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Biomedical subjects

H Mathieu

Publications and source records attributed to H Mathieu.

At least 73 records · Page 4Linked to original sources
PubMed1987

Absence of plasma prostacyclin stimulating activity deficiency in hemolytic uremic syndrome.

We compared the effect of plasma from 19 children with hemolytic uremic syndrome (HUS) on prostacyclin (PGI2) production by fresh rat aortic rings to the effect of plasma from 17 age- and sex-matched normal children, taking into account the PGI2 baseline aortic production (PGI2 release in presence of buffer, 21 determinations). After 10, 20, 30, 40, and 60 minutes incubation of rat aortic tissue with either plasma or buffer, the presence of PGI2 was studied by measuring by radioimmunoassay (RIA) the concentration of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha). 6-keto-PGF1 alpha production increased with time in the two groups of plasma samples and in the presence of buffer, but 6-keto-PGF1 alpha production (ng/mg dried tissue) after 30 minutes incubation and mean 6-keto-PGF1 alpha production (slope of regression line, ng/mg/min) were significantly (P less than 0.01) lower in the presence of normal plasma compared with buffer, and significantly (P less than 0.01) higher in the presence of HUS plasma compared with normal plasma. There was no significant difference between buffer and HUS plasma. We conclude that, under our experimental conditions, normal plasma had an inhibitory activity on 6-keto-PGF1 alpha production by rat aorta. This inhibitory activity was absent in HUS plasma.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Urinary excretion of N-acetyl-glucosaminidase and beta-2-microglobulin as early markers of gentamicin nephrotoxicity in neonates.

A prospective study in 16 healthy and 16 gentamicin-treated neonates was undertaken to compare the urinary excretion of proximal tubular markers such as beta 2-microglobulin (beta 2-m) and total N-acetyl-beta-D-glucosaminidase (NAG) and its isoenzymatic form NAGB. beta 2-m excretion was not related to postnatal age in control full-term neonates; it was significantly increased in gentamicin-treated full-term neonates. The urinary excretion of the lysosomal markers, total NAG and NAGB, rose significantly with postnatal age in control group. fMean values for total NAG and NAGB were significantly higher in the treated group but the isoenzymatic profile (NAGB/total NAG X 100) was not modified by gentamicin treatment.

Acetylglucosaminidase↗
PubMed1987

Vitamin D-dependent calcium-binding proteins (CaBPs) in human fetuses: comparative distribution of 9K CaBP mRNA and 28K CaBP during development.

The vitamin D-dependent calcium-binding protein (CaBP) cholecalcin or calbindin, has been used as a molecular marker of 1,25-dihydroxyvitamin D3 action. Mammals possess two CaBPs: a 9,000 mol wt (9K CaBP) and a 28,000 mol wt (28K CaBP). The distinct localization of each protein in the rat has been previously described with the aid of specific radioimmunoassays developed for each CaBP. Antibodies raised against the rat 28K CaBP can be used to detect this protein in a number of mammalian species including humans. In contrast, antibodies against rat 9K CaBP do not cross react with human 9K CaBP, but human 9K CaBP mRNA can be analyzed using a cDNA probe for rat 9K CaBP mRNA. Such a cross-hybridization between the rat cDNA probe and human CaBP mRNA was demonstrated by Northern analysis. We have documented the distribution and evolution of 28K CaBP and 9K CaBP mRNA in human tissues during fetal development from 14 to 32 wk of gestation. 28K CaBP was only present in kidney and cerebellum, and not detectable in duodenum. There was a 2-fold increase of 28K CaBP in the cerebellum between 14 and 24 wk of gestation. The 9K CaBP mRNA was unevenly distributed in human fetal tissues. 9K CaBP mRNA was present in classical vitamin D target tissues such as duodenum and placenta; high levels of 9K CaBP mRNA also were found in thymus and lung.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

[Importance of the study of the minimal bactericidal time of serum in the choice of optimal treatment of neonatal septicemias].

Rapid eradication of bacteria in bloodstream is critical for the outcome in neonatal bacterial sepsis. Two groups of neonates with E. coli K1 sepsis without purulent meningitis were studied. Group I (n = 14) received cefotaxime IV (100 mg.kg-1 D-1) plus netilmicin (4 mg.kg-1 D-1); group II (n = 8) received amoxicillin/clavulanic acid IV (100/10 mg.kg-1 D-1) plus netilmicin (4 mg.kg-1 D-1). Both groups were identical. For all strains MICs of cefotaxime, amoxicillin/clavulanic acid, netilmicin were less than 0.2, 4 and 1 mg/l respectively. Serum bactericidal activity (SBA) was determined for each patient (peak sample). The SBA was defined as the greatest dilution in which 99,99% of the inoculum was killed. Time-kill curves were performed with 1:16 dilutions of peak serum samples to measure the kinetic of bacterial killing. The minimal bactericidal time of serum (MBTS) was defined as the minimal time required to observe a decrease of more than 4 log CFU/ml of the bacterial inoculum. Samples (10 microliters) were taken at 1 h intervals over a 6 h period and at 24 h for quantitative culture. All patients cured. Median SBA were respectively 1/128 and 1/64 for group I and II. However, mean MBTS for groups I and II were respectively 1.2 h +/- 0.8 and 3.9 h +/- 1.4. Killing was more rapid in group I (p less than 0.01). The MBTS may be a clinically useful adjunctive test when optimal therapy would be expected.

Amoxicillin↗
PubMed1987

[Clinical study and effect of nitroxoline on fecal flora in children].

Twelve children (mean age: 4) are treated in practice office with nitroxoline (200 mg/kg/24 h) during 10 days for urinary tract infection. A study on the effect of nitroxoline against the fecal flora is undertaken in a group of 21 children who receive nitroxoline during 4 days or a long period. Bacteriological and clinical efficacy is checked when urinary concentrations of nitroxoline are greater than 16 mg/l. The results show 8 clinical and bacteriological success one true failure and 3 failure due to a non-compliance to the treatment. No qualitative and quantitative modification of the fecal flora is observed after treatment with nitroxoline.

Adolescent↗
PubMed1986

Evidence for the presence of Calbindin-D 28K (CaBP-28K) in the tibial growth cartilages of rats.

The distribution of the vitamin-D dependent calcium-binding protein (Calbindin-D 28K) (CaBP-28K) in the tibial growth plate cartilage of the rat has been studied immunohistochemically using an antibody raised against rat renal CaBP-28K. The protein was detected mainly in the nuclei of chondrocytes and occasionally in the juxtanuclear cytoplasm. The distribution was not uniform throughout the growth plate, but concentrated in the proliferatively active chondrocytes of the resting and proliferative zones. These findings raise the possibility that CaBP-28K may be involved in the mitotic activity of the chondrocytes, acting as a regulator of the proliferative process, perhaps via intranuclear calcium.

Animals↗
PubMed1986

Vitamin-D-dependent calcium-binding protein (CaBP-9K) in rat growth cartilage.

The presence of vitamin-D-dependent calcium-binding protein (CaBP-9K) in tibial growth-plate cartilage was immunohistochemically demonstrated using a specific antibody to rat duodenal CaBP-9K. The protein was found to be mainly localized in the cytoplasm of maturing chondrocytes. In hypertrophic chondrocytes, CaBP-9K concentrations decreased, and the protein was found in the cytoplasmic processes. No CaBP-specific immunoreactivity was seen in the hypertrophic chondrocytes of the lower calcified hypertrophic zone; in contrast, the protein was found in the extracellular lateral edges of longitudinal septa, i.e. where matrix vesicles are preferentially localized and where cartilage mineralization is initiated. These findings suggest that vitamin D has a direct function in this tissue. It also seems likely that CaBP-9K is an indicator of chondrocyte maturation, and that it is involved in the matrix vesicle-associated process of cartilage calcification.

Animals↗
PubMed1986

Sequential echocardiographic study prior and during antihypertensive therapy in children with severe hypertension.

This study was performed to assess myocardial involvement in 18 children with severe hypertension (HT), using two dimensional (2D) guided M mode echocardiography, prior and during therapy. All patients but 2 had renal or renovascular disease. Septal diastolic thickness (SDT) was utilized as a serial marker. Except for one case, all patients had increased SDT initially (1.03 +/- .26 cm/m2, p less than .01 vs normal). Evolution under therapy allowed subdivision of patients: Group I: 12 patients showed left ventricular (LV) hypertrophy regression, within a follow-up period of 20 +/- 9 months (final SDT: .78 +/- .12 cm/m2 vs initial 1.09 +/- .28, p less than .01). Blood pressure (BP) was normalized in 9 patients, and borderline in 3. Therapy consisted on acebutolol (n = 10), captopril (n = 1), and renal artery surgery (n = 1). Group II: LV hypertrophy was unchanged (n = 3) or increased (n = 3), within a follow-up period of 19 +/- 8 months, with persistent severe (n = 3) or mild (n = 3) HT, under acebutolol (n = 5). Treatment was changed to captopril with subsequent normal BP and echocardiogram improvement (n = 3). In the overall population, final SDT was significantly correlated to the final BP (r = .69, p less than .01). In conclusion, echocardiographic follow-up allowed serial non invasive assessment of LV hypertrophy in our severely hypertensive pediatric population. At first echocardiogram, LV hypertrophy was present in all patients but one. Antihypertensive therapy allowed simultaneous decrease of BP and LV hypertrophy in 12 patients, 10 under acebutolol.

Acebutolol↗
PubMed1986

[Optimum choice of antibiotic treatment in neonatal infections due to group B streptococci].

Morbidity and mortality among neonates with group B streptococcal infections remain high. As delays in bacterial killing may be responsible for these poor results, there is a need for studies into killing kinetics. We investigated antimicrobial sensitivity and killing effect time lags for penicillin, ampicillin and mezlocillin, alone and in combination with gentamicin or amikacin, against 20 strains of group B streptococci isolated in cultures of blood and cerebrospinal fluid from neonates. A culture of each strain (10(5) germs/ml) was exposed to the antibiotics individually or in combination. Antibiotics were used in the concentrations achieved clinically. Surviving bacteria were counted after 2 h 30, 4 h 30 and 24 h. incubation. Mean killing curves showed that the time interval until onset of a killing effect was 24 hours with either penicillin or ampicillin alone, against 4 h 30 with penicillin-amikacin or ampicillin-gentamicin. The most rapid killing effect (2 h 30) was observed with mezlocillin alone and ampicillin-amikacin. No antagonism was found between mezlocillin and aminoglycosides. Choice of the best antibiotic treatment for group B streptococcal infections should be based on both the rapidity of the in vitro killing effect and the antibiotic's diffusion into the site of the infection.

Amikacin↗
PubMed1985

Regulation of rat yolk sac 25-hydroxy- and 1,25-dihydroxyvitamin D3 24-hydroxylase activities.

The yolk sac of the pregnant rat which functions as a true placenta is a target organ for vitamin D. This tissue can hydroxylate in position 24 both 25-hydroxy- and 1,25-dihydroxyvitamin D3 (25-OHD3 and 1,25-(OH)2D3). The present report describes an in vitro model for the study of 1,25-(OH)2D3 action on the further metabolism of 25-OH[3H]D3 and 1,25-(OH)2[3H]D3 by yolk sac. The tissue explants were preincubated with 1,25-(OH)2D3 for 18 h in a serum-free culture medium. Physiological concentrations of 1,25-(OH)2D3 were the most effective in stimulating (7.5-fold) the 1,25-(OH)2D3 24-hydroxylase, while the 25-OHD3 24-hydroxylase stimulation (4-fold) required a 1,25-(OH)2D3 concentration of 10(-7) M. The stimulating effect of 1,25-(OH)2D3 on the 1,25-(OH)2D3 24-hydroxylase was temperature-dependent, and, since its was inhibited by actinomycin D and cycloheximide, required de novo protein synthesis. 1,24,25-(OH)3D3, 25-OHD3, and 24,25-(OH)2D3 were 10- to 1000-fold less potent than 1,25-(OH)2D3 in inducing the 1,25-(OH)2D3 hydroxylase. Our results strongly suggest that 1,25-(OH)2D3 regulated the 1,25-(OH)2D3 24-hydroxylase by a receptor-mediated process. Furthermore, 1,25-(OH)2D3 at 10(-9) M induced within 4 h an increase of its own degradation and the formation of an as yet unidentified major 1,25-(OH)2[3H]D3 metabolite. We conclude that the yolk sac can participate in the regulation of 1,25-(OH)2D3 concentration in the fetoplacental unit.

24,25-Dihydroxyvitamin D 3↗
PubMed1985

Impact of cefotaxime on the fecal flora in children.

A differential quantitative analysis was used to study the effect of cefotaxime on the fecal flora in 26 hospitalized children ranging from two days to four years of age. Fecal specimens were obtained before, during and after therapy. This study was evaluated in comparison to 41 patients of the same age and from the same environment without antibiotic treatment or signs of infection. The fecal flora of the control group showed qualitative and quantitative stability. Two groups of species were distinguished: a group in which the upper limit was less than or equal to 10(7) bacteria/g of stool (Klebsiella, Enterobacter, other enterobacteria, Staphylococcus, Pseudomonas) and a group with less than or equal to 10(10) bacteria/g of stool (anaerobes, Escherichia coli, Streptococcus D). This stability of the control group of subjects allowed us to interpret the variations of microbial concentrations during and after cefotaxime treatment. In previous studies, we showed in the newborn a substantial risk of septicemia of intestinal origin when overgrowth occurred, especially with Klebsiella. With cefotaxime there was a decrease or a disappearance in 65% of E. coli and a slight decrease of Klebsiella and Enterobacter. This fact was of great interest in the treatment of endogenous secondary septicemia. We observed an appearance of Pseudomonas (nine Pseudomonas aeruginosa, two Pseudomonas putida, one Pseudomonas fluorescens) in 12 cases among the 26 children treated.(ABSTRACT TRUNCATED AT 250 WORDS)

Bacteria↗
PubMed1985

Urokinase treatment of pulmonary artery thrombosis complicating the pediatric nephrotic syndrome.

Two pediatric patients with severe pulmonary thrombosis complicating a lipoid nephrosis were treated with urokinase administered either as a continuous infusion or in massive bolus doses. Both patients recovered but one died suddenly 2 yr later after recurrence of the nephrotic syndrome and probably new massive pulmonary thrombosis. These patients had severe abnormalities of hemostasis and fibrinolysis, which favored thrombosis and complicated fibrinolytic treatment.

Child↗
PubMed1985

Presence of immunoreactive vitamin D-binding protein in rat yolk sac endodermal cells.

The visceral yolk sac is, in the rat, an organ which possesses true placental functions. We recently showed that yolk sac is involved in the control of metabolism and action of vitamin D in the fetoplacental unit, since its endodermal cells contain a 24-hydroxylase for vitamin D metabolites and the 1,25-dihydroxyvitamin D receptor. In the present work, by using indirect immunoperoxidase staining, we demonstrate that an immunoreactive vitamin D-binding protein (DBP) is present in this yolk sac throughout embryonic and fetal development. It is mainly located at the apex of the endodermal cells. Immunoprecipitation studies of radioactive proteins synthesized in vitro by yolk sac explants showed that yolk sac DBP, in contrast to alpha-fetoprotein, is not synthesized in situ by yolk sac. This result, combined with the location of DBP at the apex of the endodermal cells which face the uterus, strongly suggests that yolk sac DBP is of maternal origin. The concomitant presence in the endodermal cells of this DBP, of the 1,25-dihydroxyvitamin D receptor, and of the system hydroxylating vitamin D metabolites in position 24, certainly has considerable physiological significance.

Animals↗