Objective To evaluate the safety and effectiveness of Pipeline embolization device (PED) for the treatment of large and giant intracranial aneurysms.Methods Frorn November 2014 to May 2016,the clinical and radiological data of 33 patients with intracranial aneurysm confirmed by DSA or head CT angiography (CTA) or head magnetic resonance angiography (MRA) at the Department of Neurosurgery,Changhai Hospital,the Second Military Medical University were enrolled retrospectively.Its safety and effectiveness were evaluated.Results The Pipelines were successfully released in 33 patients with 35 aneurysms,10 aneurysms were implanted by using PED alone,25 were implanted by using PED combined with coil embolization (including 2 were implanted by using Pipeline bridging technology).During the perioperative period,1 thrombotic event(one aneurysm) occurred and had hemorrhagic transformation.One(one aneurysm) died of fatal aneurysm delayed bleeding.Thirty-one patients (33 aneurysms) were followed up clinically,the follow-up time was 4-18 months,no bleeding or thrombosis events occurred.Eighteen aneurysms received a short-term postoperative imaging follow-up (3-5 months,enhanced MRA or DSA),of which 10 had neck residue or aneurysm development,and 8 aneurysms did not have development at all,and 19 achieved postoperative mid-term imaging follow-up (6-16 months,enhanced MRA or DSA).Two of them had neck residue and 17 did not develop at all.Conclusion Pipeline for the treatment of intracranial large and giant aneurysms may be safe and effective.However,the complications of intracranial hemorrhage cannot be ignored after implantation of embolization device.Its related mechanism needs to be further studied.

The objective of this study was to construct and express recombinant prokaryotic plasmid pET32a (+)- ast1 in E. coli BL21(DE3). Amastin gene was amplified from genomic DNA of Leishmania Donovani and its transmembran region was predicted by the methods of SOSUI and Tmpred; astl located in N-terminus of amastin gene was amplified and cloned into prokaryotic plasmid pET32a(+), which was named pET32a(+)-ast1, and then rAST1 was expressed in E. coli BL21(DE3). The results of SDS-PAGE and immunobloting assay showed that a fusion protein rAST1 (relative molecular mass about 27 kDa) was able to express in BL21. The recombinant prokaryotic plasmid pET32a(+)- ast1 was successfully constructed, and noted to be efficiently expressed in E. coli BL21(DE3).
Animals ; Cloning, Molecular ; Escherichia coli ; genetics ; metabolism ; Extracellular Space ; Genes, Protozoan ; Leishmania donovani ; genetics ; Plasmids ; genetics ; Protozoan Proteins ; biosynthesis ; genetics ; Recombinant Fusion Proteins ; biosynthesis ; genetics

The role of glial scar after intracerebral hemorrhage(ICH)remains unclear.This study aimed to inves-tigate whether microglia-astrocyte interaction affects glial scar formation and explore the specific function of glial scar.We used a pharmacologic approach to induce microglial depletion during different ICH stages and examine how ablating microglia affects astrocytic scar formation.Spatial transcriptomics(ST)analysis was performed to explore the potential ligand-receptor pair in the modulation of microglia-astrocyte interaction and to verify the functional changes of astrocytic scars at different periods.During the early stage,sustained microglial depletion induced disorganized astrocytic scar,enhanced neutrophil infiltration,and impaired tissue repair.ST analysis indicated that microglia-derived insulin like growth factor 1(IGF1)modulated astrocytic scar formation via mechanistic target of rapamycin(mTOR)signaling activation.Moreover,repopulating microglia(RM)more strongly activated mTOR signaling,facilitating a more protective scar formation.The combination of IGF1 and osteopontin(OPN)was necessary and sufficient for RM function,rather than IGF1 or OPN alone.At the chronic stage of ICH,the overall net effect of astrocytic scar changed from protective to destructive and delayed microglial depletion could partly reverse this.The vital insight gleaned from our data is that sustained microglial depletion may not be a reasonable treatment strategy for early-stage ICH.Inversely,early-stage IGF1/OPN treatment combined with late-stage PLX3397 treatment is a promising therapeutic strategy.This prompts us to consider the complex temporal dynamics and overall net effect of microglia and astrocytes,and develop elaborate treatment strategies at precise time points after ICH.