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Fatty acids resources:

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Eur J Pharmacol. 2002 Sep 13;451(2):191-202.
Effect of Helicobacter pylori on delay in ulcer healing induced by aspirin in rats.

Konturek PC, Brzozowski T, Kwiecien S, Drozdowicz D, Harsch IA, Meixner H, Stachura J, Hahn EG, Konturek SJ.

First Department of Medicine, University Erlangen-Nuremberg, Erlangen, Germany.

Helicobacter pylori and nonsteroidal anti-inflammatory drugs (NSAIDs) are major pathogenic factors in peptic ulcer disease but whether these two factors exert synergistic or antagonistic effects on ulcer healing has been a subject of controversy. We compared the effect of aspirin alone with that of aspirin combined with H. pylori on gastric acid secretion and healing of acetic acid gastric ulcers in rats. The H. pylori colonization of gastric mucosa was determined by viable H. pylori culture, histology and assessment of bacterial DNA using polymerase chain reaction (PCR). The area of ulcers, gastric blood flow, mucosal generation of prostaglandin E(2) and plasma gastrin levels and expression of cyclooxygenase-1, cyclooxygenase-2 and growth factors was determined. Aspirin delayed significantly the healing of chronic gastric ulcers, decreased the gastric blood flow at the ulcer margin and gastric mucosal prostaglandin E(2) generation being without significant influence on gastric acid output. H. pylori acquisition that produced moderate gastric inflammation at the ulcer margin delayed significantly the healing of gastric ulcers, decreased significantly both the gastric blood flow at the ulcer margin and the gastric secretion while raising significantly the gastric mucosal prostaglandin E(2) generation and plasma gastrin levels. H. pylori infection attenuated the aspirin-induced inhibition of ulcer healing and accompanying fall in the gastric blood flow. Both aspirin and H. pylori up-regulated significantly cyclooxygenase-2 messenger RNA (mRNA) and protein but not that of cyclooxygenase-1 at the ulcer margin. Aspirin reduced significantly the transforming growth factor alpha- and vascular endothelial growth factor mRNAs, but these effects were significantly attenuated by H. pylori. We conclude that H. pylori antagonizes, in part, aspirin-induced delay of ulcer healing due to suppression of acid secretion, the enhancement in prostaglandin E(2) possibly derived from cyclooxygenase-2 and the overexpression of transforming growth factor alpha and vascular endothelial growth factor in the ulcer area.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12231391&dopt=Abstract

Life Sci. 2002 Oct 4;71(20):2369-81.
Selective changes in DNA binding activity of transcription factors in UM-X7.1 cardiomyopathic hamsters.

Ambra R, Di Nardo P, Fantini C, Minieri M, Canali R, Natella F, Virgili F.

Free Radicals Research Group, National Institute for Food and Nutrition Research, via Ardeatina 546, 00178, Rome, Italy. ambrnran.it

UM-X7.1 hamsters (CH) are considered a representative model for human cardiomyopathy. CH display the loss of the cytoskeletal delta-sarcoglycan protein, associated with myocardium remodeling and fatal reduction of heart functional efficiency. Even though altered redox balance and calcium homeostasis have already been reported to affect cardiomyocyte function, the molecular mechanisms underlying this pathology are largely unknown. We found no significant differences in DNA binding activity of redox-related (NF-kappaB, Sp1, AP-1 and AP-2) transcription factors in heart ventricles of 90 day-old CH, compared to normal animals. On the other hand, DNA binding activity of calcium-dependent transcription factors NF-AT3 and CREB were increased and decreased respectively in CH vs. normal ventricles. Western blot experiments confirmed the down regulation of CREB levels and suggest a novel regulation mechanism for this transcription factor in the heart.Our results are consistent with recent studies on NF-AT3, GATA4 and CREB transgenic mice, and provide clues for the comprehension of pathogenetic mechanisms of hamster hereditary cardiomyopathy.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12231398&dopt=Abstract

Neurosci Lett. 2002 Sep 20;330(2):159-62.
Estrogen attenuates tumor necrosis factor-alpha expression to provide ischemic neuroprotection in female rats.

Liao SL, Chen WY, Chen CJ.

Department of Education and Research, Taichung Veterans General Hospital, No. 160, Sec. 3, Taichung-Gang Road, Taichung 407, Taiwan, ROC.

Proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) plays an important role in the pathogenesis of neurodegenerative diseases including ischemia. Circulating estrogen is positively associated with neuroprotection against ischemia in female rats. In the present study, we examined whether endogenous estrogen levels affect ischemia-induced TNF-alpha expression in normal cycling female rats. An elevated concentration of TNF-alpha was toxic to neurons. A high level of expression of TNF-alpha accompanied the decline in circulating estrogen levels in normal cycling female rats. Estrogen administration attenuated endotoxin-induced TNF-alpha expression and neuronal injury, indicating that the down-regulation of TNF-alpha expression plays a role in ischemic neuroprotection by estrogen. Therefore, we propose that one mechanism by which estrogen protects females from ischemic damage is through the regulation of TNF-alpha production.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12231436&dopt=Abstract

Neurosci Lett. 2002 Sep 20;330(2):210-3.
An association study of a functional catalase gene polymorphism, -262C-->T, and patients with Alzheimer's disease.

Goulas A, Fidani L, Kotsis A, Mirtsou V, Petersen RC, Tangalos E, Hardy J.

Department of Pharmacology, School of Medicine, Aristotle University, Thessaloniki 54124, Greece.

According to the oxidative stress hypothesis which has been proposed as one of a number of possible mechanisms underlying pathogenesis of Alzheimer's disease (AD), accumulation of hydrogen peroxide in the brain of affected individuals, due to overproduction and/or insufficient detoxification, can trigger a cascade of neurotoxic events, thus contributing to the neuronal damage characteristic of the disease. The upregulation of enzymes that are able to neutralize hydrogen peroxide (catalase, peroxidases) would then be conceivably able to offer at least some protection from the damaging effects of this agent. In this study we examined the distribution of a functional polymorphism in the gene for catalase, -262C-->T, in an independent population of 137 AD patients and 130 control individuals. The presence of the polymorphism, which results in the elimination of a SmaI restriction site, was tested with a PCR amplification/SmaI digestion-based assay. No significant difference has emerged from the comparison of either genotype or allele frequencies (P>0.5). We conclude that the catalase gene -262C-->T polymorphism does not confer a protective effect with respect to AD.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12231449&dopt=Abstract

Brain Res. 2002 Sep 27;951(1):31-5.
Stress-induced mitochondrial depolarization and oxidative damage in PSP cybrids.

Chirichigno JW, Manfredi G, Beal MF, Albers DS.

Department of Neurology and Neuroscience, Room A-503, Weill Medical College of Cornell University, 525 East 68th Street, New York, NY 10021, USA.

Increased oxidative damage and mitochondrial dysfunction have been suggested to play critical roles in the pathogenesis of progressive supranuclear palsy (PSP) yet the specific intracellular defects which cause and can result from these oxidative and bioenergetic defects remain unclear. To extend our previous PSP cybrid findings, we measured electron transport chain (ETC) activities in cell lines expressing mitochondrial genes from patients with PSP. Further, we measured changes in mitochondrial membrane potential as well as lipid peroxidation in PSP and control cybrids in response to mitochondrial toxins. We observed significant decreases in complex I+III activity in PSP cybrids as well as significant increases in markers of lipid oxidative damage as compared to control cybrids. These results coupled with previous reports from this and other laboratories strongly suggest contributory roles of mitochondrial dysfunction and oxidative damage in PSP, possibly due to genetic abnormalities and/or damage of mitochondrial DNA.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12231453&dopt=Abstract

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