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To present a consecutive 20-year series of blood blister-like aneurysms (BBAs) to show that clip-on-wrapping with a Y-shaped autologous dura mater enables treatment of BBAs with a low complication rate and a satisfactory curative result. A retrospective review was performed from patients with BBAs of the internal carotid artery (ICA) at the Affiliated Hospital of Qingdao University from 1999 to 2019. Diagnosis and treatment options were analyzed. Outcome was assessed using the modified Rankin scale (mRS). A total of 30 patients with BBAs of the ICA were included. Among these patients, 20 patients underwent microsurgical treatment (15 patients were treated by clip-on-wrapping with a Y-shaped autologous dura mater), the other 10 patients underwent endovascular treatment. All patients presented with subarachnoid hemorrhage (SAH). Four angiograms were initially negative. For all patients, intraoperative rupture occurred in five cases, but no postoperative aneurysm rupture occurred in this series. Three cases with clinical or radiologic cerebral infarctions were observed. The outcome was favorable in 26 patients. Clip-reinforced wrapping technique using a Y-shaped autologous dura mater may be an effective method for treating BBAs. [ABSTRACT FROM AUTHOR]

We report that adenovirus mediated TNF-related apoptosis-inducing ligand (TRAIL) influenced the cell growth and cell cycle in the glioma cells in vitro. After being infected with the Ad-sTRAIL, U251 cell growth was inhibited. The expression of sTRAIL was detected using immunofluorescence. The higher rate of apoptosis was demonstrated using short-term microculture tetrazoliun (MTT) assay and flow cytometry. The rate of Ad-sTRAIL-inducing U251 cell apoptosis was increased depending on the dosage and the time. The apoptosis of G0/G1 and S phase cells was more significant than that of the control groups. The growth and proliferation of U251 cell line was inhibited after the infection of Ad-sTRAIL. It is dose- and time dependent. [ABSTRACT FROM AUTHOR]

Objective: To examine the effects of intraventricular pre-treatment with a combination of recombinant adeno-associated virus vectors encoding VEGF (rAAV-VEGF) and Ang1 (rAAV-Ang1) on early stroke in a rat model of transient middle cerebral artery occlusion (tMCAO). Methods: rAAV-VEGF/rAAV-Ang1 or rAAV-VEGF/rAAV-null vector was delivered into the lateral ventricles of 48 rats. Eight weeks later, the rats were subjected to tMCAO for 2 hours. During the early stages of ischemic reperfusion, VEGF and Ang1 expression levels, blood–brain barrier (BBB) permeability and cerebral microvessel density were determined and compared statistically between groups. Cerebral infarct volume and modified neurological severity scores (NSS) were also determined to evaluate the therapeutic efficacy of rAAV-VEGF/rAAV-Ang1. Results: Intraventricular application of rAAV-VEGF/rAAV-Ang1, 8 weeks before tMCAO, resulted in VEGF and Ang1 overexpression, and significantly decreased Evans blue permeability following ischemia (p<0.05). The microvessel density in the peri-infarct zone was significantly increased in the rAAV-VEGF/rAAV-Ang1 group compared with the rAAV-VEGF/rAAV-null group (p<0.05). Cerebral infarct volume and NSS in the rAAV-VEGF/rAAV-Ang1 group were significantly decreased compared with the rAAV-VEGF/rAAV-null group (p<0.05). Conclusion: In cerebral ischemia, the combination of Ang1 and VEGF could be used early to promote the formation of mature neovessels and protect the injured cells, without inducing the side effects on BBB permeability. Early intraventricular injection of mixed rAAV-VEGF and rAAV-Ang1 may be a favorable therapeutic strategy in gene therapy for experimental stroke. [ABSTRACT FROM AUTHOR]

Objective: To examine the effects of intraventricular pre-treatment with recombinant adeno-associated virus vectors encoding VEGF (rAAV-VEGF) on early stroke in a rat model of transient middle cerebral artery occlusion (tMCAO). Methods: rAAV-VEGF, rAAV-null or physiologic saline was delivered into the lateral ventricle of 93 Wistar rats, respectively. Eight weeks later, the rats were subjected to tMCAO for 2 hours. During the early stage following ischemic reperfusion, intracranial pressure (ICP) and brain water content were measured to make a correlation analysis, T2-weighted MRI was performed to observe cerebral edema volume, and TTC-derived cerebral infarct volume and modified neurological severity scores (NSS) were determined to evaluate the therapeutic efficacy of rAAV-VEGF in tMCAO. Results: Twenty-four hours following tMCAO, the rAAV-VEGF group, with VEGF overexpression in the rats brain, showed a significantly increase in ICP, brain water content and cerebral edema volume compared with two control groups (p<0.05). The ICP significantly correlated with the brain water content in the infarct hemisphere in all three groups during 24 hours following tMCAO (r=0.93, p<0.05). Forty-eight hours following tMCAO, a 1.3-fold larger infarct volume and 1.3-fold higher NSS were observed in the rAAV-VEGF group than both control groups (p<0.05). Conclusion: Our results indicate that intraventricular rAAV-VEGF pre-treatment can result in deleterious intracranial hypertension and augment secondary ischemic insults at the early stage of tMCAO, and pre-ischemic VEGF gene transfer via intraventricular approach may not be a favorable therapeutic strategy for tMCAO which should be adopted with caution or avoided in experimental stroke. [ABSTRACT FROM AUTHOR]