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Biomedical subjects

N Fabre

Publications and source records attributed to N Fabre.

53 records · Page 3Linked to original sources
PubMed1993

Analysis of the resistance to heat and hydrogen peroxide stresses in COS cells transiently expressing wild type or deletion mutants of the Drosophila 27-kDa heat-shock protein.

The Drosophila melanogaster small heat-shock protein, hsp27 (Dhsp27) belongs to a family of polypeptides which shares a sequence related to alpha-crystallin and which protect cell against heat shock. Dhsp27 accumulates following heat shock and, in absence of stress, in the central nervous system, imaginal discs and the gonads of the developing fly. Two internal and adjacent deletion mutants in the conserved alpha-crystallin domain of Dhsp27 were constructed. Expression vectors containing either the coding sequence of Dhsp27 or that of the two deletion mutants linked to the Simian-Virus-40 late promoter were used to transfect monkey COS cells. The transient expression of Dhsp27 was found to decrease the sensitivity of COS cells to heat and hydrogen-peroxide stresses as judged by Trypan-blue staining and indirect immunofluorescence analysis. Using this rapid test, we observed that a deletion of 62 amino acids, which lies at the 5' end of the conserved alpha-crystallin domain and covers the first 41 amino acids of this region had only a weak effect on the protective activity of Dhsp27. This suggests that the N-terminal half of the conserved alpha-crystallin domain may not be essential for the protective activity of the small hsp. In contrast, Dhsp27 was no more active when the last 42 amino acids of the alpha-crystallin domain were deleted. Biochemical fractionation and indirect immunofluorescence analysis indicated that the protective function of Dhsp27 was localized at the level of the nucleus.

Animals↗
PubMed1993

DNA analysis of haemophilia A families from southern France. Experience of a hospital laboratory.

A sample of 101 individuals from 19 unrelated families from Southern France affected with haemophilia A was studied in our laboratory from 1990 to 1992. The aim of the analysis was to define the carrier status of women related to a haemophiliac, or to find an informative DNA marker for further prenatal diagnosis in obligate carriers. Three intragenic (BclT/intron 18, XbaI/intron 22, AlwNI/intron x7) and two extragenic polymorphisms (TaqI/St14, BglII/DX13) were used for this study. The tested population exhibited some original characteristics, including a lower rate of heterozygosity for the FVIII BclI polymorphism and a number of specificities for the St14 RFLP. We also compared the different methodologies available for each RFLP in a routine diagnostic service, and determined a strategy for linkage analysis in our population.

Adult↗
PubMed1993

[Creutzfeldt-Jakob disease after treatment with human extracted growth hormone. A clinicopathological study].

This report describes the pathological changes observed in the brain of a 18-year-old patient who died with Creutzfeldt-Jakob disease (CJD) of the ataxic and panencephalopathic type. Clinically, the disease began at age 17 with a rapidly progressive cerebellar syndrome, associated with myoclonus and mental deterioration. Cranial CT scan and MRI showed minor abnormalities. EEG demonstrated non specific changes. The patient became progressively demented, bedridden and died 10 months after the onset. Nine years earlier, he had been operated upon for craniopharyngioma and subsequently treated with cadaver-derived human growth hormone. Post-mortem examination of the brain revealed mild diffuse atrophy. Histology showed congophilic amyloid plaques found in both gray and white matters of the cerebrum and cerebellum, associated with spongiosis, mainly in the basal ganglia and cerebellum, and gliosis. They were immunostained with antiprion protein antibody using the immunoperoxidase method on paraffin embedded sections. The clinical findings in this case were similar to those of other cases of human growth hormone-associated CJD. However, this case is unusual because of the great number of amyloid plaques, which have been only rarely found in previous reports.

Amyloid↗
PubMed1993

Alopecia: an adverse effect of bromocriptine.

We report the cases of two patients who experienced a poorly known adverse effect of bromocriptine-alopecia. The first patient was an infertile 34-year-old woman treated with 2.5 mg of bromocriptine per day. The second patient was a 45-year-old woman with Parkinson's disease treated with 40 mg of bromocriptine per day. In both cases there was no preexisting hair loss. Hair loss ceased when bromocriptine was withdrawn and was not attributed to another etiology. Pathophysiological mechanisms are unknown.

Adult↗
PubMed1992

[Cerebral blood flow in migraine without aura].

For several years, cerebral blood flow (CBF) studies have been fueling the controversy surrounding the pathophysiology of migraine headache. The earliest studies focused mainly on migraine with aura (MA+) and provided evidence in support of the classical hemodynamic theory: a decrease in blood flow during the aura is followed by reactive vasodilation during the headache phase. Studies in migraine without aura (MA-), although less numerous, consistently demonstrated an increase in CBF during the attack. Olesen et al., gave rise to a heated debate by suggesting that hemodynamic manifestations are different in MA+ and MA-; in their view, CBF remains unchanged in MA-, whereas MA+ is associated with a wave of posterior blood flow deficiency which slowly spreads forwards in a manner reminiscent of experimental spreading depression; they interpret this hemodynamic pattern as evidence that the attack is mainly caused by a neural mechanism rather than a vascular spasm. This concept of MA- with no hemodynamic changes suggests that the pathophysiology of MA- may be completely different from that of MA+. However, most studies using stationary detectors or single photon emission computerized tomography (SPECT) with Xenon 133 or HMPAO as the tracer have demonstrated increased CBF during migraine attacks. The increase was not correlated with the side of the pain suggesting that vasodilatation is not the only cause of the pain. Current data do not seem to support the view that MA- and MA+ are different pathophysiologic entities; whether the mechanism of the attack is neural or vascular cannot be determined on the basis of CBF data.(ABSTRACT TRUNCATED AT 250 WORDS)

Cerebrovascular Circulation↗
PubMed1990

CQA 206-291: a novel dopamine agonist in the treatment of Parkinson's disease.

The antiparkinsonian efficacy and tolerability of CQA 206-291, a novel ergoline derivative with potent dopamine agonist properties, were studied during 2 months of treatment in 72 parkinsonian patients. In 36 de novo patients (patients who have not previously been treated with levodopa or dopamine agonists), CQA 206-291 was studied in an open design, while in 36 levodopa-treated patients, CQA 206-291 was studied in a randomized, double-blind, parallel-group, placebo-controlled design. CQA 206-291 induced in both groups a significant antiparkinsonian effect with an effective dose range of 5-30 mg/day. The spectrum of adverse events was similar to what is commonly observed with dopamine agonists. Further studies are required to assess the putative therapeutic advantages of CQA 206-291 when compared to other antiparkinsonian drugs.

Aged↗
PubMed1986

[Migraine and the idiopathic Raynaud phenomenon].

The successive onset of spasms of distal arteries of the limbs and complicated migraine in a young migrainous woman raised the possibility of a common mechanism for both disorders. Three similar cases have been reported and two recent epidemiological studies have shown the frequent association of migraine attacks and Raynaud's phenomenon or variant angina in a individual patient. The possible role of vasospasm in triggering the migrainous aura is discussed.

Adult↗
PubMed1983

Cerebral blood flow studied by Xenon-133 inhalation technique in parkinsonism: loss of hyperfrontal pattern.

Cerebral blood flow (grey matter flow) in parkinsonism requires further investigation. The noninvasive method of 133Xe inhalation permits study of larger numbers of subjects than previously used invasive techniques such as the intracarotid 133Xe injection method. Measurements were made in this laboratory in 30 subjects having Parkinson's disease. Mean hemispheric blood flow (F1) values were 70.4 +/- 9.3 ml/100 g/min, compared to 76.3 for a group of age-matched normal subjects, which is a decrease of -7.8%. The most striking difference was the loss of the "hyperfrontal distribution" in parkinsonism. The prefrontal F1 values were only 1.8% greater than the hemisphere grey matter flow, compared with 8.5% in controls of a similar age group.

Adult↗
PubMedDate not supplied

Dyskinesia: L-dopa-induced and tardive dyskinesia.

Neuroleptic induced tardive dyskinesia and L-dopa-induced dyskinesia are the two most common types of drug-induced abnormal involuntary movements. These two drug-induced dyskinesias are clearly different with respect to the offending drugs and the underlying disease, but they both share a number of intriguing similarities in terms of clinical phenomenology, epidemiology, risk factors, pathophysiological mechanisms and therapeutic responses. In both instances, it is believed that some dysregulation occurring at the level of the striatal dopaminergic receptors, and related non-dopaminergic neurotransmitters systems are playing a crucial role in the development and persistence of the mechanisms causing dyskinesia. These long-lasting functional changes, known as the "priming" phenomenon, are responsible for an impaired balance within the relays of the cortico-subcortical motor loops that release an inadequate output from the basal ganglia leading to an abnormal motor behavior. From a therapeutic perspective, there are also many similarities in the strategies proposed to manage these two dyskinesias. In both cases, unprimed patients not previously exposed to the offending drugs, are offered alternative medications to reduce, at least partly, the risk of occurrence of future dyskinesia: "atypical" neuroleptics in the place of "typical" neuroleptics, and dopamine agonists in the place of L-dopa. In both cases, once dyskinesias are present, in already "primed" patients, both types of dyskinesia appear to be poorly and only partly reversible. Based on limited clinical evidence, it is a common proposal to switch the dyskinetic subject from "typical" to "atypical" neuroleptics for tardive dyskinesia, or to switch from (or more pragmatically to substitute as much as possible) L-dopa to a dopamine agonist for L-dopa-induced dyskinesia. In both cases, efficacious symptomatic antidyskinetic interventions, to reduce the severity of a ready present dyskinesia, are rare. There are some uncontrolled data suggesting that dopamine depleting agents, like tetrabenazine, are possibly useful for tardive dyskinesia; however, there is more clinical evidence to support the efficacy of amantadine and functional surgery in parkinsonian patients with L-dopa-induced dyskinesia.

Antiparkinson Agents↗
PubMedDate not supplied

Cortical atrophy in Parkinson disease: correlation between clinical and CT findings with special emphasis on prefrontal atrophy.

Thirty-seven patients with Parkinson disease were evaluated clinically and with computed tomography in order to determine the incidence of prefrontal atrophy. An age-matched healthy control group was also scanned. The computed tomographic criteria used were the width of cortical sulci and ventriculocerebral indices. Parkinsonian patients with frontal cortical atrophy represent only one patient out of three. They are much older than parkinsonian patients with normal computed tomographic scans, and the onset of their illness occurs later. No significant difference was found according to gender, parkinsonian clinical triad, psychomotor study, or mean duration of illness and/or dopatherapy to the time of computed tomography. This work seems to separate two Parkinson diseases: one beginning before 65 years and damaging the nigrostriate system, and another beginning after 65 years and damaging both the nigrostriate system and the cortex, particularly the frontal cortex.

Aged↗