Drugs online research references
Eur J Pharmacol. 2002 May 3;442(1-2):125-35.
Chronic gastric ulcer healing in rats subjected to selective and non-selective cyclooxygenase-2 inhibitors.
Berenguer B, Alarcon de la Lastra C, Moreno FJ, Martin MJ.
Department of Pharmacology, Faculty of Pharmacy, University of Sevilla, Profesor Garcia Gonzalez Street, Seville, Spain.
The influence of different nonsteroidal anti-inflammatory drugs (NSAIDs) and of a proton pump inhibitor on the healing parameters of a chronic gastric ulcer was evaluated. Wistar rats were used after the induction of a chronic acetic acid ulcer. The animals were treated orally for 8 and 15 days, twice daily, with the conventional NSAID, piroxicam (0.35 mg/kg), the non-narcotic analgesic, metamizol (33 mg/kg), the selective cyclooxygenase-2 inhibitor, celecoxib (1.8 mg/kg) and the proton pump inhibitor, omeprazole (0.35 mg/kg). Macroscopic ulcer index, myeloperoxidase activity and prostaglandin E(2) content (both biochemical parameters were evaluated in ulcerated and in intact tissue) as well as histological and immunohistochemical evaluations were carried out at 8 and 15 days. Omeprazole accelerated ulcer healing at 8 and 15 days (P<0.05), while celecoxib delayed healing significantly at 15 days (P<0.01). At 8 days, the prostaglandin E2 content decreased with all NSAIDs at the ulcer site as well as in intact tissue. The same happened at 15 days except for celecoxib, which only diminished prostaglandins in intact mucosa. Immunohistochemistry showed differences in the location of cyclooxygenase-2 and -1. The highest cyclooxygenase-2 expression was found with piroxicam and the lowest expression was with celecoxib. CONCLUSIONS: Down-regulation of cyclooxygenase-2 expression as well as a possible involvement of the chemical structure of celecoxib, a 1,5-dirarylpirazole with a sulphonamide moiety, may account for the delay in ulcer healing.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12020690&dopt=Abstract
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orl.am.wroc.pl
Although the association between gastroesophageal reflux disease (GERD) and laryngeal disorders in adults is well established there is still a lack of information concerning the true extent of the laryngeal complications of GERD in children. The aim of this study was to determine the laryngeal status of children with diagnosed GERD. We sought to identify the initial appearance of their larynges and then to determine the clinical response to antireflux therapy. GERD was recognized in 90/100 children examined. Using 24-h pH monitoring we found that most of the patients experienced episodes of gastroesophageal reflux during the daytime when they were in an upright position. The hallmark of GERD affecting the larynx in our group was posterior laryngitis, which is characterized by erythema of the mucous membrane overlying the arytenoid cartilages and the posterior mucosal wall of the glottis. The findings regarding the effectiveness of therapy were that, in children with severe laryngeal alterations, voice quality improved significantly after 12 weeks of antireflux treatment (p < 0.001) and laryngeal status was significantly better after 6 weeks of treatment (p < 0.001). This study provides evidence that gastroesophageal reflux in children is the underlying cause of inflammatory and morphological lesions, and that antireflux treatment is effective in reducing or eliminating these lesions.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12030580&dopt=Abstract
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snh.go.jp
Helicobacter pylori (HP) infection is known to induce the specific immune response in the gastric mucosa. The immune response is triggered by presentation of antigen peptides on the major histocompatibility assembly of the antigen-presenting cells (APC) with the assistance of costimulatory molecules such as B7-1 (CD80) and B7-2 (CD86). Their counter-receptors or ligands on T cells are CD28 or cytotoxic lymphocyte-associated molecule-4. The aim of the present study was to clarify the localization of APC and their relation with T cells in HP-infected human gastric mucosa. Our findings suggest that the macrophages in the lamina propria may mainly act as APC in the HP-infected gastric mucosa, and the triggered immune response might be involved in the mucosal immune response in the inflamed gastric mucosa to invasive antigens related to HP organisms.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12031081&dopt=Abstract
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