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Biomedical subjects

P Richard

Publications and source records attributed to P Richard.

At least 127 records · Page 7Linked to original sources
PubMed1996

[Traumatic tricuspid insufficiency].

Traumatic tricuspid insufficiency is a rare condition. The diagnosis is difficult because of the slow progression of this pathology and the presence of more clinically acute lesions. Non-penetrating chest trauma is responsible for 90% of cases. Echocardiography is the investigation of choice for assessing the mechanism of the tricuspid regurgitation and for diagnosing associated lesions. It should be performed systematically in patients with multiple trauma. The surgical indications are difficult to determine and depend on the patients' symptoms and the type of anatomical lesions. It should be undertaken before right ventricular myocardial dysfunction. Several techniques may be used from valvuloplasty to valve replacement mainly with bioprostheses in symptomatic patients.

Adult↗
PubMed1996

Maturation of the electroretinogram in children: stability of the amplitude ratio a/b.

We report the method and results of mesopic electroretinogram (ERG) recording by corneal electrode in 75 children aged from 0 to 15 years. This method gives an overall evaluation of the electrical activity of the retina in a rapid and acceptable manner, in the awake state and without sedation. The a- and b-waves were present at birth. The amplitude of these waves increased considerably throughout the period studied. The decrease in latencies was statistically significant only for the b-wave between birth and 6 months. The presence of oscillatory potentials increased with age. The amplitude ratio a/b remained constant at about 0.25 in all age groups. This a/b ratio thus constitutes, under the recording conditions described, a criterion of normality that is independent of age.

Adolescent↗
PubMed1996

[Pleuropericarditis complicated of tamponade disclosing mixed connective tissue disease. Remission with non-steroidal anti-inflammatory agents. Apropos of a case].

Mixed connective tissue diseases or Sharp's syndrome are inflammatory diseases essentially presenting in the form of joint, muscle and skin manifestations. Pleuropericardial involvement is uncommon and rarely the presenting sign, and tamponade is exceptional. This clinical report concerns a case of pleuropericarditis complicated by tamponade in a 22-year-old man, constituting the presenting sign of Sharp's syndrome. The diagnosis of mixed connective tissue disease was based on the combination of clinical signs and a high serum anti-RNP antinuclear antibody titre. The treatment of the pericarditis is base on prescription of corticosteroids, but non-steroidal anti-inflammatory drugs were sufficient in our case. Larger effusions may require corticosteroids and pericardial drainage. We report the value of immunological assays in the aetiological assessment of pleuropericarditis in young subjects.

Adult↗
PubMed1995

ATP synthesis by the F0F1-ATPase from the thermophilic Bacillus PS3 co-reconstituted with bacteriorhodopsin into liposomes. Evidence for stimulation of ATP synthesis by ATP bound to a noncatalytic binding site.

F-type ATPase from the thermophilic Bacillus PS3, TF0F1, which was essentially free of bound nucleotides after isolation and purification, was co-reconstituted into liposomes with the light-driven proton pump bacteriorhodopsin. The time course of the light-induced ATP synthesis was biphasic; an initial slow phase accelerated to a final steady-state rate two to three times faster. Adding ATP before initiating the reaction suppressed the slow phase, suggesting that the state of occupancy of specific sites by ATP regulated the synthetic activity of TF0F1. Incubating the purified TF0F1 with ADP and ATP revealed one ADP and two ATP binding sites that were stable to gel filtration. We analyzed the time courses of light-induced ATP synthesis for the enzyme with different nucleotide content, after co-reconstitution into liposomes with bacteriorhodopsin. The two ATP sites were identified to have regulatory function. A complex containing TF0F1.ADP, 1:1, was co-reconstituted with various quantities of ATP to obtain a range of molar ratios of TF0F1.ADP:ATP of between 1:0 and 1:1.7. It was found that the initial rate of ATP synthesis increased with the level of ATP bound to the enzyme. After binding one ATP, a stimulation of ATP synthesis by a factor of 2 was observed. The second ATP site also exhibited regulatory properties. It stimulated ATP synthesis but to a much smaller extent; the stimulation did not exceed 20%. Binding of the photoreactive analogues 2-azido-[alpha-32P]ADP and 2-azido-[alpha-32P]ATP to the TF0F1 and their effects on the rate of ATP synthesis are described further.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗
PubMed1995

Viridans streptococcal bacteraemia in patients with neutropenia.

Viridans streptococcal bacteraemia is frequent in neutropenic patients. 25 neutropenic patients with viridans streptococcal bacteraemia were compared with 64 control patients. Exposure to repeated chemotherapy or cytarabine were independent risk-factors for streptococcal bacteraemia. The use of carboxyureidopenicillins and a stay in laminar-airflow rooms were protective. In a further cohort study of 49 patients, oral streptococci with the same ribotype as blood isolates were recovered from all 7 bacteraemic patients. The oral cavity is a portal of entry for viridans streptococci bacteraemia in neutropenic patients, especially after oral mucosal damage induced by repeated chemotherapy.

Anti-Bacterial Agents↗
PubMed1995

Identification of a new apolipoprotein E variant (E2 Arg142-->Leu) in type III hyperlipidemia.

A new rare apolipoprotein E mutant was identified as we were investigating the apolipoprotein E genotype of patients with type III hyperlipidemia (HLP III). The unusual DNA restriction fragment length polymorphism profile and then the sequence analysis of a PCR amplified fragment of the proband's apo E gene revealed a simple base substitution (G-->T) at nucleotide 3836. This mutation leads to the replacement of arginine by leucine at position 142 of the mature protein. The proband carried the mutant allele at the heterozygous status with an epsilon 3 allele. Subsequently, analysis of the proband's father's apo E gene showed that same mutated allele associated with an epsilon 2 allele. The two subjects presented a dysbetalipoproteinemia in which this new apo E variant could be implicated.

Aged↗
PubMed1995

Monofluorophosphate increases lumbar bone density in osteopenic patients: a double-masked randomized study.

To assess the efficacy of combined sodium monofluorophosphate and calcium therapy (FC) in increasing lumbar bone mineral density (BMD) in patients with low bone mass, we conducted a prospective double-masked randomized study in 94 patients aged 50-70 years. Patients were selected on the basis of a lumbar BMD at least 2 standard deviations (SD) below the young adult mean (T-score) but without evidence of previous vertebral fracture (severe osteopenia). They were randomly assigned to receive for 2 years, twice a day, either FC (13.2 mg F-, i.e. 100 mg sodium monofluorophosphate, and 500 mg Ca2+) or C (500 mg Ca2+). Vertebral BMD was measured by dual photon absorptiometry from L2 to L4. Comparison at final assessment in the 76 eligible patients (Student's t-test) showed a statistically significant difference between the two groups in the mean BMD increase in favour of FC. Furthermore, Student's t-test showed a significantly greater increase in lumbar BMD in FC-treated patients at 1 year, at 18 months and after 2 years (mean increase of 7.1%/year). These results were confirmed by ANOVA at 1 year, at 18 months and after 2 years of treatment. Of the FC-treated patients, 71.4% were considered to have responded (i.e. they showed an increase in lumbar BMD of more than 0.034 g/cm2). The dosage of 26.4 mg fluoride ion/day (i.e. 200 mg monofluorophosphate/day) therefore appears to be safe and to increase the BMD effectively in patients with low bone mass prior to vertebral fracture.

Absorptiometry, Photon↗
PubMed1995

Genotyping of a patient homozygous for a rare apolipoprotein E1 [Gly127-->Asp; Arg158-->Cys] (Weisgraber allele).

We examined the apolipoprotein E polymorphism of an obese patient presenting non-insulin-dependent diabetes, hypertension and moderate lipid disturbances. The apolipoprotein E genotyping carried out from leukocyte DNA using PCR amplification and restriction enzyme digestion demonstrated homozygosity for the rare apoE1[Gly127-->Asp; Arg158--> Cys] (Weisgraber allele). The nucleotide change results in a glycine to aspartic acid substitution at amino acid 127 in the apolipoprotein E2.

Alleles↗
PubMed1995

Cardiac myosin binding protein-C gene splice acceptor site mutation is associated with familial hypertrophic cardiomyopathy.

Familial hypertrophic cardiomyopathy (FHC) is an autosomal dominant disease characterized by a ventricular hypertrophy predominantly affecting the interventricular septum and associated with a large extent of myocardial and myofibrillar disarray. It is the most common cause of sudden death in the young. In the four disease loci found, three genes have been identified which code for beta-myosin heavy chain, cardiac troponin T and alpha-tropomyosin. Recently the human cardiac myosin binding protein-C (MyBP-C) gene was mapped to chromosome 11p11.2 (ref. 8), making this gene a good candidate for the fourth locus, CMH4 (ref. 5). Indeed, MyBP-C is a substantial component of the myofibrils that interacts with several proteins of the thick filament of the sarcomere. In two unrelated French families linked to CMH4, we found a mutation in a splice acceptor site of the MyBP-C gene, which causes the skipping of the associated exon and could produce truncated cardiac MyBP-Cs. Mutations in the cardiac MyBP-C gene likely cause chromosome 11-linked hypertrophic cardiomyopathy, further supporting the hypothesis that hypertrophic cardiomyopathy results from mutations in genes encoding contractile proteins.

Amino Acid Sequence↗
PubMed1995

Characterization of spontaneous and N-methyl-D-aspartate-induced calcium rise in rat cultured hypothalamic neurons.

The effect of N-methyl-D-aspartate (NMDA) on intracellular calcium concentration ([Ca2+]i) was analyzed in cultured hypothalamic neurons using the Ca(2+)-sensitive fluorescent dye Fura-2. The resting [Ca2+]i in silent neurons ranged between 35 and 100 nM and regular spontaneous [Ca2+]i oscillations were observed in 37% of neurons. Such [Ca2+]i oscillations were blocked by tetrodotoxin (TTX--the sodium channel blocker), and reduced by the voltage-sensitive calcium channel blockers omega-conotoxin (omega-CTX-GVIA) (N-type) and nifedipine (L-type). NMDA increased [Ca2+]i transients and MK-801 [(+)-5-methyl-10,11-dihydro-5H-dibenzo(a,d')cyclohepten-5,10-imine hydrogen] reduced them, in a dose-response manner. The amplitude of the NMDA-induced [Ca2+]i rise increased with increasing external Ca2+ concentrations, and was completely abolished in Ca(2+)-free medium. The role of intracellular calcium was tested by addition of intracellular Ca2+ mobilizers. In the presence or absence of external Ca2+, 2,5-di(tert-buty)-1,4-benzohydroquinone) (tBuBHQ) (25 microM) evoked a robust [Ca2+]i rise in NMDA-sensitive neurons. Preincubation (20 min) with tBuBHQ completely abolished the NMDA-induced [Ca2+]i response. Caffeine (10 mM), thapsigargin (25 microM), and ryanodine (10 microM) did not elicit any Ca2+ transients. Nifedipine and omega-CTX-GVIA did not modify NMDA-induced [Ca2+]i transients. NMDA-induced [Ca2+]i rise was not altered by 0.1 microM TTX but at 1 microM it was reduced by 20%. These data show that hypothalamic neurons in culture respond to NMDA in a dose-dependent manner by a rise in [Ca2+]i and that this response is mediated by NMDA receptor-gated channel. In addition, [Ca2+]i rise is dependent on the presence of extracellular Ca2+, and also seems to involve mobilization of Ca2+ from tBuBHQ-sensitive intracellular stores.

Animals↗
PubMed1995

Longitudinal survey of Loa loa filariasis in southern Cameroon: long-term stability and factors influencing individual microfilarial status.

A longitudinal, one-year survey of Loa loa infection was carried out in an endemic area of southern Cameroon. Parasitologic samplings (calibrated thick blood smears) were performed every two months to study the evolution of loiasis infection at both the population and the individual level. The mean number of measurements by subject was 3.8 (range 1-6). At the population level, prevalence of infection and microfilarial load were found to be very stable over time. This observation is consistent with the existence of an important reserve of parasitic material available for vectors and the maintenance of high levels of transmission. At the individual level, both the microfilarial status (microfilaremic/nonmicrofilaremic) and the level of parasitemia showed a remarkable stability over time. Age was the relevant factor that influenced the individual microfilarial status in the whole population. When only microfilaremic individuals were taken into account, age did not influence the level of microfilaremia, suggesting that loiasis could be considered as a noncumulative disease. The stability of individual microfilarial status and the pattern of infection variations observed with age support the view that genetic factors might be involved in host defense mechanisms against loiasis infection.

Adolescent↗
PubMed1995

[Neuropapillitis in Behçet disease. A case].

The authors report the case of a 34 year old woman, who developed acute neuropapillitis, which appeared to be the first ophthalmologic manifestation of Behçet's disease. One year later, this patient recurred with another neuro-ophthalmologic sign: a sixth nerve palsy.

Abducens Nerve↗