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Biomedical subjects

G Said

Publications and source records attributed to G Said.

At least 109 records · Page 6Linked to original sources
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↗
PubMed1984

Length-dependent degeneration of fibers in Portuguese amyloid polyneuropathy: a clinicopathologic study.

We investigated two patients with Portuguese amyloid polyneuropathy to learn more about the role played by amyloid in this condition. In sural nerves, axonal loss predominated in unmyelinated axons. Different abnormalities of single fibers near amyloid deposits included distortion of the myelin sheath, segmental demyelination, and wallerian degeneration. Electronmicroscopic studies showed degenerative changes of endoneurial cells in contact with fibrils of amyloid. Therefore, amyloid plays an important role in the length-dependent degeneration of fibers of this condition. Why unmyelinated fibers are so heavily affected remains unclear.

Adult↗
PubMed1983

Progressive centripetal degeneration of axons in small fibre diabetic polyneuropathy.

A clinicopathological study is presented of 5 patients with a pseudosyringomyelic dissociation of sensory loss and severe autonomic disturbances related to diabetic polyneuropathy. Sensory loss which followed a pattern that suggested a length-related degeneration of fibres was associated with spontaneous pains in 3 patients. Plantar ulcers and neurogenic arthropathies were also present in 3 patients. The pathological changes in sural nerve biopsies included a severe loss of unmyelinated and small myelinated axons which appeared to be involved earlier than larger myelinated fibres. Distal degeneration of single fibres with subsequent axonal sprouting from the proximal axon was demonstrated in all patients. This severe axonal neuropathy was associated with primary and secondary segmental demyelination. Our observations are consistent with a progressive centripetal degeneration of axons in predominantly sensory diabetic polyneuropathy.

Adult↗
PubMed1983

Different patterns of uremic polyneuropathy: clinicopathologic study.

Ten patients with a uremic polyneuropathy were investigated. Chronic renal failure was associated with a variety of neuropathies, including an acute axonal neuropathy, a progressive axonal neuropathy with secondary segmental demyelination, and a predominantly demyelinative neuropathy. All patterns were associated with distal degeneration of fibers evidenced by axonal sprouting observed on single-fiber preparations. The etiology of such variations in pathology of uremic neuropathy is still not clearly understood.

Adolescent↗
PubMed1982

Peripheral neuropathies and tremor.

We studied 14 patients with tremor and acquired peripheral neuropathies of different origin. Minimal weakness was the only clinical finding common to all patients. Sensory changes, etiology, and course of the neuropathy varied. NO unique pattern of peripheral nerve histopathology could be demonstrated. Slowing of conduction velocity of Ia fibers was found, but the role played by impairment of sensory inputs remains unclear. Tremor associated with peripheral neuropathy seems to be due to enhancement of physiologic tremor by minimal weakness.

Adult↗
PubMed1982

[Electrophysiological and morphological effects of the injection of Guillain-Barré sera in the sciatic nerve of the rat (author's transl)].

Serum from 3 of 4 patients with classical Guillain-Barré syndrome has produced conduction block in a large proportion of motor axons following subperineurial injection into 13 rat sciatic nerves. These effects, although qualitatively similar to those previously described for certain experimental sera (EAN, EAE, and anti-Gal-Cer), are notably slower in evolution. Conduction block does not begin until more than 24 hours after injection and is maximal at about 5 days. Between 6 and 8 days the appearance of long latency responses signals return of conduction in previously blocked axons. Thereafter return to control values is rapid and complete within 10 to 15 days. Six control human sera injected into 13 sciatic nerves have shown no comparable effect. Correlative morphological studies indicate that these Guillain-Barré sera produce focal demyelination which evolves pari passu with conduction block. Demyelination appears to evolve both by vesicular disruption and by macrophage mediated myelin stripping. A factor is present in the serum of some patients with Guillain-Barré syndrome, which given access to the endoneurial environment produces active demyelination with conduction block. We believe that the production of this factor could be responsible for the polyradiculoneuropathy of this disease.

Animals↗
PubMed1981

Proliferation of Schwann cells in tellurium-induced demyelination in young rats. A radioautographic and teased nerve fiber study.

This is a study of DNA synthesis of Schwann cells during the demyelination and the remyelination of peripheral nerves secondary to the intoxication of young rats with tellurium (Te). 3H-thymidine uptake of Schwann cells begins on day 4, reaches a zenith on day 7, and ends before day 20 on the Te diet despite continuation of the diet. The chronology of pathologic events is that myelin breakdown leading to segmental demyelination occurs first, followed within 24--48 h by the appearance of paralysis and by the beginning of DNA synthesis by the Schwann cells. A quantitative study on isolated nerve fiber preparations showed that more Schwann cells are produced than necessary to cope with the remyelination and that only one of four to six Schwann cells present in the demyelinated area at day 12 will participate in the remyelinating process.

Animals↗