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Biomedical subjects

J Etienne

Publications and source records attributed to J Etienne.

At least 217 records · Page 12Linked to original sources
PubMed1991

Distribution and source of lipoprotein lipase in mouse mammary gland.

During lactation lipoprotein lipase (LPL) is elevated in mammary tissue and depressed in adipose tissue to redirect lipids for incorporation into milk fat. The cellular origin of lipoprotein lipase in mammary tissue is thought to be the mammary epithelial cell which is the predominant cell type noticeable in the lactating gland; however, mammary adipocytes are also present. If lipoprotein lipase is produced by adipocytes in other sites of the body, then the question remains as to why mammary adipocytes have not been shown to produce lipoprotein lipase. In this study we present several lines of evidence that indicate that the mammary adipocyte is a source of LPL in the lactating mammary gland of mice. This evidence includes the absence of extracellular and intracellular lipoprotein lipase activity in two types of primary mammary epithelial cell cultures and a similarity in the changes of lipoprotein lipase activity in genital adipose tissue from nonpregnant mice and lactating mammary tissue to the nutritional state of the animal. Other evidence presented here includes strong localization of lipoprotein lipase protein and messenger RNA by fluorescence immunohistochemistry and in situ hybridization, respectively, to interstitial cells located between epithelial structures. We postulate that these interstitial cells are regressed, lipid-deleted mammary adipocytes.

Adipose Tissue↗
PubMed1990

Interferon-gamma inhibits lipoprotein lipase in human monocyte-derived macrophages.

Lipoprotein lipase (LPL) (EC 3.1.1.34) hydrolyzes triacylglycerols of very low density lipoproteins and chylomicrons. It is produced by several cell types, including macrophages, which are frequent in atherosclerotic lesions. The atherosclerotic plaque also contains activated T lymphocytes. We therefore investigated the possible regulatory effect of the T lymphocyte-derived lymphokine interferon-gamma (IFN-gamma) on macrophage LPL. Human monocyte-derived macrophages were treated with recombinant IFN-gamma or conditioned medium from activated peripheral blood mononuclear cells for 3 days. LPL activity was thereafter measured in the culture medium and in cell homogenates. The enzyme protein was detected at a cellular level by immunocytochemistry and immunopredicipitation. Recombinant IFN-gamma caused a profound decrease in macrophage LPL secretion. The IFN-gamma-treated cells, however, still contained immunodetectable enzyme and the decrease in secretion was apparently only partly due to an inhibited synthesis. Conditioned medium from activated peripheral blood mononuclear cells also drastically decreased the macrophage LPL secretion. When the conditioned medium was treated with antibodies against IFN-gamma, its down-regulating effect on macrophage LPL was totally removed. The data indicate that IFN-gamma is inhibiting macrophage LPL at least in part via a reduction of LPL synthesis. A local release of IFN-gamma may be important in the pathogenesis of atherosclerosis by affecting the lipid accumulation in the lesion.

Cells, Cultured↗
PubMed1990

Plasmid profiles and genomic DNA restriction endonuclease patterns of 30 independent Staphylococcus lugdunensis strains.

Extrachromosomal DNA analysis and restriction endonuclease analysis of whole cellular DNA were used to characterize 30 Staphylococcus lugdunensis strains isolated from 13 different hospitals from 1977 to 1988. All the strains were susceptible to most of the antibiotics tested, including penicillin G. A single 3.2 kilobase plasmid was detected in 13 strains and one or two plasmids, ranging from 2.3 to 6.6 kilobases, were found in 7 strains. EcoRI, PstI and PvuII restriction patterns of total cellular DNA were identical for 23 isolates, indicating strong conservation of endonuclease sites in this species. One or two additional DNA bands occurred in seven isolates. Molecular markers show rather little variations between different S. lugdunensis isolates suggesting that they are closely related.

DNA Restriction Enzymes↗
PubMed1990

Capacitance hydrophones for pressure determination in lithotripsy.

Capacitance hydrophones have been designed and applied for pressure measurements of shock waves in lithotripsy. Their working principle, properties, and design are discussed. Formulae are given, permitting the determination of pressures and calibration of hydrophones from electric measurements. Examples of comparative measurements with electrodynamic and PVDF hydrophones are presented, confirming the correctness of obtained peak pressure values. The hydrophones are characterized by high durability, small controlled nonlinearity, and a wide frequency band. However, they cause distortions in the shape of the overshoot of the measured shock wave pulses and their application is limited to measurements in the focal region.

Calibration↗
PubMed1990

Cefazolin and netilmicin serum levels during and after cardiac surgery with cardiopulmonary bypass.

The kinetics of cefazolin and netilmicin were studied in 10 patients undergoing elective cardiac surgery with hemodilution and cardiopulmonary bypass (CPB). During surgery, but before CPB, cefazolin, 25 mg/kg, and netilmicin, 2 mg/kg, were administered intravenously over 30 minutes. For the 48-hour period following CPB, cefazolin, 25 mg/kg, and netilmicin, 1 mg/kg, were administered intravenously every 8 hours. Initiation of CPB was accompanied by a 28% to 30% decrease in hematocrit and serum antibiotic levels. At the conclusion of surgery, cefazolin and netilmicin serum levels were 41 +/- 12 micrograms/L and 2.5 +/- 0.6 micrograms/mL (mean +/- SD), respectively. During the postoperative period, cefazolin levels were consistently greater than the minimum inhibitory concentration (MIC) for sensitive bacteria (4 micrograms/mL); average netilmicin levels were greater than MIC of sensitive bacteria (2 micrograms/mL) for 2 hours after antibiotic infusion. The netilmicin trough levels were 0.6 +/- 0.5 micrograms/mL. Pharmacokinetic parameters were determined using a model-independent method, and gave the following results during surgery: cefazolin--elimination half-life, 231 minutes, total body clearance, 1.05 mL/kg/min, and steady-state volume of distribution, 243 mL/kg. The values for netilmicin were 249 minutes, 1.18 mL/kg/min, and 353 mL/kg, respectively. Postoperatively there were no significant changes in the disposition of cefazolin, but the elimination half-life of netilmicin was shorter (124 minutes, P less than 0.01) and the total body clearance greater (3.58 mL/kg/min, P less than 0.01) than during surgery.

Adolescent↗
PubMed1990

Instability of characteristics amongst coagulase-negative staphylococci causing endocarditis.

Variation in typing of clinically significant isolates of coagulase-negative staphylococci (CNS) was determined by five typing methods with 143 isolates obtained from 19 patients over periods from 2 days to 1 year. In only one case did all isolates give exactly the same typing pattern by all five tests. No single method, or simple combination, provided a ready means of confirming the relatedness of separate isolates. The most frequently useful tests were antibiotic susceptibility and extrachromosomal DNA banding patterns. However, the results of biotyping, serotyping and phage typing were also helpful in showing the relationship between different isolates from a given patient. In most cases a core pattern varying by the gain or loss of a small number of features, characterised a given patient's isolates. In two causes, apparently radical changes in the infecting organism were observed, and confirmed by restriction endonuclease analysis. Care should be taken when successive isolates of CNS show distinct typing differences in deciding their clinical relevance.

Anti-Bacterial Agents↗
PubMed1990

Chronic Q fever: diagnosis and follow-up.

Sera from 40 patients (25 men, and 15 women) with clinical features compatible with the diagnosis of chronic Q fever were received. Total or partial clinical data were available. All of them had serological evidence of chronic Q fever (IgG class anti-phase I titer greater than 800). The final diagnosis was vascular infection in four cases (with two positive cultures for Coxiella burnetii), bone infection in two patients (one positive culture), chronic hepatitis in one patient, and endocarditis in 32. The last patient had an isolated fever with a chronic Q fever serologic profile. Among the 32 with endocarditis, valve replacement was performed in 59%, and valve cultures were positive in 14/18 patients. Twenty-nine of these patients had previously known valvulopathy; 23 were exposed to cattle, sheep or goats; and four had an immunocompromised situation. Ten patients died; two before any treatment, five of cardiac failure during or a few weeks after surgery, and three during the medical treatment. For antibiotic treatment, tetracycline alone was employed in seven cases. For the other patients, combined therapy including tetracycline and another drug (rifampin, fluoroquinolones, cotrimoxazole, or erythromycin) was initiated. Three patients were considered to be completely cured.

Adolescent↗
PubMed1990

Increase in native valve endocarditis caused by coagulase negative staphylococci: an Anglo-French clinical and microbiological study.

Native valve endocarditis caused by coagulase negative staphylococci has become more common. A study of 35 cases showed that the infections were usually acquired in the community and occurred in men (mean age 51 years). A pre-existing cardiac abnormality (mitral leaflet prolapse in a third of patients) was detected in 26 (74%). The source of the organisms in the community acquired infections was assumed to be the skin, though lesions were seldom demonstrated; most hospital acquired infections resulted from intravenous devices. Community acquired organisms were usually sensitive to penicillin, whereas those acquired in hospital were often multiresistant. Most infections were caused by Staphylococcus epidermidis. The frequency of acute presentation (26%) and of major neurological abnormality (23%), together with the need for valve replacement (often emergency) (51%) and the mortality (36%) suggest that coagulase negative staphylococci can be virulent aggressive pathogens, mimicking Staphylococcus aureus.

Adult↗
PubMed1990

Effects of the beta 1-adrenergic receptor partial agonist xamoterol on left ventricular diastolic function. An evaluation after 1-6 years of oral therapy.

Acute intravenous administration of the new beta 1-adrenergic receptor partial agonist xamoterol lowers left ventricular end-diastolic pressure and improves the isovolumic indexes of inotropic state and relaxation. To determine if these hemodynamic changes were maintained after prolonged administration, the dose-response relation to cumulative doses of xamoterol was determined in a group of 14 patients with mild (n = 6)-to-serve (n = 8) ischemic left ventricular dysfunction. These patients had been treated with xamoterol (200 mg, b.i.d.) for a mean of 51 +/- 17 months, and the drug had been stopped for 72 hours before testing the responsiveness to xamoterol. In these patients, xamoterol administration still induced dose-dependent decreases in left ventricular end-diastolic pressure from 21.4 +/- 8.2 to 15.8 +/- 7.7 mm Hg (p less than 0.01, vs. baseline and vs. the control data 51 +/- 17 months before). Peak positive dP/dt and dP/dt normalized to a developed pressure of 40 mm Hg [( dP/dt]/DP40) increased by 14% and 23%, respectively (p less than 0.01), whereas the rate of isovolumic pressure decrease improved by 12% (p less than 0.01). It is concluded that the myocardial response to xamoterol is maintained after years of continuous therapy, and that in patients with heart failure, this response was expressed mainly as a reduction in left ventricular end-diastolic pressure.

Administration, Oral↗
PubMed1990

["Cis" and "trans" regulator elements of transcription].

The 5'-flanking region of genes is involved in transcription regulaton. Multiple nucleotidic cis-acting sites are spread out over a region of 400 bp, (mostly) upstream of the start point. Examples are given with TATA box, GC box, CCAAT box and some octamers. Transcription factors recognize cis-acting sites and bind to them. Some are required for transcription initiation. Others affect (usually enhance) the rate of initiation. Trans-regulator proteins contain two domains. One is responsible for binding to DNA (as for instance: Zn fingers, Leu zipper, positive homeotic domain). The other one is responsible for activity on transcription (as for instance: rich in Gln, rich in Pro, acidic alpha-helix domain). Some technics used for determination of the site of transcription initiation and of protein fixation on DNA are briefly described. It is hoped that a better comprehension of transcription mechanisms will offer new possibilities of investigation for acting in some varieties of protein synthesis dysfunctionnements.

Genes, Regulator↗
PubMed1990

[Epidemiological notes: meningococcal meningitis of serogroup X in Niamey (Niger)].

From 19th February to 15th April 1990, 22 strains of meningococcus belonging to serogroup X have been identified by the Centre for Study and Research on meningitidis and Schistosomiases (CERMES) at Niamey (Niger). Serogroup X has been confirmed by the Centre Collaborating WHO of Reference and Training for Meningococci (CCOMSRFM) at Marseille (France). These strains have been isolated from cerebrospinal fluid of patients suffering from cerebrospinal meningitis and living in different neighbourhoods of Niamey. Apparition of cases of meningococcal meningitis with other serogroups than A implies identification of serogroup of meningococcus in intertropical Africa.

Humans↗
PubMed1990

Mechanism of N-formyl-methionyl-leucyl-phenylalanine- and platelet-activating factor-induced arachidonic acid release in guinea pig alveolar macrophages: involvement of a GTP-binding protein and role of protein kinase A and protein kinase C.

Various pharmacological effectors were used to investigate the mechanism of arachidonic acid release by N-formyl-methionyl-leucyl-phenylalanine (fMLP) and platelet-activating factor (PAF) in guinea pig alveolar macrophages. The fMLP- and PAF-stimulated arachidonic acid release (i) was mimicked by sodium fluoride and inhibited by Bordetella pertussis toxin, suggesting the participation of a guanine nucleotide-binding protein; ii) was mimicked by A23187 but was insensitive to the calmodulin inhibitor R24571, making the involvement of a calmodulin-dependent pathway unlikely; and (iii) was mimicked by 12-O-tetra-decanoyl phorbol 13 acetate (TPA) and was, like the TPA-stimulated release, markedly decreased when protein kinase C (PKC) had been down-regulated by TPA (65% decrease) or inhibited by sphingosine, a diacylglycerol-competitive PKC inhibitor shown to completely abolish the enzyme activity from alveolar macrophages at 40 microM. Moreover, PAF and fMLP, under conditions where they stimulated arachidonic acid release, promoted an appreciable, albeit transient, translocation of PKC, suggesting a possible involvement of the enzyme in the agonist-stimulated process. However, staurosporine, another PKC inhibitor decreasing PKC activity from alveolar macrophages by 60% at 20 nM, failed to alter fMLP- and PAF-stimulated release. These data lead us to suggest that fMLP- and PAF-stimulated arachidonic acid release is mediated by mechanisms involving either a staurosporine-insensitive PKC isoform or a sphingosine-sensitive coupling between a pertussis toxin-sensitive guanine nucleotide-binding protein and phospholipase A2. Finally, the fMLP- and PAF-stimulated arachidonic acid release was inhibited by cholera toxin and was, like A23187-stimulated release, potentiated by N-[2-(methylamino)ethyl]-5-isoquinolinesulfonamide dihydrochloride (H8), an exclusive protein kinase A inhibitor in alveolar macrophages, suggesting a negative regulation by protein kinase A.

Alkaloids↗
PubMed1990

[Acute myocardial infarction: thrombolytic efficacy of 500.000 UI of streptokinase combined with heparin].

Most reports concerning the use of streptokinase (SK) for thrombolysis in myocardial infarction (MI) have employed doses over 1,000,000 units. We evaluated the efficacy of a dose of 500,000 U in 40 patients with acute MI who received full heparin dose before, during and after SK. Thrombolytic effect, as measured by the protamine neutralized thrombin time was shown to be strong in 60% of cases, moderate in 17% and weak in 22%, and this was not modified by larger SK doses. A patent culprit artery was demonstrated at coronary arteriography performed 3 days after SK in 90% of patients. Only one instance of severe bleeding was observed. Thus, a reduced SK dose in association to heparin provides adequate lytic effect and artery patency rate in patients with MI.

Adult↗
PubMed1989

Plasmid-mediated resistance to fosfomycin in Staphylococcus epidermidis.

Staphylococcus epidermidis strain BM2641, isolated from a patient, was resistant to penicillin G, methicillin, aminoglycosides, chloramphenicol, macrolide, lincosamide and streptogramin B-type (MLS) antibiotics, and to high levels of fosmycin. Resistance to forsfomycin and/or to MLS was lost at low frequencies either spontaneously or after curing with novobiocin. The plasmid DNA from BM2641 and its cured derivatives was purified, analyzed by agarose gel electrophoresis and transferred to a nitrocellulose sheet. Comparative analysis of the resistance phenotypes with the plasmid content of the strains indicated that fosfomycin and MLS resistance were encoded by plasmids pIP1842 (2.5 kb) and pIP1843 (2.6 kb), respectively. Southern hybridization with a probe specific for gene fosA of Serratia marcescens showed that the fosfomycin resistance determinant in Staphylococcus is not homologous to that of Gram-negative bacteria.

Conjugation, Genetic↗
PubMed1989

Insulin regulation of lipoprotein lipase activity in 3T3-L1 adipocytes is mediated at posttranscriptional and posttranslational levels.

Insulin is a major regulator of lipoprotein lipase (LPL) activity. The molecular events associated with LPL regulation by insulin in 3T3-L1 adipocytes were studied by determining LPL enzyme activity, mRNA levels, protein synthetic rate, and transcription run-off activity. Adipocytes treated with insulin (10(-6) M for 48 h) had substantially higher LPL activity (mean difference compared to carrier-treated cells 146%) with little difference in LPL mRNA levels (mean level 109% of control). Insulin regulation of LPL activity was dose-dependent but changes in LPL mRNA were not. Within 2 h of hormone addition, LPL activity was higher in insulin-treated versus carrier-treated adipocytes although their LPL mRNA levels were similar. In [35S]methionine pulse-labeled adipocytes, insulin decreased LPL protein synthetic rate measured by immunoprecipitation 42-48%, although increases (75-340%) in heparin-releasable LPL activity were detected in the same cells. In contrast, during differentiation of 3T3-L1 fibroblasts to the adipocyte state, 5-80-fold increases of heparin-releasable LPL activity were closely associated with similar (8-60-fold) increases in LPL mRNA levels. LPL synthetic rate was 16-fold greater, and LPL gene transcription initiation measured by transcriptional run-off was 10-fold higher in adipocytes than in undifferentiated cells. Differentiation of 3T3-L1 fibroblasts increases transcription of the LPL gene leading to increased LPL mRNA, protein synthetic rate, and enzyme activity. Insulin regulation of LPL activity in 3T3-L1 adipocytes, however, is mediated entirely at posttranscriptional and posttranslational levels.

Adipose Tissue↗
PubMed1989

Mechanism of the hypertriglyceridemia induced by tumor necrosis factor administration to rats.

4 h after intravenous injection of recombinant HuTNF-alpha to fed rats, an increase in heart, diaphragm, and plasma lipoprotein lipase activity was observed. At the same time, a 40-60% decrease in enzymic activity in epididymal fat pad and kidney and 40% decrease in hepatic lipase activity in liver had occurred. Similar results were obtained 20 h after injection of recombinant HuTNF-alpha into fasted rats. Pretreatment with Indomethacin did not affect the changes in tissue lipoprotein lipase activity observed following recombinant HuTNF-alpha administration. Serum triacylglycerol concentration increased by 2- and 6-fold; 4 and 20 h after recombinant HuTNF-alpha administration. Disappearance of 14C-labeled triacylglycerol from the circulation after injection of small chylomicrons, biosynthetically labeled in their triacylglycerol and cholesterol moieties, was lower in TNF-treated than in control rats. However, the clearance rate of triacylglycerol was the same or even higher in recombinant HuTNF-alpha treated rats (assuming that 14C-labeled chylomicron triacylglycerol represents the serum triacylglycerol pool). The livers of recombinant HuTNF-alpha-treated rats and controls contained similar amounts of 14C-labeled lipids, but less [3H]cholesterol, suggesting that in recombinant HuTNF-alpha-treated rats, the liver took up chylomicron remnant particles enriched with triacylglycerol. Separation of the d less than 1.04 g/ml fraction of serum obtained from control and recombinant HuTNF-alpha treated rats by zonal ultracentrifugation revealed that in recombinant HuTNF-alpha-treated rats the lipoprotein particles were less lipolyzed than in controls. The secretion rate of [3H]triacylglycerol into the serum was determined 90 min after injection of [3H]palmitate albumin complex and Triton WR 1339. In recombinant HuTNF-alpha-treated rats, the secretion of [3H]triacylglycerol into plasma was 48% higher than in controls. It is suggested that the increase in lipoprotein lipase activity of heart and diaphragm resulted from an indirect effect of TNF. It is concluded that the increase in serum triacylglycerol in the recombinant HuTNF-alpha-treated rats is due mainly to an increased secretion of triacylglycerol by the liver. Impaired lipolysis, probably due to a fall in hepatic lipase could also contribute to the rise in plasma triacylglycerol.

Animals↗
PubMed1989

Effects of long-term xamoterol therapy on the left ventricular mechanical efficiency in patients with ischemic heart disease.

Myocardial oxygen uptake and an index of mechanical left ventricular efficiency were determined in basal conditions or during prolonged therapy with the new beta 1-adrenoceptor partial agonist xamoterol in 16 patients with mild to moderate ischemic heart failure. During xamoterol therapy, left ventricular end-diastolic pressure decreased from 24.4 +/- 6.5 to 17.8 +/- 8.6 mm Hg (P less than 0.01) and the isovolumic index of inotropic state (dP/dt)/DP40 increased by 14% (P less than 0.01). The heart rate increased slightly and the mean systolic and peak systolic wall stress also tended to increase (+ 7%; NS) but myocardial oxygen uptake (14.1 vs 14.7 ml/min; NS) and the index of efficiency (8.77 +/- 3.44 to 8.82 +/- 4.27; NS) were not significantly modified. In conclusion, prolonged therapy with xamoterol was not accompanied by a deterioration in the mechanical efficiency of the ventricle, even in patients with ischemic heart disease.

Adrenergic beta-Agonists↗