2010年8月10日 星期二

國立清華大學_博碩士論文_{以基因轉殖大腸桿菌ABLE C製備硫化鎘奈米粒子 (Biosynthesis of Cadmium Sulfide Nanoparticle in Gene Modified Escherichia coli ABLE C)} [2007](IR91)

 
國立清華大學_博碩士論文_{以基因轉殖大腸桿菌ABLE C製備硫化鎘奈米粒子 (Biosynthesis of Cadmium Sulfide Nanoparticle in Gene Modified Escherichia coli ABLE C)} [2007](IR91)

http://nthur.lib.nthu.edu.tw/handle/987654321/32424

National Tsing Hua University Institutional Repository >
工學院 > 化學工程學系所 > 博碩士論文 > Item 987654321/32424

Please use this identifier to cite or link to this item:
http://nthur.lib.nthu.edu.tw/dspace/handle/987654321/32424

Title:
以基因轉殖大腸桿菌ABLE C製備硫化鎘奈米粒子
Other Titles: Biosynthesis of Cadmium Sulfide Nanoparticle in Gene Modified Escherichia coli ABLE C
Authors:
田俊文

Chun-Wen Tien
Description:
碩士
國立清華大學
化學工程學系
GH000943606
Date: 2007
Keywords:
硫化鎘
奈米粒子
Glutathione
大腸桿菌
生物法

Abstract:
本研究以基因轉殖大腸桿菌進行CdS奈米粒子的製備,研究內容結合生物科技以及奈米技術兩個領域。CdS為擁有直接能隙的II-V半導體材料,粒徑小於6 nm以下時,有明顯的量子侷限效應,被視為新一代的LED發光材料。除此之外,CdS奈米粒子應用於各類感測器以及生物螢光標定中的研究也相當的多。

本研究首次利用基因工程的手法,將gshA及gshB基因片段以重組載體送入細胞中,分別表現glutathione合成酵素γ-GCS及GS,藉此促進大腸桿菌中glutathione的含量,來量產CdS奈米粒子。GSH分子為生物合成CdS奈米粒子之關鍵,其含量之增加有助於細胞生成CdS粒子。我們證實,大腸桿菌ABLE C生成之CdS奈米粒子粒徑介於2~5 nm之間。經過基因轉殖的菌株,細胞中GS合成酵素含量增加,細胞中CdS粒子產量有顯著提升。

粒子特性方面,基因轉殖大腸桿菌所生產的CdS奈米粒子由於粒子表面有較多的GSH包覆,因此在水溶液中分散性更為提升,而重組蛋白的產生對所生成CdS的粒徑無太大影響。在此我們證明了以大腸桿菌生產CdS奈米粒子的可行性,透過基因轉殖細胞能更近一步增進產量和改善產物性質。在實驗過程中,我們也證實了GSH含量的多寡,確實引響細胞生產CdS的能力,對於此系統背後生理機制的釐清也有所助益。

Cadmium sulfide nanoparticles were synthesized intracellularly in gene modified Escherichia coli ABLE C. The nanoparticles, a known semiconducting material, which have unique optical and electronic properties, have potential for application in the emerging field of nanoelectronics. To produce nanomaterial cheaply and efficiently, biological methods of synthesis are being explored. Schizosaccharomyces pombe were found having the capacity to synthesize CdS nanoparticles intracellularly in 1983. Recently, in 2004, Sweeney found that E. coli also have ability to synthesize CdS nanoparticles. Morever, in his study, he pointed out that the cellular glutathione can enhance the formation of nanoparticles. Inspried by Sweeney, we constructed a gene modified E. coli ABLE C which could use for glutathione overproduction and attempt to figure out how this parameter can enhance the synthesis of nanoparticles within bacterial cells. Our results showed that nanoparticles biosynthesis increased about 1.6 –fold in gene modified cells compared to wild type cells. HRTEM data showed that the nanoparticles had a Wurtzite hexagonal lattice structure and most of the nanoparticles were in the size range of 2-5 nm. We also observed that nanoparticles synthesized in gene modified cells were dispersed better in water than these in wild type cells. The well dispersion behavior was due to more glutathione coated on the nanoparticles. To our best knowledge, this is the first report using genetic modification to enhance biosynthsis of CdS nanoparticles and to unravel the siginificance of glutathione in this procedure. By understanding parameters of nanoparticles synthesis, it might be possible to modulate the properties of biosynthesized nanopartilces, such as size, shae, and crystal structure.

Appears in Collections: [
化學工程學系所] 博碩士論文

2010年3月23日 星期二

查詢 美國史丹佛大學 (Stanford University) 的專業資料庫 HighWire

查詢 美國史丹佛大學 (Stanford University) 的專業資料庫 HighWire
Query professional database HighWire at Stanford University, USA

Glutathione, depletion

穀胱甘肽,耗盡


使用
關鍵字 {Glutathione, depletion (穀胱甘肽,耗盡)} 去查詢 美國史丹佛大學 (Stanford University) 的專業資料庫 HighWire

Glutathione, depletion, cancer

穀胱甘肽,耗盡,癌症

使用
關鍵字 {Glutathione, depletion, cancer (穀胱甘肽,耗盡,癌症)} 去查詢 美國史丹佛大學 (Stanford University) 的專業資料庫 HighWire

Title of this page:

查詢
美國史丹佛大學 (Stanford University) 的專業資料庫 HighWire
Query professional database HighWire at Stanford University, USA

Version of this page:

Version 1.00.02; Last Updated on [2010-03-23-PM-09-10-56]

2010年2月28日 星期日

Glutathione, oxidative stress and neurodegeneration. [2000](IR92)


Glutathione, oxidative stress and neurodegeneration [2000](IR92)

Eur J Biochem. 2000 Aug;267(16):4904-11.

Glutathione, oxidative stress and neurodegeneration.
Schulz JB, Lindenau J, Seyfried J, Dichgans J.
http://www.ncbi.nlm.nih.gov/pubmed/10931172?dopt=Abstract

Neurodegeneration Laboratory, Department of Neurology, University of Tübingen, Germany. joerg.b.schulz@uni-tuebingen.de

There is significant evidence that the pathogenesis of several neurodegenerative diseases, including Parkinson's disease, Alzheimer's disease, Friedreich's ataxia and amyotrophic lateral sclerosis, may involve the generation of reactive oxygen species and mitochondrial dysfunction. Here, we review the evidence for a disturbance of glutathione homeostasis that may either lead to or result from oxidative stress in neurodegenerative disorders. Glutathione is an important intracellular antioxidant that protects against a variety of different antioxidant species. An important role for glutathione was proposed for the pathogenesis of Parkinson's disease, because a decrease in total glutathione concentrations in the substantia nigra has been observed in preclinical stages, at a time at which other biochemical changes are not yet detectable. Because glutathione does not cross the blood-brain barrier other treatment options to increase brain concentrations of glutathione including glutathione analogs, mimetics or precursors are discussed.

PMID: 10931172 [PubMed - indexed for MEDLINE]

2010年1月19日 星期二

We are living in a world, not in an invisible box. So, please step out of the box!


2010-01-20


「We are living in a world, not in an invisible box. So, please step out of the box!」

「我們是生活在一個世界裡面,而不是住在一個隱形的盒子裡。所以,請 從盒子裡面走出來。」

「我們是生活在一個世界裡面,而不是住在一個隱形的盒子裡。所以,請 從盒子裡面走出來,看看這個世界和自己周遭的環境。然後,摸摸自己的良心,問問自己,我們有把其他的人看成,就像是我們自己的兄弟姊妹一樣,去善待他們嗎? 請務必記得, 神 對我們的教導是: 要 愛人如己 而且要 公平地去對待每一個人,把他們當成是 一個人,一個擁有 天賦人權 和 為人之尊嚴 的人,並且善待他們。」

湯偉晉 (WeiJin Tang) 親手原創性地寫作於 西元 2010-01-20

File name of the attached file:
WeiJin Tang - {We are living in a world, not in an invisible box. So, please step out of the box!}[2010-01-20](IR90).gif

我們是生活在一個世界裡面,而不是住在一個隱形的盒子裡。所以,請 從盒子裡面走出來。


2010-01-20


「We are living in a world, not in an invisible box. So, please step out of the box!」

「我們是生活在一個世界裡面,而不是住在一個隱形的盒子裡。所以,請 從盒子裡面走出來。」

「我們是生活在一個世界裡面,而不是住在一個隱形的盒子裡。所以,請 從盒子裡面走出來,看看這個世界和自己周遭的環境。然後,摸摸自己的良心,問問自己,我們有把其他的人看成,就像是我們自己的兄弟姊妹一樣,去善待他們嗎? 請務必記得, 神 對我們的教導是: 要 愛人如己 而且要 公平地去對待每一個人,把他們當成是 一個人,一個擁有 天賦人權 和 為人之尊嚴 的人,並且善待他們。」

湯偉晉 (WeiJin Tang) 親手原創性地寫作於 西元 2010-01-20

File name of the attached file:
WeiJin Tang - {We are living in a world, not in an invisible box. So, please step out of the box!}[2010-01-20](IR90).gif

2010年1月18日 星期一

The Relationship Between Plasma Levels of Oxidized and Reduced Thiols and Early Atherosclerosis in Healthy Adults [2006](IR92)


January 18, 2010; 07:34:10 p.m. Taipei Time

The Relationship Between Plasma Levels of Oxidized and Reduced Thiols and Early Atherosclerosis in Healthy Adults [2006](IR92)

Glutathione redox state (Eh GSH/GSSG), an in vivo measure of intracellular oxidative stress, is an independent predictor for the presence of early atherosclerosis in an otherwise healthy population.

atherosclerosis
【醫】動脈硬化症, 動脈粥狀硬化症

File name:
The Relationship Between Plasma Levels of Oxidized and Reduced Thiols and Early Atherosclerosis in Healthy Adults [2006](IR90).png

Glutathione redox state (ratio of GSH over GSSG), an in vivo measure of intracellular oxidative stress, is an independent predictor for the presence of early atherosclerosis in an otherwise healthy population [2010-01-18](IR90).png

2009年11月4日 星期三

Depletion (耗盡) of reduced glutathione (穀胱甘肽) precedes inactivation of mitochondrial enzymes following limbic status epilepticus (癲癇持續狀態) in the rat hippocampus [2006](IR91)


Depletion (
耗盡) of reduced glutathione (穀胱甘肽) precedes inactivation of mitochondrial enzymes following limbic status epilepticus (癲癇持續狀態) in the rat hippocampus [2006](IR91)

Depletion (
耗盡) of reduced glutathione (穀胱甘肽) precedes inactivation of mitochondrial enzymes following limbic status epilepticus (癲癇持續狀態) in the rat hippocampus [2006](IR91)

穀胱甘肽

Depletion (
耗盡) of reduced glutathione (穀胱甘肽) precedes inactivation of mitochondrial enzymes following limbic (邊緣的) status epilepticus (癲癇持續狀態) in the rat hippocampus (海馬(大腦中被認為是感情和記憶中心的部分)).

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(Memo Item created on November 4, 2009 04:12 PM)
- - - Begin title or keyword:
Depletion (
耗盡) of reduced glutathione (穀胱甘肽
) precedes inactivation of mitochondrial enzymes following limbic status epilepticus in the rat hippocampus.

http://highwire.stanford.edu/cgi/medline/pmid;16290321?maxtoshow=&HITS=&hits=&RESULTFORMAT=1&andorexacttitle=and&fulltext=glutathione%2C+depletion%2C+epilepsy&andorexactfulltext=and&searchid=1&FIRSTINDEX=0&sortspec=relevance&resourcetype=HWCIT

- - - End title or keyword:

Depletion (
耗盡) of reduced glutathione (穀胱甘肽
) precedes inactivation of mitochondrial enzymes following limbic status epilepticus in the rat hippocampus.

H Sleven, JE Gibbs, S Heales, M Thom, and HR Cock
Neurochem Int, January 1, 2006; 48(2): 75-82.    

Abstract

Epilepsy Group, Centre for Clinical Neurosciences, St. George's, University of London, Cranmer Terrace, London SW17 0RE, UK.

The time course and critical determinants of mitochondrial dysfunction and oxidative stress following limbic status epilepticus (SE) were investigated in hippocampal sub-regions of an electrical stimulation model in rats, at time points 4-44h after status. Mitochondrial and cytosolic enzyme activities were measured spectrophotometrically, and reduced glutathione (
穀胱甘肽) (GSH) concentrations by HPLC, and compared to results from sham controls. The earliest change in any sub-region was a fall in GSH, appearing as early as 4h in CA3 (-13%, p<0.05), and persisting at all time points. This was followed by a transient fall in complex I activity (CA3, 16h, -13%, p<0.05), and later changes in aconitase (CA1,-18% and CA3, -22% at 44h, p<0.05). The activity of the cytosolic enzyme glyceraldehyde-3-phosphate-dehydrogenase was unaffected at all time points. It is known that GSH levels are dependent both on redox status, and on the availability of the precursor cysteine, in turn dependent on the cysteine/glutamate antiporter, for which extracellular glutamate concentrations are rate limiting. Both mechanisms are likely to contribute indirectly to GSH Depletion (耗盡) following seizures. That a relative deficiency in GSH precedes later changes in the activities of complex I and aconitase in vulnerable hippocampal sub-regions, occurring within a clinically relevant therapeutic time window, suggests that strategies to boost GSH levels and/or otherwise reduce oxidative stress following seizures, deserve further study, both in terms of preventing the biochemical consequences of SE and the neuronal dysfunction and clinical consequences.

Publication Types:

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

Animals
Chromatography, High Pressure Liquid
Electric Stimulation
Electroencephalography
glutathione (
穀胱甘肽)
Male
Mitochondria
Rats
Rats, Sprague-Dawley
Status Epilepticus
PMID: 16290321

--------------------------------------------------------------------------------
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