Neuroprotective Effects of MicroRNA-210 on Hypoxic-Ischemic Encephalopathy

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Neuroprotective Effects of MicroRNA-210 on Hypoxic-Ischemic Encephalopathy

OBJECTIVES To reveal the effect of microRNA-210 on cell apoptosis caused by HIE. METHODS Postnatal day 7 rats after HI injury were intraventricularly injected with microRNA-210 mimic, microRNA-210 inhibitor, or physiological saline. 72 h after the injection, rats were sacrificed and the left hemispheres were collected. The expression level of microRNA-210 was identified by quantitative real-t...

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Neuroprotective Strategies after Neonatal Hypoxic Ischemic Encephalopathy

Neonatal hypoxic ischemic encephalopathy (HIE) is a devastating disease that primarily causes neuronal and white matter injury and is among the leading cause of death among infants. Currently there are no well-established treatments; thus, it is important to understand the pathophysiology of the disease and elucidate complications that are creating a gap between basic science and clinical trans...

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Stem Cell Therapy in Hypoxic Ischemic Encephalopathy

Introduction there are one million deaths from asphyxia in newborn annually. Management of this newborn is only supportive. Autologuse stem cell therapy may reduce mortality and long term morbidity. Outcome of asphyxiated newborn is related to damage CNS cells. Stem cells prevent Apoptosis and induce repairmen of injured neurons. Methods in a review study all article related to three keyword...

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Hypothermia: a neuroprotective therapy for neonatal hypoxic-ischemic encephalopathy.

t he incidence of hypoxic ischemic encephalopathy in the United States is 2.8/1000 live births of which 10–15% of the infants succumb and 25–30% suffer permanent neurologic damage: mental retardation, cerebral palsy and epilepsy. The incidence is tenfold higher in the developing world [1-3]. Experimental evidence has confirmed that HIE is an evolving process lasting hours to weeks. Understandin...

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ژورنال

عنوان ژورنال: BioMed Research International

سال: 2013

ISSN: 2314-6133,2314-6141

DOI: 10.1155/2013/350419