Drugs online research references
Dig Dis Sci. 2001 Mar;46(3):581-6.
Peptic ulcer occurrence in follow-up of chronic gastritis in patients with treated and not eradicated CagA-positive Helicobacter pylori infection.
Carratu R, Iuliano D, Iovene MR, Ferraraccio F, Esposito P, Russo MI, Montella F, Abbate G, Tufano MA.
Microbiology Institute, Second University of Naples, Italy.
The aim of the present prospective investigation was to study 49 dyspeptic Helicobacter pylori (HP)-positive (HP+) or -negative (HP), CagA+ and CagA- patients with a normal pattern or pure chronic gastritis at initial histology as well as normal features or hyperemic gastropathy at initial endoscopy in a two-year follow up. All the HP+ patients were treated with omeprazole 20 mg twice a day plus amoxicillin 1 g twice a day for two weeks. No substantial change was seen in gastritis in CagA+ patients in whom the infection was not eradicated, and, in contrast, a progressive improvement in 13/14 successfully treated patients was found. At endoscopy, a progressive change to a normal picture was seen in 8 and no change in 6 of 14 patients whose HP infection was eradicated, in contrast a worsening in the 9 HP+ patients who were still infected was observed. In particular, peptic lesions arose in 6 of 21 CagA+ patients in whom the infection was not eradicated. In conclusions, the lack of change in chronic gastritis at histology and the progressive worsening of endoscopic hyperemic gastropathy (with peptic lesions arising in 28,6%) when HP+ CagA+ infection is not eradicated, unlike the progressive improvement of the anatomoclinical condition in the patients whose infection was eradicated, draws attention to the relevance of eradicating HP in CagA+ patients even when no peptic lesion is found at initial endoscopy.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11318536&dopt=Abstract
Enzyme Microb Technol. 2000 Nov 1;27(8):576-582.
Course of pH during the formation of amoxicillin by a suspension-to-suspension reaction.
Diender MB, Straathof AJ, van der Does T, Zomerdijk M, Heijnen JJ.
Delft University of Technology, Kluyver Laboratory for Biotechnology, Julianalaan 67, NL-2628 BC, Delft, The Netherlands
Amoxicillin can be produced in an enzymatic suspension-to-suspension reaction in which the substrate(s) and product(s) are mainly present as solid particles, while the reaction takes place in the liquid phase. During these suspension-to-suspension reactions different subprocesses take place, such as dissolution/crystallization of substrates and products, enzymatic synthesis of the product(s), and undesired enzymatic hydrolysis of substrates and/or products. All these subprocesses are influenced by pH and also influence the pH because the reactants are weak electrolytes. This paper describes a quantitative model for predicting pH and concentrations of reactants during suspension-to-suspension reactions. The model is based on mass and charge balances, pH-dependent solubilities of the reactants, and enzyme kinetics. For the validation of this model, the kinetically controlled synthesis of amoxicillin from 6-aminopenicillanic acid and D-(p)hydroxyphenylglycine methyl ester was studied. The pH and the dissolved concentrations took a very different course at different initial substrate amounts. This was described quite reasonably by the model. Therefore, the model can be used as a tool to optimize suspension-to-suspension reactions of weak electrolytes.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11024520&dopt=Abstract [PubMed - as supplied by publisher]
Antimicrob Agents Chemother. 2001 Jan;45(1):196-202.
Effects of amoxicillin, gentamicin, and moxifloxacin on the hemolytic activity of Staphylococcus aureus in vitro and in vivo.
Worlitzsch D, Kaygin H, Steinhuber A, Dalhoff A, Botzenhart K, Doring G.
Institute of General and Environmental Hygiene, Faculty of Medicine, University of Tubingen, Tubingen, Germany.
In Staphylococcus aureus infection hemolysis caused by the extracellular protein alpha-toxin encoded by hla is thought to contribute significantly to its multifactorial virulence. In vitro, subinhibitory concentrations of beta-lactam antibiotics and fluoroquinolones increase the levels of hla and alpha-toxin expression, whereas aminoglycosides decrease the levels of hla and alpha-toxin expression. In the present study we investigated the effects of subinhibitory concentrations of amoxicillin, gentamicin, and moxifloxacin on hla and alpha-toxin expression and total hemolysis of S. aureus strain 8325-4, a high-level alpha-toxin producer, and its alpha-toxin-negative mutant, DU 1090, in vitro and in a rat model of chronic S. aureus infection. The levels of expression of hla and alpha-toxin and total hemolysis did not differ significantly when amoxicillin, gentamicin, or moxifloxacin was added to cultures of S. aureus strain 8325-4. In vivo, strain 8325-4 induced a significantly increased level of hemolysis in infected pouches compared to that in uninfected control pouches, but the hemolysis was reduced to control levels by treatment with doses of amoxicillin, gentamicin, or moxifloxacin that reduced bacterial numbers by 2 orders of magnitude. Additionally, the effects of subinhibitory concentrations of the three antibiotics on total hemolysis of four methicillin-resistant S. aureus and three methicillin-sensitive S. aureus (MSSA) clinical isolates were assessed in vitro. A significant increase in total hemolysis was observed for only one MSSA strain when it was treated with amoxicillin but not when it was treated with moxifloxacin or gentamicin. When purified alpha-toxin was incubated with purified human neutrophil elastase, alpha-toxin was cleaved nearly completely. The results suggest that the penicillin-induced increases in S. aureus alpha-toxin expression are strain dependent, that reduction of bacterial numbers in vivo counteracts this phenomenon effectively, and finally, that in localized S. aureus infections alpha-toxin activity is controlled by neutrophil elastase.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11120965&dopt=Abstract
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