(J Vase Surg 2011;54:609-15.)”
“BACKGROUND: The literature is controversial on whether intraventricular bleeding has a negative impact on the prognosis of spontaneous intracerebral hemorrhage. Nevertheless, an association between intraventricular bleeding and spontaneous intracerebral hemorrhage volumes has been consistently reported.
OBJECTIVE: To evaluate the prognostic value of intraventricular bleeding in deep intraparenchymal hypertensive spontaneous hemorrhage with a bleeding volume < 30 cm(3).
Of the 320 patients Selleckchem LDC000067 initially evaluated, 33 met the inclusion criteria and were enrolled in this prospective study. The volume of intraparenchymal hemorrhage was calculated by brain computed tomography (CT) image analysis, and the volume of intraventricular bleeding
was calculated by the LeRoux scale. Clinical learn more data, including neurological complications, were collected daily during hospitalization. Neurological outcome was evaluated 30 days after the event by using the Glasgow outcome scale. Patients were assigned to 1 of 3 groups according to intraventricular bleeding: Control, no intraventricular bleeding; LR 1, intraventricular bleeding with LeRoux scale scores of 1 to 8; or LR 2, intraventricular bleeding with LeRoux scale scores > 8.
RESULTS: There were no significant differences among groups concerning
age, mean blood pressure, and time from onset to brain CT scan. Patients with greater intraventricular bleeding presented lower initial Glasgow coma scale scores, increased ventricular index and width of temporal horns, increased number of clinical and neurological complications, and longer hospitalization. Furthermore, their relative risk for unfavorable clinical outcome was 1.9 (95% confidence interval 1.25-2.49).
CONCLUSION: Intraventricular bleeding with a LeRoux scale score > 8 appears to have almost a negative effect on deep spontaneous intraparenchymal cerebral hemorrhage of small volume.”
“Caspase-2, the most conserved member of the caspase family, has long been recognized as an important protein in the regulation of apoptosis. However, due to a lack of phenotype in caspase-2 knock-out mice, its precise role has been questioned. Recently, several publications have described new mechanisms regulating caspase-2 activation, including its role within an activating complex named the PIDDosome, linking caspase-2 function to p53. Consistent with this, evidence is accumulating for potential roles of caspase-2 in non-apoptotic processes, including cell cycle regulation and DNA repair. In addition, a tumor-suppressor function has been suggested for caspase-2.