Titlebook: Nimodipine; Pharmacological and Alexander Scriabine,G. M. Teasdale,Wise Young Conference proceedings 1991 Springer-Verlag Berlin Heidelber

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L. P. Huyghens,W. A. Buylaert,M. T. Rosseel,M. G. Bogaertesponsibilities, and mitigation activities to stakeholders. The decision of what and when to disclose is specific to each setting; companies make disclosure decisions while considering internal objectives, external pressure, and regulatory requirements. The motivations that drive reporting are often

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W. A. Buylaert,L. P. Huyghens,M. T. Rosseel,M. G. Bogaerting down cost in supply chain relationships, supplier relationships may suffer. In addition, through outsourcing and global sourcing, companies have not only created highly complex supply chains, but also supply chains that are not transparent. When irregularities arise, such as child labor and envi

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M. Forsmanesponsibilities, and mitigation activities to stakeholders. The decision of what and when to disclose is specific to each setting; companies make disclosure decisions while considering internal objectives, external pressure, and regulatory requirements. The motivations that drive reporting are often

CUMB

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The Effect of Nimodipine Pretreatment on Focal Cerebral Ischemia in the Hypertensive Ratnesthetized rat [12]. Nimodipine pretreatment can also provide long-lasting (24 h) protection against focal cerebral ischemia in conscious rats given continuous treatment [9]. How cytoprotection is maintained with prolonged ischemia is not clear, but work in our laboratory suggests that at a critica

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Etymology

Dihydropyridines Attenuate Slow Excitatory Amino Acid Neurotoxicityy resulting from certain acute insults to the central nervous system, including hypoglycemia, hypoxia-ischemia, epilepsy, and trauma [17, 22, 5]. While glutamate activates at least three types of ionophore-linked postsynaptic receptors, .-methyl-.-aspartate (NMDA), kainate, and alpha-amino-3-hydroxy

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The Pathophysiology of Arterial Narrowing and Delayed Ischemic Deficit After Subarachnoid Hemorrhagend mortality following subarachnoid hemorrhage (SAH) have remained unacceptably high, due in large part to ischemic complications resulting from cerebral vasospasm. The clinical syndrome of vasospasm is well described; in those patients surviving the initial ictus of ruptured intracranial aneurysm.