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Biomedical subjects

J Etienne

Publications and source records attributed to J Etienne.

At least 289 records · Page 16Linked to original sources

[Bacteriological diagnosis of infectious endocarditis. Evaluation of a system for eliminating antibiotics in the blood].

We carried out 310 blood-cultures on samples from patients receiving antibiotics for either known or suspected infective endocarditis or suspected septicaemia. The culture bottles were inoculated either directly or after the antibiotics had been removed from the blood sample by the Antimicrobial Removal Device System. Out of 63 bacterial isolates from 21 patients (15 infective endocarditis and 6 septicaemias), 45 were made by both methods, 16 only after treatment with the Antimicrobial Removal Device System and two only after conventional culture. Of the 45 paired isolates, eight were cultured more rapidly after Antimicrobial Removal Device System treatment compared with none by conventional culture. The Antimicrobial Removal Device System thus significantly increased the number of positive cultures and the speed of their isolation. In practice, Antimicrobial Removal Device System treatment proved useful in five of the 21 cases, but delayed culture in one. Its greatest value was in showing persistent bacteraemia in patients being treated for prosthetic valve endocarditis.

Anti-Bacterial Agents↗

Importance of the different steps of glycosylation for the activity and secretion of lipoprotein lipase in rat preadipocytes studied with monensin and tunicamycin.

Lipoprotein lipase synthesized by cultured rat preadipocytes is present in three compartments: an intracellular, a surface-related 3-min heparin-releasable, and that secreted into the culture medium. 30 min after addition of 6 microM monensin, the lipoprotein lipase activity in the heparin-releasable compartment starts to decrease; by 4 h of monensin treatment the lipoprotein lipase activity in the heparin-releasable pool and in the culture medium is about 10% of that found in control dishes. The intracellular activity, which had been identified as lipoprotein lipase by an antiserum to lipoprotein lipase, increases slowly and doubles by 24 h. However, since the cellular compartment accounts for 10-25% of total activity, this increase does not account for the missing enzyme activity. To determine whether this enzyme molecule is synthesized but is not active, incorporation of labeled leucine, mannose and galactose into immunoadsorbable lipoprotein lipase was studied in control, monensin- or tunicamycin-treated cells. Addition of tunicamycin (5 micrograms/ml) for 24 h caused a 30-50% reduction in immunoadsorbable lipoprotein lipase, but the enzyme activity was reduced by 90%. On the other hand, 4 h monensin treatment reduced both incorporation of [3H]leucine into immunoadsorbable lipoprotein lipase and heparin-releasable and medium lipoprotein lipase activity by 57 to 77%. The immunoadsorbable lipoprotein lipase in the intracellular compartment has a [14C]mannose to [3H]galactose ratio of 0.15 and this ratio increased 6-fold in monensin-treated cells. The intracellular lipoprotein lipase in monensin-treated cells had the same affinity for both the native and synthetic substrate as the lipoprotein lipase in control cells, yet its spontaneous secretion into the culture medium and its release by 3 min heparin treatment was markedly decreased. The present results indicate that: the presence of asparagine-linked oligosaccharide (formation of which is inhibited by tunicamycin) is mandatory for the expression of lipoprotein lipase activity; lipoprotein lipase is active also in a high mannose form; and terminal glycosylation and oligosaccharide processing, which is inhibited by monensin, may be important for the appearance of heparin-releasable lipoprotein lipase and secretion of lipoprotein lipase into the medium.

Adipose Tissue↗

Maturation and secretion of lipoprotein lipase in cultured adipose cells. I. Intracellular activation of the enzyme.

The intracellular pathway and the activation of lipoprotein lipase have been examined in differentiated Ob17 cells. These adipose cells were previously shown to secrete lipoprotein lipase during exposure to heparin. Treatment of the cells with cycloheximide and heparin leads to enzyme depletion, as shown by activity measurement and immunofluorescence microscopy. The repletion phase has been studied in the presence of monensin or carbonyl cyanide m-chlorophenylhydrazone, ionophores known to affect the intracellular transport of membrane and secretory proteins. Monensin-treated cells synthesize fully active lipoprotein lipase. Under these conditions the antigen accumulates in the Golgi apparatus and the heparin-stimulated enzyme release is extensively reduced. Carbonyl cyanide m-chlorophenylhydrazone-treated cells do not contain any enzyme activity but show detectable antigen which accumulates in the endoplasmic reticulum. Competition for binding to immobilized anti-lipoprotein lipase antibodies of mature and endoplasmic reticulum-sequestered antigens is observed. Carbonyl cyanide m-chlorophenylhydrazone removal is rapidly followed by a transient burst of enzyme activity and a redistribution of the antigen in the different subcellular compartments. Therefore, the results show that the activation of lipoprotein lipase is an intracellular event taking place after the enzyme exits from the endoplasmic reticulum and before it reaches the trans-Golgi cisternae.

Adipose Tissue↗

Antibody against rat adipose tissue lipoprotein lipase.

To facilitate detailed studies of rat adipose tissue lipoprotein lipase regulation, a high titre polyclonal antibody was raised against purified rat adipose tissue lipoprotein lipase (in a goat). The first stage of the purification of the lipoprotein lipase was carried out with heparin-Sepharose affinity chromatography. In the second stage we took advantage of the binding property of lipoprotein lipase to ampholytes. These ampholytes, used during this second step, do not have to be eliminated prior to injecting the enzyme preparation into the animal. They have neither toxic nor antigenic effects on the animal; moreover, their presence does not affect the antigenic potency of the lipoprotein lipase. When pre-incubated with a constant amount of adipose tissue lipoprotein lipase (8 mU/75 microliter), an equal volume of the antiserum raised either pure or diluted up to 1/50 resulted in complete inhibition of enzyme activity, and half maximal inhibition was observed at a dilution of 1/800. The antibody was effective in inhibiting rat heart lipoprotein lipase but not salt-resistant hepatic lipase. Immunodiffusion revealed a single line of precipitation between this antibody and the adipose tissue lipoprotein lipase.

Adipose Tissue↗

The in-vitro activity of pristinamycin against Haemophilus influenzae and Neisseria meningitidis.

The in-vitro activity of erythromycin, oleandomycin, spiramycin, josamycin and pristinamycin was tested by a plate-dilution method against strains of Haemophilus influenzae and Neisseria meningitidis. Pristinamycin was the most active product tested with minimal inhibitory concentrations (MIC) ranging between 0.5 and 4 mg/l for H. influenzae (modal value 1 mg/l) and between 0.03 and 0.12 mg/l for N. meningitidis (modal value 0.06 mg/l).

Anti-Bacterial Agents↗

Prophylaxis of infective endocarditis for dental procedures. Report of a working party of the European Society of Cardiology.

Bacterial endocarditis still remains a serious disease with significant morbidity and mortality. In patients with known valve disease, most cases are caused by oral viridans streptococci. These organisms are present in vast numbers on the gum margins and in gum pockets. They cause transient bacteraemia during eating and tooth brushing. More substantial, but short-lived bacteraemia can occur during dental treatment such as extraction and scaling. Bacteria may then become attached to abnormal endocardium leading to the development of infective endocarditis. Prophylaxis of endocarditis during dental procedures in patients with known valve disease should thus be aimed at reducing the number of bacteria entering the blood stream and eliminating those that get there. This can be sought first by good oro-dental hygiene and secondly by the use of prophylactic antibiotics. In this paper, we set out simple guidelines for practitioners in those countries that do not already have recommendations of their own. They are based on guidelines already in use in the United Kingdom, France, Switzerland and the United States.

Anti-Bacterial Agents↗

Adipose conversion of ob17 cells and hormone-related events.

The ob17 preadipocyte clonal line has been established from the adipocyte fraction of the epididymal fat pads of adult C57 BL/6J ob/ob mice. In vivo, injection of ouabain-resistant mutant cells (ob 17OR11 cell line) into athymic mice is followed by the formation of fat pads containing ouabain-resistant mature fat cells. In vitro, ob17 cells develop after confluence biochemical and morphological characteristics of adipocytes. The adipose conversion process is best represented by a stochastic model in which a pool of stem cells (adipoblasts) give rise to clusters of adipose cells and to additional stem cells that remain in the population. The role of the different factors involved in such conversion is discussed; (1) factors that enhance the number of susceptible cells (ACF or ACF-like compounds), (2) factors without which no adipose conversion takes place (triiodothyronine, growth hormone and other factors still to be characterized), (3) factors that enhance the expression of the differentiation program (insulin). The early emergence of lipoprotein lipase occurs normally in insulin-depleted medium. The separation of ob17 cells by isopycnic centrifugation shows that lipoprotein lipase is present at high levels in early differentiating cells which are still devoid of late markers, ie glycerol-3-phosphate dehydrogenase and triglycerides. These results are discussed with respect to the determination of cellularity during development of adipose tissue in vivo.

Adipose Tissue↗

Modulation of lipoprotein lipase in the intact rat by cholera toxin--an irreversible agonist of cyclic AMP.

Rats were injected intravenously with cholera toxin, a potent stimulator of adenylate cyclase, and lipoprotein lipase was determined in various organs and plasma. 16 h after cholera toxin injection, lipoprotein lipase activity increased 2-6-fold in heart, diaphragm and lung and decreased to one-third in adipose tissue. An increase in lipoprotein lipase activity was seen in the plasma and in the liver, as determined by antiserum to lipoprotein lipase. The increase in heart lipoprotein lipase was preceded by a rise in cyclic AMP and continued for 24 h when cyclic AMP returned to base-line levels. Both heparin-releasable and residual lipoprotein lipase increased in the heart, but to an unequal extent. The more pronounced rise in residual activity (up to 10-fold) could have contributed to an increase in the t1/2 of heart lipoprotein lipase from 1.5 to 2.6 h. The relatively lower increase in heparin-releasable lipoprotein lipase could have been due to a loss of the enzyme from this compartment into the circulation. The effect of cholera toxin on heart and adipose tissue lipoprotien lipase was observed in fasted, fed and super-fed animals and thus appears to be independent of the nutritional state of the animal. Since cholera toxin not only mimics hormonal stimulation, but causes an exaggerated response to hormones, it made studies on some aspects of regulation of both the functional and storage forms of lipoprotein lipase in the intact organism possible.

Adipose Tissue↗

Inhibitory factor of phospholipase A2 in normal human serum.

Normal human serum and plasma were shown to contain a factor inhibiting phospholipase A2. This factor has been separated from human serum and plasma by chromatography on a Blue-Ultrogel column and was eluted by tris-HCl buffer (pH 7.2); the proteins eluted by 1 M NaCl-tris HCl buffer exhibited phospholipase A2 activity. This activity was abolished when the inhibitory factor was added to proteins possessing such activity. The inhibitory factor was not dialysable, sensitive to both heat and trypsin treatment, suggesting that it is a protein. In vitro, the same factor inhibited phospholipase A2 rat serum.

Animals↗

Bacterial endocarditis presenting as acute vertebral osteomyelitis: 14 cases.

Association between bacterial endocarditis (BE) and vertebral osteomyelitis (VO) has infrequently been noted. In a retrospective analysis of BE (280 cases) and VO (150 cases) 14 cases were found to have this association. There were 12 males and 2 females, ages ranging from 39 to 72 years, mean age 56.6. Blood cultures were positive for Streptococcus viridans (6 cases). Str. faecalis (4 cases), staphylococcus (2 cases), Gram negative bacteria (1 case). Organism was not isolated in one case. Fever and severe back pain antedate the diagnosis of VO 3.5 and 2.5 months. X rays films of the spine and bone scans (4 cases) revealed lumbar (6 cases) or cervical (4 cases), or dorsal (3 cases) or combined cervical and dorsal (1 case) locations. History of murmur (4 cases) and development of mitral (8 cases) or aortic (4 cases) or combined mitral and aortic (2 cases) insufficiencies were consistent with concomitant BE. Echocardiogram revealed vegetations in 6 out of 9 cases. Patients received antibiotic therapy for 3.5 months. Ten patients were cured with antibiotics only, 4 required valve replacement. One died. Thus age, sex, history of heart disease, valvular involvement, duration of symptoms prior to admission and bacteriological pictures are the same in BE with VO as in BE without VO. Survival rates are also the same if early recognition of BE and VO with prompt and prolonged antibiotic therapy may prevent severe haemodynamic or vertebral problems.

Acute Disease↗

Prognosis of native valve infective endocarditis: a review of 253 cases.

Forty years after the first 'recoveries' obtained by antibiotherapy and twenty years after the first success of early valvular replacement, the mortality of infective endocarditis (IE) is still significant. The present study has been undertaken to clarify the factors which influence the prognosis of IE.

Acute Disease↗

Indices of effectiveness of medical and surgical treatment in 40 cases of prosthetic valve endocarditis.

Forty patients with prosthetic valve endocarditis (PVE) presenting during a 12-year period at a single hospital were studied. Twenty-six were male and 14 female and ages ranged from 19 to 67 years. During the first six post-operative months, most episodes were caused by staphylococci (38%) and Gram negative bacilli (24%). Between 6 and 11 months no episodes were seen, but thereafter streptococci predominated (50%). The overall mortality was 58% (66% during first six months; 36% thereafter). Nine of 23 patients undergoing re-operation died, most deaths occurring in patients in cardiac failure prior to surgery. Eleven deaths occurred in the 17 patients treated with antibiotics alone. Six of these were pyrexial at death and all but one was infected by a virulent organism. The remaining five were apyrexial at death and all had staphylococcal PVE. Our findings suggest: (1) all cases occurring during the first six months should be initially treated as 'early' PVE; (2) in staphylococcal PVE, apyrexia may not mean cure; (3) the principal guides to prognosis in PVE are the patient's cardiac status and the nature of the infecting organism.

Adult↗