Drugs online research references
Helicobacter. 2001 Jun;6(2):125-9.
Inhibitory action of a novel proton pump inhibitor, rabeprazole, and its thioether derivative against the growth and motility of clarithromycin-resistant Helicobacter pylori.
Ohara T, Goshi S, Taneike I, Tamura Y, Zhang HM, Yamamoto T.
Department of Bacteriology, School of Medicine, Niigata University, Niigata, Japan.
BACKGROUND: Clarithromycin-resistant Helicobacter pylori (CRHP) has increasingly been isolated from patients in Japan. The aim of our study was to test whether proton pump inhibitors (PPIs) and their thioether derivatives, which are secreted into the gastric mucosa, could inhibit the growth and motility (a factor in colonization) of CRHP. MATERIALS AND METHODS: CRHP was isolated from patients who had experienced gastritis or peptic ulcers in Tokyo and Niigata. Drugs and related agents tested were omeprazole, lansoprazole, rabeprazole, the thioether derivative of rabeprazole (rabeprazole-TH), clarithromycin, amoxicillin and metronidazole. The MICs of the drugs and agents for H. pylori strains were determined by the agar dilution METHOD: Bacterial swimming in a liquid layer was examined under an inverted, phase-contrast microscope. RESULTS: The PPIs and rabeprazole-TH, but not the anti-H. pylori agents, inhibited the motility of CRHP at both pH 7.4 and 6.0. The concentrations (microg/ml) necessary to inhibit 50% of the motility at pH 7.4 were 0.25-0.5, 8-32, 8-16 and 128-256 for rabeprazole-TH, rabeprazole, lansoprazole and omeprazole, respectively. Rabeprazole-TH exhibited the strongest inhibitory effect against the growth of CRPH (MIC, 0.5 microg/ml). CONCLUSION: Rabeprazole-TH, which is secreted into the gastric mucosa, had the strongest inhibitory action against both the growth and motility of CRHP, suggesting that it is a potential novel agent for CRHP eradication.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11422467&dopt=Abstract
knusun.kangnung.ac.kr
Amoxicillin is one of the most frequently recommended antibiotics for prophylaxis of infective endocarditis in dental/oral procedures. In this study, the postantibiotic effect (PAE), postantibiotic sub-MIC (PASME) and sub-MIC effect (SME) of amoxicillin on oral streptococci, Streptococcus gordonii and Streptococcus sanguis, which are two of the major etiological agents in infective endocarditis, were investigated. The PAE was induced by 10 x MIC of amoxicillin for 2 h and the antibiotic was eliminated by washing. The PASMEs were studied by addition of 0.1, 0.2 and 0.3 x MICs during the postantibiotic phase of the bacteria, and the SMEs were studied by exposing bacteria to amoxicillin at the sub-MICs only. The PAE of amoxicillin was 2.0 h with S. gordonii DL1 and 0.7 h with S. sanguis MPC1. The PASME and SME of amoxicillin were observed both for S. gordonii DL1 and for S. sanguis MPC1. However, the durations of effects for S. sanguis MPC1 were shorter than those for S. gordonii DL1. The PASME values for both strains increased as the concentration of amoxicillin increased. The PASME values for both strains were substantially longer than the SME values. The present study illustrates the existence of PAE, PASME and SME for amoxicillin against S. gordonii and S. sanguis, thereby extending the pharmacodynamic advantages of amoxicillin for these bacteria in the prophylaxis procedures of infective endocarditis.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11128556&dopt=Abstract
J Invest Dermatol. 2000 Oct;115(4):647-52.
T cells isolated from positive epicutaneous test reactions to amoxicillin and ceftriaxone are drug specific and cytotoxic.
Yawalkar N, Hari Y, Frutig K, Egli F, Wendland T, Braathen LR, Pichler WJ.
Clinic of Rheumatology and Clinical Immunology/Allergology, Inselspital, Bern, Switzerland.
In order to investigate the function of T cells in cutaneous adverse drug reactions, skin-derived T cells were analyzed in two patients with a drug-induced exanthem. Skin biopsy specimens were obtained from positive epicutaneous test reactions to amoxicillin and ceftriaxone. Immunohistochemical analysis revealed that the majority of the cell infiltrate in both biopsy specimens was composed of activated T cells, of which some expressed perforin. By limiting dilution 36 amoxicillin-specific and 10 ceftriaxone-specific T cell clones were raised. All of these T cell clones expressed CD4/T cell receptor alphabeta. Cytokine analysis after antigen stimulation of the seven best proliferating T cell clones (four specific for amoxicillin and three for ceftriaxone) revealed that these cells secrete high amounts of interleukin-5 and mostly lower or no amounts of tumor necrosis factor alpha, interleukin-4, and interferon-gamma. A part of these CD4+ T cell clones were cytotoxic, i.e., two selected ceftriaxone-specific T cell clones killed target cells after antigen stimulation. The amoxicillin-specific T cell clones failed to show drug-specific cytotoxicity, but killed target cells in the presence of concanavalin A, indicating a principal ability to be cytolytic. In correlation with the in situ expression of perforin on T cells, the ceftriaxone-specific T cell clones also expressed perforin in vitro. In conclusion, a substantial part of the T cells in drug-induced epicutaneous test reactions are drug specific and are composed of a heterogeneous cell population. Drug-specific T cells producing interleukin-5 may contribute to eosinophilia, whereas cytotoxic CD4+ T cells may account for tissue damage. These data underline the role of T cells in delayed-type cutaneous adverse drug eruptions and drug-induced epicutaneous test reactions.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10998137&dopt=Abstract
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