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Biomedical subjects

M Corbo

Publications and source records attributed to M Corbo.

At least 37 records · Page 2Linked to original sources
PubMed1994

[The Cytobrush and Ayre spatula in taking cervical-vaginal specimens].

The authors prepare 131 cervicovaginal cytologic specimens with Ayre and Cytobrush spatulas and 94 with only the Ayre spatula and results are tested evaluating the percentage of specimens containing cells from the transformation area. The results of such tests show that the sampling methods with Cytobrush and the Ayre spatulas together is to be preferred to the use of the Ayre spatula alone for the higher presence in these specimen of cells from the transformation area, and consequently with the reduction in the number of tests to be repeated and the increase in the percentage of positive diagnoses and decrease of false negatives.

Adolescent↗
PubMed1994

[Chlamydia trachomatis and sterility].

The infection caused by Chlamydia is one of the sexually transmitted diseases and the correlation between Chlamydia infection and sterility has long been known. In this work, the authors discuss how frequent the isolation of Chlamydia is in women with organic tubal damage, a datum supporting the hypothesis which sees tubal damage as secondary to the rooting of Chlamydia in the tube itself.

Adult↗
PubMed1994

[Beta interferon in clinical practice].

Intramuscular interferon beta determines a positive therapeutic effect on the moderate dysplasia of the when associated with infection by HPV. The therapeutic effect is expressed mainly by progressive viral regression. Also our results show a satisfactory answer to the treatment with intramuscular interferon beta: in fact, the patients we treated had a positive reaction in terms of regression of the infection distinctly superior to what is the spontaneous regression of the infection itself.

Adult↗
PubMed1993

The gp120 glycoprotein of human immunodeficiency virus type 1 binds to sensory ganglion neurons.

Using immunofluorescence microscopy we found that gp120 binds to the surface of rat dorsal root ganglia neurons and human neuroblastoma cells but not to rat fibroblasts or glial cells. The binding of gp120 to neurons was eliminated by pretreatment with trypsin, which removes cell-surface proteins, but not with chloroform: methanol, which removes glycolipids. As control, neuronal staining by antisulfatide antibodies was eliminated by pretreatment with chloroform: methanol but not with trypsin. The gp120 binding to neurons was also inhibited by the mouse monoclonal antibody 01, which binds to galactocerebroside and cross-reactive glycoproteins. These studies suggest that the receptor for gp120 on the surface of the dorsal root ganglia neurons is a glycoprotein. This interaction may mediate the effects of human immunodeficiency virus type 1 in sensory neuropathy.

Animals↗
PubMed1993

Conduction abnormalities induced by sera of patients with multifocal motor neuropathy and anti-GM1 antibodies.

Increased titers of anti-GM1 antibodies have been associated with motor neuron disease and motor neuropathy with or without conduction block. To investigate the pathogenetic role of anti-GM1 antibodies we injected into rat tibial nerves sera from patients with multifocal motor neuropathy and conduction block (MMN) or progressive spinal muscular atrophy (PMA), both presenting anti-GM1 antibodies. Sera of patients with MMN produced reduction of amplitude and dispersion of compound muscle action potential from proximal stimulation. Morphometry revealed demyelination in 6.2% of fibers. Sera of patients with PMA did not produce clear-cut electrophysiological or morphological changes. Differential effects of sera from patients presenting high-titer anti-GM1 antibodies, but with distinct clinical syndromes, might depend on differences in anti-GM1 antibody affinity, valency, or ability to fix complement. Alternatively, circulating factors other than, or in addition to, anti-GM1 antibodies present in sera of patients with MMN, but not of PMA patients, might be responsible for conduction abnormalities and reproduce them after passive transfer.

Animals↗
PubMed1993

Effect of hypothyroidism on rat peripheral nervous system.

The function and structure of the peripheral nervous system of Sprague-Dawley rats, 3 months after the induction of hypothyroidism by administration of N-propylthiouracil in drinking water, has been studied. The motor action potential amplitude of the caudal nerve showed a significant reduction (p < 0.001) when compared with an age-matched control group of animals. Computer-assisted morphometric analysis of sciatic nerves of hypothyroid rats showed normal distribution and density of myelinated fibers, and a normal axon/myelin ratio. Electron microscopy revealed only minor alterations in axons of myelinated fibers characterized by a dissolution of neurotubules. After two months of substitution therapy these effects were reversed. The present data suggest that early impairment of nerves induced by hypothyroidism is rare and could be related to metabolic alterations rather than to structural changes and is reversible with hormone treatment.

Action Potentials↗
PubMed1993

Lambert-Eaton myasthenic syndrome and polyneuropathy in a patient with epidermoid carcinoma of the lung.

We describe a patient affected by the Lambert-Eaton myasthenic syndrome, sensory motor axonal neuropathy and epidermoid carcinoma of the lung. Serum autoantibodies to voltage-operated calcium channels were detected. After lobectomy, voltage-operated calcium channel-related structures were demonstrated in the patient's tumor. By immunocytochemistry, the patient's IgG reacted with neural structures and particularly with intermediate filaments. We think that these autoantibodies may be implicated in the pathogenesis of the neurological symptomatology.

Aged↗
PubMed1993

Localization of GM1 and Gal(beta 1-3)GalNAc antigenic determinants in peripheral nerve.

Anti-GM1 antibodies in patients with motor neuropathy or motor neuron disease frequently recognize the Gal(beta 1-3)GalNAc epitope, which is shared by several glycoproteins in peripheral nerve. In this study, cholera toxin (CT), which is specific for GM1, and the lectin peanut agglutinin (PNA), which binds to Gal(beta 1-3)GalNAc-bearing glycoproteins, were used in tissue section and intraneural injection studies to examine the distribution of GM1 and Gal(beta 1-3)GalNAc epitopes in human and rat peripheral nerve by epifluorescence and confocal microscopy. In tissue sections, CT stained the compact myelin in both human and rat nerves, whereas PNA was localized at the outer edge of the myelin sheath or Schwann cell membrane. Following intraneural injection into rat sciatic nerves, both CT and PNA bound to the nodes of Ranvier, although CT was concentrated in the paranodal myelin region whereas PNA was concentrated at the nodal gap. These structures may be targets for anti-GM1 antibodies in peripheral nerve.

Animals↗
PubMed1993

Expression of a cell death marker (Clusterin) in muscle target fibers.

We report, for the first time, the expression of immunoreactivity to clusterin in skeletal muscle. Clusterin, a protein probably related to the process of programmed cell death (apoptosis), was specifically very highly expressed in target fibers. All target fibers found in 50 muscle biopsy samples from a variety of neuromuscular disorders expressed a high concentration of clusterin in the middle of the targets. Clusterin was not expressed in any targetoid fibers or cores. Acute denervation, where targets are mostly seen, may be the beginning of apoptosis. Hence our findings support the concept that targets are harbingers of acute denervation.

Cell Death↗
PubMed1992

Experimental conduction block induced by serum from a patient with anti-GM1 antibodies.

Increased titers of antibodies to GM1 ganglioside in humans are associated with lower motor neuron disease and predominantly motor neuropathy with or without conduction block. To investigate the possible mechanism of these antibodies, we injected the serum of a patient with anti-GM1 antibodies who had motor neuron disease and multifocal motor conduction block, into rat sciatic nerve. When injected with fresh human complement, the serum-induced conduction block with temporal dispersion and deposits of immunoglobulin were detected at the nodes of Ranvier. Electron microscopic studies revealed demyelination in 6.5% of the fibers. After preabsorption with GM1, the serum had no effect, suggesting that the anti-GM1 antibodies were responsible for the conduction abnormalities.

Animals↗
PubMed1992

Patterns of reactivity of human anti-GM1 antibodies with spinal cord and motor neurons.

Human anti-GM1 antibodies from patients with lower motor neuron disease or predominantly motor neuropathy recognize carbohydrate determinants shared by GM1 and related glycolipids and glycoproteins, but the identity of the antigens to which they bind in tissue is unknown. We examined the binding of anti-GM1 antibodies with differing fine specificities to spinal cord, isolated motor neurons, and dorsal root ganglia neurons in order to characterize the tissue antigens. All anti-GM1 antibodies tested bound to the surface of bovine spinal motor neurons and immunostained the gray matter of unfixed sections of spinal cord. The staining was blocked by cholera toxin, which is specific for GM1, indicating that GM1 itself was the target antigen. Binding to white matter was more variable and depended on fixation and the fine specificities of the antibodies. The anti-GM1 antibodies did not bind to dorsal root ganglia neurons in tissue sections or in culture. These studies suggest that the autoantibodies might exert their effect, in part, by binding to GM1 on the surface of motor neurons, and that the absence of binding to dorsal root ganglia neurons might explain the lack of sensory abnormalities in affected patients.

Animals↗
PubMed1992

Peripheral nerve involvement in Churg-Strauss syndrome.

Peripheral neuropathy associated with bronchial asthma, multisystem organ dysfunction and idiopathic hypereosinophilia may be found in Churg-Strauss syndrome, hypereosinophilic syndrome and polyarteritis nodosa. Some authors have diagnosed their patients according to the presence in tissue biopsies of the three histological criteria of Churg and Strauss (necrotizing vasculitis, tissue eosinophilic infiltration, extravascular granulomas). We have observed three patients with a common history of a prodromal phase of allergic diseases (bronchial asthma and rhinitis) followed by a vasculitic phase with mononeuritis multiplex, purpura and arthritis, associated with hypereosinophilia of more than 1500 cells/mm3. All responded well to steroid treatment. Sural nerve biopsy revealed true vasculitis in two of these cases and a mild perivascular inflammatory infiltration in the other. On the basis of their characteristic clinical pattern, we think that our cases best fit the diagnosis of Churg-Strauss syndrome even though the typical histological features were not found in the sural nerves examined.

Adolescent↗
PubMed1992

Anti-sulfatide antibodies in neurological disease: binding to rat dorsal root ganglia neurons.

Increased titers of anti-sulfatide antibodies were detected by ELISA in 5 of 200 patients and control subjects. All 5 patients had sensory impairment; 4 had neuropathy, and one had multiple sclerosis. Of the patients with neuropathy, 2 had a clinical syndrome of small fiber sensory neuropathy with normal electrophysiological or nerve biopsy studies, 1 had a sensorimotor axonal neuropathy associated with IgM monoclonal gammopathy, and 1 had sensorimotor neuropathy with multifocal motor conduction block and anti-GM1 antibodies. The anti-sulfatide antibodies bound to the surface of unfixed rat dorsal root ganglia neurons and human neuroblastoma cells, and to fixed sections of central and peripheral myelin. No binding was detected following intraneural injection into rat sciatic nerves. Pre-absorption with sulfatide but not with galactocerebroside eliminated the tissue binding activity. These findings indicate that increased titers of anti-sulfatide antibodies are found in patients with sensory impairment but are not restricted to a particular neurological syndrome or type of neuropathy. The significance of anti-sulfatide antibodies is uncertain although sulfatide on dorsal root ganglia neurons may be a target antigen.

Aged↗
PubMed1992

Peripherin and neurofilament protein coexist in spinal spheroids of motor neuron disease.

We have compared the immunolocalization of neurofilament protein (NF) with two other neuronal-specific intermediate filament proteins in large spinal axonal swellings (spheroids) of motor neuron disease and controls. All spheroids labeled each of the three different subunits of NF, the low, middle, and high molecular weight polypeptides. In doublelabel immunofluorescence, 300 axonal swellings were immunostained for NF, and 87% of them contained the intermediate protein peripherin. The pattern of immunostaining of NF and peripherin was indistinguishable at a high resolution viewed in 1 microns optical sections by confocal microscopy. A minority of the spheroids contained alpha-internexin, another intermediate protein, but it was weakly immunoreactive. The immunostaining of axonal swellings was similar for all epitopes tested in motor neuron disease and control subjects. The findings suggest that peripherin as well as neurofilament protein are major components of the proliferated intermediate filaments in spheroids.

Axons↗
PubMed1992

[Screening of endometrial carcinoma].

The Authors analyse the characteristics of the carcinoma of the endometrium concluding that this neoplasia has the necessary requirements to undergo a screening by means of endometrial cytology. The Authors believe that this test should be combined with those carried out to prevent cervical and mammary neoplasia, applying a total screening to the gynaecological neoplasia.

Age Factors↗
PubMed1991

Identification of glycoconjugates which are targets for anti-Gal(beta 1-3)GalNAc autoantibodies in spinal motor neurons.

Human IgM anti-Gal(beta 1-3)GalNAc antibodies which bind to GM1 and GD1b, are implicated in the pathogenesis of predominantly motor neuropathy or motor neuron disease. By immunofluorescence microscopy, the human antibodies immunostain the surface of motor neurons from bovine spinal cord. The motor neurons are also immunostained by cholera toxin (CT), which is specific for GM1. Glycolipid analysis using thin-layer chromatography (TLC) and immunostaining reveals that the relative concentration of GM1 and GD1b in motor neurons is greatly reduced in comparison to whole spinal cord, and that other motor neuron gangliosides are unreactive with the anti-Gal(beta 1-3)GalNAc antibodies. By Western blot analysis, the antibodies react with several protein bands in motor neuron extracts, and many of the same proteins are also recognized by PNA. These data suggest that both glycoproteins and glycolipids might be targets for anti-Gal(beta 1-3)GalNAc antibodies in spinal motor neurons.

Animals↗