Observational Study - ILM Peeling

2010-07-15 17:00:00 | BioPortfolio


This observational study investigates the effects of epimacular membrane peeling on the structure and function of the retina.

Study Design

Observational Model: Cohort, Time Perspective: Prospective


Epimacular Gliosis


Centre for Ophthalmology, University Hospital Tuebingen




University Hospital Tuebingen

Results (where available)

View Results


Published on BioPortfolio: 2010-07-15T17:00:00-0400

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PubMed Articles [45 Associated PubMed Articles listed on BioPortfolio]

Predictors of seizure outcome following resective surgery for drug-resistant epilepsy associated with focal gliosis.

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Pretreatment with Korean red ginseng or dimethyl fumarate attenuates reactive gliosis and confers sustained neuroprotection against cerebral hypoxic-ischemic damage by an Nrf2-dependent mechanism.

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Reduction of microglial progranulin does not exacerbate pathology or behavioral deficits in neuronal progranulin-insufficient mice.

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Medical and Biotech [MESH] Definitions

The production of a dense fibrous network of neuroglia; includes astrocytosis, which is a proliferation of astrocytes in the area of a degenerative lesion.

Non-specific white matter changes in the BRAIN, often seen after age 65. Changes include loss of AXONS; MYELIN pallor, GLIOSIS, loss of ependymal cells, and enlarged perivascular spaces. Leukoaraiosis is a risk factor for DEMENTIA and CEREBROVASCULAR DISORDERS.

Heterogeneous group of neurodegenerative disorders characterized by frontal and temporal lobe atrophy associated with neuronal loss, gliosis, and dementia. Patients exhibit progressive changes in social, behavioral, and/or language function. Multiple subtypes or forms are recognized based on presence or absence of TAU PROTEIN inclusions. FTLD includes three clinical syndromes: FRONTOTEMPORAL DEMENTIA, semantic dementia, and PRIMARY PROGRESSIVE NONFLUENT APHASIA.

Parkinsonism following encephalitis, historically seen as a sequella of encephalitis lethargica (Von Economo Encephalitis). The early age of onset, the rapid progression of symptoms followed by stabilization, and the presence of a variety of other neurological disorders (e.g., sociopathic behavior; TICS; MUSCLE SPASMS; oculogyric crises; hyperphagia; and bizarre movements) distinguish this condition from primary PARKINSON DISEASE. Pathologic features include neuronal loss and gliosis concentrated in the MESENCEPHALON; SUBTHALAMUS; and HYPOTHALAMUS. (From Adams et al., Principles of Neurology, 6th ed, p754)

An inherited disorder of copper metabolism transmitted as an X-linked trait and characterized by the infantile onset of HYPOTHERMIA, feeding difficulties, hypotonia, SEIZURES, bony deformities, pili torti (twisted hair), and severely impaired intellectual development. Defective copper transport across plasma and endoplasmic reticulum membranes results in copper being unavailable for the synthesis of several copper containing enzymes, including PROTEIN-LYSINE 6-OXIDASE; CERULOPLASMIN; and SUPEROXIDE DISMUTASE. Pathologic changes include defects in arterial elastin, neuronal loss, and gliosis. (From Menkes, Textbook of Child Neurology, 5th ed, p125)

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