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J Duval

Publications and source records attributed to J Duval.

At least 127 records · Page 7Linked to original sources

In vitro [3H]-erythromycin binding to Staphylococcus aureus.

Characteristics of erythromycin binding to Staphylococcus aureus were determined by using kinetics and equilibrium binding experiments. Both methods yielded identical values of the dissociation constant, i.e. 0.1 muM. This value was in accord with that found with a bacterial extract of ribosomes which are the organelles where erythromycin exerts its action. This good agreement shows that the dissociation constant of erythromycin determined with intact bacteria is a good reflect of specific bacterial receptors of macrolides, i.e. ribosomes. In addition, mechanism of uptake of the antibiotic by Staphylococcus aureus was investigated. Passive diffusion process was shown to be mainly responsible for this phenomenon.

Erythromycin↗

Antiestrogen binding within different pituitary cell populations. Comparison with androgen and estrogen receptors.

Gonadotrope-enriched populations were prepared from 42-day old male rats by centrifugal elutriation. They contained 4.8 +/- 0.7% of the cells, 51 +/- 10% of the LH and less than 3% of the PRL (n = 4). Gonadotrope-depleted fractions were also obtained that contained most of PRL cells. Specific antiestrogen binding sites (AEBS) were quantitated in these populations after destruction of estrogen receptor. Results showed the presence of a distinct, specific high affinity binding site for antiestrogen in dispersed pituitary cells and in enriched fractions. However, AEBS are not specific of a pituitary cell type. Thus, AEBS appear different from estrogen receptors in pituitary gland: by the thermal stability of AEBS, by the localization of AEBS in particulate material, by the uniform distribution of AEBS in different populations which differ markedly for E2 binding sites. Whereas the ratio of binding AE/E2 averaged 11.4 in the initial cell suspension it reached only 2.9 in the gonadotropes. The dissociation constants for AEBS were in the same range (1.16 - 2.27 X 10(-9) M) for the different populations.

Animals↗

LHRH promotes the synthesis and release of a 87,000 Da protein (GP-87) by enriched gonadotrophs.

Protein secretion by cultured pituitary cells from 14-day-old female rats was estimated using [35S]methionine incorporation followed by either one- or two-dimensional electrophoresis and autoradiography. Stimulation of total cells or gonadotrophs by LHRH promoted the synthesis and release of a specific polypeptide (apparent molecular weight 87,000, pI = 4.6). Silver staining of cellular proteins from both gonadotroph-enriched and gonadotroph-depleted populations prepared by centrifugal elutriation revealed a high concentration of this polypeptide in the gonadotrophs and a very low level in the other cell population. This species was thus called Gonadotrope Polypeptide GP-87. Release of labeled GP-87 by gonadotrophs was both time dependent (up to 4 h) and LHRH dose dependent (from 10(-9) M to 10(-7) M) as was the release of LH. Attempts to precipitate GP-87 from the incubation medium with anti-LH antiserum were unsuccessful suggesting that GP-87 is not a 'big' form of LH. TRH neither stimulated the release of GP-87 from gonadotrophs nor from lactotrophs though it did stimulated PRL release. From these data, we conclude that gonadotrophs in culture synthesize a specific polypeptide (GP-87), LHRH stimulates both the synthesis and release of GP-87, and the pituitary cell response is peptide specific. The LHRH-induced synthesis and release of GP-87 could be an important step in the molecular processes that regulate gonadotrophin secretion.

Animals↗

[Multicenter study of the activity of pefloxacin on bacteria isolated in a hospital milieu].

Minimal inhibitory concentrations (MICs) of pefloxacin were evaluated by agar dilution for 3422 bacterial strains isolated in nine hospitals. Enterobacteriaceae proved very sensitive to pefloxacin: 62 p. 100 of 1743 strains tested had MIC less than or equal to 0.12 and 90 p. 100 less than or equal to 1 microgram/ml; but the percent of strains with MIC greater than or equal to 2 varied among the different groups of Enterobacteriaceae: 2.7 p. 100 for E. coli to 39 p. 100 for Serratia. 55 p. 100 for Pseudomonas and 81 p. 100 of Acinetobacter were inhibited by 1 micrograms/ml or less (mode MIC 1 and 0.5 micrograms/ml). Haemophilus sp.: 0.03 and 0.06 micrograms/ml and Gonococci were very sensitive to pefloxacin. The spectrum of pefloxacin extended to Gram positive cocci: MIC of Staphylococci were 0.06 to 8 micrograms/ml (mode MIC: 0.5); Enterococci, other Streptococci and Pneumococci were less sensitive: 2 and 4 micrograms/ml for the majority of strains. Concerning anaerobic bacteria, pefloxacin was more active against Clostridium (0.5 to 1 microgram/ml generally), than against Bacteroides (4 to 16 micrograms/ml).

Bacteria↗

Blood-borne pulmonary infection with Nocardia asteroides in a heroin addict.

Nocardia asteroides frequently causes primary lung infection with possible hematogenous dissemination to various organs, especially in patients with altered immune responses. The preponderance of pulmonary infections suggests an airborne route of contamination. We report a case of pulmonary nocardiosis in a previously healthy intravenous heroin abuser. The clinical and epidemiologic data strongly suggest a paraphernalia blood-borne infection in this patient, a mode of contamination which has not been previously reported.

Adolescent↗

[Effect of LHRH on the synthesis and phosphorylation of proteins in gonadotropic cells].

Protein secretion by cultured pituitary cells from 14 day-old female rats was estimated using [35S]-méthionine incorporation, electrophoresis and autoradiography. Stimulation by LHRH promoted biosynthesis and fast release of a protein of apparent molecular weight 87,000 daltons and pI 4.6. Gonadotrophs enriched by centrifugal elutriation were particularly rich in this polypeptide which was thus called GP-87 (Gonadotrope polypeptide). Cells were then cultured with [32P]-orthophosphate and proteins were analyzed. Our first results tend to show that GP-87 is phosphorylated, at least in the cells. We suggest that this specific protein, the secretion of which is correlated with LH release, participates to the response mechanisms of gonadotrope cells stimulated by LHRH.

Animals↗

[Multicenter study of ofloxacin activity on bacteria isolated from a hospital environment].

Minimal inhibitory concentrations (MICs) of ofloxacin were evaluated by agar dilution for 1508 bacterial strains isolated in five hospitals. For Enterobacteriaceae sensitive to nalidixic acid, MICs ranged from 0.008 to 1 microgram/ml (mode MIC: 0.12); the different species of Enterobacteriaceae exhibited similar mode MICs (0.12) with the exception of E. coli (0.06-0.12), P. mirabilis (0.5) and Providencia (0.25). Among strains intermediate and resistant to nalidixic acid, most of which were Serratia, Providencia and Citrobacter, 41% had a MIC within the susceptibility range, while the others had a MIC of 2 to 8 micrograms/ml, or even 64 micrograms/ml in a few instances. Ofloxacin also exhibited satisfactory activity against P. aeruginosa, with MICs ranging from 0.25 to 16 micrograms/ml (mode MIC: 2) for 87% of strains, and A. calcoaceticus, with MICs from 0.25 to 2 micrograms/ml (mode MIC: 1). Haemophilus sp. (MIC: 0.008 to 0.06 microgram/ml; mode MIC: 0.03), Gonococci (mode MIC: 0.008), and Meningococci (mode MIC: 0.016) were very sensitive to ofloxacin. The spectrum of ofloxacin included Gram positive cocci: MICs of Staphylococci were 0.06 to 2 micrograms/ml (mode MIC: 0.5); Enterococci, other Streptococci and Pneumococci were less sensitive, with MICs of 2 to 4 micrograms/ml for the majority of strains. As for anaerobic bacteria, ofloxacin proved more active against Clostridium (0.5 to 2 micrograms/ml) than Bacteroides (0.5 to 16 micrograms/ml).

Bacteria↗

[In vitro activity of a new 3d-generation cephalosporin, cefodizime, on hospital bacteria].

Minimal inhibitory concentrations (MICs) of cefodizime were evaluated by agar dilution for 746 bacterial strains isolated in two hospitals. For enterobacteriaceae MICs ranged from 0.008 micrograms/ml to more than 128 micrograms/ml (mode MIC: 0.25); mode MICs varied across species, ranging from 0.016 micrograms/ml for Proteus mirabilis to 1 microgram/ml for Citrobacter; MICs ranged from 0.12 to 8 for most Enterobacter and from 1 to 64 for Serratia. The rare cefotaxime-resistant strains, most of which were Citrobacter or Enterobacter, also showed resistance to cefodizime. Cefodizime was noticeably less active against Pseudomonas aeruginosa and Acinetobacter, with MICs ranging from 32 to more than 128. Haemophilus sp. and Gonococci, regardless of beta-lactamase-production status, as well as Neisseria meningitidis, were highly susceptible (MIC less than or equal to 0.008-0.016). Cefodizime was moderately active against methicillin-susceptible Staphylococci (MIC: 2 to 16 micrograms/ml) and failed to inhibit methicillin-resistant strains. Enterococci were slightly susceptible or resistant. Whereas the other Streptococci and Pneumococci had low MICs (0.03-0.12). A fairly wide range of MICs was found for anaerobes, with lower values for Clostridium (0.008 to 1) than for Bacteroids (8 to 128 mu g/ml). Our results show that cefodizime has the same properties as other third-generation cephalosporins: cefotaxime-resistant Enterobacteriaceae strains also exhibit resistance to cefodizime.

Bacteria↗

[Antibacterial activity in vitro of 10 quinolones against 20 strains of Legionella pneumophila].

Minimal inhibitory concentrations (MICs) of 10 quinolones were determined by dilution method on BCYE, for 20 strains of Legionella pneumophila. Since the BCYE Agar medium reduces the antibacterial activity of some antimicrobials, a correction factor was calculated. It was found to be 1 to 16 according to the antibiotic tested. The following mode adjusted MIC show the good in vitro antibacterial activity of quinolones on L. pneumophila: ofloxacin, pefloxacin, ciprofloxacin, norfloxacin, A 56620 cMIC: 0.06 microgram/ml), A 56619, enoxacin (cMIC: 0.12 microgram/ml), rosoxacin (cMIC: 0.25 microgram/ml). Pipemidic acid (cMIC: 2 micrograms/ml) and nalidixic acid (cMIC: 1 microgram/ml) were the least active.

Anti-Bacterial Agents↗

Evolution and epidemiology of MLS resistance.

Within the framework of this symposium, it is not feasible to present an exhaustive description of the present state of knowledge regarding the sensitivity and resistance of bacterial species to macrolides, lincosamides and streptogramins (MLS). This paper is limited to a description of the evolution of different types of resistance in the light of decisive factors described in previous papers, in order to deduce, if at all possible, trends in future strategy in therapeutics. Only acquired resistance lends itself to epidemiological study, in contrast to natural resistance which is, by definition, characteristic of a species or a genus, and not liable to change. Three groups will therefore be studied in turn: Staphylococcus aureus, streptococci and Bacteroides fragilis. There is as yet insufficient accumulated data to draw conclusions regarding the epidemiology and evolution of MLSB resistance observed in Clostridium perfringens and Corynebacterium diphtheriae, or regarding the high-level resistance to erythromycin due to enzymatic inactivation recently described in Escherichia coli.

Anti-Bacterial Agents↗

Plasmid-mediated resistance to lincomycin by inactivation in Staphylococcus haemolyticus.

Staphylococcus haemolyticus BM4610 was resistant to high levels of lincomycin and susceptible to macrolides, clindamycin, and streptogramins. This resistance phenotype, not previously reported for a human clinical isolate, was due to inactivation of the antibiotic. The gene conferring resistance to lincomycin in strain BM4610 was carried by a 2.5-kilobase plasmid, pIP855, which was cloned in Escherichia coli. Plasmid pIP855 caused inactivation of both lincomycin and clindamycin in S. haemolyticus and in E. coli but conferred detectable resistance to lincomycin only in S. haemolyticus and to clindamycin only in E. coli.

Clindamycin↗

Luteinizing hormone and prolactin release by cultured pituitary cells and by gonadotrope- and lactotrope-enriched populations in the presence of modulators of adenylate cyclase.

The effects of 3 compounds previously known to alter the adenylate cyclase activity in various tissues were tested on rat pituitary. Forskolin increased while RMI 12,330 A and SQ 22,536 decreased enzyme activity of pituitary homogenates. Forskolin (10(-5) M) promoted in cultured cells a massive synthesis of cyclic adenosine monophosphate (cAMP) and intense output of the nucleotide in the medium; at the same concentration, RMI 12,330 A decreased the cell content of cAMP while release was unaffected, and SQ 22,536 exerted no effect on the cyclic nucleotide amount of both cell and medium. The basal release of plated total cells or enriched gonadotropes was slightly stimulated by forskolin (10(-7) - 10(-5) M) though the level of stimulation never attained the one produced by 10(-7) M luteinizing hormone-releasing hormone (LHRH); it was affected neither by RMI 12,330 A (10(-7) - 10(-5) M) nor by SQ 22,536 (10(-7) - 10(-4) M). The LHRH-stimulating effect was slightly amplified during the 1st h (sensitivity response of cells) by low concentrations of forskolin (10(-7) and 10(-6) M) but the overall luteinizing hormone (LH) release after 4 h of incubation (capacity response of cells) was unmodified. Higher concentrations of the diterpene inhibited the LHRH effect as seen with total cells and with enriched gonadotropes. RMI 12,330 A at 10(-5) M significantly inhibited the LHRH-promoted LH release from total cells and from gonadotropes but a higher concentration (10(-4) M) promoted a large unspecific release that masked the LHRH effect. SQ 22,536 never modified the cell response to LHRH, whatever the drug concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenine↗

Differential distribution of androgen and estrogen receptors in rat pituitary cell populations separated by centrifugal elutriation.

The distribution of 5 alpha-dihydrotestosterone (DHT)-binding sites within specific pituitary cell populations, as compared with the estradiol (E2)-binding sites distribution, could be estimated after gonadotrope cell enrichment. Centrifugal elutriation allowed the purification of large gonadotropes from 42-day-old male rat pituitaries; this population contained 5.3 +/- 1.0% of the cells, 54 +/- 3% of the LH, and less than 5% of PRL. A gonadotrope-depleted fraction was also defined that contained more than 92% of the total PRL and was thus called the lactotrope population though it still contained small gonadotropes and most somatotropes. DHT and E2 receptors were quantified by multidose saturation analysis. The association constants (Ka) ranged from 0.2-0.5 X 10(9) M-1 both for E2 and DHT independent of the cell population. The binding of DHT was mainly observed in the gonadotropes (50-100 fmol/10(6) cells), while it was very low in the other cells (0.9-3 fmol/10(6) cells). E2-binding sites measured within the same cell populations showed a broader distribution than DHT-binding sites. Whereas the ratio of binding DHT/E2 averaged 0.86 +/- 0.01 in the gonadotropes, it reached only 0.35 +/- 0.07 in the lactotropes. Thus, using enriched cell populations, our results demonstrate for the first time a quantitative selective distribution of androgen-binding sites as compared with the estrogen sites.

Animals↗

[LHRH stimulates the secretion of an 87 K protein by cultured gonadotrophic cells].

The biosynthesis of proteins secreted by cultured pituitary cells was studied using (35S)-methionine. The intracellular and released proteins were analyzed by polyacrylamide gel electrophoresis followed by autoradiography. The LHRH-stimulated release is accompanied by the synthesis and release of a 87,000 dalton molecule (87 K protein). This peculiar secretion is particularly evidenced when using enriched gonadotrophs obtained by centrifugal elutriation. The 87 K protein could be involved in the release process of gonadotropins.

Animals↗

[Activity of the amoxicillin-clavulanic acid (augmentin) combination on strains of hospital isolates].

All strains of Staphylococcus aureus and Gram negative bacilli (Enterobacteriaceae, Pseudomonas aeruginosa, Acinetobacter) isolated from 01.01 to 03.31.83 were studied using agar diffusion with augmentin-impregnated discs (amoxicillin 20 micrograms + clavulanic acid 10 micrograms). Augmentin is active against penicillinase-producing Staphylococci susceptible to methicillin, whereas methicillin-resistant strains are also resistant to augmentin. According to the susceptibility of strains to amoxicillin, carbenicillin and cefalotin, Enterobacteriaceae can be divided into five main phenotypes, of which four are resistant. "RSR" and "RRR" phenotypes, which are cephalosporinase producers, are chiefly found among Enterobacter, Serratia, Citrobacter and indole + Proteus; in these groups a change in inhibition diameters indicating activity of augmentin is observed only in a significant number of Proteus vulgaris strains. "RRS" and "RRI" strains are penicillinase producers found mainly among E. coli, Klebsiella pneumoniae and oxytoca, and Proteus mirabilis; they emerge as very susceptible to augmentin. Pseudomonas aeruginosa is never susceptible to augmentin. Augmentin is slightly more active than amoxicillin on some Acinetobacter strains but the difference is too inconsiderable to be of clinical significance.

Acinetobacter↗

[Comparative effect of a new calcium antagonist, BRL 40015, and verapamil on LH secretion from cultured pituitary cells].

Effects of the new calcium antagonist with antianginal properties BRL 40015 A (-1-(4-diethoxyphenyl) methyl-3,4-(dihydro-6,7 bis (methylethoxy)-isoquinoline, hydrochloride) on luteinizing hormone (LH) release from cultured rat pituitary cells were investigated and compared with those of verapamil. BRL 40015 A provoked a dose-dependent inhibition of LHRH-stimulated LH release; IC50 (50% inhibition) was found to be 2 X 10(-6)M whereas it was ten times greater with verapamil (2 X 10(-5)M). Inhibition was reversible, partially at least, when BRL 40015 A was removed from the incubation medium. Contrarily to what occurred with verapamil, an increase in extracellular Ca2+ concentration (5mM) provoked the disappearance of BRL 40015 A--induced inhibition. Such effects of BRL 40015 A were observed in absence of cytotoxicity. Thus, while confirming that Ca2+ mobilization plays an essential role in LH release, results suggest that the mechanism of action of BRL 40015 A on calcium channels is however different from that of verapamil.

Animals↗

[Development and current status of Pseudomonas aeruginosa sensitivity to antibiotics].

The response of Pseudomonas aeruginosa to antibacterial drugs is remarkably stable and is characterized by multiresistance. This organism is uniformly resistant to ampicillins, first and second generation cephalosporins and kanamycin and most often resistant to streptomycin, tetracyclines, chloramphenicol, nalidixic acid, sulphonamides, co-trimoxazole and nitrofurans. Very few of the conventional antibiotics are active against Pseudomonas spp.: polymyxin is virtually always active in vitro but gives disappointing therapeutic results; little change has been observed over years in the incidence of strains resistant to carbenicillin and to some aminoglycosides, such as gentamicin, tobramycin and amikacin. Recently developed antibacterial agents of the beta-lactam and quinolone groups offer hopes of better therapeutic effectiveness. Among beta-lactam antibiotics, new penicillins, including azlocillin, are more active than carbenicillin and some third generation cephalosporins, notably cefoperazone, cefsulodin and ceftazidime, also show anti-Pseudomonas activity. The same applies to new beta-lactam antibiotics with a novel structure, such as thienamycins and monobactams. Several new quinolones are active in vitro against Ps. aeruginosa; these are rosoxacin, norfloxacin, enoxacin, pefloxacin, ciprofloxacin and ofloxacin.

Ampicillin↗