Checkerboard fields in multiple sclerosis.
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Adult↗
Biomedical subjects
C E Markowitz
Publications and source records attributed to C E Markowitz.
Neuronal cell injury precedes brain atrophy in multiple sclerosis.
Global brain atrophy estimated using MRI and whole brain N-acetylaspartate (WBNAA) concentration measured with proton MR spectroscopy were obtained in 42 patients with relapsing-remitting multiple sclerosis and 41 matched control subjects. Patients exhibited cross-sectional atrophy (0.5%; p = 0.033) and WBNAA decline (1.8%/y; p = 0.005) vs disease duration. The 3.6-fold rate disparity between the two processes suggests that neuronal/axonal dysfunction (N-acetylaspartate decline) precedes parenchyma loss, not its consequence (i.e., is an earlier, more sensitive specific metric of the ongoing disease activity).
Adult↗
Contrast letter acuity as a visual component for the Multiple Sclerosis Functional Composite.
BACKGROUND: Visual dysfunction is one of the most common causes of disability in multiple sclerosis (MS). The Multiple Sclerosis Functional Composite (MSFC), a new clinical trial outcome measure, does not currently include a test of visual function. OBJECTIVE: To examine contrast letter acuity as a candidate visual function test for the MSFC. METHODS: Binocular contrast letter acuity testing (Sloan charts) was performed in a subgroup of participants from the International Multiple Sclerosis Secondary Progressive Avonex Controlled Trial (IMPACT Substudy) and in MS patients and disease-free control subjects from a cross-sectional study of visual outcome measures (Multiple Sclerosis Vision Prospective cohort [MVP cohort]). High-contrast visual acuity was measured in both studies; MVP cohort participants underwent additional binocular testing for contrast sensitivity (Pelli-Robson chart), color vision (D-15 desaturated test), and visual field (Esterman test, Humphrey Field Analyzer II). RESULTS: Contrast letter acuity (Sloan charts, p < 0.0001, receiver operating characteristic curve analysis) and contrast sensitivity (Pelli-Robson chart, p = 0.003) best distinguished MS patients from disease-free control subjects in the MVP cohort. Correlations of Sloan chart scores with MSFC and Expanded Disability Statue Scale (EDSS) scores in both studies were significant and moderate in magnitude, demonstrating that Sloan chart scores reflect visual and neurologic dysfunction not entirely captured by the EDSS or MSFC. CONCLUSIONS: Among clinical measures, contrast letter acuity (Sloan charts) and contrast sensitivity (Pelli-Robson chart) demonstrate the greatest capacity to identify binocular visual dysfunction in MS. Sloan chart testing also captures unique aspects of neurologic dysfunction not captured by current EDSS or MSFC components, making it a strong candidate visual function test for the MSFC.
Adult↗
Antagonism of beta-endorphin-induced prolactin release by alpha-melanocyte-stimulating hormone and corticotropin-like intermediate lobe peptide.
The ability of two proopiomelanocortin-derived peptides, alpha MSH and corticotropin-like intermediate lobe peptide (CLIP) [ACTH (18-39)] to antagonize the stimulation of PRL secretion by beta-endorphin (beta EP) was studied in the rat. When 50 ng beta EP were injected into the lateral cerebral ventricle, plasma PRL rose from a mean baseline of 1.87 +/- 0.43 ng/ml (+/- SEM) to a peak of 23.0 +/- 3.67 ng/ml 10 min after the injection. When the same animals received 500 ng alpha MSH together with 50 ng beta EP, the peak concentration of PRL was reduced by 74% to 6.05 +/- 1.43 ng/ml (P less than 0.005). After the injection of 500 ng CLIP together with 500 ng beta EP, the peak concentration of PRL was reduced by 47% to 12.8 +/- 3.09 ng/ml (P less than 0.01). Total PRL release, determined by calculating the areas under the plasma PRL concentration curves, was also significantly reduced by the injection of alpha MSH or CLIP. A dose of 100 ng alpha-MSH or CLIP also antagonized the stimulation of PRL secretion by 50 ng beta EP. PRL release was reduced by 62% after administration of 100 ng alpha MSH (P less than 0.001) and by 43% after 100 ng CLIP (P less than 0.05). When 100 ng alpha MSH and 100 ng CLIP were injected together, there was an additive effect in blocking the stimulation of PRL release by beta EP, and the peak plasma PRL concentration was reduced by 81%. Des-acetyl alpha MSH, the predominant form of alpha MSH in the hypothalamus, was also very effective in antagonizing beta EP-induced PRL release. The peak PRL concentration was reduced by 52% after administration of 100 ng des-acetyl alpha MSH plus 50 ng beta EP compared with that after beta EP alone (P less than 0.005). We conclude that relatively low doses of both alpha MSH and CLIP can effectively antagonize the actions of beta EP on pituitary PRL release. These findings suggest the possibility that differential posttranslational processing of proopiomelanocortin may serve as a regulator of anterior pituitary function.
Adrenocorticotropic Hormone↗