No abstract

We describe a refined animal model of human intracerebral aneurysms for testing endovascular devices for interventional neuroradiological procedures. Saccular aneurysms resulting from a stump of the right common carotid artery (CCA) were created in 15 New Zealand White rabbits by intraluminal incubation of elastase that was applied to the CCA after distal ligation of the CCA and proximal occlusion of the vessel using a pliable balloon. Subsequently a microcatheter was advanced to a position cranial to the balloon and the elastase was infused under fluoroscopic guidance to avoid retrograde flow to the trachea via aberrant vessels. Contrast-enhanced (CE) MRA at 1.5 T and conventional digital subtraction angiography was performed to test for aneurysm size, morphology and neck anatomy. In all 15 animals aneurysms resulted from the stump of the right CCA, ranging in size from 2.0 to 9.9 mm (mean 6.3 mm) in craniocaudal direction, 1.0 to 5.5 mm (mean 3.8 mm) in mediolateral direction and 1.0 to 3.8 mm (mean 2.4 mm) in neck diameter. Aneurysm morphology could be adequately demonstrated using CE MRA. On histological evaluation a loss of the internal elastic lamina was noted. The described method represents an easy, reliable, and reproducible method of aneurysm creation in the rabbit in an area of high shear stress. These aneurysms can be used for testing new endovascular devices for embolization of intracranial aneurysms.

This study demonstrates the possible shortcomings and problems of emerging stent techniques to treat intracerebral aneurysms, shows where technical advances have to be made, and describes in which cases of aneurysm morphology caution has to be exercised when considering an endovascular approach using stents.

BackgroundNeovascularization and peritumoral edema are hallmarks of glioblastoma (GBM). Programmed cell death 10 (PDCD10) plays a pivotal role in regulating apoptosis, neoangiogenesis and vessel permeability and is implicated in certain tumor signaling pathways. However, little is known about PDCD10 in GBM. We aimed to investigate the expression pattern of PDCD10 and to identify the association of its expression with some molecular and clinical parameters in human GBM.MethodsmRNA and protein expression of PDCD10 were examined respectively by real-time RT-PCR and Western blotting in GBM (n = 27), astrocytoma grade II (n = 13) and control (n = 11). The protein level of p-Akt and GFAP was detected by Western blot. Double-imunofluorecent staining was performed to reveal the cellular expression profile of PDCD10. Brain edema and microvascular density (MVD) were respectively analyzed based on pre-operative MRI and after laminin immnostaining. MGMT promoter methylation was detected by methylation specific PCR.ResultsmRNA and protein levels of PDCD10 were significantly downregulated in GBM, concomitantly accompanied by the activation of Akt. PDCD10 immunoreactivity was absent in proliferating tumor cells, endothelial cells and GFAP-positive cells, but exclusively present in the hypoxic pseudopalisading cells which underwent apoptosis. Moreover, loss of PDCD10 was associated with a higher MVD and a more severe peritumoral edema but not with MGMT promoter methylation in GBM.ConclusionWe report for the first time that PDCD10 expression is downregulated in GBM, which is associated with the activation of Akt signaling protein. PDCD10 is potentially implicated in tumor proliferation and apoptosis, hyperangiogenesis and peritumoral edema in GBM.