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Biomedical subjects

J Etienne

Publications and source records attributed to J Etienne.

At least 235 records · Page 13Linked to original sources
PubMed1989

Clinical isolates of Staphylococcus lugdunensis and S. schleiferi: bacteriological characteristics and susceptibility to antimicrobial agents.

The bacteriological characteristics and susceptibility to antimicrobial agents of 108 clinical isolates of Staphylococcus lugdunensis and Staphylococcus schleiferi are described. Fifty out of 108 isolates were considered to be responsible for 16 documented infections, including some severe infections (endocarditis, bacteraemia, osteitis). A number of bacteriological characteristics enabled the identification of these species in the clinical microbiology laboratory: the absence of coagulase and protein A, and the presence of a fibrinogen affinity factor and thermonuclease along with other biochemical characteristics (ornithine and arginine decarboxylases, carbohydrate acidification, novobiocin susceptibility) differentiated these new species from other staphylococci; however, they did not possess virulence markers such as toxins or haemagglutinin, but were haemolytic. In this series, almost all isolates were susceptible to 22 antibiotics and 4 antiseptics representative of the main groups of antimicrobial agents. More information is needed on the ecology and epidemiology of these new opportunistic pathogens.

Adult↗
PubMed1989

Oxacillin and tobramycin serum levels during cardiopulmonary bypass.

Antibiotic prophylaxis in cardiac surgery is recommended to combat acquired infections caused by staphylococci and gram-negative bacilli. Prophylaxis seems effective provided blood levels are greater than minimal inhibitory concentrations (MIC). In this study, two doses of antibiotics were compared in 45 patients with normal renal function during cardiopulmonary bypass (CPB). All patients received 50 mg/kg of oxacillin. Group 1 (30 patients) also received 1 mg/kg of tobramycin, while group 2 (15 patients) received 2 mg/kg of tobramycin. Blood samples were taken after the administration of antibiotics, as well as at the onset and conclusion of CPB. Additional samples were taken before and after heparin injection before CPB, and from the arterial and venous cannulae of the bubble oxygenator during CPB. In both groups, oxacillin serum levels were constantly greater than MIC for susceptible bacteria. In group 1, tobramycin levels less than 2 micrograms/mL (MIC for most susceptible bacteria) occurred in four patients before CPB, in 14 patients at the onset of CPB, and in 19 patients at the conclusion of CPB. These low levels were not explained by heparin administration or absorption onto the CPB circuit, but were the result of hemodilution. In group 2, in which all the tobramycin levels were higher than 2 micrograms/mL, serum levels decreased from 9.9 +/- 3.4 (mean +/- SD) to 3.7 +/- 0.7 micrograms/mL throughout the procedure. Plasma creatinine did not change significantly in either group. It is concluded that in patients with normal renal function, doses as high as 50 mg/kg of oxacillin and 2 mg/kg of tobramycin may be necessary before CPB to provide adequate serum levels throughout CPB.

Adult↗
PubMed1989

Hospital dispersion of Staphylococcus epidermidis isolates resistant to a fluoroquinolone, pefloxacin.

Since 1985, nosocomial infections have been frequently treated with a new fluoroquinolone, pefloxacin, at the Cardiological and Neurological Hospital in Lyon. From 1986 to 1988, the incidence of resistance of clinical Staphylococcus epidermidis strains to pefloxacin increased from 31 to 57%. Dispersion of these resistant strains in the hospital environment was recognized when they were detected on 22% of staff members' fingers (139 samples were investigated) and in 28% of the environmental samples (180 were investigated). There was an association between carriage rate and work place. Most of the pefloxacin-resistant S. epidermidis were resistant to oxacillin, gentamicin, erythromycin, cotrimoxazole and fosfomycin. Intensive use of pefloxacin selected multiresistant S. epidermidis which became ubiquitous in the hospital environment.

Carrier State↗
PubMed1989

Production of tumor necrosis factor by rat mesangial cells in response to bacterial lipopolysaccharide.

Tumor necrosis factor (TNF) is a cytokine which is produced by mononuclear phagocytes upon activation by bacterial lipopolysaccharide (LPS) and various other stimuli. In immune-mediated glomerulonephritis, infiltration of glomeruli by monocytes-macrophages is associated with production of TNF. The purpose of the present experiments was to determine whether mesangial cells could also contribute to glomerular TNF synthesis. TNF activity has been determined in the culture medium of rat mesangial cells using a L-929 fibroblast lytic assay. This activity was detectable only when the cells were exposed to LPS (0.1 to 10 micrograms/ml) and for periods longer than one hour. The cytotoxic factor was identified as TNF since: (1) the lytic activity was completely inhibited by an anti-mouse TNF polyclonal antibody and was associated with suppression of lipoprotein lipase activity in adipocytes; (2) its molecular weight (110,000 daltons) corresponded to that observed for murine TNF under non-denaturing conditions; and (3) mRNA encoding TNF was expressed by mesangial cells two hours after addition of LPS. To assess the mechanisms whereby TNF production was regulated, the role of prostaglandin E2 (PGE2) was determined. LPS caused a dose-dependent increase of PGE2 synthesis by mesangial cells. Treatment by indomethacin promoted a suppression of PGE2 production together with an increase of TNF synthesis, indicating that PGE2 acted in a negative feedback manner to regulate the production of TNF. Addition of PGE2 (0.1 to 300 nM) or 8-bromo cyclic AMP (0.1 to 100 microM) induced similar dose-dependent reductions of TNF synthesis. Thus the inhibitory effect of PGE2 probably required in part cyclic AMP accumulation.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1989

Organization of the human lipoprotein lipase gene and evolution of the lipase gene family.

The human lipoprotein lipase gene was cloned and characterized. It is composed of 10 exons spanning approximately equal to 30 kilobases. The first exon encodes the 5'-untranslated region, the signal peptide plus the first two amino acids of the mature protein. The next eight exons encode the remaining 446 amino acids, and the tenth exon encodes the long 3'-untranslated region of 1948 nucleotides. The lipoprotein lipase transcription start site and the sequence of the 5'-flanking region were also determined. We compared the organization of genes for lipoprotein lipase, hepatic lipase, pancreatic lipase, and Drosophila yolk protein 1, which are members of a family of related genes. A model for the evolution of the lipase gene family is presented that involves multiple rounds of gene duplication plus exon-shuffling and intron-loss events.

Amino Acid Sequence↗
PubMed1989

Susceptibilities to ceftriaxone of streptococcal strains associated with infective endocarditis.

We determined the bactericidal activity of ceftriaxone on 20 streptococci isolated from patients with infective endocarditis and that of penicillin G on 5 strains. The MICs of ceftriaxone were less than or equal to 2 micrograms/ml and the MBCs were low for 5 nontolerant strains (less than or equal to 2 micrograms/ml) and high for 15 tolerant strains (greater than or equal to 16 micrograms/ml). The maximal reduction of the viable bacterial counts after 24 h of exposure to antibiotic was achieved for a concentration of ceftriaxone of 4, 32 and 256 micrograms/ml, respectively for 5, 10 and 19 strains. The activity of penicillin G was similar.

Ceftriaxone↗
PubMed1989

Effects of pimobendan (UD-CG 115 BS) on left ventricular inotropic state in conscious dogs and in patients with heart failure.

The purpose of this study was to examine the time course of the changes in left ventricular inotropic state after intravenous pimobendan administration. In conscious dogs, cumulative doses of 1 and 2.5 mg of pimobendan significantly increased heart rate and the isovolumic indices of inotropic state and relaxation. The maximal effect, however, required 2 h to be present. The changes in cardiac index and capillary wedge pressure after the intravenous administration of 5 mg to patients with heart failure confirmed this slightly delayed action of pimobendan. Accordingly, the effects of pimobendan on left ventricular inotropic state in patients with moderate to severe heart failure were determined during cardiac catheterization 130-150 min after injection of 5 (n = 3) or 2.5 (n = 4) mg. After drug administration, heart rate increased slightly (+7 beats/min; NS) while left ventricular end-diastolic and systolic pressure both decreased significantly (from 22.7 to 9.2 mm Hg, p less than 0.007 and from 123 to 90 mm Hg, p less than 0.025, respectively). The isovolumic index of contractility (dP/dt)/DP40 increased by 19.6 +/- 14.7% (p less than 0.02) and the slope of the late systolic stress-volume relationship improved by 48% (p less than 0.05). It is concluded that pimobendan is a positive inotropic agent in the failing human heart as well as a powerful veno- and arteriodilator.

Animals↗
PubMed1989

[Staphylococcal endocarditis on a heart valve prosthesis. Apropos of 28 cases].

The purpose of this retrospective study of 28 cases of staphylococcal endocarditis on cardiac valve prosthesis was to evaluate the prognosis of that disease and the possible causes of its recent improvement. Between March 1977 and May 1987, 69 patients were treated for bacterial endocarditis on cardiac valve prosthesis. Among these, 28 patients (19 men, 9 women, mean age 53.2 +/- 14.3 years) had staphylococcal endocarditis (Staph. epidermidis in 18 cases, Staph. aureus in 10 cases) of early (10 cases) or late (18 cases) onset. Complications were present in no less than 27 out of 28 patients, the most frequent being heart failure, embolism or neurological disorders. The mortality rate was high (61 p. 100). Among the clinical variables studied, only a state of shock seemed to be predictive of death. Mortality was higher in the group treated medically (100 p. 100) than in the group treated surgically (50 p. 100). Since 1984, however, a significant decrease of mortality was noted; it coincided with the systematic use of vancomycin but also with surgical treatment in all cases. As a result of this study, we suggest that all patients with staphylococcal endocarditis on cardiac valve prosthesis should be operated upon and that this should be done as soon as possible, before the end of the classical antibiotic therapy period.

Adolescent↗
PubMed1989

[Recurrent infective endocarditis].

Between August, 1974 and May, 1987, 486 patients were treated for infective endocarditis. In 16 of these patients (12 men, 4 women, mean age 44.3 +/- 18.0 years at the time of the first episode) the endocarditis recurred: once in 14 patients, twice in 2 patients. The time elapsed between recovery from the first episode and onset of the recurrence varied from 6 to 159 months (mean 54.3 +/- 35.1 months). Among the 18 recurrences, 10 affected native valves (mitral 6, aortic 4) and 8 aortic prostheses. In all but one case the organism isolated during the recurrence (Streptococcus in 14 cases, Staphylococcus in 3 cases, Rickettsia in 1 case) was different from the organism responsible for the previous infection. The 16 patients were followed up for periods of 28 to 203 months (mean 107.0 +/- 58.0 months), counting from the onset of the first episode. Ten patients were treated medically during the second episode: 4 died and 2 had a second recurrence, lethal in one of them (time elapsed between the onset of the first episode and the date of death: 32 to 149 months). Six patients were operated upon (valve replacement in 5 cases, closure of a left aorto-ventricular fistula in 1 case) without deaths. Nine of the 11 survivors are now asymptomatic. The actuarial survival rate in recurrent endocarditis (75 p. 100, 10 years after the onset of the first episode) is not different from that observed in non-recurrent endocarditis.

Adult↗
PubMed1988

Modulation of lipoprotein lipase activity in mouse peritoneal macrophages by recombinant human tumor necrosis factor.

Thioglycollate-elicited mouse peritoneal macrophages spontaneously secrete lipoprotein lipase during culture. Exposure of the cultures to 50 ng/ml of recombinant human tumor necrosis factor (rTNF) for 48 h resulted in a 69% reduction in lipoprotein lipase activity in the culture medium with a concomitant decrease in cellular enzyme activity. The decrease in enzyme activity was not the result of rTNF-dependent reduction in the total protein synthesis, since the presence of rTNF did not affect [3H]leucine incorporation into cellular proteins. The effect of rTNF on lipoprotein lipase was reversible; upon TNF withdrawal, enzyme activity returned to basal levels after 60 h. The reduction of lipoprotein lipase in rTNF-treated cultures could be completely prevented by preincubation with a specific antiserum against recombinant human TNF. The late onset of decrease of lipoprotein lipase (LPL) activity suggests that rTNF might induce a mediator, which in turn suppresses LPL production. While rTNF was very effective in reducing lipoprotein lipase activity in mouse peritoneal macrophages, it did not affect lipoprotein lipase activity when added to the murine J774 cell line and to CT2 macrophage-like cells, a variant of the J774 cell line.

Animals↗
PubMed1988

Tunicamycin-treated rat heart cell cultures synthesize an inactive nonreleasable lipoprotein lipase.

Cells isolated from newborn rat hearts were cultured in the presence of 100 mM Hepes (4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid). Lipoprotein lipase activity was present in an intracellular and heparin-releasable pool and was also secreted into the culture medium. Treatment of the cultures with 5 micrograms/ml tunicamycin caused almost complete loss of lipoprotein lipase activity in all three compartments. In control cultures, immunoblotting of lipoprotein lipase derived from all three pools revealed a single band of lipoprotein lipase with an apparent Mr of 56,000. In the tunicamycin-treated cultures, the enzyme appeared only intracellularly and had an apparent Mr of 49,000. No immunoreactive enzyme was found in the medium. Thus, glycosylation of lipoprotein lipase in heart cell cultures is mandatory for enzyme activity and translocation from an intracellular to the heparin-releasable pool and for secretion into the medium.

Animals↗
PubMed1988

Lipoprotein lipase in heart cell cultures is suppressed by bacterial lipopolysaccharide: an effect mediated by production of tumor necrosis factor.

Exposure of rat heart cell cultures, consisting mainly of nonbeating mesenchymal cells, to 50 ng/ml of bacterial lipopolysaccharide (LPS) for 24 h resulted in a more than 80% reduction in lipoprotein lipase activity. The loss of enzymic activity was accompanied by a concomitant reduction in enzyme protein, as shown by immunoblotting. Addition of LPS to the culture medium resulted also in the production of tumor necrosis factor (TNF), and the fall in lipoprotein lipase in LPS-treated cultures could be prevented by an antibody to TNF. Addition of recombinant human TNF to the heart cell cultures also depressed lipoprotein lipase activity. LPS treatment of preadipocytes in culture resulted in a fall in lipoprotein lipase activity and TNF production. Since TNF is known as a macrophage product, the cultures were tested for phagocytic capacity, and only 0.2-1.3% of the cells were shown to engulf Staphylococcus albus. Immunofluorescent staining with monoclonal antibodies OX-1, which identify leukocyte common antigen, was negative, and only 0.1 +/- 0.07% of the cells were positive after staining with OX-42 antibody to iC3b receptor. Both antibodies stained more than 98% of rat peritoneal macrophages used as controls. Since LPS treatment of macrophages at numbers comparable to or exceeding the number of phagocytic cells present in the heart cell cultures did not induce measurable amounts of TNF, it is suggested that in the heart cell cultures, TNF may be produced by cells other than macrophages.

Animals↗
PubMed1988

Increased lipoprotein lipase content in the adipose tissue of suckling and weaning obese Zucker rats.

The aim of this study was to determine whether the increase in lipoprotein lipase activity displayed by the adipose tissue of obese (fa/fa) rats as compared with that of lean (Fa/fa) rats could be ascribed to a change in the content or in the catalytic properties of the enzyme. The question was addressed in rats of two ages: in 7-day-old suckling and in 30-day-old post-weaning pups. Inguinal fat-pads were removed surgically (7 days of age) or after killing (30 days of age), and acetone-extract powders were prepared. The relative quantity of enzyme was assessed by immunotitration using an antiserum raised in goat against purified lipoprotein lipase from rat adipose tissue. The results indicate that increases in enzyme activity in obese animals were strictly paralleled by increases in the amount of enzyme in suckling as well as in post-weaning pups. Moreover, the apparent Km values of lipoprotein lipase for its substrate triacylglycerol were identical in the two genotypes. In conclusion, the genotype-mediated increase in lipoprotein lipase activity in adipose tissue of obese Zucker rats was fully accounted for by an increase in the content of the enzyme. In addition, this work documents the mechanism of the increase in lipoprotein lipase activity during weaning, which is mediated mainly through changes in the adipose-tissue enzyme content.

Adipose Tissue↗
PubMed1988

Regulation of lipoprotein lipase activity in the sand rat: effect of nutritional state and cAMP modulation.

The sand rat (Psammomys obesus) is a desert rodent in which obesity and diabetes mellitus appeared only subsequent to feeding laboratory animal chow. To study the role of lipoprotein lipase in the development and maintenance of obesity in the sand rat, enzyme activity in various organs and in plasma of sand rats or albino rats was determined following a 20-hour fast, or 16 hours after injection of cholera toxin. Despite comparable change in body weight, an altered pattern of enzyme distribution and regulation was observed in the sand rat. Neither fasting nor cholera toxin had an effect on heart and daiphragm muscle lipoprotein lipase activity of the sand rat, but caused a 1.5- to 2-fold increase in the treated albino rats. By using an isolated perfused heart system, we were able to measure enzyme activity present in the heparin-releasable fraction that represents the functional pool of the enzyme. In both species, the heparin-releasable fraction of the heart increased twofold following fasting, though initial values were lower in sand rat. In both species, fasting and cholera toxin administration resulted in an increase in plasma and liver lipoprotein lipase activity. Adipose tissue lipoprotein lipase activity of sand rat, unlike the albino rats, was similar in the various fat regions and was not lowered by food deprivation or cholera toxin administration. After both treatments, sand rat plasma insulin levels exceeded fivefold those of albino rats. Adipose tissue lipoprotein lipase activity of fed and fasted normal and diabetic sand rats correlated negatively with plasma insulin and glucose levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗