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Preparation and characterization of active site protected poly(ethylene glycol)-avidin bioconjugates.
Biochim Biophys Acta
October 2005
Department of Pharmaceutical Sciences, University of Padova, Via F. Marzolo 5, 35131 Padova, Italy.
Avidin was modified with poly(ethylene glycol) in the presence of a biotin binding site protective agent synthesised by imminobiotin conjugation to branched 20 kDa PEG. Avidin was incubated with imminobiotin-PEG and reacted with high amounts of 5, 10 or 20 kDa PEG to modify the protein amino groups. Circular dichroism demonstrated that the extensive PEGylation does not alter the protein conformational structure.
View Article and Find Full Text PDFA comparative overview of the adverse effects of antiulcer drugs.
Drug Saf
February 1995
University of Sydney, New South Wales, Australia.
During the past 2 decades, great advances have been made in the treatment of ulcer disease. This has involved the development of new drugs that are not only well tolerated, but are relatively inexpensive. The lack of significant adverse effects has revealed a degree of tolerability that, to write a review of the adverse effects, poses a difficult task.
View Article and Find Full Text PDFFasciculin inhibition of acetylcholinesterase is prevented by chemical modification of the enzyme at a peripheral site.
Biochim Biophys Acta
December 1994
Instituto de Investigaciones Biológicas Clemente Estable, Montevideo, Uruguay.
Fasciculin 2 (FAS) is a 61 amino acid peptide present in Dendroaspis angusticeps snake venom, with a selective and potent inhibitory activity towards acetylcholinesterase (AChE). The specific interaction of FAS with peripheral sites present in Electrophorus electricus AChE (Ki = 0.04 nM FAS) was investigated by chemical modification with N,N-dimethyl-2-phenylaziridinium (DPA) in the presence of active or peripheral anionic site protective agents.
View Article and Find Full Text PDFTopically active agents (i.e., colloidal bismuth subcitrate and sucralfate) have proved to be effective in promoting the healing of both gastric and duodenal ulcers and in relieving ulcer symptoms.
View Article and Find Full Text PDF[No acid, no ulcer: such a simple axiom?].
An Med Interna
September 1991
Divisione di Gastroenterologia, Ospedale Generale Regionale, Bolzano, Italia.
According to the traditional view gastric acid and pepsin are a sine qua non for ulcer development. Acid suppression, however, is far from being the only successful therapeutic approach, and similar healing rates are achieved by drugs with substantially different mechanisms of action--antacids, H2-antagonists, antimuscarinics, cytoprotective and site-protective agents--thus denoting a multifactorial pathogenesis. Even with the antisecretory compounds, the relationship between gastric acid and ulcer healing gives rise to perplexity: antacids prove effective at widely varying doses; pirenzipine and H2-blockers, which are clinically equieffective, differ considerably in antisecretory efficacy; H2-antagonist studies on early vs late postprandial dosing yield contradictory clinical results; morning and bedtime single administrations of H2-antagonists prove equiactive on ulcer healing, leading to a reappraisal of the alleged importance of nocturnal acidity.
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