Journal of neurosurgical anesthesiology
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J Neurosurg Anesthesiol · Jul 2008
Admission microalbuminuria and neurologic outcomes in intensive care unit patients with spontaneous intracerebral hemorrhage.
This study was performed to determine the prevalence and the prognostic significance of microalbuminuria in patients admitted to intensive care unit (ICU) after spontaneous intracerebral hemorrhage (ICH). From May 2004 to April 2006, we studied 59 consecutive ICH patients verified using computed tomography and admitted to our ICU within a day after stroke. General clinical, neurologic data, and Glasgow Coma Scale (GCS) were recorded at admission to ICU. ⋯ The areas under the receiver operator characteristic curves showed that the urinary microalbumin/creatinine ratio [0.81 (95% CI, 0.70-0.92)] and the GCS score [0.78 (95% CI, 0.66-0.90)] at admission were significant predictors of unfavorable neurologic outcome at hospital discharge. The threshold value, sensitivity, specificity, and likelihood ratio for the urinary microalbumin/creatinine ratio were 200 mg/g, 51% (95% CI, 39-64), 96% (95% CI, 90-100), and 11.3 (95% CI, 7.9-16.0); and those for the GCS score were 11, 46% (95% CI, 36-61), 96% (95% CI, 90-100), and 10.1 (95% CI, 7.2-14.1), respectively. This study confirmed a high prevalence of microalbuminuria in ICH patients in ICU, and suggested that the urinary microalbumin/creatinine ratio >200 mg/g was comparable to the GCS score <11 at admission to the ICU with regard to its prognostic characteristics after ICH.
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J Neurosurg Anesthesiol · Apr 2008
Biography Historical Article2008 Wood Library-Museum Laureate of Anesthesia History.
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J Neurosurg Anesthesiol · Apr 2008
Glutamate-induced c-Jun expression in neuronal PC12 cells: the effects of ketamine and propofol.
Transcription factor c-Jun affects neuronal cell death and survival in mammalian brain. As general anesthetics, such as ketamine and propofol, are thought to provide some degree of neuroprotection, this study was intended to test whether the protection of injured neuronal PC12 cells by ketamine and propofol is related to the inhibition of phospho-c-Jun. Using neuronal PC12 cells from rat pheochromocytoma cells differentiated with nerve growth factor, we found that 24 hours of exposure to glutamate (1 to 100 mM) induced concentration-dependent cell death as determined by an ability to reduce the tetrazolium derivative, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) into a blue formazan salt. ⋯ Glutamate-induced cell death was reduced by ketamine (0.1, 1.0 mM) in a dose-dependent manner and also by propofol (0.5, 5.0 microM). In addition, the expression of phospho-c-Jun was substantially reduced by ketamine (0.1, 1.0 mM) and propofol (0.5, 5.0 microM), respectively, as determined by Western blot assay. These results suggest that inhibition of c-Jun activity is involved in the neuroprotective effects of ketamine and propofol on glutamate-induced injury in neuronal PC12 cells.