employees Neurologist on the division of Veterans Affairs better la Healthcare method. His curiosity in mechanisms of nerve mobilephone demise within the mind begun in the course of a two-year epilepsy learn fellowship with Dr. Claude Wasterlain, from 1981 to 1983. he's a Fellow of the yank Academy of Neurology and is a member of the yank Epilepsy Society, American Neurological organization, foreign Society for Cerebral Blood stream and Metabolism, and the Society for Neuroscience.

Show description

Read or Download Acute Neuronal Injury: The Role of Excitotoxic Programmed Cell Death Mechanisms PDF

Similar microbiology books

Cell Motility: From Molecules to Organisms (Life Sciences)

Fresh advances in molecular and biophysical concepts, quite fluorescence and stay mobile imaging, are revolutionizing the learn of cellphone motility. New bioprobes not just show uncomplicated intracellular localization, but additionally comprise information of post-translational variations, conformational country and protein-protein interactions.

Microbiology: A Systems Approach, 2nd Edition

Microbiology: A platforms procedure is a microbiology textual content for non-science/allied future health majors with a physique platforms method of the ailment chapters. It has develop into recognized for its attractive writing type, tutorial paintings application and concentrate on lively studying. we're so excited to provide a strong studying software with student-focused studying actions, permitting the coed to control their studying if you simply deal with their evaluate.

Analytical Microbiology Methods: Chromatography and Mass Spectrometry

The 1st foreign Symposium at the Interface among Analytical Chemistry and Microbiology: purposes of Chromatography and Mass Spectrometry used to be held June 1987 on the collage of South Carolina, Columbia, SC, U. S. A. the aim of the "Interface" assembly used to be to forge connections among analytical chemists and microbiologists which are utilizing chromatography and mass spectrometry to unravel universal difficulties.

Extra resources for Acute Neuronal Injury: The Role of Excitotoxic Programmed Cell Death Mechanisms

Sample text

Elegans: Gain of function mutations in deg-1 induce necrosis in a group of interneurons of the posterior touch sensory circuit (Chalfie and Wolinsky 1990). mec-4 gain of function mutations cause similar effects in the six touch receptor neurons, which are required for the sensation of gentle touch of the body (Syntichaki and Tavernarakis 2004). Both genes belong to the family of degenerins, which induce cell degeneration when mutated to a hyperactive form. Dying cells exhibit the typical morphological characteristics of necrotic cell death.

AIF is here a mitochondrial FAD-dependent oxidoreductase that plays a role in oxidative phosphorylation (Mate et al. 2002; Vahsen et al. 2004; Miramar et al. 2001). However, after a cellular insult, AIF is cleaved by calpains and/or cathepsins to yield tAIF (truncated AIF) a 57 kDa form of AIF (Otera et al. 2005; Polster et al. 2005; Yuste et al. 2005a). tAIF then translocates from mitochondria to cytosol and further to the nucleus, where it interacts with DNA and causes caspase-independent chromatin condensation and participates in large-scale (~50 kb) DNA fragmentation (Susin et al.

Oxford University press, Oxford Juhasz G, Sass M (2005) Hid can induce, but is not required for autophagy in polyploid larval Drosophila tissues. Eur J Cell Biol 84:491–502 Juhasz G, Erdi B, Sass M, Neufeld TP (2007a) Atg7-dependent autophagy promotes neuronal health, stress tolerance, and longevity but is dispensable for metamorphosis in Drosophila. Genes Dev 21:3061–3066 Juhasz G, Puskas LG, Komonyi O, Erdi B, Maroy P, Neufeld TP, Sass M (2007b) Gene expression profiling identifies FKBP39 as an inhibitor of autophagy in larval Drosophila fat body.

Download PDF sample

Rated 4.24 of 5 – based on 27 votes