Chronic Akt activation, increased myocardial expression of endostatin, and impaired growth factor signaling may account for the diminished endogenous angiogenic response observed with atorvastatin treatment.”
“The objective of this study is to reevaluate the clinical significance of 1-C-11-acetate (ACE) positron emission CHIR-99021 molecular weight tomography (PET) in patients with brain glioma, in comparison with F-18-fluorodeoxyglucose (FDG) PET.
Methods: Ten patients with histologically proven glioma were included in this study. They underwent PET examination with both FDG and ACE on separate days. For ACE PET, 20-min data acquisition was performed just after the administration
of 740 MBq of ACE; 10-20-min data were used for the analysis. FDG PET data acquisition for 10 min started 60 min postinjection of 370 MBq of FDG, approximately. Both reconstructed images were converted to standardized uptake value (SUV) images for patient body weight and injected dose.
Regions of interest were placed on the tumor and the contralateral cerebral cortex, and SUV and tumor-to-cortex ratio (T/C) were calculated; these values were compared between high- and low-grade gliomas.
Results: SUV and T/C of ACE PET showed significant difference (SUV: 2.63 +/- 0.46 vs. 1.85 +/- 0.56, P=.03; T/C: 2.36 +/- 0.63 vs. 1.14 +/- 0.36, P=.02). In contrast, FDG PET AZD4547 mouse revealed no significant difference in SUV or T/C between high- and low-grade gliomas (SUV: 7.13 +/- 4.31 vs. 4.71 +/- 1.27, P=.31; T/C: 0.98 +/- 0.55 vs. 0.62 +/- 0.09, P=.22).
Conclusion: This preliminary study revealed that ACE PET is a promising tracer for the grading of Levetiracetam brain glioma. (c) 2008 Elsevier Inc. All rights reserved.”
“Objective: Mitochondrial permeability transition pore opening plays a critical role in mediating the mitochondrial response to ischemia/reperfusion injury and initiation of apoptosis. We tested whether inhibition of mitochondrial permeability transition pore opening with cyclosporine A prevented apoptosis-related
alterations in mitochondrial structure and function after cardioplegic arrest.
Methods: Newborn piglets (age similar to 14 days) underwent cardiopulmonary bypass, cardioplegic arrest (60 minutes), weaning from bypass, and 6-hour reperfusion. Comparison was made among cold crystalloid cardioplegia (n = 5), cold crystalloid cardioplegia with cyclosporine A pretreatment (n = 5), and noncardiopulmonary bypass (n = 5) groups.
Results: Early apoptosis signaling events (Bax translocation to the mitochondria) were prominent in cold crystalloid cardioplegia and prevented in cold crystalloid cardioplegia + cyclosporine A myocardium. Mitochondrial release of cytochrome c, determined by Western blot of cytosolic fractions and confocal quantitative colocalization analysis, was also prominent in cold crystalloid cardioplegia but prevented in cold crystalloid cardioplegia + cyclosporine A myocardium.