Results 91 to 100 of about 150,877 (243)

TREATMENT OF FOCAL CEREBRAL ISCHEMIA WITH HYPERBARIC OXYGEN

open access: gold, 1965
David H. Ingvar, Niels A. Lassen
openalex   +1 more source

Neurogenic Regulation of Cerebral Blood Flow Following Ischemia [PDF]

open access: bronze, 1976
Nicholas T. Zervas   +3 more
openalex   +1 more source

A subset of OPCs do not express Olig2 during development which can be increased in the adult by brain injuries and complex motor learning

open access: yesGlia, Volume 71, Issue 2, Page 415-430, February 2023., 2023
Main Points A subset of OPCs do not express Olig2, of which population peaks in the juvenile brain while wanes with age. Plastic changes of the brain by acute injuries or complex motor learning stop the expression of Olig2 in OPCs. Abstract Oligodendrocyte precursor cells (OPCs) are uniformly distributed in the mammalian brain; however, their function ...
Li‐Pao Fang   +7 more
wiley   +1 more source

A Clinical Evaluation of Transient Focal Cerebral Ischemia with Some Comments on Its Concept

open access: bronze, 1965
Kosuke Mori   +9 more
openalex   +2 more sources

Distinct cerebral cortical perfusion patterns in idiopathic normal‐pressure hydrocephalus

open access: yesHuman Brain Mapping, Volume 44, Issue 1, Page 269-279, January 2023., 2023
The present study investigates cerebral blood flow (CBF) and cortical thickness using surface‐based analysis of early‐phase 18F‐florbetaben PET and MRI in patients with idiopathic normal‐pressure hydrocephalus (INPH). INPH patients had significantly increased CBF with a concomitant increase in cortical thickness in areas located in the high convexity ...
Kyunghun Kang   +10 more
wiley   +1 more source

Protective Action of Phenytoin in Cerebral Ischemia

open access: bronze, 1979
John P. Cullen   +3 more
openalex   +1 more source

ENPP1 deficiency: A clinical update on the relevance of individual variants using a locus‐specific patient database

open access: yesHuman Mutation, Volume 43, Issue 12, Page 1673-1705, December 2022., 2022
Abstract Loss‐of‐function variants in the ectonucleotide pyrophosphatase/phosphodiesterase family member 1 (ENPP1) cause ENPP1 Deficiency, a rare disorder characterized by pathological calcification, neointimal proliferation, and impaired bone mineralization. The consequence of ENPP1 Deficiency is a broad range of age dependent symptoms and morbidities
Stephanie A. Mercurio   +8 more
wiley   +1 more source

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