Search PubMed⌕ Search

Biomedical subjects

G Said

Publications and source records attributed to G Said.

At least 91 records · Page 5Linked to original sources
PubMed1989

[Poisoning by beta,beta'-iminodipropionitrile (IDPN) in the rat: an experimental model for elective lesions of peripheral motoneurons].

Chronic or acute intoxication of rats with beta,beta'-iminodipropionitrile induces characteristic lesions of axons of anterior horn cells. Swellings of proximal axons are associated with disorganization of the cytoskeleton which includes a disorientation of neurofilaments which are segregated in the periphery of the axon, while microtubules and mitochondria are clustered centrally. Slow axonal transport, which is markedly reduced, results in accumulation of neurofilaments in the proximal part of the peripheral motoneuron and distal atrophy. In chronically intoxicated rats, proliferation of Schwann cells with onion bulb formation were observed in the anterior spinal roots after 10 months on diet. In distal sciatic nerve, axonal degeneration was associated with accumulation of neurofilaments, organelles and glycogen. Axonal regeneration occurred in spite of sustained intoxication. The intensity of the lesions induced by IDPN in the proximal part of the axon of the spinal motoneuron are reminiscent of those observed in degenerative motor neuron disease. However, the abnormalities of the myelin sheath and the proliferation of Schwann cells encountered in IDPN-intoxicated rats do not occur in degenerative motor neuron diseases in humans.

Animals↗
PubMed1988

The peripheral neuropathy of necrotizing arteritis: a clinicopathological study.

We have reviewed the clinical and morphological data from 100 patients with necrotizing arteritis in muscle and/or in nerve samples taken by biopsy. The neuropathy occurred in the context of a multisystem disorder (Group 1) or in apparent isolation (Group 2). The average age of patients was 59 in Group 1 and 61 in Group 2. Females were more commonly affected than males, especially in the first group. Necrotizing arteritis complicated the course of rheumatoid arthritis in 25 patients. In 3 patients necrotizing arteritis was associated with infection with the human immunodeficiency virus, the agent of AIDS. Tests for hepatitis B surface antigen were positive in 19 patients. Mononeuritis was present in 13, mononeuritis multiplex in 62, and distal symmetrical sensory or sensorimotor neuropathy in 19 patients. In both groups of patients, the muscle biopsy was more frequently diagnostic for arteritis than was the nerve biopsy (80% versus 55%). The average incidence of isolated fibers undergoing axonal degeneration was 64.8%; that of demyelinated/remyelinated fibers was 1.9%. We conclude that the combination of nerve and muscle sampling increases the chance of visualizing characteristic arterial lesions in vasculitic neuropathy.

Adult↗
PubMed1988

Inflammatory lesions of peripheral nerve in a patient with human T-lymphotropic virus type I--associated myelopathy.

In a patient with tropical spastic paraparesis associated with a positive titer for human T-lymphotropic virus type I, electrophysiological study detected a mixed, axonal and demyelinating, multifocal neuropathy. Perineural and perivascular infiltrates, moderate axon loss, wallerian degeneration, and demyelinating lesions of isolated fibers were present in the nerve biopsy specimen. These inflammatory lesions resembled those found in the central nervous system of patients with tropical spastic paraparesis.

Deltaretrovirus Infections↗
PubMed1988

POEMS syndrome presenting as systemic sclerosis. Clinical and pathologic study of a case with microangiopathic glomerular lesions.

A rare form of plasma cell dyscrasia characterized by the various association of polyneuropathy, organomegaly, endocrinopathy, monoclonal protein, and skin changes has been termed POEMS syndrome. The pathogenesis of the multisystemic features of this syndrome remains unclear. Herein is reported a case of POEMS syndrome with striking clinical similarities with scleroderma, and microangiopathic glomerular lesions, as well as diffuse perivascular non-amyloid deposits, which could explain certain features of the syndrome, including peripheral nerve demyelination. It is proposed that a pathogenic role might be played by a non-immunoglobulin vasculotoxic component.

Adult↗
PubMed1988

Persistence of Trypanosoma cruzi antigens in the inflammatory lesions of chronically infected mice.

Different tissues and organs of mice infected with Trypanosoma cruzi trypomastigotes have been examined for the presence of parasites and parasitic antigens during both the acute and the chronic phases of infection. Specimens of skeletal and cardiac muscles, spleen, liver, brain and sciatic nerves were studied by histological and immunological methods. During the acute phase of infection, the parasites were commonly observed in these tissues. In the chronic phase of the experimental infection, pseudocysts filled with amastigotes were seen in less than 1% of the tissue sections, while immunohistological methods showed that T. cruzi antigens were present in 11% of the inflammatory infiltrates. These findings suggest that antigenic stimulation persists throughout the chronic phase, even though the parasites are not morphologically detectable.

Animals↗
PubMed1988

Cellular immunity to Trypanosoma cruzi is mediated by helper T cells (CD4+).

The infection of mice with Trypanosoma cruzi has been used as an experimental model for human Chagas disease, because the murine and human infections have similar acute and chronic phases generating similar immunopathological phenomena. Histopathological studies of murine tissues showed that the inflammatory lesions were small during the acute phase and composed mainly of mononuclear cells. During the chronic phase, cellular infiltrates were clustered in large granulomata consisting of mononuclear and polynuclear neutrophil cells. Characterization of the infiltrating cells by surface markers showed that about 6% were Thyl.2+ T cells, and CD4+(Lyt 1+) T cells (T helper/DTH subset) were more numerous than CD8+(Lyt 2+) T cells. These observations suggest that delayed type hypersensitivity plays a role in the pathology of Chagas disease.

Animals↗
PubMed1988

Schwann cell degeneration induced by doxorubicin (adriamycin).

Doxorubicin is an anthracycline antineoplastic antibiotic that acts at the cell nucleus by intercalating between base pairs of DNA, thus inhibiting DNA-directed mRNA synthesis. Intraneural micro-injection of 0.19-0.38 micrograms of this substance into rat sciatic nerve results in a delayed subacute demyelination that is secondary to focal Schwann cell degeneration. Remyelination eventually occurs but is not complete until at least days 60-75 postinjection. Toxic Schwann cell disorders produced by agents such as doxorubicin may serve as useful models in understanding the pathogenesis of human demyelinative neuropathies.

Action Potentials↗
PubMed1987

L3T4+ T cells able to mediate parasite-specific delayed-type hypersensitivity play a role in the pathology of experimental Chagas' disease.

During the chronic phase of infection with the parasite Trypanosoma cruzi, mice develop inflammatory lesions in the heart and skeletal muscles, as well as in peripheral nerves and the liver. We demonstrated the presence, in the blood of chronically infected mice, of L3T4+ T cells able to transfer a specific T. cruzi delayed-type hypersensitivity (DTH) reaction. Transfer of the chronic inflammatory lesions was obtained by injecting Lyt-2+-depleted lymphocytes from either lymph node or blood of infected mice. T cell lines were established from the chronically infected mice by culturing peripheral blood lymphocytes or lymph node cells with either T. cruzi extracts (TC) or mouse peripheral nerve extracts (PN). Those cell lines that presented an L3T4+ phenotype were also able to specifically transfer a local DTH reaction to naive recipients. Examination of the antigen specificities of these TDTH lines revealed three types: those that mediated a DTH reaction to TC, those that responded to both TC and PN and those that provoked a DTH response when injected with subinflammatory doses of an irrelevant antigen. Some of the lines, when injected into the sciatic nerve of naive recipients, provoked demyelination of the type observed in chronically infected animals. These results suggest that T. cruzi and the host nervous system share common epitopes that can be recognized by TDTH cells.

Animals↗
PubMed1987

[Acquired metabolic neuropathies (2): Kidney failure, hypothyroidism and hypoglycemia].

This is the second part of a review article on metabolic neuropathies. The frequency and severity of neuropathy due to chronic renal failure have dramatically decreased during the last ten years, as a result of improvement in management of patients with renal failure, even though the mechanism leading to development of the neuropathy is not well understood. Measurement of nerve conduction velocity does not appear to be appropriate to the detection of axonal neuropathy and follow-up of patients with neuropathy associated with chronic renal failure. Peripheral neuropathy observed in association with hypoglycaemia and with hypothyroidism are briefly reviewed.

Humans↗
PubMed1986

Hypotrophic and dying-back nerve fibers in Friedreich's ataxia.

Eight patients with Friedreich's ataxia showed profound reduction in the density of large myelinated fibers in sural nerve biopsies. The density of small myelinated fibers was normal, but the axonal size and myelin thickness were reduced. Demyelination, presumably secondary to axonal dysfunction, was observed in 3% of the isolated fibers. There was axonal degeneration, including dying-back axons isolated in three specimens, in 2.6% of the isolated fibers. The low incidence of degenerating fibers did not account for loss of myelinated fibers in children. There is probably a defect in maturation of fibers, followed by a dying-back process.

Adult↗
PubMed1985

Neuropathy associated with experimental Chagas' disease.

Mice were acutely and chronically infected with Trypanosoma cruzi and then examined histologically for the presence of lesions in the peripheral nervous system. In acutely infected animals, small lymphocytic and macrophagic infiltrates were found in the nerves in association with intracellular parasites. Little or no nerve damage was present at this stage. In chronically infected animals, large perivascular granulomatous infiltrates were found in association with multifocal, predominantly demyelinative lesions of neighboring nerve fibers. Similar inflammatory infiltrates were present in muscles and were frequently associated with vasculitis and destruction of muscle fibers. Our pathological findings and the negative results produced by intraneural injections of sera from chronically infected animals and the positive results following injections of small numbers of live trypanosomes suggest that the demyelination is not due to circulating serum factors such as antibodies cross-reacting with peripheral myelin. Delayed-type hypersensitivity may be induced by the presence of the parasites, a notion supported by the development of granulomas in naive mice injected intravenously with helper T cells from chronically infected animals.

Animals↗
PubMed1985

[Metabolic neuropathies. I. Diabetic neuropathies].

This is a review article on diabetic neuropathy. The different patterns of diabetic neuropathies, including focal and multifocal, distal symmetrical and autonomic neuropathy are exposed. Length dependent degeneration of fibers is suggested by the pattern of sensory loss and by morphological findings. The various hypotheses on the mechanisms of the neuropathy, including the possible role played by ischemia and by the accumulation of sorbitol in Schwann's cells, are reviewed. The therapeutic implications of the clinical, pathological and biochemical abnormalities are discussed.

Cranial Nerve Diseases↗