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J Antel

Publications and source records attributed to J Antel.

8 recordsLinked to original sources
PubMed1991

Proton magnetic resonance spectroscopy for metabolic characterization of plaques in multiple sclerosis.

We are investigating the potential of in vivo proton magnetic resonance spectroscopy for noninvasive characterization of the chemical pathology of plaques in magnetic resonance brain images from patients with multiple sclerosis. Spectra localized to chronic, irreversible plaques showed a decrease in the ratio of N-acetyl/creatine resonance intensities relative to normal-appearing white matter. Spectra localized to active plaques showed different metabolite changes as compared with spectra from identical, plaque-free volumes in the contralateral hemispheres. Some active plaques showed either no abnormalities or only an increase in tissue lactate. Spectra from others showed an increased ratio of choline/creatine resonance intensities, with or without a decreased N-acetyl/creatine resonance intensity ratio. In one case, serial observations showed an evolution of changes in spectra from a single plaque from an increased choline/creatine ratio to a decreased N-acetyl/creatine ratio. These observations suggest that proton magnetic resonance spectroscopy may be able to distinguish acute or active from chronic plaques and to characterize the pathologic evolution of active plaques by measurement of local tissue metabolite levels.

Choline↗
PubMed1990

Proton magnetic resonance spectroscopy of human brain in vivo in the evaluation of multiple sclerosis: assessment of the load of disease.

Image localized, water-suppressed proton magnetic resonance spectra were obtained from affected brain in patients with multiple sclerosis. In patients with moderate to severe chronic disease, spectra revealed a decreased ratio of N-acetylaspartate to creatine resonance intensities. A normal ratio was obtained from a large recently symptomatic MRI plaque that resolved without sequelae. We propose that the observed metabolite changes can be useful as an index of irreversible CNS injury.

Aspartic Acid↗
PubMed1988

Activated suppressor cell function in multiple sclerosis--clinical correlations.

Activated suppressor cell function mediated by either freshly isolated peripheral blood mononuclear cells (MNCs), freshly isolated CD8+ lymphocytes or by CD8+ cell lines, has previously been found to be reduced compared to controls in multiple sclerosis (MS) patients with progressive disease (MS-P). In this study, we found that suppressor activity mediated by CD8+ cell lines, derived from MS patients with stable disease (MS-S) patients and maintained in culture for 14 days, was significantly greater (45 +/- 6%) compared to that mediated by MS-P patients' CD8+ cells (11 +/- 4%, P less than 0.005). The MS-S suppressor values were, however, suggestively reduced compared to controls (60 +/- 6%, P less than 0.05). MNC-mediated suppressor values for the MS-S group (61 +/- 5%) did not differ from the control group (67 +/- 6%). Values for the MS-P group (7 +/- 6%) were significantly reduced compared to MS-S and control groups. Cytotoxic activity mediated by CD8+ cell lines showing defective suppressor function did not differ from control values. The cell lines in MS and control did not differ with respect to their rate of proliferation in the presence of IL-2 and OKT3. Suppressor function in this assay was ablated if exogenous IL-2 was removed from the culture media. These data suggest that defective activated suppressor function is characteristic of the progressive form of MS, although a suppressor defect is also partially expressed in stable MS patients when CD8+ cell lines are studied.

Adult↗
PubMed1986

Defective suppressor cell function mediated by T8+ cell lines from patients with progressive multiple sclerosis.

Activated suppressor cell function, induced with either concanavalin A or OKT3 and mediated by either unfractionated mononuclear cells or "panning" enriched T8+ cells, freshly isolated from peripheral blood, is reduced in patients with progressive multiple sclerosis (MS) as compared with control donors. In this study, we generated T8+ cell lines from the peripheral blood of these same patients and controls. Suppressor activity, mediated by T8+ cells exposed to OKT3 on days 1, 7, and 14 of culture and then treated with mitomycin C on day 16, was significantly reduced in the MS group (mean percent suppression 13% +/- 5) as compared with the control group (68% +/- 6, n = 8, p less than 0.001). No differences were noted in [3H]thymidine uptake by the OKT3-stimulated T8+ cell lines of MS and control groups. Mean percent suppression mediated by T4+ cell lines did not differ between MS and control groups (15% +/- 4, n = 3, vs 22% +/- 2, n = 4). These current data suggest that the previously observed defect in T8+ cell-mediated activated suppressor cell function in MS is a persistent one, favoring the postulate that the defect reflects intrinsic alterations in this cell population rather than a transient effect of serum factors on T8+ cell function.

Antigens, Differentiation, T-Lymphocyte↗