大鼠自体异体表皮细胞悬液混合移植的实验研究

目的　探讨自、异体表皮细胞悬液混合移植技术在创面修复中的应用。　方法　 30只大鼠随机配成 15对后 ,分成细胞悬液移植组 (A组 ,10对 )和细胞膜片移植组 (B组 ,5对 )。取每只大鼠全厚皮 ,分离表皮细胞 ,并根据配对情况按 1∶1的细胞比例混合 ,体外常规培养。 4d后收获A组混合细胞悬液 ,14d后收获B组混合细胞膜片。将此细胞悬液和膜片分别转移至A、B组相应供体大鼠的去全厚皮创面。随后A组每对大鼠的创面交叉覆盖配对方的异体全厚皮 ;B组创面覆盖胶原膜及“优妥”敷料。比较移植后 2～ 3周两组的创面修复情况。　结果　术后 2～ 3周 ,A组创面大多愈合 ,表面光滑 ,与皮下连接紧密。术后第 5天 ,B组创面部分细胞膜片脱落 ,部分成活 ,膜片成活的创面后期再次出现小创面 ,经久不愈。　结论　自、异体表皮细胞悬液混合移植是一种可行的、体内构建皮肤、修复创面的方法。     

显微锁孔手术治疗脑干及其周围病变

目的 将显微锁孔手术应用于脑干及其周围病变的外科治疗，探求以最小的创伤来取得最佳的手术疗效。方法 采用颞下锁孔人路、乳突后锁孔人路、枕下正中锁孔人路，以20mm左右直径的骨窗进行脑干及其周围病变的显微手术治疗。结果 本组16例例病人术后3d内均行MRI或DSA检查，肿瘤或动静脉畸形全切除11例，次全切除3例，部分切除1例，1例小脑后下动脉瘤成功夹闭。术中输血3例。并发脑脊液耳漏1例，硬膜下积液1例，1例术后持续昏迷40d苏醒，无死亡及感染病例。结论 锁孔人路微创技术处理脑干及其周围病变，因其手术创伤小，疗效佳，费用节省，值得临床推广应用。     

老年人食道病变呈心绞痛样胸痛13例分析

13例有心绞痛样胸痛的住院病人入院均诊有冠心病心绞痛,后均经ECG、8例心脏“B”超、核素心肌灌注及24小时动态ECG各2例,确诊冠心病5例,不支持冠心病8例;后均行GI,并同时行胃镜、食管24小时pH测定及压力测定各2例,确诊有胃食管反流疾病(GERD),本组自胸痛症状出现至GERD确诊病程平均29.5个月(0.5～120个月),报告2例典型病例,讨论了误漏诊原因,探讨了老年人食管性胸痛的诊疗程序。     

单侧鼻前庭切口经蝶切除垂体腺瘤

对１６例垂体腺瘤采用单侧鼻前庭切口经蝶切除，效果满意，既可减少手术创伤，又缩短了手术距离，且避免了美容缺陷，是一种设计巧妙，较为实用的手术方法，尤其适用于生长激素腺瘤。     

Potential contribution of nuclear factor-kappaB to cerebral vasospasm after experimental subarachnoid hemorrhage in rabbits.

Nuclear factor-kappaB (NF-kappaB) plays a key role in inflammation, which is involved in the development of cerebral vasospasm after subarachnoid hemorrhage (SAH). In the present study, we assessed the potential role of NF-kappaB in regulation of cerebral vasospasm. Nuclear factor-kappaB DNA-binding activity was measured in cultured vascular smooth muscle cells (VSMCs) treated with hemolysate and pyrrolidine dithiocarbamate (PDTC, 80 micromol/L), an inhibitor of NF-kappaB. Forty-two rabbits were divided into three groups: control, SAH, and PDTC groups (n=14 for each group). The caliber of the basilar artery was evaluated. Nuclear factor-kappaB DNA-binding activity and the gene expression levels of cytokines and adhesion molecules in the basilar artery were measured. Immunohistochemical study was performed to assess the expression and localization of tumor necrosis factor (TNF)-alpha, intercellular adhesion molecule (ICAM)-1, and myeloperoxidase (MPO). It was observed that NF-kappaB DNA-binding activity was significantly increased by treatment with hemolysate in cultured VSCMs, but this increase was suppressed by pretreatment with PDTC. Severe vasospasm was observed in the SAH group, which was attenuated in the PDTC group. Subarachnoid hemorrhage could induce increases of NF-kappaB DNA-binding activity and the gene expression levels of TNF-alpha, interleukin (IL)-1 beta, ICAM-1, and vascular cell adhesion molecule (VCAM)-1, which were reduced in the PDTC group. Immunohistochemical study demonstrated that the expression levels of TNF-alpha, ICAM-1, and MPO were all increased in the SAH group, but these increases were attenuated in the PDTC group. Our results suggest that NF-kappaB is activated in the arterial wall after SAH, which potentially leads to vasospasm development through induction of inflammatory response.     

Adeno-associated virus vector-mediated systemic delivery of IFN-beta combined with low-dose cyclophosphamide affects tumor regression in murine neuroblastoma models.

PURPOSE: Type I IFNs (IFN-alpha/beta) have shown significant antitumor activity in preclinical models but limited efficacy and significant toxicity in clinical trials. We hypothesized that the antitumor activity of type I IFNs could be enhanced by chronic, low-dose systemic delivery and sought to test this in murine neuroblastoma models. EXPERIMENTAL DESIGN: Continuous liver-generated expression of human IFN-beta (hINF-beta) was achieved through a gene therapy-mediated approach using adeno-associated virus vectors encoding hIFN-beta (AAV hINF-beta). Orthotopic localized retroperitoneal and disseminated models of neuroblastoma were established using three different xenografts. Immunohistochemical analysis and ELISA were used to evaluate the antiangiogenic effect of therapy. RESULTS: The development of both localized orthotopic (retroperitoneal) and disseminated neuroblastoma was prevented in all mice expressing hINF-beta. Continued growth of established retroperitoneal tumors, treated with AAV hINF-beta as monotherapy, was significantly restricted, and survival for mice with established, disseminated disease was significantly prolonged following administration of AAV hINF-beta. Analysis of treated tumors revealed a significant antiangiogenic effect. Mean intratumoral vessel density was diminished and expression of the angiogenic factors vascular endothelial growth factor and basic fibroblast growth factor were both decreased. Finally, combination therapy in which AAV hIFN-beta was used together with low-dose cyclophosphamide resulted in regression of both established retroperitoneal and disseminated disease. CONCLUSIONS: AAV-mediated delivery of hIFN-beta when used as monotherapy was able to restrict neuroblastoma growth due in part to inhibition of angiogenesis. When used in combination with conventional chemotherapy, AAV hIFN-beta was able to effect complete tumor regression.