End-to-end revascularization between the occipital Artery(OA) and the p1 segment of posterior inferior cerebellar Artery(PICA) for a patient with posterior circulation ischemia via a far-lateral approach:2-Dimensional Operative video.

Vertebral artery （VA）Aneurysms involving the origin of the posterior inferior cerebellar artery (PICA) ,occasionally, induce cerebellum and brainstem infarction due to intraluminal thrombus and calcific VA stenosis. At times, vessel occlusion and revascularization is necessary for successful obliteration of these aneurysms.2 The occipital artery (OA) is often the preferred donor graft for lesions of the posterior fossa. Although most OA-PICA bypasses can be performed using the p3 segment as the recipient site for an end-to-side anastomosis, a more feasible alternative to conventional OA-p3 PICA bypass in cases of high-riding caudal loops , aberrant anatomy or p3 multiple perforators is to free the p1 PICA, transpose it away from the lower cranial nerves, and perform an end-to-end OA-p1 PICA bypass instead. This video captures the dissection of the OA using an orientational anterograde harvesting technique and the end-to-end anastomosis of the OA to the PICA at the p1 segment. This was performed in a 56-year-old man who presented with posterior circulation ischemia from a fusiform aneurysm with calcific vertebral artery stenosis located at the origin of the right PICA. The patient tolerated the procedure well and suffered no major complications related to the operation. He did experience some mild, posterior neck rigidity at the time of his 6-month follow-up, likely due to nerve injury that occurred while harvesting the OA. Overall, the patient remains in good neurologic status 1 year after the operation. The operation proved the feasibility of end-to-end bypass in OA-p1 PICA.

circRPPH1_025 Overexpression Promotes Migration and Invasion of Glioblastoma Multiforme.

Objective: To study the effect of circ_0000512 (circRPPH1_025) on the tumorigensis and development of glioblastoma and its molecular mechanism. Methods: The expression levels of circ_0000512 in normal astrocytes (NHA) and human glioblastoma cell lines (U87, U251, and A172) and the expression levels of circ_0000512 and linear RNA RPPH1 in U87 cells after RNase R treatment were detected by qRT-PCR. The effects of circ_0000512 knockdown or overexpression on the proliferation, migration, invasion, and epithelial-mesenchymal transition of U87 cells were detected by CCK-8 assay, cell colony formation assay, transwell invasion assay, wound healing assay, and western blot. Results: The expression of circ_0000512 was upregulated in glioblastoma cells, and the overexpression of circ_0000512 was beneficial to the proliferation, migration, invasion, and epithelial-mesenchymal transition of U87 cells, while knockdown of circ_0000512 showed the opposite results. Conclusion: circ_0000512 can be used as a potential target for early diagnosis and targeted therapy of glioblastoma multiforme.

Protective effect of isoliquiritigenin against cerebral injury in septic mice via attenuation of NF-κB.

BACKGROUND: The study was conducted to scrutinize the outcome of isoliquiritigenin (ISL) against cerebral injury in septic mice. METHODS: The sepsis was introduced using cecal ligation and puncture (CLP) method in experimental mice. The effect of ISL was quantified using the content of brain water and blood brain barrier (BBB) permeability. The effect on the levels of myeloperoxidase (MPO), superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione (GSH) in brain homogenates was also determined. The effect of ISL on the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, and IL-6 in serum was also estimated. The levels of various inflammatory biomarkers (COX-2 and PGE2) were also studied. The expression of NF-κB signalling cascade and inducible nitric oxide synthase (iNOS) was estimated by Western blot. RESULTS: Compared with CLP group, the brain water content was found to be reduced significantly together with the enhanced BBB integrity in ISL treated group. The level of MDA was reduced together with enhanced level of SOD and GSH in the ISL treated group. The levels of TNF-α, IL-1ß, and IL-6 were also found to be modulated in ISL group. The level of COX-2 and PGE2 was reduced to near normal after ISL administration together with increase in the IκBα expression and reduction of p65 and p-p65 expression in a concentration-dependent manner. The expression of iNOS was also found to be reduced in ISL group. CONCLUSION: These results demonstrate that ISL causes protection of CLP-induced sepsis in experimental mice via multiple pathways.