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Biomedical subjects

A Robert

Publications and source records attributed to A Robert.

At least 19 recordsLinked to original sources
PubMed1992

[Use of conventional and complementary medical care in patients with chronic non-cancerous pain].

The use of medical care was surveyed among 157 chronic pain patients. Half of them had consulted more than 6 and up to 17 specialists in "conventional" medicine for their pain problem. Moreover, 46% had used "complementary" medicine. They had tried many different "alternative" therapies in 40% of the cases. The users of "complementary" medicine, mostly females, also sought care from a significantly higher number of "conventional" therapists, had more physiotherapy, took drugs more frequently and had tried a larger number of different medications, even though their pain characteristics were similar to those of the other patients studied. Interestingly, they remained significantly more active professionally than patients who had never used "complementary" medicine. These characteristics could be attributed to a more active manner of coping with chronic pain.

Adaptation, Psychological↗
PubMed1992

l-folinic acid versus d,l-folinic acid in rescue of high-dose methotrexate therapy in children.

BACKGROUND: At this time, folinic acid (FA) is commercially available as the racemic mixture d,l-FA, whose biological activity is supported by natural l-FA. The administration of d,l-FA results in the accumulation of d-FA in plasma relative to the active l-FA form; in vitro studies have shown that d-FA can compete with the polyglutamation of methotrexate (MTX). PURPOSE: Our purpose was to compare, on a pharmacokinetic, biological, and clinical basis, the racemic mixture d,l-FA with the pure l-FA in rescue of high-dose MTX therapy (5 g/m2) in children with acute lymphocytic leukemia (ALL). METHODS: Eighteen children with ALL were entered in this trial, which was planned with a crossover design. Four cycles of MTX were administered to each patient, and rescue was achieved orally every 6 hours at a dose of 12 mg/m2 for d,l-FA and 6 mg/m2 for pure l-FA. The d,l-FA and l-FA rescues were alternated from one cycle to the next. d-FA, l-FA, and the active metabolite 5-methyltetrahydrofolate (5-MTHF) were measured in plasma using a stereospecific high-performance liquid chromatography assay. RESULTS: Considering total active folate levels (l-FA + 5-MTHF), mean residual concentrations were similar for rescue by d,l-FA and l-FA, after two and six intakes, respectively: 92 and 186 nM for d,l-FA rescue versus 100 and 184 nM for l-FA rescue. Intra-individual comparison of total active folates (l-FA + 5-MTHF) did not show any significant difference between d,l-FA rescue and l-FA rescue. After administration of d,l-FA, the accumulation of d-FA in plasma was confirmed. For both types of FA rescue, MTX terminal half-lives were identical (average value, 13.9 hours). Considering each type of toxic effect (hematologic, hepatic, renal, and digestive), there was no significant difference in the proportion of toxic cycles following l-FA rescue or d,l-FA rescue. CONCLUSION: The administration of the pure l-FA, compared with the administration of the racemic mixture, results in comparable blood profiles of active folates and MTX, leads to equivalent treatment tolerance, and avoids the plasma accumulation of d-FA.

Adolescent↗
PubMed1992

Proteolytic susceptibility of the central domain in chicken gizzard and skeletal muscle dystrophins.

We investigated proteolytic susceptibility of the central domain in dystrophin molecules from chicken smooth and skeletal muscles. Dystrophin-enriched preparations from both muscles were made as described in Pons et al. (Proc. Natl. Acad. Sci. USA (1990) 87, 7851-7855). These preparations contained other protein components in addition to dystrophin. Three enzymes (Staphylococcus aureus proteinase, chymotrypsin and trypsin) having different proteolytic specificities were used. Time-courses of proteinase degradation were examined by the Western immunoblot technique using a specific polyclonal serum directed against a fragment (residues 1173-1728) of the dystrophin central domain. We observed accumulation of some major proteinase-resistant fragments, in the 110-160 kDa range originating from that central region of the molecule. Cleavage patterns of the smooth and skeletal muscle preparations were quite similar, but molecular weights of the breakdown products differed slightly. Interpretation of the results was based on two predictive structural models of the dystrophin central domain (Koenig and Kunkel (1990) J. Biol. Chem. 265, 4560-4566 and Cross et al. (1990) FEBS Lett. 262, 87-90). Skip residues at the end of repeat 13 (around the 1740th residue of the dystrophin amino acid sequence), as hypothesized in the Cross model, constitute probably the most sensitive site within the dystrophin central domain for any exogenous (or even endogenous) proteinase. Variations observed between dystrophins from skeletal and smooth muscles also suggest that the structures of both dystrophins differ slightly even within the dystrophin central domain. This precise identification of proteinase-resistant dystrophin fragments of variable lengths is a first step towards further physicochemical studies on the very large and rare dystrophin molecule.

Animals↗
PubMed1992

trans,trans-Muconic acid, a reliable biological indicator for the detection of individual benzene exposure down to the ppm level.

trans,trans-Muconic acid (2,4-hexadienedioic acid) (t,t-MA) is a minor benzene metabolite which can be used as a biological indicator for benzene exposure. The purpose of the study was to evaluate the limits of use of t,t-MA for detection and quantification of occupational exposures to benzene, particularly on an individual scale, phenol being used as the metabolite of reference. A simple and sensitive method previously described by the authors was carried out to analyse t,t-MA in 105 end-of-shift urinary samples from 23 workers exposed to benzene used as an extraction solvent for "concretes" recovery in the perfume industry. Good correlations were found between atmospheric benzene and both metabolites (uncorrected or corrected for creatinine) or between the metabolites themselves, with correlation coefficients from 0.81 to 0.91 (P < 0.0001). Correlation- coefficients were not improved after correction for creatinine. The overall individual benzene exposure range, median, and arithmetic mean were respectively 0.1-75, 4.5, and 9.0 ppm with corresponding t,t-MA excretion of 0.1-47.9, 5.2 and 8.9 mg/l (uncorrected) and phenol excretion of 1.4-298, 30.9, and 42.2 mg/l (uncorrected). In the control group (145 determinations for t,t-MA and 76 for phenol from 79 individuals) the range, median, and arithmetic mean were respectively < 0.04-0.66, 0.08, and 0.13 mg/l (uncorrected t,t-MA) and 1.5-42.0, 9.85 and 11.3 mg/l (uncorrected phenol). t,t-MA was far more specific than phenol and could be easily and practically used to estimate with a given probability the upper or lower corresponding benzene concentrations down to around the ppm level.(ABSTRACT TRUNCATED AT 250 WORDS)

Air Pollutants, Occupational↗
PubMed1992

Prognostic significance of karyotype in a twelve-year follow-up in childhood acute lymphoblastic leukemia.

We report a follow-up of 49 children with acute lymphoblastic leukemia (ALL) diagnosed between 1972 and 1978 (follow-up 12-18 years). This series allowed us to analyze the predictive value of karyotype in a long-term follow-up. Karyotypes were abnormal in 33 cases (67.3%): pseudodiploidy in 11 (22.4%), hyperdiploidy > 50 chromosomes in 8 (16.3%), hyperdiploidy 47-50 chromosomes in 11 (22.4%), and hypodiploidy in 3 cases (6.1%). Event-free survival (EFS) and survival studies showed that the outcome of patients was determined only by treatment and karyotype. Eleven patients have survived, nine in first remission (6 years 5 months to 15 years 2 months), and two are in second remission (3 years 8 months and 8 years 2 months). All ploidy groups are represented in these patients. Late relapses can occur in the hyperdiploid > 50 group, thus accounting for shorter EFS than expected, but because of the unusually long second remission of one patient, the rate of surviving patients was higher for this ploidy group than for all other ploidy groups together. Conversely, patients with only numerical abnormalities (no matter which ploidy group they belonged to), had a better outcome than did patients with structural changes or normal karyotypes and no discrepancy between EFS and survival curves was observed in this chromosomal group. Thus, our results suggest that numerical changes only should be considered an indicator of low risk factor, but our results, based on partially banded karyotypes, need to be verified by a current method and therapy.

Adolescent↗
PubMed1992

Prognostic significance of silent exertional myocardial ischaemia in symptomatic men without previous myocardial infarction.

A total of 360 consecutive male patients with complaints of chest pain and documented coronary artery disease underwent a maximal exercise test combined with thallium myocardial scintigraphy. Patients with a history of previous myocardial infarction were excluded. During follow-up (46 months; from 12 to 96) 27 patients died and 26 had a first non-fatal myocardial infarction. The 6-year survival rate and the 6-year event-free rate were 81 and 71%. Four variables contributed independently to the prognosis (Cox Model): the number of diseased vessels, the angiographic ejection fraction, the age and a multivariate score of the exercise test. From these patients, 227 had an abnormal response to exercise (ST-segment depression greater than or equal to 0.1 mV); in 138 patients, angina pectoris was induced during exercise while 89 patients had no pain during exercise (silent ischaemia). These 89 patients with silent exertional ischaemia were matched to 89 patients with exertional angina pectoris, according to the above-mentioned four prognostic predictors. The two groups of patients had similar signs of ischaemia during exercise (ST-segment depression and thallium perfusion score). The 6-year survival rates (81 and 81.5%) and the 6-year event-free rates (71 and 70.5%) were similar in the two groups. Thus, in men without previous myocardial infarction, silent exertional ischaemia bears the same prognosis as exertional ischaemia attended by angina pectoris.

Adult↗
PubMed1992

Expression of recombinant proteins on the surface of the coagulase-negative bacterium Staphylococcus xylosus.

An expression system to allow targeting of heterologous proteins to the cell surface of Staphylococcus xylosus, a coagulase-negative gram-positive bacterium, is described. The expression of recombinant gene fragments, fused between gene fragments encoding the signal peptide and the cell surface-binding regions of staphylococcal protein A, targets the resulting fusion proteins to the outer bacterial cell surface via the membrane-anchoring region and the highly charged cell wall-spanning region of staphylococcal protein A. The expression system was used to secrete fusion proteins containing sequences from a malaria blood-stage antigen and a streptococcal albumin-binding receptor to the cell surface of S. xylosus. Analysis of the recombinant cells by immunogold staining and immunofluorescence revealed that both the receptor and the malaria peptide were properly processed and exposed on the surface of the host cells. However, only approximately 40 to 50% of the recombinant cells were strongly stained with antiserum reactive with the albumin-binding receptor, while approximately 10 to 15% of the cells were stained with antiserum reactive with the malaria peptide. The incomplete staining of some of the cells suggests steric effects that make the recombinant fusion proteins inaccessible to the reactive antibodies because of variable cell wall structures. However, the results demonstrate for the first time that recombinant techniques can be used to express heterologous receptors and immunogens on the surface of gram-positive cells.

Amino Acid Sequence↗
PubMed1992

Morphological and functional gastric cytoprotection by prostaglandin in rats receiving absolute ethanol orally.

Pretreatment with prostaglandins at non-antisecretory doses protects the gastric mucosa, including the parietal cells, from deep necrosis produced by intragastric administration of necrotising agents such as absolute ethanol. Whether the parietal cells also retained their ability to secrete acid when rats were pretreated with a prostaglandin, in spite of exposure to ethanol, was investigated. Gastric acid secretion was abolished 4 hours after ethanol, and secretion returned to control values only after 5-6 days. Pretreatment with a single, non-antisecretory dose of 16, 16-dimethyl prostaglandin E2 (dm PGE2) maintained acid secretion, in spite of exposure to absolute ethanol. Absolute ethanol caused histological changes - extensive gastric mucosal necrosis (through the muscularis mucosae), oedema, haemorrhages, polymorphonuclear infiltration, and formation of granulation tissue - that were maximal 24-48 hours after ethanol and persisted for 2 to 4 weeks. None of these changes were present in animals treated with the prostaglandin. It is concluded that a single oral pretreatment with dmPGE2 protects the gastric mucosa against not only the morphological damage of absolute ethanol (preventing necrosis, haemorrhages, and polymorphonuclear infiltration) but also the functional damage (maintaining the acid secretory function of parietal cells).

16,16-Dimethylprostaglandin E2↗
PubMed1992

Low-dose endothelin-1 potentiates volume-induced secretion of atrial natriuretic factor.

To evaluate the role of calcium in volume-induced secretion of atrial natriuretic factor (ANF), effects of verapamil and endothelin-1 (ET-1), both known to influence free intracellular calcium, were studied during saline infusion in seven conscious instrumented dogs. Fifteen minutes after intravenous injection of placebo or verapamil (0.25 mg/kg) or during continuous ET-1 infusion (at 5 ng.kg-1.min-1), saline (10% body wt) was infused during 40 min. Saline produced a rise (P less than 0.001) of plasma ANF from 28.1 +/- 6.3 to 50.4 +/- 12.9 pM after placebo, from 30.2 +/- 6.1 to 51.1 +/- 8.5 pM after verapamil, and from 31.2 +/- 6.1 to 81.0 +/- 12.9 pM with ET-1. This increase was comparable after placebo and verapamil, but was 80% greater with ET-1 (P less than 0.02). Plasma ET-1, unchanged after placebo, rose (P less than 0.001) from 1.7 +/- 0.5 to 38.3 +/- 9.2 pM with ET-1. In the three experiments, heart rate and left atrial pressure (LAP) increased (P less than 0.001) similarly. The linear relation between ANF and LAP was steeper with ET-1 than with saline or verapamil (both P less than 0.05), indicating that the enhanced ANF secretion with ET-1 was occurring at all levels of LAP. Thus volume-induced secretion of ANF is not suppressed by verapamil, but is directly enhanced by low-dose ET-1, known to activate the phosphoinositide pathway.

Angiotensin II↗
PubMed1992

Regional oxidative metabolism in patients after recovery from reperfused anterior myocardial infarction. Relation to regional blood flow and glucose uptake.

BACKGROUND: Enhanced uptake of the glucose analogue 18F-fluorodeoxyglucose (FDG) in relation to flow has been proposed as an accurate method of identifying viable myocardium. The evaluation of myocardial oxidative metabolism could be an alternate way to identify reversible injury. The aim of the present study was to investigate in patients with reperfused anterior infarction whether differences in regional oxidative metabolism exist among regions with and without flow-metabolism mismatch. METHODS AND RESULTS: Fifteen patients with reperfused anterior myocardial infarction were studied between 2 weeks and 3 months after the acute event. Regional myocardial blood flow (13N-ammonia; three-compartment model), oxidative metabolism (11C-acetate; monoexponential clearance), and glucose uptake (FDG, linear graphic analysis) were evaluated with dynamic positron emission tomography. Flow-metabolism patterns were used to differentiate reversibly (FDG/flow greater than 1.2) from irreversibly injured myocardium (FDG/flow less than 1.2) using circumferential profile technique. Relative 13N-ammonia uptake was reduced in 71 of 90 anterior and/or septal segments, including 24 with (seven patients) and 38 without (eight patients) flow-metabolism mismatch. Acetate clearance (k), reflecting oxidative metabolism, was reduced by 51% in the center of the infarct area versus remote segments (27 +/- 12 versus 55 +/- 13 min-1.10(-3), p less than 0.001). Compared with infarct segments without flow-metabolism mismatch, segments exhibiting increased glucose uptake relative to flow had faster acetate clearance (35 +/- 14 versus 23 +/- 9 min-1.10(-3), p less than 0.01). Similarly, myocardial blood flow was better preserved in segments with flow-metabolism mismatch (54 +/- 13 versus 45 +/- 8 ml/min/100 g, p less than 0.01) compared with segments without mismatch. However, at similar levels of hypoperfusion, there was no significant difference in acetate clearance among segments with and those without flow-metabolism mismatch: 37 +/- 14 versus 41 +/- 15 min-1.10(-3), respectively. A positive correlation (r = 0.89, p less than 0.001) was found between absolute myocardial blood flow and acetate clearance, regardless of the flow-metabolism pattern. CONCLUSIONS: In patients with reperfused myocardial infarction studied between 2 weeks and 3 months after the acute event, regional oxidative metabolism is reduced in proportion to residual myocardial blood flow and does not differ significantly among similarly hypoperfused segments with and without flow-metabolism mismatch.

Acetates↗
PubMed1992

Systematic use of aprotinin in cardiac surgery: influence on total homologous exposure and hospital cost.

To assess the impact of systematic use of aprotinin, 115 consecutive adults undergoing cardiac surgery were randomly allocated with a sealed envelope technique. Treated (T) patients (n = 58) received 2.10(6) Kallikrein Inactivating Units (KIU) before incision, 2.10(6) prior to bypass, and 5.10(5) KIU.hr-1 for 5 hrs, whereas control (C) cases (n = 57) received nothing. Surgeons, perfusionists, ICU and ward physicians were blinded. Postoperative blood loss decreased from 1198 ml (C) to 698 ml (T) (p less than 0.001). Total transfusional needs were 7.25 (C) and 4.9 (T) units (p less than 0.01), where from 65% were autologous in group T, versus 51% in group C (p less than 0.02). Total homologous exposure decreased from 4.5 (C) to 2.7 (T) units on the average, from 3 to 1 units as a median (p less than 0.01). Multiple Stepwise Regression Analysis showed treatment as the most important variable influencing postoperative blood loss, but duration and type of procedures were more important to explain transfusion needs. Both groups were comparable for other pre- and intra-operative variables. For coronary operations (n = 75), aprotinin showed the strongest negative association with blood loss, the number of arterial conduits being the second influencing variable. No evidence was found for increased early graft thrombosis. The average hospital bill was 9% lower in the treated group, an unexplained finding needing independent confirmation.

Adult↗
PubMed1992

Vasomotor response to ergometrine and nitrates of saphenous vein grafts, internal mammary artery grafts, and grafted coronary arteries late after bypass surgery.

BACKGROUND: In vitro studies have shown that the vasomotor response of internal mammary artery to vasoactive agents differs from that of saphenous vein. METHODS AND RESULTS: To assess whether the response in vivo to methylergometrine and to nitrates differs in saphenous vein grafts, internal mammary artery grafts, and coronary arteries, 25 patients were studied more than 6 months (range, 6-96 months) after surgery. Angiograms of saphenous vein grafts (n = 11) or mammary artery grafts (n = 14) were obtained in basal conditions, after intravenous infusion of 0.4 mg methylergometrine, and after intragraft infusion of 1 mg isosorbide dinitrate. Computerized quantitative angiography was used to assess the changes in luminal diameter of the bypass graft and of the grafted coronary artery (n = 11). Methylergometrine reduced the diameter of saphenous vein grafts by 6.9 +/- 7.4%, from 3.26 +/- 0.71 to 3.05 +/- 0.76 mm (p < 0.01), and that of grafted coronary arteries by 9.3 +/- 7.2% (NS compared with saphenous vein grafts), from 2.08 +/- 0.49 to 1.89 +/- 0.49 mm (p < 0.005). The diameter of internal mammary artery grafts did not change significantly, from 3.27 +/- 0.42 to 3.25 +/- 0.44 mm (-0.3 +/- 5.1%, p < 0.02 compared with saphenous vein grafts and p < 0.002 compared with coronary arteries). After isosorbide dinitrate, the diameter of both grafted coronary arteries and mammary artery grafts increased significantly (respectively to 2.46 +/- 0.62 mm and 3.44 +/- 0.43 mm), the vasodilatation being greater (p < 0.002) in coronary arteries (+17.8 +/- 9.8% in proportion to basal diameter, p < 0.001) than in mammary grafts (+5.5 +/- 3.3%, p < 0.001). The diameter of saphenous vein grafts returned to control values (3.28 +/- 0.70 mm, NS compared with basal); the changes in luminal diameter after nitrates (+0.7 +/- 3.1%, NS) were significantly smaller than for mammary artery grafts (p < 0.01) and for grafted coronary arteries (p < 0.001). CONCLUSIONS: Unlike internal mammary artery grafts, saphenous vein grafts constrict in response to methylergometrine and do not dilate in response to nitrates. These differences in vasomotor response could reflect heterogeneity in the sensitivity of vascular smooth muscle to these agents or differences in the basal level of vasomotor tone.

Cardiac Catheterization↗
PubMed1992

Mitoxantrone and high dose Ara-C for the treatment of ANLL in childhood: a pilot study of the EORTC CLCG (EORTC 58 872).

Since January 1988, 91 children with ANLL have been treated with a polychemotherapy regimen containing Mitoxantrone (MTZ), excluding other anthracyclines. Induction consisted of Ara-C, MTZ, and VP 16. Consolidation lasted 6 weeks with Vincristine, MTZ, Ara-C and 6-thioguanine (6TG), and was followed by 2 intensification courses combining High-dose Ara-C with respectively MTZ or VP 16. Maintenance therapy associated 6TG, Ara-C and MTZ up to a cumulative dose of 150 mg/m2. 91 patients are evaluable: 70 (76.9%) achieved complete remission, 59 (64.8%) after induction alone. There were 7 early deaths, 5 deaths in complete remission, and 17 relapses. Major toxic side effects were observed during the consolidation phase, mainly infectious complications, and the median duration of neutropenia was 82 days in this phase, leading to decrease the MTZ dose from 10 to 8 mg/m2. The event-free survival at three years is 38%. Cardiac toxicity is presently absent in children without previous cardiopathy.

Adolescent↗
PubMed1992

[Extracellular matrix and vascular pathologies. Role of proteases and oxygenated free radicals].

Vessel walls contain several types of mesenchymatous cells and many representatives of the 4 groups of macromolecules of the extracellular matrix secreted by those cells. Under normal conditions, a proportion of the macromolecules of the vascular wall is broken down by the neosynthesis of an equivalent amount of the same macromolecules which are then integrated into functional structures. Under pathological conditions, an excessive amount of macromolecules is broken down by proteases and free radicals, without any compensatory increase in biosynthesis and without the integration of biosynthesised compounds into functional structures. Thus, for example, a varicose saphenous vein may lose as much as 60 per cent of the collagen of its wall. Attempts at symptomatic treatment designed to combat this loss of substance, a notable cause of weakening of he vessel wall, are based upon three principles: inhibition of catabolic enzymes, chiefly proteases (e.g. leucocyte elastase), responsible for excessive breakdown; uptake of oxygenated free radicals; "substrate protection" designed to preserve undamaged fibrous proteins and to help the integration of neosynthesized compounds into functional structures. Only medications which act as "substrate protectors" are capable of coping at one and the same time with the effects of proteases and those of oxygenated free radicals.

Aging↗
PubMed1991

A homologue of dystrophin is expressed at the neuromuscular junctions of normal individuals and DMD patients, and of normal and mdx mice. Immunological evidence.

Polyclonal and monoclonal antibodies, which recognize different regions and epitopes of the dystrophin molecule, bind to a protein of Mr 400,000 which is present in extracts of mdx muscle from regions which contain neuromuscular junctions (NMJ) and is absent from those which do not. This NMJ-associated homologue of dystrophin has at least 2 epitopes which are different to usual Xp21 form of dystrophin expressed along the sarcolemma of muscle fibres in normal muscles. This protein is also expressed at the NMJ of a DMD patient who lacks the first 52 exons of the Xp21 dystrophin gene and it must therefore be translated from a different gene transcript.

Animals↗