“To elucidate the time course of neuronal cell death after

“To elucidate the time course of neuronal cell death after the clinical criteria for brain death are met, the authors reviewed FK866 cost serial changes of serum neuron-specific enolase levels in 3 children (age range, 3-15 years) clinically diagnosed as brain dead due to cardiopulmonary arrest. All patients survived for more than 2 months after brain death. Children with brain death had higher peak neuron-specific enolase values (1069-2849 ng/mL) than did 3 control children (256-1800 ng/mL)

who did not become brain dead but had poor neurological outcome (1 death, 2 vegetative state) after cardiopulmonary arrest. A major finding is that children with brain death showed persistent elevation of neuron-specific enolase at 4 weeks (> 400 ng/mL) and 8 weeks (> 50 ng/mL) after cardiopulmonary arrest, in comparison with 2 surviving

patients without brain death (< 50 ng/mL at 4 weeks). This prolonged elevation of neuron-specific enolase suggests that total brain YH25448 ic50 necrosis might not be present at the time of clinical diagnosis of brain death.”
“Purpose: To assess patients with chronic portal vein thrombosis (PVT) with respect to transcapsular collateral veins, the communication between these veins and ectopic varices, and the cause of PVT.

Materials and Methods: This study was approved by the institutional review committees, and written informed consent was obtained. From November 2003 to March 2008, 145 consecutive patients with chronic PVT due to a variety of causes were assessed for transcapsular collaterals and ectopic varices with ultrasonography (US). Analysis of contingency tables was performed with the Fisher exact test.

Results: Transcapsular collaterals were detected in 15 (10.3%) of 145 patients with chronic PVT. They were restricted to patients with a history of hepatobilary surgery, severe pancreatitis, or abdominal surgery (n Sapanisertib solubility dmso = 21) and were not detected in patients with liver cirrhosis,

systemic coagulopathy, extrahepatic malignancy, idiopathic PVT, chronic pancreatitis, or infectious or inflammatory diseases (n = 124) (P < .001). Ectopic varices were infrequent in 70 patients with liver cirrhosis (n = 2, 3%) but were common in 14 patients with PVT after hepatobiliary surgery (n = 9, 64 %) (P < .001, odds ratio = 21.4). Direct communication between transcapsular collaterals and ectopic varices was visible in all nine patients in this cohort. In eight of these patients, ectopic varices were found to be the bleeding source in gastrointestinal hemorrhage.

Conclusion: Transcapsular collaterals frequently occur in patients with chronic PVT due to hepatobilary surgery or necrotizing pancreatitis. They are associated with ectopic varices; therefore, awareness of transcapsular collaterals in this patient subgroup will help to localize ectopic varices as potential bleeding source.

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