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Fatty acids resources:

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Plant Mol Biol. 2000 Jul;43(4):429-38.
cDNA cloning and characterization of a plant protein that may be associated with the harpinPSS-mediated hypersensitive response.

Chen CH, Lin HJ, Ger MJ, Chow D, Feng TY.

Institute of Botany, Academia Sinica, Taipei, Taiwan.

Hypersensitive response-assisting protein (HRAP) is a novel plant protein that can intensify the harpinPSS-mediated hypersensitive response (HR) in harpinPSS-insensitive plants, such as the vegetative stage of sweet pepper. In this report, we identified a HRAP cDNA clone from sweet pepper (Capsicum annuum cv. ECW). The sequence of this cDNA clone showed no appreciable similarity to any other known sequences. However, it contained three positively charged regions, a typical signal peptide and a cAMP-dependent phosphorylation site. The hrap mRNA accumulated preferentially during the incompatible interaction of sweet pepper leaves with a pathogenic bacterium, Pseudomonas syringae pv. syringae. When the hrap gene transcription level was high, the sweet pepper leaves readily expressed the harpinPSS-mediated HR. The hrap gene transcription level in sweet pepper was also higher during the reproductive stage than during the vegetative stage. The HRAP distribution in an individual plant and different plant species was investigated. We found that all the organs of sweet pepper, except fruit, could express two different forms of HRAP. Moreover, the hrap gene was presented in many plant species including tobacco, Arabidopsis, and rice. In conclusion, our results suggest that the hrap gene is widely distributed throughout the plant world and its transcription level correlates with plant sensitivity to harpinPSS. The interaction between HRAP and harpinPSS reveals a novel way to interpret the interaction mechanism between plants and bacterial pathogens.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11052195&dopt=Abstract

Transpl Int. 2000;13(5):357-62.
Plasma levels of endothelin-1 in patients with the hepatorenal syndrome after successful liver transplantation.

Bachmann-Brandt S, Bittner I, Neuhaus P, Frei U, Schindler R.

Department of General and Transplant Surgery, Universitatsklinikum Charite, Berlin, Germany.

The hepatorenal syndrome (HRS) is characterized by renal vasoconstriction leading to deterioration of renal function in patients with liver disease. A possible role of endothelin-1 (ET-1) in the pathogenesis of HRS has been suggested, but a correlation between ET-1 plasma levels and the development of HRS as well as the recovery from HRS following OLT has not been shown yet. We performed longitudinal measurements of ET-1 plasma levels in four groups of patients, 5 patients with HRS before and after orthotopic liver transplantation (OLT), 10 patients without HRS undergoing OLT, 20 patients with chronic renal failure but without liver disease, and 12 healthy controls. Before OLT, plasma levels of ET-1 were higher in patients with HRS (19.5 +/- 8.6 ng/l, P < 0.001; n = 5) compared to patients without HRS (4.9 +/- 1.1 ng/l; n = 10), normals (1.2 +/- 0.18 ng/l; n = 12), and patients with chronic renal failure (2.4 +/- 0.4 ng/l; n = 20). Patients with HRS compared to patients without HRS had higher levels for creatinine (2.42 +/- 0.6 vs. 0.89 +/- 0.05 mg/dl, P < 0.05), creatinine clearance (107 +/- 9 ml/min vs. 44.6 +/- 5.5 ml/ min, P < 0.001), and bilirubin (11.4 +/- 3.8 vs. 3.7 +/- 1 mg/dl, P < 0.05) before OLT. Within one week after OLT, there was a rapid decrease in ET-1 levels in patients with HRS while creatinine and bilirubin levels decreased slower. Regression analysis revealed a weak correlation between serum creatinine and ET-1 (r = 0.192, P = 0.04) and a significant correlation between serum bilirubin and ET-1 (r = 0.395, P < 0.001). The means of the ET-1 levels decreases rapidly with improvement of liver function after OLT. Levels of ET-1 correlate with excretory liver function assessed by bilirubin. The fall in ET-1 levels preceding improvement of renal function further strengthens the concept of ET-1 being a causative factor in HRS.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11052272&dopt=Abstract

Vaccine. 2003 May 16;21(17-18):1862-6.
Evaluation of endotoxin content of diphtheria-tetanus-acellular pertussis combined (DTaP) vaccines that interfere with the bacterial endotoxin test.

Ochiai M, Kataoka M, Toyoizumi H, Kamachi K, Yamamoto A, Horiuchi Y.

Department of Bacterial Pathogenesis and Infection Control, National Institute of Infectious Diseases, 4-7-1 Gakuen, Musashimurayama, 208-0011, Tokyo, Japan

Applicability of the endotoxin test to diphtheria-tetanus-acellular pertussis combined (DTaP) vaccines was examined. We found some DTaP vaccines that strongly interfered with Limulus amoebocyte lysate (LAL) activity of endotoxin without affecting lethal activity of endotoxin in D-galactosamine-treated mice. LAL activity that was interfered in such vaccines increased apparently after the treatment with phosphate buffer at 4 degrees C for a week. The DTaP vaccines that interfered with the endotoxin test showed no significant effect on endotoxin activity in inducing tumor necrosis factor-alpha (TNF-alpha) in rabbit peripheral blood. The in vitro TNF-alpha induction assay was, therefore, suggested to be an appropriate assay method for the quantitative detection of the endotoxin activity in DTaP vaccines.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12706670&dopt=Abstract [PubMed - in process]

Dig Dis Sci. 2000 Sep;45(9):1774-80.
Cytoskeletal rearrangements induced by Helicobacter pylori strains in epithelial cell culture: possible role of the cytotoxin.

Ashorn M, Cantet F, Mayo K, Megraud F.

Laboratoire de Bacteriologie, Universite Victor Segalen Bordeaux II, France.

The relationship between Helicobacter pylori adherence, cytotoxin production, and modification of the cytoskeletal structure was investigated by studying the effects of 12 H. pylori strains cocultured with Hep-2 epithelial cells. Bacterial strains were isolated from patients with peptic ulcer disease or nonulcer dyspepsia. Presence of the cag pathogenicity island and vacA subtypes of the strains were determined as was the production of vacuolating cytotoxin. We found that cytoskeletal rearrangements, as observed by confocal microscopy after double staining of the bacteria and the cell actin with Texas red and fluorescein-conjugated phalloidin, respectively, occurred essentially when the strains were cytotoxin producers and that the supernatants alone could also lead to these modifications.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11052319&dopt=Abstract

Dig Dis Sci. 2000 Sep;45(9):1820-7.
Experimental ulcerative colitis impairs antioxidant defense system in rat intestine.

Nieto N, Torres MI, Fernandez MI, Giron MD, Rios A, Suarez MD, Gil A.

Department of Biochemistry, University of Granada, Spain.

Increasing attention has been given recently to the role of free radicals in the pathogenesis of ulcerative colitis, since the inflamed intestine is exposed to oxidative stress generated by infiltrating macrophages and neutrophils within the lamina propia. The overall goal of this study was to evaluate whether experimental ulcerative colitis induces significant changes in the antioxidant defense system in an experimental model induced by the intrarectal administration of 2,4,6-trinitrobenzenesulfonic acid. Twenty rats were treated with 80 mg/kg body weight of trinitrobenzenesulfonic acid and 20 with the same volume of 0.9% NaCl. Rats were killed at one and two weeks after treatment to evaluate colon damage by light and electron transmission microscopy. The degree of tissue injury and inflammation was determined by measuring alkaline phosphatase, gamma-glutamyltranspeptidase, and myeloperoxidase activities and prostaglandin E2 and leukotriene B4. Glutathione levels and the activity of the enzymes of the antioxidant defense system were determined. Enzymatic markers of colon injury showed higher activities in rats with ulcerative colitis. Concentrations of prostaglandin E2 and leukotriene B4 were higher in the groups treated for one week with trinitrobenzenesulfonic acid and markers decreased after two weeks of treatment. All antioxidant enzyme activities were higher at one and two weeks after treatment; however, a significant decrease in total glutathione content was also observed. In conclusion, ulcerative colitis induced by trinitrobenzenesulfonic acid damages the intestinal mucosa and is accompanied by a shift in the antioxidant enzyme activities, and low levels of glutathione. This deficiency in glutathione could be a target for new therapies to treat ulcerative colitis.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11052326&dopt=Abstract

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