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Biomedical subjects

J B Cosgrove

Publications and source records attributed to J B Cosgrove.

17 recordsLinked to original sources
PubMed1985

Clinical sub-groups of multiple sclerosis in relation to HLA: DR alleles as possible markers of disease progression.

We have examined the distribution of HLA antigens in 70 multiple sclerosis (MS) patients divided in three groups defined according to clinical criteria: benign MS, severe MS, cerebellar MS. We have found a significant association between severe MS and HLA-DR2, and between benign MS of more than 15 years of evolution and HLA-DR3. We review previous work along the same line and conclude that the association of HLA antigens with "clinical subgroups of MS" could indicate a genetically based heterogeneity of the disease and offer help in establishing a prognosis.

Cerebellar Diseases↗
PubMed1979

Short-latency somatosensory responses in multiple sclerosis.

Cervical and cortical somatosensory evoked potentials were measured in 80 patients with suspected or established multiple sclerosis (MS). The cervical response was a more sensitive diagnostic indicator than the cortical response, and was abnormal in 86.7 percent of patients with definite MS and in 40.9 percent of MS suspects. The complementary value of measuring both responses was greatest (89.3 percent) in early probable or latent MS. Comparing the responses obtained from stimulation of the left and right extremities increased the overall diagnostic yield by 25 percent. Abnormal responses were frequently obtained from clinically normal limbs.

Adolescent↗
PubMed1978

Sensitization to myelin basic protein in attacks of multiple sclerosis. A preliminary report.

Recent attempts to detect the presence of antibody to encephalitogenic basic protein in multiple sclerosis have generally been unsuccessful. The utilization of a new system of double immunodiffusion in detecting such antibody in EAE serum prompted us to apply this method in the search of such antibody MS sera. In our preliminary investigation of 67 sera, antibody was detectable in MS sera, but it was most often found during convalescence rather than an acute exacerbation of illness. Antibody was also found in several myasthenic patients, and occasionally in subjects with other neurological disease.

Antibodies↗
PubMed1977

Direct leukocyte migration inhibition by myelin basic protein in exacerbations of multiple sclerosis.

Studies in 13 normal subjects, 9 patients with multiple sclerosis (MS) within 3 weeks of exacerbation and 16 others 1 to 6 months after onset were carried out for evidence of cell-mediated hypersensitivity to myelin basic protein. Ten patients with stroke and 10 with Guillain-Barré syndrome were studied as additional controls. Peripheral leukocytes obtained by leukapheresis were packed into capillary tubes and allowed to migrate out onto glass in the presence or absence of myelin basic protein. Cells of patients within 3 weeks of an MS episode gave a mean migration index of 68 +/- 9%, and those 1 to 6 months after onset, 93 +/- 21%. For the entire MS group the mean index was 88 +/- 20%, for those with Guillain-Barré, 103 +/- 7%; and for the stroke patients, 107 +/- 11%. Results for the acutely ill MS patients were significant (P less than 0.005). The data are similar to those obtained using the migration inhibition factor assay but show that sensitized lymphocytes also elaborate a second mediator during acute exacerbations of illness. These observations strengthen evidence that sensitization to this potent encephalitogen occurs simultaneously with exacerbations of clinical illness.

Acute Disease↗
PubMed1977

Multiple sclerosis: sensitization of a myelin basic protein fragment (peptide T) encephalitogenic to primates. A preliminary report.

Myelin basic A1 protein is the sole antigen of the central nervous system capable of inducing experimental allergic encephalitis (EAE), but sensitization with peptide fragments of the molecule may also induce disease. Using the macrophage migration inhibition factor (MIF) assay we have compared sensitization to portions of the molecule active in inducing EAE in monkeys with results obtained concomitantly using the intact protein. Cellular sensitization to human myelin A1 protein, peptide L (residues 1-116), peptide T (residues 117-170), and petide Y (residues 154-170) was studied using the Thor-Rocklin MIF assay system. Lymphocytes of 10 normal subjects, 10 multiple sclerosis patients 0-3 weeks after onset, 10 4 weeks to 3 months after and 10 6 months or longer after onset of an acute exacerbation were assayed. Results of the investigation reveal evidence of cellular sensitization to myelin basic protein encephalitogenic peptide T occurring during attacks of multiple sclerosis. Peptide L, relatively nonencephalitogenic to primates, failed to induce a significant lymphocyte response, whereas peptide Y which is encephalitogenic gave irregular results.

Adult↗
PubMed1976

Multiple sclerosis and cell-mediated hypersensitivity to myelin A1 protein.

Cellular hypersensitivity to myelin basic (A1) protein was evaluated using the MIF assay in 246 subjects. Of 100 with multiple sclerosis positive results are seen in relationship to acute exacerbations of illness. Normal control subjects gave a mean value of 100 +/- 9% whereas patients studied within 4 weeks of onset of illness gave a result of 59 +/- 12.5%. A convalescent group studied between 5 and 12 weeks after an attack gave results of 86 +/- 22.2%. A chronic group gave a mean of 91 +/- 8.2%. Positive values were also seen in a number of other patients with central or peripheral nervous system disease especially those with "autoimmune disease". However, results of this study clearly establish a temporal relationship between in vitro evidence of hypersensitivity to A1 protein and clinical expression of disease.

Acute Disease↗
PubMed1976

Cerebrospinal fluid T and B lymphocyte kinetics related to exacerbations of multiple sclerosis.

Cerebrospinal fluid T and B lymphocyte populations were identified in 21 patients with relapsing and 10 patients with stable multiple sclerosis. The results indicate that the percentage of T cell is largest in the acute stage of a relapse (65 percent) and diminishes by the second week (41 percent). Conversely, the stable patients had a lower percentage of T cells (30 percent) and a relatively high percentage of nonreacting cells (66 percent). The proportion of T cells in the cerebrospinal fluid varies directly with the clinical activity of the disorder, further implicating cellular immune mechanisms in the pathogenesis of multiple sclerosis.

Adult↗
PubMed1975

Cellular hypersensitization to peripheral nervous antigens in the Guillain-Barré syndrome.

The macrophage migration inhibition factor assay was used as a specific measure of cellular hypersensitivity to peripheral nervous system antigen in a large group of Guillain-Barre patients and control subjects. Lymphocytes from 34 patients with Guillain-Barre syndrome, 33 with other peripheral nervous system disease, and 33 normal controls were assayed for production of macrophage migration inhibition factor. A mean of 101 +/- 7.2 was obtained in the control group, 70 +/- 16.3 in the Guillain-Barre syndrome group, and 96 +/- 11.3 in those with other peripheral nervous system disease. Twenty-six of the 34 patients with Guillain-Barre syndrome, two patients with myeloradiculitis, and two with Bell's palsy gave significant values. These results support the hypothesis that cellular hypersensitization to peripheral nervous system antigens is a pathogenetic factor in Guillain-Barre syndrome.

Antigens↗