“Pleckstrin (plek)-null platelets from a knockout mouse ha


“Pleckstrin (plek)-null platelets from a knockout mouse have been shown to be defective in granule secretion, aggregation and actin polymerization. However, the mechanism

of plek signaling is currently unknown. Therefore, we sought to identify plek-binding proteins in platelets by using GST pulldown assays and immunoprecipitation to isolate proteins from extracts of protein kinase C-activated or inhibited human platelets. Co-purified plek-binding proteins were resolved by SDS-PAGE and identified via nanospray quadruple TOF MS. Identified proteins may be involved in various cellular Daporinad research buy processes including cytoskeletal reorganization (moesin, radixin and a-actinin) and signal transduction (serum deprivation response protein, 17 beta-hydroxysteroid dehydrogenase 4 and factor XIIIA). Both platelet aggregation and/or secretion require actin polymerization. However, studies have shown no direct

association between plek and actin. Based on our findings we propose indirect associations between plek and actin through 17 beta-hydroxysteroid dehydrogenase 4, a-actinin, moesin, radixin and factor XIIIA, which in turn suggest new roles for plek AZD3965 mouse in platelet biology.”
“BACKGROUND: During external ventricular drainage (EVD) weaning, cranial computed tomography (cCT) is necessary to evaluate ventricle width. Because intrahospital transfer of critically ill patients is associated with higher mortality, bedside techniques are necessary to evaluate ventricle width. Transcranial sonography is able to show the ventricles in patients with sufficient temporal acoustic window. Contrast-enhanced ultrasound (CEUS) is able to overcome the limitations of insufficient insonation.

OBJECTIVE: We demonstrate the feasibility of bedside transcranial CEUS ventriculography to measure ventricles and verify the passage Vorinostat in vivo of cerebrospinal fluid

(CSF) through the foramen of Magendie into the subarachnoid space during EVD weaning in critically ill patients.

METHODS: Six patients were examined by transcranial and transnuchal CEUS. Harmonic imaging with low mechanical index was used. One milliliter of an ultrasound contrast agent was administered via EVD line. Comparison with the cCT scans at the time of discharge was used to confirm CEUS-ventriculography results.

RESULTS: Ventricles were visualized in all patients. CSF transmission via the foramen of Magendie was demonstrated in 5 patients. Mean ventricle width (centimeters) was 0.67 (CEUS) vs 0.73 (cCT) (standard deviation 0.43, 0.45, P = .116) [third ventricle], 0.88 vs 1.02 (0.28, 0.22, P = .055) [fourth ventricle], 1.40 vs 1.37 (0.56, 0.54, P = .620) [left lateral ventricle], 1.37 vs 1.37 (0.55, 0.54, P = .952) [right lateral ventricle], 2.33 vs 2.23 (0.51, 0.58, P = .169) [left anterior horn], and 2.25 vs 2.07 (0.56, 0.64, P = .204) [right anterior horn].

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