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This observational study investigates the effects of epimacular membrane peeling on the structure and function of the retina.
Observational Model: Cohort, Time Perspective: Prospective
Centre for Ophthalmology, University Hospital Tuebingen
University Hospital Tuebingen
Published on BioPortfolio: 2010-07-15T17:00:00-0400
Patients and clinicians need better options to prevent the weight regain that almost universally follows a weight loss intervention. In lay terms, a new, higher "set point" seems to occur ...
Wet age-related macular degeneration is the most common cause of blind registration in the UK. Standard treatment involves regular eye injections of a drug called ranibizumab (Lucentis). ...
This study evaluates the safety of Next Generation Ophthalmic Irrigating Solution compared to BSS PLUS for use during surgery for removal of epimacular membrane and vitrectomy.
Alzheimer disease (AD) is a dementing illness characterized by progressive neuronal degeneration, gliosis, and the accumulation of intracellular inclusions and extracellular deposits of am...
Numerous terms have been used to describe epiretinal membrane (ERM): macular pucker, epimacular membrane, surface-wrinkling retinopathy, cellophane maculopathy and preretinal macular fibro...
OBJECTIVE The authors studied the clinical characteristics and postoperative outcomes of drug-resistant epilepsy associated with focal gliosis. METHODS From their epilepsy surgery database, the author...
In adults, hypothalamic gliosis has been documented using quantitative T2 neuroimaging, whereas functional magnetic resonance imaging (fMRI) has shown a defective hypothalamic response to nutrients. N...
The transcriptional factor Nrf2, a master regulator of oxidative stress and inflammation that are tightly linked to the development and progression of cerebral ischemia pathology, plays a vital role i...
Loss-of-function mutations in progranulin (GRN), most of which cause progranulin haploinsufficiency, are a major autosomal dominant cause of frontotemporal dementia (FTD). Individuals with loss-of-fun...
Spinal muscular atrophy (SMA) is characterized by the loss of α-motoneurons (MNs) with concomitant muscle denervation. MN excitability and vulnerability to disease are particularly regulated by choli...
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)