By Philip M. Parker
In March 2001, the nationwide Institutes of well-being issued the next caution: ''The variety of sites delivering health-related assets grows on a daily basis. Many websites supply helpful details, whereas others could have details that's unreliable or misleading.'' additionally, a result of fast raise in Internet-based details, many hours should be wasted looking out, deciding upon, and printing. due to the fact basically the smallest fraction of knowledge facing Amyotrophic lateral sclerosis is listed in se's, reminiscent of www.google.com or others, a non-systematic method of web examine will be not just time eating, but additionally incomplete. This publication used to be created for doctors, scholars, and participants of most of the people who are looking to behavior scientific study utilizing the main complicated instruments on hand and spending the smallest amount of time doing so.
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Extra resources for Amyotrophic Lateral Sclerosis - A Bibliography and Dictionary for Physicians, Patients, and Genome Researchers
We propose to study transgenic mouse models that have an altered expression of androgen receptors in skeletal muscle fibers to better understand how hormones regulate the survival of motoneurons. ; Professor; Waisman Ctr/Mr & Human Devlmt; University of Wisconsin Madison Suite 6401 Madison, Wi 537151218 Timing: Fiscal Year 2004; Project Start 01-DEC-1998; Project End 31-MAR-2009 Summary: (provided by applicant): This is a proposal to study the articulatory underpinnings of speech intelligibility deficits in the neurogenic speech disorders associated with Parkinson disease (PD) and amyotrophic lateral sclerosis (ALS).
Secondary endpoints include the rate of decline of forced vital capacity (FVC, percent predicted), the change in the ALS functional rating scale (ALSFRS-R), the SF-12 (quality of life instrument), and the safety and tolerability of creatine. ; Professor & Vice Chairman; Neurology; University of Pittsburgh at Pittsburgh 350 Thackeray Hall Pittsburgh, Pa 15260 Timing: Fiscal Year 2004; Project Start 01-JUN-1999; Project End 31-MAY-2008 Summary: (provided by applicant): Cyclooxygenase, the enzyme that catalyzes the production of prostaglandins from arachidonic acid, has long been thought to play a 36 Amyotrophic Lateral Sclerosis role in exacerbating injury due to cerebral ischemia via its vascular and inflammatory effects.
Preliminary data implicates astrocytic synthesis of nerve growth factor (NGF) and its precursor form proNGF in triggering motor neuron apoptosis through activation of the "low affinity" NGF receptor p75NTR. We hypothesize that zinc-deficient SOD plus nitric oxide will activate astrocytes and contribute to the progression of motor neuron death through activating NGF/p75NTR signaling. To test this hypothesis, we propose to characterize whether zinc deficient SOD can make astrocytes reactive and induce NGF synthesis and secretion.