The Secret of Life and Death - a Scientific Approach (生老病死的秘密 - 從科學的觀點切入) [2009-05-06]

The Secret of Life and Death - a Scientific Approach  (生老病死的秘密 - 從科學的觀點切入) [2009-05-06]

The Secret of Life and Death - a Scientific Approach
生老病死的秘密 - 從科學的觀點切入

Title of the presentation WeiJin Tang (湯偉晉) presented to the 5070退休樂活論壇 at Taipei on May 6, 2009

Nitric Oxide and Peroxynitrite in Health and Disease (IR93)[2007]; 我們應該高度讚賞和尊崇，這些科學家的勤奮與努力，和他們既傑出又驚人的偉大貢獻。

April 14, 2009; 03:58:07 p.m. Taipei Time

Nitric Oxide and Peroxynitrite in Health and Disease (IR93)[2007]; 我們應該高度讚賞和尊崇，這些科學家的勤奮與努力，和他們既傑出又驚人的偉大貢獻。

We should highly appreciate and respect the diligent efforts and phenomenal contributions of these scientists.
(我們應該高度讚賞和尊崇，這些科學家的勤奮與努力，和他們既傑出又驚人的偉大貢獻。)

湯偉晉 (WeiJin Tang) 親手逐字地寫於 西元 2009-04-14


Nitric Oxide and Peroxynitrite in Health and Disease (IR93)[2007] 001.PNG
Nitric Oxide and Peroxynitrite in Health and Disease (IR93)[2007] 002.PNG
Nitric Oxide and Peroxynitrite in Health and Disease (IR93)[2007] 003.PNG
Nitric Oxide and Peroxynitrite in Health and Disease (IR93)[2007] 01.PNG
Nitric Oxide and Peroxynitrite in Health and Disease (IR94)[2007] 02.PNG
Progression of heart failure and the role of oxidative stress and peroxynitrite [2007](IR88).PNG

盡心盡力地教導自己的部屬，讓他們也可以像自己一樣地成長和茁壯。

盡心盡力地教導自己的部屬，讓他們也可以像自己一樣地成長和茁壯。


只要你是一個移動的目標，你的部屬將永遠追不上你。所以，請您務必盡心盡力，好好地教導和幫助您的部屬，讓他們可以與您一起成長和茁壯。

湯偉晉 (WeiJin Tang) 親手逐字地寫於 西元 2009-04-29

盡心盡力地教導自己的部屬，讓他們也可以像自己一樣地成長和茁壯。
Version 1.00.01; Last Updated on [2009-04-29-AM-00-23-14]

2009-04-29

File Index: 0001
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GUID file name:
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Keywords:
盡心盡力地教導自己的部屬，讓他們也可以像自己一樣地成長和茁壯。

Number of attached files: 
1

Chemical Biology of DNA Damage Associated with Inflammation - Problems and Prospects of Using DNA Lesions as Biomarkers of Oxidative and Nitrosative Stress [2006](IR90)

April 14, 2009; 03:20:22 p.m. Taipei Time

Chemical Biology of DNA Damage Associated with Inflammation - Problems and Prospects of Using DNA Lesions as Biomarkers of Oxidative and Nitrosative Stress [2006](IR90) 01.PNG
Chemical Biology of DNA Damage Associated with Inflammation - Problems and Prospects of Using DNA Lesions as Biomarkers of Oxidative and Nitrosative Stress [2006](IR90) 02.PNG
Chemical Biology of DNA Damage Associated with Inflammation - Problems and Prospects of Using DNA Lesions as Biomarkers of Oxidative and Nitrosative Stress [2006](IR90) 03.PNG

Atherosclerosis is the principal cause of heart disease and a leading cause of stroke, making it the most common cause of death in the U.S. [2008](IR92)_FNKWs_{hydrogen peroxide, H2O2}

Atherosclerosis is the principal cause of heart disease and a leading cause of stroke, making it the most common cause of death in the U.S. [2008](IR92)

Atherosclerosis is the principal cause of heart disease and a leading cause of stroke, making it the most common cause of death in the U.S. [2008](IR92)_FNKWs_{hydrogen peroxide, H2O2}
http://www.vascularpath.org/projects.htm

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Essentially all risk factors for atherosclerosis result in the enhanced generation of hydrogen peroxide in the vessel wall by the activation of membrane bound NADPH oxidases (NOX). The NADPH oxidases generate superoxide in the extracellular space that both inactivates nitric oxide and is dismutated into hydrogen peroxide by extracellular superoxide dismutase (ECSOD).

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(Memo Item created on January 15, 2009 02:33 PM)
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Atherosclerosis is the principal cause of heart disease and a leading cause of stroke, making it the most common cause of death in the U.S.

http://www.vascularpath.org/projects.htm
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Home | Projects | Lab Members | Publications | Links | Biographical Sketch | Contact

Projects

Atherosclerosis is the principal cause of heart disease and a leading cause of stroke, making it the most common cause of death in the U.S. The laboratory is seeking to understand the biochemical processes resulting in atherosclerosis in order to combat this pervasive disease.

Atherosclerosis is characterized by the development of necrotic/lipid cores within the intima of arteries at particular sites in the circulation. These necrotic/lipid cores form in the setting of a pre-existing intimal hyperplasia, characterized by the proliferation of smooth muscle-like cells within the intima. The laboratory is investigating both the mechanisms of signal transduction responsible for the formation of the pre-atherosclerotic intimal hyperplasia, as well as the factors stimulating the formation of intimal necrotic/lipid cores. Signal Transduction with Hydrogen Peroxide in Vascular Cells

Essentially all risk factors for atherosclerosis result in the enhanced generation of hydrogen peroxide in the vessel wall by the activation of membrane bound NADPH oxidases (NOX). The NADPH oxidases generate superoxide in the extracellular space that both inactivates nitric oxide and is dismutated into hydrogen peroxide by extracellular superoxide dismutase (ECSOD). These low physiologic levels of hydrogen peroxide are mitogenic, stimulating vascular cell growth and proliferation.

The mechanisms by which low endogenous levels of hydrogen peroxide stimulate cellular proliferation are currently poorly understood. The laboratory is using proteomic approaches with cultured vascular cells to identify signal transduction pathways activated by low physiologic levels of hydrogen peroxide. One target protein identified is the nuclear pre-mRNA binding protein hnRNP-C. Low physiologic levels of hydrogen peroxide stimulate the hyperphosphorylation of the acidic C-terminal domain of hnRNP-C, resulting in diminished ability of the protein to bind mRNA. The effect is mediate by protein kinase CK1 Other groups have previously shown that hnRNP-C is hyperphosphorylated during mitosis, and that CK1 entry into the nucleus is required for cell cycle progression. Proteomic Analyses of Intimal Hyperplasia from Atherosclerosis-Prone and Atherosclerosis-Resistant Human Arteries

Pre-atherosclerotic intimal hyperplasia forms at branch sites both in arteries prone to develop atherosclerosis, such as the internal carotid and coronary arteries and also in vessels remarkably resistant to the formation of atherosclerosis, such as the internal thoracic artery and the distal ulnar artery. The structural variations in intimal hyperplasia that may facilitate the development of atherosclerosis have been unclear. Proteoglycans have been implicated as playing a direct role in atherosclerosis, both by binding and retaining lipoproteins in the vessel wall and by regulating cell growth. One project in the laboratory has been to analyze by mass spectrometry the extracellular proteoglycans present in pre-atherosclerotic intimal hyperplasia from atherosclerosis-prone arteries as well as atherosclerosis-resistant arteries. This project has revealed the proteoglycan composition of human intimal hyperplasia to be more complex than previously realized with eight distinct proteoglycans present: perlecan, versican, aggrecan, biglycan, decorin, fibromodulin, lumican, and prolargin. Importantly, while most of the proteoglycans are present at similar levels in the two arterial types, there is a selective enhanced deposition of lumican proteoglycan in the pre-atherosclerotic intimal hyperplasia from the atherosclerosis-prone artery compared with the intimal hyperplasia from the atherosclerosis-resistant artery. This data suggests that lumican may play a central role in the development of atherosclerotic lesions in humans, and may partly account for site-specific susceptibility to atherosclerosis. Home | Projects | Lab Members | Publications | Links | Biographical Sketch | Contact

Massachusetts General Hospital | Simches Building, Rm 8236
185 Cambridge Street, CPZN | Boston, MA 02114
Phone: 617-726-8303 | Fax: 617-726-2365

©2007 James R. Stone Lab - Department of Pathology - Massachusetts General Hospital

Site by: AlternaSite

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2009-03-17

File Index: 0001
Original file name (原始的檔案名稱):
Atherosclerosis is the principal cause of heart disease and a leading cause of stroke, making it the most common cause of death in the U.S. [2008](IR92)_FNKWs_{hydrogen peroxide, H2O2} 01.PNG
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FN_A2CF01CC1B6F4534A8DADDFEC29A9CE5.PNG

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Atherosclerosis is the principal cause of heart disease and a leading cause of stroke, making it the most common cause of death in the U.S. [2008](IR92)_FNKWs_{hydrogen peroxide, H2O2} 02.png
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Atherosclerosis is the principal cause of heart disease and a leading cause of stroke, making it the most common cause of death in the U.S. [2008](IR92)_FNKWs_{hydrogen peroxide, H2O2} 03.png
GUID file name:
FN_C87B4CCEB3624598A61178DB66955278.png

Keywords:
Hydrogen peroxide, increased, glutathione (GSH), L-Cysteine, Atherosclerosis (【醫學】動脈粥狀硬化), cardiovascular (【醫學】心血管性的), stroke (中風)

Number of attached files: 
3

The major determinants (決定因素) of GSH synthesis are the availability of cysteine, and the activity of the rate-limiting enzyme, g-glutamylcysteine synthetase (GCS)[1999](IR90)

 

The major determinants (決定因素) of GSH synthesis are the availability of cysteine, and the activity of the rate-limiting enzyme, g-glutamylcysteine synthetase (GCS)[1999](IR90)

 

Regulation of hepatic glutathione synthesis: current concepts and controversies SHELLY C. LU

USC Liver Disease Research Center, the Division of Gastrointestinal (胃腸的) and Liver Diseases, Department of Medicine, University of Southern California School of Medicine, Los Angeles, California 90033, USA

 

ABSTRACT

 

Glutathione (GSH) is an important intracellular peptide with multiple functions ranging from antioxidant defense to modulation of cell proliferation. GSH is synthesized in the cytosol (【生物學】細胞溶質) of all mammalian (哺乳動物(的)) cells in a tightly regulated manner. The major determinants (決定因素) of GSH synthesis are the availability of cysteine, the sulfur amino acid precursor, and the activity of the rate-limiting enzyme, g-glutamylcysteine synthetase (GCS). In the liver, major factors that determine the availability of cysteine are diet, membrane transport activities of the three sulfur amino acids cysteine, cystine and methionine, and the conversion of methionine to cysteine via the trans-sulfuration pathway. Many conditions alter GSH level via changes in GCS activity and GCS gene expression. These include oxidative stress, activators of Phase II detoxifying enzymes, antioxidants, drug-resistant tumor cell lines, hormones, cell proliferation, and diabetes mellitus (糖尿病). Since the molecular cloning (複製) of GCS, much has been learned about the regulation of this enzyme. Both transcriptional and post-transcriptional mechanisms modulate the activity of this critical cellular enzyme.

 

Lu, S. C. Regulation of hepatic glutathione synthesis: current concepts and controversies. FASEB J. 13, 1169-1183 (1999)

 

Key Words:

g-glutamylcysteine synthetase , cysteine availability , detoxification , antioxidant

Effect of ageing on human plasma glutathione concentrations as determined by high-performance liquid chromatography with fluorimetric detection [1995](IR94).doc

Effect of ageing on human plasma glutathione concentrations as determined by high-performance liquid chromatography with fluorimetric detection [1995](IR94).doc

Effect of ageing on human plasma glutathione concentrations as determined by high-performance liquid chromatography with fluorimetric detection [1995](IR94)

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Effect of ageing on human plasma glutathione concentrations as determined by high-performance liquid chromatography with fluorimetric detection [1995](IR94)

http://highwire.stanford.edu/cgi/medline/pmid;8749248?maxtoshow=&HITS=&hits=&RESULTFORMAT=&fulltext=Effect+of+ageing+on+human+plasma+glutathione+concentrations&andorexactfulltext=and&searchid=1&FIRSTINDEX=0&resourcetype=HWCIT
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Effect of ageing on human plasma glutathione concentrations as determined by high-performance liquid chromatography with fluorimetric detection.
CS Yang, ST Chou, L Liu, PJ Tsai, and JS Kuo
J Chromatogr B Biomed Appl, December 1, 1995; 674(1): 23-30.    

Department of Medical Research. Taichung Veterans General Hospital Taiwan (台中榮民總醫院).

A convenient method for the determination of reduced glutathione (GSH) and oxidized glutathione (GSSG) in human plasma by high-performance liquid chromatography with fluorescence detection is reported. This assay involves direct addition of human plasma to methanolic monobromobimane, for simultaneous protein precipitation and thiol derivatization. The assay was validated by addition of authentic GSH and GSSG to plasma samples. Plasma glutathione levels in Chinese male and female volunteers were found to decrease with increasing age (age groups 20-30, 30-40, 40-50, 50-60, and > 60; mean +/- S.E.M. 0.95 +/- 0.03, 0.77 +/- 0.02, 0.67 +/- 0.03, 0.51 +/- 0.02, 0.48 +/- 0.02 microM for male volunteers and 1.11 +/- 0.06, 0.76 +/- 0.03, 0.61 +/- 0.03, 0.53 +/- 0.04 and 0.43 +/- 0.04 microM for female volunteers). GSSG levels, in both males and females, did not show a correlation with age. There were no significant differences in GSH or GSSG levels among male and female volunteers of the same age group. These results suggest that elderly persons might be more susceptible to oxidative injury due to decreased plasma glutathione levels.

Publication Types:

Journal article
Research support, non-u.s. gov't
MeSH Terms:

Adult
Aged
Aging
Bicyclo Compounds
Chromatography, High Pressure Liquid*
Dithiothreitol
Ethylmaleimide
Female
Fluorometry
Glutathione
Humans
Male
Middle Aged
Reproducibility of Results
Sulfhydryl Reagents
PMID: 8749248

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