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Pathol Biol (Paris). 1982 Jun;30(6 Pt 2):543-8.
[Haemagglutinins and adhesins of Escherichia coli strains isolated from urine: inhibitory effect of sub-inhibitory concentrations of tetracycline, doxycycline and minocycline. Preliminary results ]

[Article in French]

Chabanon G, Archambaud M, Marty N, Enjalbert L.

The present work concerned the study of the sub-minimal inhibitory doses of tetracyclin, doxycyclin and minocyclin on both hemagglutinating activity and adhesion capacity demonstrated in three E. coli strains isolated from urine. Two different types of hemagglutinins, mannose-resistant (HAMR) and mannose-sensitive (HAMS), were associated in two strains; HAMR was present in the third strain. Adhesion capacity was detected, in vitro, with uroepithelial cells spontaneously eliminated in urine. Whatever the antibiotic used, HAMR titers clearly decreased. In contrast, the effect of these antibiotics on the HAMS titers was inconstant, according to the bacterial strain or the antibiotic used. Adhesion capacity was inhibited particularly in the presence of tetracyclin and doxycyclin. Minocyclin was not a very good inhibitor molecule. The analysis of coefficient of correlation showed that the ability of adhering to uroepithelial cells was related to the HA titers. But it is impossible to say if the same bacterial structure migt be considered as mediator for both HA and adhesion capacity.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6750523&dopt=Abstract




J Periodontol. 1982 Sep;53(9):557-61.
The effect of short-term administration of minocycline HCl on gingival inflammation and subgingival microflora.

Ciancio SG, Slots J, Reynolds HS, Zambon JJ, McKenna JD.

The purpose of this investigation was to determine the efficacy of minocycline hydrochloride in the management of subgingival microorganisms and periodontal disease. In a double-blind, split-mouth study, minocycline or placebo was administered systemically for 7 days to 26 adults with moderate-to-serve periodontitis. Four study groups were examined: (i) minocycline-scaled, (ii) minocycline-unscaled, (iii) placebo-scaled, and (iv) placebo-unscaled. The minocycline-scaled group responded most favorably, with improved gingival health for at least 49 days and with marked reductions in total bacterial counts and proportions of spirochetes for at least 70 days (termination of the study). Minocycline administration with no periodontal scaling and root planing also resulted major, long-lasting shifts in the subgingival microflora. Scaling alone was least effective in changing the microflora. The data indicated that minocycline may be a useful adjunct in the treatment of periodontal disease. Further studies are needed, however, to determine the long-term effect of minocycline therapy on the periodontal attachment level.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6752371&dopt=Abstract




Antimicrob Agents Chemother. 1982 Nov;22(5):791-9.
Transport of the lipophilic analog minocycline differs from that of tetracycline in susceptible and resistant Escherichia coli strains.

McMurry LM, Cullinane JC, Levy SB.

Plasmids which specify resistance to tetracycline offer much less resistance to its more lipophilic analog, minocycline. Resistance to minocycline varies for different plasmids. In the case of plasmid R222 (bearing the class B tetracycline resistance determinant on Tn10), minocycline resistance is comparatively high (10 microgram/ml, or 6% of the tetracycline resistance level). For plasmid pIP7 (bearing the class A determinant), minocycline resistance is only 1% of the tetracycline resistance level. To understand the basis for these differences, we compared the transport of the two tetracyclines by susceptible cells and by resistant cells. Uptake of minocycline by susceptible cells was 10 to 20 times more rapid than uptake of tetracycline and occurred largely via an energy-dependent route. This host-mediated energy-dependent uptake of both analogs was still present in tetracycline-resistant cells. In resistant cells, the same plasmid-mediated active efflux system previously described for tetracycline also exported minocycline. The 15-fold greater susceptibility of tetracycline-resistant R222-bearing cells to minocycline as compared with tetracycline could be explained at least in part by the more rapid influx of minocycline, which more easily overcame the efflux system. The particularly low minocycline resistance offered by pIP7 was due to a weak efflux for minocycline, 10-fold less effective than that mediated by R222. The rate-limiting step for uptake of both analogs appeared to be the outer membrane. That the lipophilic minocycline should cross this membrane more rapidly than tetracycline stands in contrast with other studies which show the outer membrane to be a barrier for entry of lipophilic substances.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6758689&dopt=Abstract













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