类风湿病中左心室收缩功能障碍：一种未被认识的负荷？

目的:本研究旨在明确左心室收缩功能障碍在临床类风湿病(RD)患者中是否较正常人群中更常见,并评价脑利钠肽(BNP)的诊断价值。背景:RD患者罹患缺血性心脏病的风险增加,而采用超声心动图评估RD患者心功能不全的大型研究却少见。假定左心室收缩功能障碍在RD患者中较正常人群中更为     

肝移植术后胆道并发症的介入治疗

目的 探讨原位肝移植术后胆道并发症的介入治疗疗效。方法 回顾性分析我院2002年6月至2005年9月诊治的173例原位肝移植患者的临床资料。结果 术后出现胆道并发症14例（8．1％），其中胆管狭窄6例．胆管狭窄合并胆漏1例，胆泥淤积或结石3例，肝断面胆漏2例（劈离式肝移植患者），T管拔除后胆漏1例，Oddi括约肌功能失常1例。除1例胆道狭窄再次行肝移植，因发生严重感染导致肝功能衰竭死亡外．其余患者经介入治疗均获得满意的效果。结论 介入治疗是诊断和治疗肝移植术后胆道并发症的首选方法。     

Lethal effect of mononuclear cells derived from human umbilical cord blood differentiating into dendritic cells after in vitro induction of cytokines on neuroblastoma cells

BACKGROUND: Dendritic cell is the most major antigen presenting cell of organism. It is proved in recent studies that human umbilical cord blood mononuclear cells induced and cultured in vitro by recombinant human granulocyte-macrophage colony stimulating factor (rhG-MCSF) and recombinant human interleukin-4(rhIL-4) can generate a great many dendritic cells and promote the lethal effect of T cells on human neuroblastoma, but it is unclear that whether the lethal effect is associated with the most proper concentration of dendritic cells. OBJECTIVE: To investigate the lethal effect of human umbilical cord blood mononuclear cells induced in vitro by cytokines differentiating into dendritic cells on human neuroblastoma, and its best concentration range. DESIGN: Open experiment. SETTING: Department of Pediatrics, the Medical School Hospital of Qingdao University. MATERIALS: The study was carried out in the Shandong Provincial Key Laboratory (Laboratory for the Department of Pediatrics of the Medical School Hospital of Qingdao University) during September 2005 to May 2006. Human umbilical cord blood samples were taken from the healthy newborn infants of full-term normal delivery during October to November 2005 in the Medical School Hospital of Qingdao University, and were voluntarily donated by the puerperas. Main instruments: type 3111 CO2 incubator (Forma Scientific, USA), type 550 ELISA Reader (Bio-Rad, USA). Main reagents: neuroblastoma cell line SK-N-SH (Shanghai Institute of Life Science, Chinese Academy of Sciences), RPMI-1640 culture fluid and fetal bovine serum (Hyclone), rhIL-4 (Promega, USA), rhG-MCSF (Harbin Pharmaceutic Group Bioengineering Co.Ltd), rat anti-human CD1a monoclonal antibody and FITC-labeled rabbit anti-rat IgG (Xiehe Stem cell Gene Engineering Co.Ltd). METHODS: ① Human umbilical cord blood mononuclear cells obtained with attachment methods differentiated into human umbilical cord blood dendritic cells, presenting typical morphology of dendritic cells after in vitro induction by rhG-MCSF and rhIL-4. ② Different concentrations of dendritic cells[ dendritic cells: neuroblastoma cells=20∶1,50∶1,100∶1（2×108 L-1，5×108 L-1，1×109 L-1）], 1×109 L-1 T cells and 1×107 L-1 neuroblastoma cells were added in the experimental group. 1×109 L-1 T cells and 1×107 L-1 neuroblastoma cells were added in the control group. ③ Main surface marker CD1a molecules of dendritic cells were detected with indirect immunofluorescence, and the percent rate of dendritic cells was counted with ultraviolet light and expressed as the expression rate of CD1a+ cells. ④ Single effector cells and target cells were respectively set in the experimental group and control group to obtain the lethal effect. The lethal effect of dendritic cells on neuroblastoma cells was indirectly evaluated by detecting cellular survival with MTT assay. The lethal effect(%)=（1-A experimental well-A effector cell well/A target cell well）×100%.⑤The experimental data were presented as Mean ±SD, and paired t test was used. MAIN OUTCOME MEASURES: ① Morphological characters of dendritic cells in the process of induction and differentiation. ②CD1a+ cellular expression rate. ③Lethal effect of dendritic cells on neuroblastoma cells. RESULTS: ①Morphological characters of dendritic cells in the process of induction and differentiation: On the 15th day after human umbilical cord blood mononuclear cells were induced by rhG-MCSF and rhIL-4, typical morphology of dendritic cells could be seen under an inverted microscope. ②Expression rate of CD1a+ cells was （43.12±5.83）%. ③Lethal effect of dendritic cells on neuroblastoma cells: Lethal effect of dendritic cells stimulated T cells in each experimental group ( dendritic cells: neuroblastoma cells=100∶1,50∶1,20∶1 respectively) on neuroblastoma cells was significantly higher than that in control group[（31.00 ±4.41）%，（30.92±5.27）%，(33.57±5.35)%,(26.23±5.20)%, t=3.51，2.98，4.24, P < 0.01）; But the lethal effect of dendritic cells on neuroblastoma was significantly lower when their ratio was 100∶1 and 50∶1 in comparison with 20:1 （t=2.01，2.36, P < 0.05）, and no significant difference in lethal effect existed between the ratio at 100∶1 and 50∶1（t=0.06,P > 0.05）. CONCLUSION: Dendritic cells differentiated from human umbilical cord blood mononuclear cells after in vitro induction of cytokines can promote the lethal effect of T cells on neuroblastoma cells. The lethal effect is associated with the concentration of dendritic cells within some range.     

胸腰椎骨折术后内固定松动、断裂的原因及预防

目的 探讨椎弓根螺钉系统用于胸腰椎骨折术后出现松动、断裂的原因，并提出相应的预防对策。方法 12例胸腰椎骨折术后内固定失效病例，采用RF系统3例，AF系统9例。均未行植骨融合，AF系统中未按要求安装横连结3例，术后伤椎前缘高度平均恢复至正常的85．2％。结果 术后8—21个月出现棒断裂4例，螺钉断裂3例，钉帽松动5例。结论 内固定物的自身问题、术者的经验欠缺及操作不规范是胸腰椎骨折术后椎弓根螺钉系统松动、断裂的原因，但伤椎骨结构未能得到良好重建及术后椎间盘退变可能是其更重要的因素。因此重视内固定物的选择、加强规范操作，强调对损伤椎体及椎间盘的全面处理是预防内固定失效的有效措施。     

The use of the facial translocation technique in the management of tumors of the paranasal sinuses and skull base.

OBJECTIVE: We sought to assess the efficacy of facial translocation in the management of tumors of the skull base and paranasal sinuses. STUDY DESIGN AND SETTING: From July 1993 to December 1999, 75 patients, aged 3 to 102 years old, underwent facial translocation. Thirty-three (44%) patients also underwent a combined neurosurgical procedure. Nineteen (25%) had previous surgery. These patients were followed up to 6 years. RESULTS: There were 21 benign and 54 malignant tumors. There were no perioperative deaths. The morbidity rate was 31%. Of the 54 patients with malignant tumors, the actuarial 3-year survival rate was 59%, whereas the local control rate was 54%. CONCLUSION: The facial translocation technique offers favorable exposure of the critical zones of the anterior and middle cranial base, thus facilitating extensive resection and reconstruction. SIGNIFICANCE: This study demonstrates that facial translocation is one of the best surgical approaches to the skull base.     

外伤性股动脉栓塞继发肾功能衰竭32例的综合治疗

目的 探讨外伤性股动脉栓塞后继发急性肾功能衰竭的临床综合治疗。方法 对32例外伤性股动脉栓塞术后继发急性肾功能衰竭病例均进行急诊手术切开取栓、血管吻合术，术后均予以综合治疗。结果住院时间7天-3个月，平均41d。最终截肢6例，死亡2例，24例修复成功。结论 术前准确判断预后，正确选择手术方式、术中筋膜减张性切开、术后及时清除坏死组织、术后利尿合剂应用和及时必要的血透是影响外伤性股动脉栓塞保肢术后急性肾功能衰竭预后的重要因素。     

The upregulation of glial glutamate transporter-1 participates in the induction of brain ischemic tolerance in rats.

Glial glutamate transporter-1 (GLT-1) plays an essential role in removing glutamate from the extracellular space and maintaining the glutamate below neurotoxic level in the brain. To explore whether GLT-1 plays a role in the acquisition of brain ischemic tolerance (BIT) induced by cerebral ischemic preconditioning (CIP), the present study was undertaken to observe in vivo changes in the expression of GLT-1 and glial fibrillary acidic protein (GFAP) in the CA1 hippocampus during the induction of BIT, and the effect of dihydrokainate (DHK), an inhibitor of GLT-1, on the acquisition of BIT in rats. Immunohistochemistry for GFAP showed that the processes of astrocytes were prolonged after a CIP 2 days before the lethal ischemic insult, which could protect pyramidal neurons in the CA1 hippocampus against delayed neuronal death induced normally by lethal ischemic insult. The prolonged processes extended into the area between the pyramidal neurons and tightly surrounded them. These changes made the pyramidal layer look like a 'shape grid'. Simultaneously, the prolonged and extended processes showed a great deal of GLT-1. Western blotting analysis showed significant upregulation of GLT-1 expression after the CIP, especially when it was administered 2 days before the subsequent lethal ischemic insult. Neuropathological evaluation by thionin staining showed that DHK dose-dependently blocked the protective role of CIP against delayed neuronal death induced normally by lethal brain ischemia. It might be concluded that the surrounding of pyramidal neurons by astrocytes and upregulation of GLT-1 induced by CIP played an important role in the acquisition of the BIT induced by CIP.