Objective:To evaluate the effect of surgery on 47 patients with moyamoya disease by retrospective analysis.Methods:A total of 47 patients with moyamoya disease were enrolled from August,2010 to According to the improved treatment in August,2013,all cases were divided into two groups:a pre-improved group and a post-improved group.According to different surgical methods,they were divided into two subgroups:an indirect revascularization subgroup and a combined revascularization subgroup.Results:The cerebral ischemia in 77.4％ of patients was relieved after the surgery.There was significant difference in outcomes of patients between the pre-improved group and the post-improved group (P＜0.05),while there was no significant difference between the pre-improved indirect revascularization subgroup and the pre-improved combined revascularization subgroup.There was also no significant difference between the post-improved indirect revascularization subgroup and the post-improved combined revascularization subgroups (P＞0.05).Conclusion:Surgical treatment can improve the outcomes of patients with moyamoya disease,but there is no significant difference in surgical effects between indirect and combined revascularization.

OBJECTIVE: To explore the microsurgical techniques for insular glioma without damaging its surrounding normal structures. METHODS: We retrospectively analyzed 54 patients with insular gliomas who underwent microsurgical operation by trans-syvian fissure approach between May, 2003 and August, 2008 in Xiangya Hospital. We discussed the techniques in the operation and summarized how to protect the key blood vessels, distinguish and protect the surrounding normal structures. RESULTS: There were 36 complete removals,14 secondary complete removals, and 4 partial removals.Six patients had complications after the craniotomy who had temporal speech disorder (aphasia mostly began to recover about 10 days after the craniotomy),4 patients had opposite side paralysis worsening (3 recovered normally and 1 improved after 6 months),4 had light paralysis, and another 3 had paralysis and speech disorder. CONCLUSION The microsurgery by means of trans-syvian fissure approach can well expose the anatomical relation between tumor and its surrounding structures,so that we can remove the tumor and protect the surrounding normal tissues as much as we can.
Adolescent ; Adult ; Brain Neoplasms ; pathology ; surgery ; Cerebral Cortex ; pathology ; surgery ; Female ; Glioma ; pathology ; surgery ; Humans ; Male ; Microsurgery ; methods ; Middle Aged ; Neurosurgical Procedures ; methods ; Retrospective Studies ; Young Adult

Chondrosarcoma original from the zygomatic arch is a very rare disease with high malignancy. Surgery is the main means of treatment at present for duo to its poor sensitivity to radiochemotherapy. We reported a young patient who was recovery well in a 4-years follow-up without radiochemotherapy after a total resection of the tumor.
Bone Neoplasms ; Chemoradiotherapy ; Chondrosarcoma ; Humans ; Self Concept ; Zygoma

ObjectiveTo investigate the effects of berbamine hydrochloride on sorafenib resistance in hepatocellular carcinoma cells and the underlying mechanisms. MethodThe sorafenib-resistant cell line SMMC-7721/S was selected by the concentration increment method starting at 1.25 μmol·L^-1 sorafenib. Both SMMC-7721 and SMMC-7721/S cells were treated with 0， 2.5， 5， 10， 15， 20 μmol·L^-1 sorafenib， and the cell counting kit-8 （CCK-8） assay was employed to determine the half maximal inhibitory concentration （IC₅₀） and calculate the resistance index （RI）. Western blot was conducted to compare the expression of proteins involved in autophagy and phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin （PI3K/Akt/mTOR） signaling pathway between SMMC-7721 and SMMC-7721/S cells. Furthermore， SMMC-7721/S cells were treated with 5 μmol·L^-1 berbamine hydrochloride alone or in combination with 2.5， 5， 10 μmol·L^-1 sorafenib， and the cell growth was assessed by the CCK-8 assay. In addition， SMMC-7721 and SMMC-7721/S cells were treated with 5 μmol·L^-1 berbamine hydrochloride alone or in combination with 5 μmol·L^-1 sorafenib， and the cell proliferation was examined by the colony formation assay. The immunofluorescence assays with Microtubule-associated protein 1 light chain 3 （LC3） and LysoTracker as probes were employed to assess the lysosomal acidification in SMMC-7721 cells treated with 5 μmol·L^-1 berbamine hydrochloride or 0.1 μmol·L^-1 autophagy inhibitor bafilomycin A1 （Baf）. Further， the expression of proteins involved in autophagy and PI3K/Akt/mTOR signaling pathway was determined by Western blot and compared between groups. ResultSorafenib showed the IC₅₀ of 9.56 mol·L^-1 （P<0.01） and 7.99 mol·L^-1 for SMMC-7721/S and SMMC-7721 cells， respectively， at 24 h. The resistance index （RI） of SMMC-7721/S for sorafenib was 1.20 （P<0.01）， which indicated mild resistance. Compared with SMMC-7721 cells， SMMC-7721/S cells exhibited up-regulated expression of p-mTOR， p-Akt， and LC3Ⅱ， down-regulated expression of p62 protein （P<0.01）， and unchanged Akt protein level. CCK-8 and colony formation assays demonstrated that the combination of berbamine hydrochloride and sorafenib exhibited a synergistic effect （Q>1.15）， with berbamine hydrochloride partially reversing the resistance of liver cancer cells to sorafenib. The immunofluorescence detection of LC3 revealed that berbamine hydrochloride and Baf significantly increased LC3 in SMMC-7721 cells. The detection with LysoTracker as the probe showed that berbamine hydrochloride inhibited the acidity of lysosomes in SMMC-7721 cells （P<0.01）， indicating the suppression of autophagy. Berbamine hydrochloride further enhanced the downregulation of p-mTOR and p-Akt protein levels and did not change the Akt protein level in SMMC-7721 cells exposed to sorafenib. Berbamine hydrochloride inhibited the increase in p-mTOR expression， down-regulated the p-Akt protein level， and did not change the total Akt protein level in the SMMC-7721/S cells exposed to sorafenib. ConclusionBerbamine hydrochloride can ameliorate the resistance of liver cancer cells to sorafenib by inhibiting cellular autophagy and the PI3K/Akt/mTOR signaling pathway.