Drugs online research references
Acta Biochim Pol. 1995;42(4):481-96.
Targeting the fungal plasma membrane proton pump.
Monk BC, Mason AB, Kardos TB, Perlin DS.
Department of Oral Biology and Oral Pathology, University of Otago, Dunedin, New Zealand.
The need for new mechanistic classes of broad spectrum antifungal agents has prompted development of the membrane sector and ectodomain of the plasma membrane proton pumping ATPase as an antifungal target. The fungal proton pump is a highly abundant, essential enzyme in Saccharomyces cerevisiae. It belongs to the family of P-type ATPases, a class of enzymes that includes the Na+,K(+)-ATPase and the gastric H+,K(+)-ATPase. These enzymes are cell surface therapeutic targets for the cardiac glycosides and several anti-ulcer drugs, respectively. The effects of acid-activated omeprazole show that extensive inhibition of the S. cerevisiae ATPase is fungicidal. Fungal proton pumps possess elements within their transmembrane loops that distinguish them from other P-type ATPases. These loops, such as the conformationally sensitive transmembrane loop 1+2, can attenuate the activity of the enzyme. Expression in S. cerevisiae of fully functional chimeric ATPases that contain a foreign target comprising transmembrane loops 1+2 and/or 3+4 from the fungal pathogen Candida albicans suggests that these loops operate as a domain. The chimera containing C. albicans transmembrane loops 1+2 and 3+4 provides a prototype for mutational analysis of the target region and the screening of inhibitors directed against opportunistic fungal pathogens. Panels of mutants with modified ATPase regulation or with altered cell surface cysteine residues are also described. Information about the ATPase membrane sector and ectodomain has been integrated into a model of this region.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8852338&dopt=Abstract
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Gut. 1998 Dec;43(6):747-51.
Eradication of Barrett's mucosa with argon plasma coagulation and acid suppression: immediate and mid term results.
Van Laethem JL, Cremer M, Peny MO, Delhaye M, Deviere J.
Department of Gastroenterology, Erasme University Hospital, Brussels, Belgium.
BACKGROUND: Intestinal metaplastic mucosa in Barrett's oesophagus can be replaced by squamous epithelium after mucosal thermal ablation associated with acid suppression therapy. AIMS: To assess whether restoration of squamous epithelium can be obtained after ablation of Barrett's oesophagus using argon plasma coagulation (APC) associated with proton pump inhibitor (PPI) therapy. METHODS: Thirty one patients with Barrett's oesophagus received APC. Omeprazole (40 mg/day) was given from the first APC application to one month after completion of the treatment, then given symptomatically. Twenty four hour pH-metry was performed during endotherapy. RESULTS: Complete re-epithelialisation was visualised at endoscopy in 25/31 patients (81%) after a mean number of 2.4 APC sessions (range 1-4). Only partial squamous re-epithelialisation was observed in three patients and three others had no eradication. At histological assessment, eradication of Barrett's oesophagus was only confirmed in 19/31 patients (61%) due to the presence of a few residual Barrett's glands under the new squamous epithelium. Complete eradication was related to a Barrett's oesophagus segment length of less than 4 cm and the absence of circumferential extension but not to the normalisation of oesophageal acid exposure under PPI therapy. Seventeen patients with apparently complete endoscopic and histological eradication of Barrett's oesophagus were re-evaluated at one year; eight (47%) disclosed relapsing islands of Barrett metaplasia despite continuous omeprazole therapy (10-40 mg/day). CONCLUSIONS: APC combined with 40 mg omeprazole daily can eradicate Barrett's mucosa with apparent squamous re-epithelialisation in the majority of patients even in the absence of normalisation of oesophageal acid exposure. However, one year after endotherapy for Barrett's oesophagus, relapse is frequent but limited in extent.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9824599&dopt=Abstract
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Digestion. 1986;35 Suppl 1:98-105.
Alterations in gastric mucosal morphology induced by long-term treatment with omeprazole in rats.
Blom H.
The effects of long-term treatment with omeprazole on the gastric mucosal morphology was studied. Eighty male Sprague-Dawley rats were used and divided into 4 equal groups. Half of the animals in 3 of the groups were given omeprazole, 40 mumol/kg body weight, orally once daily for 130 days. The remaining rats in these groups served as controls. Half of the rats in the fourth group were given subcutaneous injections with pentagastrin, this group received vehicle only. At the end of the treatment period, all animals were killed by vascular perfusion with fixative and the gastric corpus mucosae prepared for light and electron microscopy. Quantitative morphometry was used to evaluate eventual effects of treatment on the different epithelial cell types which are present in the corpus mucosa. Omeprazole treatment resulted in an increased mucosal thickness as a result of a proportional increase in all types of epithelial cells with the exception of the endocrine cells. These cells increased in number by 100%. A similar increase was seen after pentagastrin treatment. In the omeprazole-treated rats, there was also an increase in the size and number of pepsinogen granules within the zymogen cells. All changes in gastric mucosal morphology seen after 130 days of treatment with omeprazole turned out to be reversible and were not seen after a recovery period of 3 months.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3792675&dopt=Abstract
note: kwd match prilosec online literature
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