Neuroprotection

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Neuroprotection with

Members of the Bcl-2 proto-oncogene family have been identified as major modulators of programmed cell death, with Bcl-2 gene products either enhancing or diminishing the likelihood of neuronal survival. This regulation appears to be essential to normal brain development, where programmed cell death may eliminate up to 50% of neurons as a part of selective pruning during formation of neuronal n...

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Perinatal neuroprotection

Fetal or neonatal brain injury can result in lifelong neurologic disability. The most significant risk factor for perinatal brain injury is prematurity; however, in absolute numbers, full-term infants represent the majority of affected children. Research on strategies to prevent or mitigate the impact of perinatal brain injury ("perinatal neuroprotection") has established the mitigating roles o...

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Argon neuroprotection

Certain noble gases, though inert, exhibit remarkable biological properties. Notably, xenon and argon provide neuroprotection in animal models of central nervous system injury. In the previous issue of Critical Care, Loetscher and colleagues provided further evidence that argon may have therapeutic properties for neuronal toxicity by demonstrating protection against both traumatic and oxygen-gl...

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Rethinking Neuroprotection in Severe Traumatic Brain Injury: Toward Bedside Neuroprotection

Neuroprotection after traumatic brain injury (TBI) is an important goal pursued strenuously in the last 30 years. The acute cerebral injury triggers a cascade of biochemical events that may worsen the integrity, function, and connectivity of the brain cells and decrease the chance of functional recovery. A number of molecules acting against this deleterious cascade have been tested in the exper...

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Neuroprotection does not work!

For more than 2 decades neurologists have searched for a drug that protects ischemic brain tissue from cell death— without success so far. The list of drugs tested in phase II and III trials is long. One of the first substances that showed a neuroprotective effect in experimental ischemia was the NMDA-antagonist MK-801,1 which protected hippocampal CA1 and CA2 pyramidal neurons. Besides NMDA an...

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ژورنال

عنوان ژورنال: THE JOURNAL OF JAPAN SOCIETY FOR CLINICAL ANESTHESIA

سال: 2007

ISSN: 0285-4945,1349-9149

DOI: 10.2199/jjsca.27.588