[Superficial pemphigus in children. Induction role of amoxicillin?].
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Biomedical subjects
Publications and source records attributed to D Lambert.
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Corrinoids were extracted with hot ethanol from human plasma and faeces and separated by high-performance liquid chromatography. The corrinoids (cobalamin and cobalamin analogues) were quantified in the eluted fractions by a dual radioisotope assay using as binders intrinsic factor and haptocorrin to detect cobalamin and total corrinoids, respectively. Recoveries ranged from 37.7 +/- 5.1% for hydroxycobalamin to 75.0 +/- 9.1% for cyanocobalamin. In plasma, the main forms of cobalamin were the coenzymes methylcobalamin and 5'-deoxyadenosylcobalamin (32.1 +/- 13.4 and 28.4 +/- 12.3%, respectively, of total corrinoids). The cobalamin analogue fraction of plasma was eluted with a retention time close to that of cobinamide and of deoxyadenosylcobalamin. In the faeces, most of the corrinoids separated were detected better by the haptocorrin assay than by the intrinsic factor assay. One corrinoid peak was eluted with the same retention time as cobinamide. This peak was detected by haptocorrin assay but not by intrinsic factor assay. It could therefore correspond to cobinamide.
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Glutathione peroxidase (GPX), superoxide dismutase (SOD) and catalase are the most important enzymes of the cell antioxidant defense system. However, these molecules are themselves susceptible to oxidation. The aim of this work was to estimate to what extent this system could be inactivated by its own substrates. We tested the effect of hydrogen peroxide, cumene hydroperoxide, t-butyl hydroperoxide and hydroxyl and superoxide radicals on GPX, SOD and catalase. For GPX, a 50% inactivation was observed at 10(-1) M (30 min, 37 degrees C) for hydrogen peroxide, 3 x 10(-4) M (15 min, 37 degrees C) for cumene hydroperoxide and 5 x 10(-5) M (11 min, 37 degrees C) for t-butyl hydroperoxide. Unlike the hydroxyl radicals, superoxide anions did not inactivate this enzyme. Catalase was inactivated by hydroxyl radicals and by superoxide anions but organic peroxides had no effect. SOD was inactivated by 50% by hydrogen peroxide at 4 x 10(-4) M (20 min, 37 degrees C), but organic peroxides and hydroxyl radicals were ineffective on this enzyme. Since the three enzymes of the antioxidant system are susceptible to at least one of the oxidative reactive molecules, in the case of high oxidative stresses such an inhibition could take place, leading to an irreversible autocatalytical process in which the production rate of the oxidants will continuously increase, leading to cell death.
Early and accurate detection of prosthetic arterial graft infection is important because this serious complication of vascular surgery carries high morbidity and mortality rates. This report describes the use of a new method of isotopic imaging to detect graft infection using 99mTc-hexametazime-labelled leucocytes. Seventeen patients with potentially infected arterial grafts were imaged in addition to routine investigations but were managed according to our normal surgical practice. 99mTc-imaging was positive in eight patients with proven graft infection and falsely positive in one patient with a groin haematoma (89 per cent specificity). There were no false negatives (100 per cent sensitivity) after an average follow-up of 6 months (range 3-9 months). This technique has proved a reliable and rapid method of confirming graft infection.
Antioxidant enzymes (catalase, superoxide dismutase and glutathione peroxidase) have been injected into human fibroblasts exposed to 2 atm O2 in order to test if the threshold of oxidative damage versus antioxidant defenses could be modulated and if the damage remains reversible beyond the threshold. Cell damage was estimated by thymidine incorporation and cell survival curves. The proportion of dividing cells, measured by thymidine incorporation, rapidly decreased after O2 incubation: no cells could divide after 15 h of hyperoxia. However, cells incubated for a short time and injected with a high concentration of any of the three enzymes divided like non-oxygen-incubated cells: the enzymes could protect the cells against their loss of division potential. However, when cells were incubated for a longer period and/or when the injected enzyme concentration was lower, cells were either less or not protected and could no longer divide. These results suggest the presence of a threshold for the oxidative damage which cannot be totally repaired and which impairs the cell division; this threshold can, however, be modulated by supplementation of antioxidant enzymes, glutathione peroxidase being the most efficient.
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The thrombosis rate after long-term cannulation of the radial artery was assessed prospectively in 48 intensive care patients randomly assigned to groupe A (polyethylene Leader-Cath 115-09 catheter; n = 50, aged 55 +/- 20 years, 74% male patients) or groupe B (Teflon Viggo Floswitch 4441 catheter; n = 48, aged 58.6 +/- 16 years, 73% male patients). Bedside angiography was carried out with 10 to 15 ml Hexabrix before removal of the catheter. The two groups were similar with regard to anthropometric parameters, used drugs, pathological events during the stay in ICU, arterial cannulation technique and its duration. There was no case of clinically significant ischaemia. The rate of X-ray total arterial thrombosis was 20% in group A, and 2% in group B (p less than 0.01). There was no difference in the rate of partial thrombosis (54% vs. 41.7% respectively, NS) and of lack of thrombosis (26% vs. 56.3% respectively, NS). The overall rate of thrombosis was greater in group A than in group B, but not significantly (74% vs. 43.7% respectively). The duration of arterial cannulation did not influence the rate of thrombosis. However it was higher in males of Group A than in those of Group B (p less than 0.01), when heparin was not given (p less than 0.05); when vaso-active drugs were used (p less than 0.05); and when the time required for cannula insertion was greater than 5 min (p less than 0.01). It is concluded that Teflon catheters are more biocompatible than polyethylene catheters.
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Percutaneous balloon angioplasty offers an alternative to surgery for the alleviation of symptoms in upper limb arterial disease. This report documents 28 per-femoral dilatation procedures in 27 patients for 33 subclavian, two innominate, and two axillary lesions. Thirty-four stenoses and three occlusions were treated, with multiple dilatations in five patients. Indications for treatment were: arm ischaemia (15 patients); neurological (steal syndrome) symptoms (8); and combined ischaemia plus steal (5). Angioplasty was technically successful in 27 procedures with symptomatic relief in 25 cases up to a mean follow-up of 24 months (median 20 months, range 2-90 months). One patient had successful repeat angioplasty for recurrent ischaemic symptoms after 30 months. Angioplasty improved pulse deficits in all but two patients and reduced arm blood pressure differential to less than 30 mmHg in all but three patients. There were three complications: a femoral artery occlusion and a groin haematoma required surgical intervention and another patient suffered an extension of a contralateral stroke. Percutaneous balloon angioplasty has proved safe and effective. We recommend angioplasty as the first line treatment for ischaemic or neurological symptoms in upper limb vascular disease.
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Pharmacokinetics and tissue penetration of cefotetan were studied after a single injection of 2 g for antibiotic prophylaxis in colo-rectal surgery. Beta half-life was 4.3 +/- 1 h, total body clearance was 0.74 +/- 0.2 ml/kg/min and volume of distribution was 270 +/- 76 ml/kg. At time of laparotomy, cefotetan concentration was 14.2 +/- 7 micrograms/g in abdominal wall fat and 16.4 +/- 1 micrograms/g in epiploic fat. In the colonic wall, cefotetan concentration was 33.3 +/- 16 micrograms/g. At time of abdominal closure, cefotetan concentrations were 6.3 +/- 3 micrograms/g in the abdominal wall fat and 6.1 +/- 4 micrograms/g in the epiploic fat.
The pharmacokinetics of ofloxacin was studied in 12 intensive care patients, 6 of whom being under mechanical ventilation. All patients had a creatinine clearance greater than 60 ml/min/1.73 m2 and they were given 3 mg/kg. IV ofloxacin within 30 mn, with a twice daily regimen for 7 days. Pharmacokinetic studies were performed on day 1 (D1) and 7 (D7). Between D1 and D7 a significant increase in T 1/2 beta, AUC and blood levels were observed together with a decrease in total body clearance. Creatinine clearance was not modified between D1 and D7 but ofloxacin renal clearance was considerably altered. Abnormalities in ofloxacin renal tubular secretion may account for the drug cumulation which was observed during repeated administration in intensive care patients.
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The plasma, in addition to the liver, is a major site of hydrolysis of aspirin. Human plasma and liver aspirin esterase activities in samples from a group of patients varied over a two fold range and there was a significant correlation between individual plasma and liver activities. Human liver aspirin esterase was present in the cytosolic and microsomal fractions. Cytosolic and microsomal enzymes had different activities and apparent affinities for aspirin.