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Biomedical subjects

J F Pelissier

Publications and source records attributed to J F Pelissier.

18 recordsLinked to original sources
PubMed1999

Fish oil supplementation prevents diabetes-induced nerve conduction velocity and neuroanatomical changes in rats.

Diabetic neuropathy has been associated with a decrease in nerve conduction velocity, Na,K-ATPase activity and characteristic histological damage of the sciatic nerve. The aim of this study was to evaluate the potential effect of a dietary supplementation with fish oil [(n-3) fatty acids] on the sciatic nerve of diabetic rats. Diabetes was induced by intravenous streptozotocin injection. Diabetic animals (n = 20) were fed a nonpurified diet supplemented with either olive oil (DO) or fish oil (DM), and control animals (n = 10) were fed a nonpurified diet supplemented with olive oil at a daily dose of 0.5 g/kg by gavage for 8 wk. Nerves were characterized by their conduction velocity, morphometric analysis and membrane Na, K-ATPase activity. Nerve conduction velocity, as well as Na,K-ATPase activity, was improved by fish oil treatment. A correlation was found between these two variables (R = 0.999, P < 0.05). Moreover, a preventive effect of fish oil was observed on nerve histological damage [endoneurial edema, axonal degeneration (by 10-15%) with demyelination]. Moreover, the normal bimodal distribution of the internal diameter of myelinated fibers was absent in the DO group and was restored in the DM group. These data suggest that fish oil therapy may be effective in the prevention of diabetic neuropathy.

Animals↗
PubMed1997

Phenotypic expression of diabetes secondary to a T14709C mutation of mitochondrial DNA. Comparison with MIDD syndrome (A3243G mutation): a case report.

OBJECTIVE: To analyze the clinical and biochemical features of a recently described point mutation of mitochondrial DNA associated with diabetes. This mutation, characterized by a T14709C transition of a highly conserved nucleotide in the region coding for the glutamic acid tRNA, is heteroplasmic. RESEARCH DESIGN AND METHODS: The phenotypic expression in the insulin-requiring diabetic proband from the pedigree was compared to that of diabetic probands from three families with the classic A3243G mtDNA mutation (maternally inherited diabetes and deafness [MIDD] syndrome). The same investigations to evaluate pancreatic neurosensorial and muscle involvement were performed in all four patients. RESULTS: The natural courses of the diabetes and the hearing defects were not different between the two mutations. The patient with the 14,709 mutation, however, exhibited a milder alteration of pigmentary epithelium of retina and a much more severe muscle involvement, as attested by the clinical expression and the concurrent anomalies of muscle energy production evidenced by 31P magnetic resonance spectroscopy, confirming the profound impairment of oxidative processes. CONCLUSIONS: This novel mutation has to be added to the other known mtDNA anomalies in order to ascribe some diabetes suspected to arise from mitochondrial defects to this nosological framework.

Adult↗
PubMed1995

Extra-pancreatic manifestations in diabetes secondary to mitochondrial DNA point mutation within the tRNALeu(UUR) gene.

OBJECTIVE: A point mutation in the mitochondrial genome has been identified as a cause of diabetes and deafness. We report two pedigrees with and A-to-G transition at nucleotide 3243 of mtDNA within the tRNALeu(UUR) gene and focus our investigations on other localizations of the anomaly, particularly muscle and retina. RESEARCH DESIGN AND METHODS: Muscular localization has been studied in probands by invasive and noninvasive methods, including muscle biopsy (evaluation of the proportion of mutated mtDNA in comparison to blood cells, measurement of respiratory chain complex activities and histological and histochemical aspects) and 31P-nuclear magnetic resonance (NMR) spectroscopy. Ophthalmic and angiographic examination of retina, electroretinography, and visual evoked potentials were performed in five subjects. RESULTS: This mutation, previously described in patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS), was expressed more abundantly in muscle than in nucleated blood cells. This low expression in blood cells could hamper the diagnosis for some patients. In addition, despite poor clinical expression, muscle was found to be highly affected. Ragged red fibers and dystrophic mitochondria were observed in muscle biopsy. Histochemical assays showed decreased activity of respiratory chain complexes, and 31P-NMR in vivo data further confirmed the defect of muscle oxidative processes. Exercise-induced lactate production was increased. Finally, in both families, an atypical "salt and pepper" pigmentary retinopathy was observed without consequences on visual acuity. CONCLUSIONS: In diabetes secondary to 3243 mtDNA mutation, infraclinical muscular and ocular lesions are frequent. These two locations of the disease, which are easily investigated by simple methods, can help in the diagnosis of this new type of diabetes.

Adult↗
PubMed1995

Genetic linkage heterogeneity in myotubular myopathy.

Myotubular myopathy is a severe congenital disease inherited as an X-linked trait (MTM1; McKusick 31040). It has been mapped to the long arm of chromosome X, to the Xq27-28 region. Significant linkage has subsequently been established for the linkage group comprised of DXS304, DXS15, DXS52, and F8C in several studies. To date, published linkage studies have provided no evidence of genetic heterogeneity in severe neonatal myotubular myopathy (XLMTM). We have investigated a family with typical XLMTM in which no linkage to these markers was found. Our findings strongly suggest genetic heterogeneity in myotubular myopathy and indicate that great care should be taken when using Xq28 markers in linkage studies for prenatal diagnosis and genetic counseling.

Chromosome Mapping↗
PubMed1984

[Association of polymyositis, myasthenia, and thymoma. A case and review of the literature].

We report the case of a 51 years old woman with myositis, myasthenia gravis and thymoma. First apparent sign is myositis in 1976 but chest X ray show a mediastinal opacity and the patient reports an intermittent diplopia since 1973. The evolution of myositis occurs in two bouts in 1976 and 1981, Myasthenia gravis restricted to diplopia from 1973 to 1979 grow worse first alone then in association with increase of myositis signs in 1981. The mediastinal opacity seen on chest X ray in 1976 don't change and is revealed to be a thymoma at operation in 1981. After thymoma ablation myasthenic and myositis signs decrease. This pathologic association is found 24 times in literature and involves "giant cells" in muscle biopsy in about 50 p. 100 of cases and a myocarditis also with "giant cells". Those "giant cells" unusual in common myositis appears to have a prognostic value.

Adult↗
PubMed1979

Duchenne type muscular dystrophy and consanguinity: difficulties in pedigree analysis.

We report the case of a 2-year-old girl who had signs of Duchenne type muscular dystrophy on clinical, electromyographic, laboratory, and pathological examination. The parents of the child are first cousins. A brother and nephew of the mother also had Duchenne type muscular dystrophy. Karyotype analysis in the proband showed both X chromosomes to be morphologically normal. The mother had very high plasma CK levels, equivalent to those observed in carriers of the disease. We discuss different hypothetical mechanisms designed to account for the family pedigree.

Biopsy↗
PubMed1977

[Experimental study of neural and neuro-muscular conduction during simulated diving in dogs and rabbits: anatomo-pathologic correlations].

Five dogs and twelve rabbits were submitted to simulated diving at 6 ATA (compressed air) and 13-15 ATA (normoxic oxygen + nitrogen). Progressive decompressions were carried on for the first, rapid for the lasts. Motor nerve conduction velocity and nerve-muscle delays were measured. No variations could be observed neither for nerve conduction velocity nor for muscular and nerve action potentials. Nevertheless optic and electronic microscopy observations shew some nerve, neuronal and a few muscular alterations occuring during rapid decompression.

Action Potentials↗
PubMed1977

[The brain in the aged].

Under the very broad term of brain in the elderly, we cannot consider exhaustively all the anatomical, physiopathological and pathological aspect and, still less, the therapeutic possibilities in diseases of the anesthetist should know concerning the special characteristics of this aging organ. First are recalled the anatomical, macro and microscopic data of the senile brain. The metabolic characteristics are then considered. Investigations which may give the clinician information concerning the organic state and metabolic capacities of the brain of the elderly subject, e.g. cerebral blood flow, fundus oculi, E.E.G. brain arteriography, tacography or tomodensitometry by scanner, are consideres. But in practice, they are difficult to use and their data are only relatively reliable, i.e. clinical examination is of great imporatnce and the overall impression prevails. The therapeutic possibilities are limited and in these elderly subjects with cerebral metabolism in unstable equilibrium, one should be circumspect and careful in treatment.

Aged↗