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G Satta

Publications and source records attributed to G Satta.

144 records · Page 8Linked to original sources
PubMedDate not supplied

Evaluation of in vitro antimicrobial activity of lomefloxacin against staphylococci, enterococci, Enterobacteriaceae, and Pseudomonas aeruginosa.

In vitro antimicrobial activity of lomefloxacin and other antibiotics (norfloxacin, beta-lactams, cotrimoxazole, netilmicin, and miokamycin) was evaluated against 317 clinical isolates including Staphylococcus aureus, enterococci, Enterobacteriaceae, and Pseudomonas aeruginosa. Lomefloxacin showed a high in vitro activity against a wide variety of bacterial species. Against Enterobacteriaceae, lomefloxacin displayed the highest activity (MIC90S, less than or equal to 1 microgram/ml), and it was usually more active than ampicillin and netilmicin, and often more active than cotrimoxazole. Lomefloxacin showed a good antimicrobial activity also against both methicillin-susceptible and methicillin-resistant S. aureus, as it was able to inhibit 90% of staphylococcal strains at a concentration less than or equal to 2 micrograms/ml. Against enterococci and P. aeruginosa, lomefloxacin was usually less active (MIC90S, 8 micrograms/ml). As compared to norfloxacin, lomefloxacin displayed an overall similar activity against staphylococci and enterococci, but appeared less active against Gram-negative bacteria. Bactericidal activity of lomefloxacin against E. coli, when assayed by a novel method, proved to be high, and results indicate that an oral dose of 200 mg of lomefloxacin should exert a very high bactericidal activity against E. coli in urinary tract infections, even in those sustained by large bacterial populations.

4-Quinolones↗
PubMedDate not supplied

Interactions between lateral wall elongation and septum formation during cell cycle in Klebsiella pneumoniae.

In this study, we evaluated the effect of three different beta-lactams on peptidoglycan synthesis and cell division of synchronously growing rods of the pH conditional morphology mutant MirM7 and its parental strain MirA12. We have found that mecillinam, when added at varying times to synchronous MirM7 rods during the first 30 min of the cell cycle, inhibits peptidoglycan synthesis but has no effect when added afterwards while cells form septa and divide. Addition to the above cells of piperacillin for 30 min from the very beginning of the cell cycle did not cause any delay in cell division. On the contrary, when this antibiotic was added to synchronous cells for 15 min, starting 35 min after the beginning of the cell cycle, cell division occurred with an approximate 15-min delay. Addition of cefaloridine to synchronous cells at varying times during the cell cycle invariably caused a delay in cell division equal to the time during which the antibiotic was maintained in the culture. These findings are interpreted as supporting a previous hypothesis for shape regulation in bacterial rods and are discussed in terms of the interaction between lateral wall elongation and septum formation during the cell cycle.

Amdinocillin↗
PubMedDate not supplied

Comparative effects of L-methionine, S-adenosyl-L-methionine and 5'-methylthioadenosine on the growth of preneoplastic lesions and DNA methylation in rat liver during the early stages of hepatocarcinogenesis.

Male Wistar rats, initiated with diethylnitrosamine (DENA), were subjected to a selection treatment, according to the "resistant hepatocyte" model, followed or not followed by phenobarbital (PB). Rats received, for 3 weeks after selection, 4 i.m. doses (96 mmol/kg) of L-methionine, S-adenosyl-L-methionine (SAM), or 5'-methylthioadenosine (MTA), a SAM catabolite formed during polyamine synthesis or by spontaneous splitting of SAM at physiologic temperature and pH. They were then killed. In some rats, SAM and MTA treatments were started 20 weeks after initiation. The animals were killed 3 weeks later and persistent (neoplastic) nodules (PN) were collected. Some rat groups received 1/2 and 1/4 of the above SAM and MTA doses, or 1/8 of the above MTA dose. SAM and MTA, but not methionine, caused a dose-dependent decrease in number and surface area of gamma-glutamyltranspeptidase (GGT)-positive foci, and in labeling index (LI) of focal cells, coupled with remodeling. SAM and MTA liver contents, SAM/S-adenosylhomocysteine (SAH) ratio and overall methylation of liver DNA were low during the development of GGT-positive foci. SAM, but not methionine, caused a dose-dependent recovery of SAM content and DNA methylation, and a partial reconstitution of liver MTA pool. Exogenous MTA only induced the reconstitution of MTA pool, without affecting SAM level and DNA methylation. Recovery of SAM and MTA pool and DNA methylation was found in the rats subjected to SAM plus MTA, indicating the absence of inhibition of DNA methyltransferases in vivo by MTA. MTA also inhibited liver reparative growth in partially hepatectomized rats, without modifying SAM content and DNA methylation of regenerating liver (RL). A high activity of ornithine decarboxylase (ODC) was found in the liver, during the development of preneoplastic foci, and in PN. This activity was inhibited by SAM and MTA treatments. Although MTA was more effective than SAM, the decrease in ODC activity was coupled with a larger fall in DNA synthesis in SAM-treated than in MTA-treated rats. Thus the antipromotion effect of SAM could not merely depend on its (spontaneous) transformation into MTA. Although MTA production may play a role in the SAM antipromotion effect, other mechanisms could be involved. A role of DNA methylation in the inhibition of growth by SAM is suggested. MTA is a potential chemopreventive agent for liver carcinogenesis.

Adenosine↗