11 results match your criteria: "National Institute for Neurological Diseases and Stroke[Affiliation]"

Patients with von Hippel Lindau (VHL) disease develop multiple central nervous system hemangioblastomas (HB). The surgical resection of VHL-HBs is the standard of clinical care when these HBs become symptomatic due to tumor growth, edema, or cyst formation. VHL-HBs frequently present at the obex of the brainstem, making this a challenging surgical problem.

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Stroke Hospital Characteristics in the Florida-Puerto Rico Collaboration to Reduce Stroke Disparities Study.

South Med J

July 2017

From the University of Miami Miller School of Medicine, Miami, Florida, University of Miami School of Architecture, Coral Gables, Florida, the National Institute for Neurological Diseases and Stroke, Bethesda, Maryland, Hospital HIMA San Pablo, Caguas, Puerto Rico, American Heart Association Greater Southeast Affiliate, San Juan, Puerto Rico, and the Barrow Neurological Institute, Phoenix, Arizona.

Objectives: Although disparities in stroke care and outcomes have been well documented nationally, state-based registries to monitor acute stroke care in Florida (FL) and Puerto Rico (PR) have not been established. The FL-PR Collaboration to Reduce Stroke Disparities (CReSD) was developed to evaluate race-ethnicity and regional disparities in stroke care performance. The objective of this study was to assess and compare hospital characteristics within a large quality improvement registry to identify characteristics associated with better outcomes for acute ischemic stroke care.

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Screening for GPR101 defects in pediatric pituitary corticotropinomas.

Endocr Relat Cancer

June 2016

C Stratakis, Program on Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, United States

Cushing disease (CD) in children is caused by adrenocorticotropic hormone (ACTH)-secreting pituitary adenomas. Germline or somatic mutations in genes such as MEN1, CDKIs, AIP, and USP8 have been identified in pediatric CD, but the genetic defects in a significant percentage of cases are still unknown. We investigated the orphan G protein-coupled receptor GPR101, a gene known to be involved in somatotropinomas, for its possible involvement in corticotropinomas.

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Rescue of an in vitro neuron phenotype identified in Niemann-Pick disease, type C1 induced pluripotent stem cell-derived neurons by modulating the WNT pathway and calcium signaling.

Stem Cells Transl Med

March 2015

National Institute of Arthritis and Musculoskeletal and Skin Diseases, NeuroTherapeutics Development Unit, National Institute for Neurological Diseases and Stroke, Genetic Disease Research Branch, National Human Genome Research Institute, Eunice Kennedy Shriver National Institute for Child Health and Human Development, and Center for Regenerative Medicine, National Institutes of Health, Bethesda, Maryland, USA

Niemann-Pick disease, type C1 (NPC1) is a familial disorder that has devastating consequences on postnatal development with multisystem effects, including neurodegeneration. There is no Food and Drug Administration-approved treatment option for NPC1; however, several potentially therapeutic compounds have been identified in assays using yeast, rodent models, and NPC1 human fibroblasts. Although these discoveries were made in fibroblasts from NPC1 subjects and were in some instances validated in animal models of the disease, testing these drugs on a cell type more relevant for NPC1 neurological disease would greatly facilitate both study of the disease and identification of more relevant therapeutic compounds.

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Multiple sclerosis (MS) is an immunological disorder of the CNS. Linked to an initial transient inflammation as the result of blood-brain barrier leakage, the disease progresses into a neurodegenerative phase. MRI is the most powerful paraclinical tool for diagnosing and monitoring MS.

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Theories of fatigue: application in HIV/AIDS.

J Assoc Nurses AIDS Care

June 2006

National Institute for Neurological Diseases and Stroke, National Institutes of Health, Bethesda, MD, USA.

A number of theoretical fatigue frameworks have been developed by nurse scientists with the intention of guiding research, practice, and education in fatigue. However, there is a significant gap between theory development and research utilization of fatigue frameworks in clinical and intervention trials. The purpose of this report is to assess an example of an inductive fatigue framework and a deductive symptom management model: The Integrated Fatigue Model (IFM) and the revised University of California, San Francisco, Symptom Management Model (UCSF-SMM), to investigate their potential to guide future nursing research projects on fatigue.

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Immunopathogenesis of the multiple sclerosis lesion.

Curr Neurol Neurosci Rep

May 2001

Neuroimmunology Branch, National Institute for Neurological Diseases and Stroke, National Institutes of Health, Building 10, Room 5B-16, 10 Center Drive MSC 1400, Bethesda, MD 20892-1400, USA.

Multiple sclerosis (MS) is thought to be an autoimmune disease with a chronic inflammatory response directed against central nervous system (CNS) myelin antigens. Immunologic studies indicate that autoreactive CD4+ lymphocytes migrate into the CNS causing blood brain barrier (BBB) disruption, an initial event in the evolution of the MS lesion. Subsequent antigen recognition within the CNS initiates inflammatory responses that, through the multiple effector mechanisms, lead to demyelination.

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Rats were trained on an olfactory and a control modality (auditory or visual) discrimination task and brain membrane-associated protein kinase C (mPKC) was subsequently assessed using quantitative autoradiography of radiolabelled phorbol ester binding. In rats which received olfactory-cued training, mPKC showed a highly significant lateralization in the piriform cortex but not in the hippocampus. Both olfactory-trained rats and control modality rats showed a significant increase in mPKC in the hippocampus when compared to naive rats.

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Expression of vascular permeability factor/vascular endothelial growth factor in normal rat tissues.

Am J Physiol

April 1993

Surgical Neurology Branch, National Institute for Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland 20892.

Vascular permeability factor (VPF)/vascular endothelial growth factor (VEGF) is a approximately 43-kDa secreted protein that has been shown in bioassays to induce endothelial proliferation, angiogenesis, and capillary hyperpermeability. VPF has been suggested to play an important role in the physiology of normal vasculature. To further elucidate the natural functions of VPF in vivo, the expression of VPF in normal tissues was examined using Northern blot analysis and in situ hybridization histochemistry.

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Imaging endoplasmic reticulum in living sea urchin eggs.

Methods Cell Biol

January 1994

Laboratory of Neurobiology, National Institute for Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Maryland 20892.

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Twinning and neurologic morbidity.

Am J Dis Child

September 1992

Neuroepidemiology Branch, National Institute for Neurological Diseases and Stroke, National Institutes of Health, Bethesda, Md 20892.

Objective: To review the literature regarding neurologic morbidity among twins.

Research Design: Review of medical literature and data from the National Center for Health Statistics.

Conclusions: The twinning rate is increasing concurrent with an increase in the survival of twins.

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