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Y Chapman

Publications and source records attributed to Y Chapman.

15 recordsLinked to original sources
PubMed1995

Anti-neuronal antibodies in antiphospholipid syndrome with central nervous system involvement: the difference from systemic lupus erythematosus.

The presence of antineuronal antibodies was compared in 43 patients with primary aPLS and 57 patients with neuropsychiatric SLE. Fifty-eight patients with Guillain-Barré syndrome and 72 normal healthy donors served as control groups. Seventeen patients in the study group had aPLS associated with CNS involvement. Antineuronal antibodies were studied in the sera employing a novel flow cytometric assay. The frequency of antineuronal antibodies in patients with aPLS and CNS involvement was not significantly different from that of patients with aPLS without CNS disease or from that found in the control groups (12%, 19% and 7%, respectively). However, it was significantly different from that found in SLE patients with CNS involvement (60%) (P < 0.001). Our results provide further evidence that unlike CNS-SLE, the major mechanism of CNS involvement in patients with primary aPLS might not be autoantibody (antineuronal) mediated, but rather 'thrombotic' in origin, or due to yet unknown factors.

Antiphospholipid Syndrome↗
PubMed1993

Autoantibodies to phospholipids and brain extract in patients with the Guillain-Barre syndrome: cross-reactive or pathogenic?

Guillain-Barre syndrome (GBS) is a transient neurological disorder characterized by an inflammatory demyelination of peripheral nerves. Although the pathogenesis of GBS has not been elucidated, there is increasing evidence pointing to an autoimmune etiology. We have studied the reactivity of GBS sera with various phospholipids which are known to be important constituents of myelin, and serve as autoantigens in other autoimmune conditions. Sixteen Guillain-Barre syndrome (GBS) sera were studied for the presence of autoantibodies to ssDNA, dsDNA, cardiolipin (CL), phosphatidyl-ethanolamine (PE), phosphatidyl-choline (PC), phosphatidyl-serine (PS), and brain extract. Six of the 16 GBS sera had autoantibodies to one or more of the antigens studied. Three of the sera contained autoantibodies to brain extract (p < 0.05), two of the sera had autoantibodies to dsDNA, ssDNA, CL and PE, and one serum had autoantibodies to PC, and PS. As expected a significant proportion of the lupus sera contained autoantibodies to ssDNA and dsDNA, while the frequency of autoantibodies to different phospholipids was significantly high in sera of patients with systemic lupus erythematosus (SLE) and cerebritis. Absorption of GBS sera with cardiolipin, phosphatidyl-choline, or brain extract inhibited the binding of the sera to cardiolipin. Our results demonstrate that some GBS patients produce autoantibodies to various phospholipid and nuclear antigens. However, these autoantibodies are probably produced as a result of the myelin damage rather than cause the demyelination.

Adolescent↗
PubMed1991

Reduction of exploratory behavior by intraperitoneal injection of interleukin-1 involves brain corticotropin-releasing factor.

The behavior of mice was scored in a multicompartment chamber one hour following intraperitoneal injection of recombinant human interleukin-1 (IL-1). Both IL-1 alpha and IL-1 beta dose-dependently reduced the mean duration for which mice were in contact with novel stimuli without altering measures of locomotor activity, such as movements between the compartments or rears. These behavioral changes resemble those previously observed with prior restraint or intracerebroventricular (ICV) injection of corticotropin-releasing factor (CRF). Effective doses were in the range 0.1-10 ng for IL-1 alpha, and 1-10 ng for IL-1 beta. The reduction in stimulus-contact times induced by 1 ng of IL-1 beta was reversed by prior ICV injection of the CRF antagonist, alpha-helical CRF9-41, suggesting that IL-1 causes secretion of brain CRF which in turn elicits the behavioral changes. These results indicate that peripheral administration of IL-1 alpha or IL-1 beta in low doses can alter behavior. They provide additional evidence that IL-1 administration stimulates brain CRF secretion, and that brain CRF can modulate exploratory behavior, and thus reinforces the concept that IL-1 administration can induce stress.

Analysis of Variance↗
PubMed1989

Immunologic assessment of a cluster of asymptomatic HTLV-I-infected individuals in New Orleans.

PURPOSE: Although clusters of individuals infected with the human T-cell lymphotrophic virus type I (HTLV-I) have been identified in the United States, no systematic evaluation of the immunologic status of these persons has been reported. We therefore studied a group of 11 HTLV-I-infected former intravenous drug abusers who were long-term participants in a methadone maintenance program in New Orleans, Louisiana, to determine the effects of HTLV-I and chronic opiate use on immunity. PATIENTS AND METHODS: Mitogenic responses and results of serologic studies, cell phenotype analysis, and cytotoxicity assays were compared to those in two other HTLV-I seronegative groups: a similar group of 17 methadone users and 15 healthy age-, sex-, and race-matched control subjects. All study participants were seronegative for human immunodeficiency virus type 1. RESULTS: Percentages and numbers of total T lymphocytes (CD2+,CD3+), T-suppressor/cytotoxic lymphocytes (CD8+), cytotoxic lymphocytes (Leu7+, Leu11+, NKH-1+) and B lymphocytes (B4+) were similar among the study groups. Although percentages and numbers of total T-helper lymphocytes (CD4+) were also similar among the groups, HTLV-I-infected subjects had higher percentages and proportions of helper/inducer cells (CD4:4B4+) than did HTLV-I seronegative methadone users. Both methadone using groups had decreased percentages and numbers of suppressor/inducer T lymphocytes (CD4:2H4+). Major histocompatibility complex unrestricted T-cell cytotoxicity (lectin-dependent cellular cytotoxicity), natural killer cell function, and mitogenic responses to the T-cell mitogen phytohemagglutin were similar among the three study groups. Pokeweed mitogen responses were severely depressed in the HTLV-I-infected population. CONCLUSIONS: We conclude that HTLV-I infection is associated with abnormalities in T-cell-dependent B-cell proliferative responses. Furthermore, both long-term methadone use and HTLV-I infection are associated with abnormalities in the distribution of CD4+ cell subpopulations. The increase in the helper/inducer and T-cell cell populations and decrease in the pokeweed mitogenic response noted in HTLV-I-infected subjects appear to be markers for infection with this retrovirus.

Adult↗
PubMed1988

Natural killer cell activity in asbestos workers. Interactive effects of smoking and asbestos exposure.

Both the numbers and function of natural killer (NK) cells in 60 were evaluated in asbestos cement workers grouped by smoking history and chest roentgenogram findings (ILO profusion scores less than 1/0 or greater than or equal to 1/0, or isolated pleural plaques). Worker and control subjects who smoked had smoking histories of less than 27 pack-years, a level of smoking lower than that previously determined to adversely affect NK function. Asbestos workers who did not smoke had percentages and total numbers of NK cells and NK function not different from that of nonsmoker control subjects. Workers who smoked and had evidence of asbestosis (ILO profusion category greater than or equal to 1/0) had significantly lower total numbers of NK cells and mononuclear cell NK activity than did smoker control subjects or smokers with pleural plaques only (p less than or equal to 0.05). Numbers of NK cells and NK cell function were not decreased in either of the asbestos-exposed smoking groups without asbestosis when compared to nonsmoker controls. We conclude that smoking and asbestos exposure interact to decrease mononuclear cell NK function in workers with levels of asbestos exposure sufficient to induce asbestosis. This finding may explain in part the previously reported synergistic effect of smoking and asbestos exposure on the risk of lung cancer. Furthermore, the data presented here clarify previous conflicting reports on NK function where asbestos exposed groups have not been stratified for analysis of data.

Adult↗
PubMed1987

Diminished natural killer-cell activity of interstitial pulmonary cell populations from patients with carcinoma of the lung.

Natural killer-cell activity of fresh interstitial pulmonary cell populations from patients with squamous cell and adenocarcinoma of the lung and carcinoma metastatic to the lung was assessed and compared to that of apparently normal lung. No increase in the percentage of lymphoid cell populations was noted in the interstitium of lung contiguous with tumor, and the cytotoxic capacity of the cells present was depressed as compared to that of normal lung. Natural killer-cell function appears to be down regulated in lung cancer and may be amenable to therapies which activate such cytotoxicity in vivo.

Adenocarcinoma↗
PubMed1987

Cytotoxic cell function in bronchogenic carcinoma.

Biologic response modifiers (BRM) such as interleukin-2 (Il-2) and gamma-interferon (gamma IFN) can augment preexisting or initiate new cytotoxic capacity of human lymphocytes against tumor cells. Although in vivo therapy with BRM or adoptive immunotherapy with BRM-treated cells seems logical in the treatment of bronchogenic carcinoma, recent studies have shown that lymphocytes from the lung and tumor tissues of patients with bronchogenic carcinoma have defective cytotoxic function. We sought to determine if defects in lung cytotoxic cell function are primary or secondary to local tumor effects, and if peripheral blood lymphocyte populations from patients can serve as a source for BRM-stimulated cytotoxic cells. We evaluated the natural killer (NK) cell and lymphokine (Il-2) activated killer cell activity (LAK) activity of mononuclear cell populations from 11 patients with newly diagnosed bronchogenic carcinoma and three control groups. Cultured human squamous cell and adenocarcinoma cell lines proved useful in evaluating LAK activity in these studies. Levels of NK and LAK activity in patients compared favorably with both those of non-smokers in two different age ranges and with smokers. Peripheral blood cytotoxic cell function remains intact and responsive to augmentation by BRM in patients with recently diagnosed bronchogenic carcinoma. Reported defects in patient lung cell cytotoxic function appear to be local tumor-related defects not present in peripheral blood lymphocytes.

Adult↗
PubMedDate not supplied

A phase II trial of irinotecan in hormone-refractory prostate cancer.

Irinotecan is a DNA topoisomerase I inhibitor that has a wide spectrum of activity against human tumors in both preclinical and clinical studies. To evaluate the efficacy of irinotecan in hormone-refractory prostate cancer, we conducted a phase II study in 15 men with metastatic, PSA-progressive disease after primary androgen deprivation. Irinotecan was administered at a dose of 125 mg/m2 weekly for four weeks followed by a two-week rest period; cycles were repeated every six weeks. Response was assessed by evaluation of serial changes in the serum PSA. None of fifteen patients had a decline in PSA of greater than 50%; eight patients had stable disease as a best response. None of three patients with measurable disease had a partial or complete response. Toxicity was primarily hematologic and gastrointestinal, with 40% of patients requiring dose modification due to granulocytopenia and 20% requiring intravenous fluid supplementation after development of diarrhea. There were no treatment-related deaths. We conclude that irinotecan in the dose and schedule used in this trial does not have significant activity against hormone-refractory prostate cancer.

Aged↗