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Stanton B. Elias

Researcher at Henry Ford Health System

Publications -  40
Citations -  2115

Stanton B. Elias is an academic researcher from Henry Ford Health System. The author has contributed to research in topics: Myasthenia gravis & Experimental autoimmune encephalomyelitis. The author has an hindex of 19, co-authored 40 publications receiving 1947 citations. Previous affiliations of Stanton B. Elias include University of Texas at Austin & Baylor College of Medicine.

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Glatiramer acetate in primary progressive multiple sclerosis: Results of a multinational, multicenter, double-blind, placebo-controlled trial

Jerry S. Wolinsky, +82 more
- 01 Jan 2007 - 
TL;DR: To determine whether glatiramer acetate slows accumulation of disability in primary progressive multiple sclerosis, a new drug is developed that acts as a ‘spatially aggregating agent’ to reduce the risk of disease progression.
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Human bone marrow stromal cell treatment improves neurological functional recovery in EAE mice.

TL;DR: Data indicate that hBMSC treatment improved functional recovery after EAE in mice, possibly, via reducing inflammatory infiltrates and demyelination areas, stimulating oligodendrogenesis, and by elevating BDNF expression.
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Central pontine myelinolysis and pontine lesions after rapid correction of hyponatremia: a prospective magnetic resonance imaging study.

TL;DR: It is concluded that the correction rate of hyponatremia plays a significant role in the pathogenesis of pontine lesions in individuals with profound hypon atremia who undergo large increases in sodium concentration as a result of severe initial hyponAtremia.
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Bone marrow stromal cells reduce axonal loss in experimental autoimmune encephalomyelitis mice

TL;DR: It is indicated that hBMSCs improve functional recovery and may provide a potential therapy aimed at axonal protection in EAE mice, in which NGF may play a vital role.
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Accelerated degradation of acetylcholine receptor from cultured rat myotubes with myasthenia gravis sera and globulins

TL;DR: It is suggested that circulating globulins in myasthenia gravis may contribute to the functional defects of neuromuscular transmission by accelerating the rate of internationalization and degradation of surface membrane acetylcholine receptors.