Results 301 to 310 of about 184,954 (326)
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Cellular and Molecular Neurobiology, 2003
1. Stimulation of the rostral-ventromedial pole of the cerebellar fastigial nucleus exerts powerful effects on systemic and cerebral circulation. 2. Excitation of fibers passing through the fastigial nucleus evokes sympathoactivation and increases in arterial pressure. 3.
Eugene V, Golanov, Ping, Zhou
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1. Stimulation of the rostral-ventromedial pole of the cerebellar fastigial nucleus exerts powerful effects on systemic and cerebral circulation. 2. Excitation of fibers passing through the fastigial nucleus evokes sympathoactivation and increases in arterial pressure. 3.
Eugene V, Golanov, Ping, Zhou
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Best Practice & Research Clinical Anaesthesiology, 2010
The endpoint of all cerebral injuries like stroke, global cerebral ischemia during cardiac arrest, cardiac, vascular, or brain surgery or head trauma is the inadequate supply of the brain with oxygen and glucose, which triggers a characteristic pathophysiologic cascade leading to neuronal death. Many methods and agents have been investigated to produce
Klaus Ulrich, Klein, Kristin, Engelhard
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The endpoint of all cerebral injuries like stroke, global cerebral ischemia during cardiac arrest, cardiac, vascular, or brain surgery or head trauma is the inadequate supply of the brain with oxygen and glucose, which triggers a characteristic pathophysiologic cascade leading to neuronal death. Many methods and agents have been investigated to produce
Klaus Ulrich, Klein, Kristin, Engelhard
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Current Drug Targets, 2007
Ischemic brain injury can be anticipated in a number of clinical settings such as procedures associated with a high-risk for stroke, patients with transient ischemic attacks or minor strokes who are at substantial risk for early recurrence and patients with multiple vascular risk factors with an enhanced risk for ischemic stroke over many years.
Savitz, Sean I., Fisher, Marc
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Ischemic brain injury can be anticipated in a number of clinical settings such as procedures associated with a high-risk for stroke, patients with transient ischemic attacks or minor strokes who are at substantial risk for early recurrence and patients with multiple vascular risk factors with an enhanced risk for ischemic stroke over many years.
Savitz, Sean I., Fisher, Marc
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Cerebrovascular Diseases, 2000
The current goal of acute stroke therapy is to restore cerebral perfusion and to protect cerebral tissue before the development of an irreversible damage. This latter is due to the duration and the severity of cerebral ischemia [1]. Recanalization operated by thrombolysis represents the most intuitive and effective treatment of acute cerebral ischemia.
MOSTARDINI C +5 more
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The current goal of acute stroke therapy is to restore cerebral perfusion and to protect cerebral tissue before the development of an irreversible damage. This latter is due to the duration and the severity of cerebral ischemia [1]. Recanalization operated by thrombolysis represents the most intuitive and effective treatment of acute cerebral ischemia.
MOSTARDINI C +5 more
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2017
Abstract Acute cerebral injury sets into motion a cascade of deleterious biochemical events that cause further neuronal damage and amplify deleterious effects. This cascade develops over time and potentially may be attenuated or limited by pharmacologic manipulation.
Stocchetti, Nino, Carbonara, Marco
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Abstract Acute cerebral injury sets into motion a cascade of deleterious biochemical events that cause further neuronal damage and amplify deleterious effects. This cascade develops over time and potentially may be attenuated or limited by pharmacologic manipulation.
Stocchetti, Nino, Carbonara, Marco
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Physical Medicine and Rehabilitation Clinics of North America, 1999
Although basic research has revealed many mechanisms involved in the repair or elimination of damaged neurons, turning these mechanisms into clinically useful neuroprotective interventions is a slow process. Numerous neurotrophic factors seem to mediate neuronal repair and viability, but because the neurotrophic factors are proteins or polypeptides ...
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Although basic research has revealed many mechanisms involved in the repair or elimination of damaged neurons, turning these mechanisms into clinically useful neuroprotective interventions is a slow process. Numerous neurotrophic factors seem to mediate neuronal repair and viability, but because the neurotrophic factors are proteins or polypeptides ...
openaire +2 more sources