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IFNbeta-1a 44 micro g subcutaneously tiw was more effective than IFNbeta-1a 30 micro g IM qw on all primary and secondary outcomes investigated after 24 and 48 weeks of treatment.

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ABSTRACT125I-Ap812s (specific activity, 3-6 x 106 dpm/;.g) in a final volume of 20 pI of phosphate-buffered saline (PBS) at pH 7.4 at 37TC. Samples were analyzed by SDS/PAGE. A 12% Tris-glycine gel was used for analysis of complexes AP3 with CSF proteins and a 13% gel in Tricine buffer was used for analysis of A( aggregation. The gel was then dried and exposed to an x-ray X-Omat film from Kodak. The purification of Ad binding activity was monitored using 'mI-A1i_28 and electrophoresis in SDS/PAGE gel and included three steps.Step 1: 5 ml of CSF was subjected to ion-exchange chromatography on a 5-ml column with DEAE-Sepharose equilibrated with 50 mM Tris-HCl (pH 7.4). The peak of AP3 binding activity was eluted at 0.4 M NaCl.Step 2: the peak fractions were combined, diluted five times, and further passed through a heparin-Sepharose column in 50 mM NaCl/50 mM Tris HCl, pH 7.4. The AP binding activity appeared in unbound fractions.Step 3: the combined fractions containing A(3 binding activity were chromatographed on a FPLC-mono Q column with a gradient of0.1-0.3 M NaCl in 50 mM Tris HCl (pH 7.4 iTo whom reprint requests should be addressed. 8368The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

Objective: To determine whether glatiramer acetate (GA) slows accumulation of disability in primary progressive multiple sclerosis. Methods: A total of 943 patients with primary progressive multiple sclerosis were randomized to GA or placebo (PBO) in this 3-year, double-blind trial. The primary end point was an intention-to-treat analysis of time to 1-(entry expanded disability status scale, 3.0 -5.0) or 0.5-point expanded disability status scale change (entry expanded disability status scale, 5.5-6.5) sustained for 3 months. The trial was stopped after an interim analysis by an independent data safety monitoring board indicated no discernible treatment effect on the primary outcome. Intention-to-treat analyses of disability and magnetic resonance imaging end points were performed. Results: There was a nonsignificant delay in time to sustained accumulated disability in GA-versus PBO-treated patients (hazard ratio, 0.87 [95% confidence interval, 0.71-1.07]; p ϭ 0.1753), with significant decreases in enhancing lesions in year 1 and smaller increases in T2 lesion volumes in years 2 and 3 versus PBO. Post hoc analysis showed that survival curves for GA-treated male patients diverged early from PBO-treated male subjects (hazard ratio, 0.71 [95% confidence interval, 0.53-0.95]; p ϭ 0.0193). Interpretation:The trial failed to demonstrate a treatment effect of GA on primary progressive multiple sclerosis. Both the unanticipated low event rate and premature discontinuation of study medication decreased the power to detect a treatment effect. Post hoc analysis suggests GA may have slowed clinical progression in male patients who showed more rapid progression when untreated.