※ 引述《albertwang (會思考的魚)》之銘言：
: Journal Title - Inflammopharmacology(只有成大醫有,線上成大醫的同學謝謝囉)
: Article Title - Oxidative stress in Helicobacter pylori-induced gastric
: cell injury
: Volume :13
: Issue :1
: Page :63- 74
: Link - http://www.springerlink.com/content/90372211694u5j28
ok
摘要：
Helicobacter pylori has been identified in the pathogenesis of chronic active
gastritis and peptic ulcer disease and is epidemiologically linked to gastric
cancer and lymphoma. Our previous studies have demonstrated enhanced
production of reactive oxygen species (ROS) in cultured gastric
adenocarcinoma cells (ATCC CRL/1739) in association with H. pylori. Recently,
we have isolated and cultured normal human gastric mucosal cells (GMC) from
H. pylori-negative endoscopic biopsies. The integrity of these mucosal cells
was determined by periodic acid-Schiff staining. We assessed the effects of
various H. pylori strains including 60190 (a 87-kDa cytotoxin producing
strain), ATCC 43504, and 60190-v1 (in which the cytotoxin gene has been
disrupted) on the primary culture of human gastric mucosal cells. The
induction of ROS and DNA fragmentation in the mucosal cells in association
with these H. pylori strains were assessed by cytochrome c reduction (an
index of superoxide anion production), hydroxyl radical production, and DNA
fragmentation. Following incubation of the mucosal cells with 1:0.5 and 1:1
ratios of H. pylori strain 60190, approximately 6.2- and 9.9-fold increases
were observed in cytochrome c reduction, respectively, as compared to mucosal
cells in the absence of H. pylori, demonstrating the production of superoxide
anion. The detection of hydroxyl radicals based on the formation of
2,3-dihydroxybenzoic acid and 2,5-dihydroxybenzoic acid was determined by
using a high-performance liquid chromatograph equipped with an
electrochemical detector. Approximately 3.5- and 7.7-fold increases in
hydroxyl radical production were observed following incubation of the mucosal
cells with 1:0.5 and 1:1 ratios of H. pylori, respectively. Approximately
3.6- and 4.5-fold increases in DNA fragmentation were observed in gastric
mucosal cells following incubation with 1:0.5 and 1:1 ratios of H. pylori,
respectively. The effects of culture supernatant preparations from H. pylori
strains 60190 and 60190-v1 on the enhanced production of ROS and increased
DNA fragmentation in mucosal cells were also investigated. Culture
supernatant preparations, the prime source of the 87-kDa cytotoxin, from both
H. pylori strains 60190 and 60190-v1 were extracted under identical
conditions to determine the role of 87-kDa cytotoxin on the enhanced
production of ROS and DNA fragmentation. The cytotoxin rich-H. pylori strain
60190 induced greater production of ROS and DNA fragmentation in mucosal
cells as compared to the supernatant preparation from H. pylori strain
60190-v1, in which the cytotoxin gene has been disrupted. This study
demonstrates that H. pylori induces enhanced production of ROS and DNA damage
in association with human gastric mucosal cells andthat the 87-kDa cytotoxin
protein plays a prime role in the induction of oxidative stress and DNA
damage.
http://0rz.tw/ea3sm
: Journal Title: Scand J Gastroenterol.
: 2003 Apr;38(4):380-6.
: Article Title:
: Stimulated murine macrophages as a bioassay for H. pylori-related inhibition
: of nitric oxide production.
這篇期刊網站有點問題
這個issue 的選項有問題....(用電子全文期刊模式搜尋)
用endnote 搜尋 web of knowledge 她的連接是顯示是有電子原文
可是連過去書商：Page Not Found
I am sorry but we cannot locate the page you are looking for.
這篇的問題可能要寫電子郵件請他們處理一下
同作者找到的是：
Selected: Choose an Action: Add to shopping cart Add to marked list
Download Citation
Helicobacter pylori induces gastritis and intestinal metaplasia but no
gastric adenocarcinoma in Mongolian gerbils
Anders Elfvin; Ingrid Bölin; Charlotte Von Bothmer; Manfred Stolte;
Hidenobu Watanabe; Lars Fändriks; Michael Vieth
Scandinavian Journal of Gastroenterology, Volume 40, Issue 11, 2005, Pages
1313 – 1320
DOI: 10.1080/00365520510023611
ACCESS
Helicobacter pylori Infection Inhibits Antral Mucosal Nitric Oxide
Production in Humans
C. von Bothmer; A. Edebo; H. Lönroth; L. Olbe; A. Pettersson; L. Fä
ndriks
Scandinavian Journal of Gastroenterology, Volume 37, Issue 4, 2002, Pages
404 – 408
DOI: 10.1080/003655202317316024
ACCESS
Intragastric Nitric Oxide/Nitrite in Helicobacter pylori-Infected Subjects
L. Fändriks; C. von Bothmer; A. Åneman; L. Olbe; A. Pettersson
Scandinavian Journal of Gastroenterology, Volume 36, Issue 4, 2001, Pages
347 – 350
DOI: 10.1080/00365520119610
狀況正常
: Journal Title: Am J Physiol Gastrointest Liver Physiol.
: 2007 Nov;293(5):G1004-12
: Toll-like receptor (TLR) 2 induced through TLR4 signaling initiated by
: Helicobacter pylori cooperatively amplifies iNOS induction
: in gastric epithelial cells.
: http://ajpgi.physiology.org/cgi/content/full/293/5/G1004
摘要：
Cell- surface Toll- like receptors ( TLRs) initiate innate immune responses,
such as inducible nitric oxide synthase ( iNOS) induction, to microorganisms'
surface pathogens. TLR2 and TLR4 play important roles in gastric mucosa
infected with Helicobacter pylori ( H. pylori), which contains
lipopolysaccharide ( LPS) as a pathogen. The present study investigates their
physiological roles in the innate immune response of gastric epithelial cells
to H. pylori- LPS. Changes in the expression of iNOS, TLR2, and TLR4, as well
as downstream activation of mitogen-activated protein kinases and nuclear
factor-kappa B (NF-kappa B), were analyzed in normal mouse gastric mucosal
GSM06 cells following stimulation with H. pylori-LPS and interferon-gamma.
Specific inhibitors for mitogen-activated protein kinases, NF-kappa B, and
small interfering RNA for TLR2 or TLR4 were employed. The
immunohistochemistry of TLR2 was examined in human gastric mucosa. H. pylori-
LPS stimulation induced TLR2 in GSM06 cells, but TLR4 was unchanged. TLR2
induction resulted from TLR4 signaling that propagated through extracellular
signal- related kinase and NF-kappa B activation, as corroborated by the
decline in TLR4 expression on small interfering RNA treatment and
pretreatment with inhibitors. The induction of iNOS and the associated nitric
oxide production in response to H. pylori- LPS stimulation were inhibited by
declines in not only TLR4 but also TLR2. Increased expression of TLR2 was
identified in H. pylori- infected human gastric mucosa. TLR4 signaling
initiated by H. pylori- LPS and propagated via extracellular signal-
regulated kinase and NF-kappa B activation induced TLR2 expression in gastric
epithelial cells. Induced TLR2 cooperated with TLR4 to amplify iNOS
induction. This positive correlation may constitute a mechanism for
stimulating the innate immune response against various bacterial pathogens,
including H. pylori- LPS.
http://0rz.tw/b13sf
那個電子PDF檔的部份點了以後我會有當機現象= =~~
所以我把 FULL HTML 印了下來
歡迎大家討論這幾篇吧^^
: MAIL:firewaterwang@yahoo.com.tw
: ※ 編輯: albertwang 來自: 61.216.40.217 (12/17 20:15)
: 推 kissinwang:我先去台中~回來幫你看看^^ 12/17 22:40
: → albertwang:謝謝先 12/17 23:36
--
個人網站 http://www.fst.ntu.edu.tw/kissinwang/index.htm
my blog http://kissinwangblog.spaces.live.com/
留言給我 http://www.hkflash.com/gb/gb.asp?id=kissinwang
化學/化學工程/生化科技BBS網路資源中心 http://groups.msn.com/chemicalBBScenter
歡迎將本板加入我的最愛：(C)lass【 分組討論區 】→11國家研究院 政治, 文學, 學術
→1 Academy 研究 Σ科學學術研究院 → 2ˇBiology 生命 ●全國生物科技轉信討論區●
--
※ 發信站: 批踢踢實業坊(ptt.cc)
◆ From: 140.112.98.14