骨纤维结构不良的诊断和治疗进展

目的:对长期以来关于骨纤维结构不良大量相关研究及文献进行回顾,综述骨纤维结构不良的诊断和治疗的最新进展。资料来源:通过计算机互联网检索OVID数据库1966-01/2006-10关于骨纤维结构不良的文献,检索词:Osteofibrous dysplasia,限定语言种类为English。同时检索1994-01/2006-10中国全文期刊数据库有关骨纤维结构不良的文献,检索词为:骨纤维结构不良,限定语言种类为中文。资料选择:选择与骨纤维结构不良相关的观察对比研究、经验总结、个案报道、最新研究进展等文献,力求资料全面,排除重复研究。资料提炼:共收集相关国内外文献41篇,排除重复性研究11篇,采用30篇,包括关于骨纤维结构不良定义、发病机制、病理、诊断及治疗等。资料综合:①骨纤维结构不良是一种起源于纤维组织的良性骨肿瘤。发病率低、误诊率高。目前具体发病机制不明,现认为与常染色体显性遗传有关。②骨纤维结构不良好发于胫骨,症状为局部肿块。特征性影像学表现为胫骨中段前侧皮质膨胀性密度减低。确诊方法为病理检查。重点与骨纤维异常增殖症、造釉细胞瘤相鉴别,现有大量研究证明该病与造釉细胞瘤有联系。③治疗上过去认为10岁以前应保守治疗,10岁后选择手术治疗,目前倾向于早期骨膜外切除手术治疗。结论:骨纤维结构不良发病率低,对该病认识较少,误诊率较高,重点需与骨纤维异常增殖症、造釉细胞瘤相鉴别,应提高对该病的认识与重视程度,对可疑者行病理检查,确诊者行骨膜外切除,切除范围较大的病例行重建手术。     

白藜芦醇对动物离体心房收缩力和心率作用的种属差异性比较

目的:观察白藜芦醇对豚鼠、小鼠和家兔离体心肌收缩力和心率的影响。方法:实验于2005-08/2006-12在河北医科大学西校区实验中心完成。①实验分组:离体豚鼠、小鼠和家兔心肌各分为9组:空白对照组、溶剂对照组、递增累积浓度白藜芦醇组(浓度为10-6,3×10-6,10-5,3×10-5,10-4,3×10-4mol/L),白藜芦醇对照组(5×10-5mol/L),ATP敏感性钾通道阻断剂格列苯脲(5×10-5mol/L)预孵育 白藜芦醇组,钙激活钾通道阻断剂四乙胺(10-3mol/L)预孵育 白藜芦醇组,电压依赖性钾通道阻断剂4-氨基吡啶(10-3mol/L)预孵育 白藜芦醇组,内向整流钾通道阻断剂氯化钡(10-4mol/L)预孵育 白藜芦醇组,乙酰胆碱调节钾通道阻断剂阿托品(10-5mol/L)预孵育 白藜芦醇组。②实验方法:不同类型的钾通道阻断剂均预孵育15min后,分别加入白藜芦醇(终浓度为5×10-5mol/L),连续记录30min,与相应动物白藜芦醇对照组相比较。③评估指标:分析不同阻断剂与白藜芦醇联用对心房收缩力下降率及心率抑制率的影响。结果:①白藜芦醇可降低豚鼠和小鼠离体心肌收缩力和心率(P<0.05),并被ATP敏感性钾通道阻断剂格列苯脲和钙激活钾通道阻断剂四乙胺部分阻断。②白藜芦醇可降低家兔离体心肌心率,格列苯脲可阻断白藜芦醇的负性变时作用。③电压依赖性钾通道阻断剂4-氨基吡啶、内向整流钾通道阻断剂氯化钡、乙酰胆碱调节钾通道阻断剂阿托品均不能阻断白藜芦醇对3种不同动物离体心房收缩力和心率的作用(P>0.05)。结论:白藜芦醇可呈剂量依赖性减慢豚鼠、小鼠和家兔的心率,白藜芦醇可减弱豚鼠心肌收缩力,其作用是与开放ATP敏感性钾通道有关,而与电压依赖性钾通道、内向整流钾通道和乙酰胆碱调节钾通道无关。同时,钙激活钾通道也参与了白藜芦醇对豚鼠和小鼠离体心房收缩力和/或心率的抑制作用。白藜芦醇对离体心肌收缩力和心率的作用有种属差异性。     

超声微泡造影影像学及治疗作用的研究进展

包裹型气体微泡已经发展为临床应用的超声造影剂.微泡造影剂不仅已广泛用于血池和组织灌注显像,其治疗作用也日渐突显,例如溶栓和作为药物或基因的载体.造影剂微泡的平均直径小于红细胞直径,因而能够自由运行于微循环.微泡能将生物活性物质(例如药物或基因)结合在其内或其外膜表面,并将此物质转运于体内特定组织,例如将抗肿瘤药物转运并结合于特定肿瘤组织.靶向性微泡能将肽段等特定性配体结合于其微泡表面,这种特定性配体可特异性地与血管壁表达的受体相结合,微泡因而在靶组织区域积聚[1].     

Granulocyte-macrophage colony-stimulating factor mRNA stabilization enhances transgenic expression in normal cells and tissues

To increase transgenic production of granulocyte-macrophage colony- stimulating factor (GM-CSF), we mutated the mRNA's 3'-untranslated region, AUUUA instability elements. Expression vectors containing human or murine GM-CSF cDNAs coding for wild-type (GM-AUUUA) or mutant versions with reiterated AUGUA repeats (GM-AUGUA) were transfected into cells in culture or animals using particle-mediated gene-transfer technology. Normal peripheral blood mononuclear cells accumulated 20- fold greater levels of GM-CSF mRNA and secreted comparably greater amounts of cytokine after transfection with hGM-AUGUA expression vectors versus hGM-AUUUA. hGM-AUGUA mRNA was fivefold more stable (t 1/2 = 95 minutes) than hGM-AUUUA mRNA (t 1/2 = 20 minutes), accounting for elevated steady-state levels. Transfection site extracts and serum samples obtained 24 hours after gene transfer of hGM-AUGUA cDNA into mouse skin contained greater than 32 ng/mL and 650 pg/mL of GM-CSF protein, respectively, compared with 0.33 ng/mL and less than 8 pg/mL for hGM-AUUUA cDNA. GM-CSF produced from mGM-AUGUA cDNA transfected into rat abdominal epidermis induced a profound neutrophil infiltrate. These data suggest a novel strategy for enhanced production of biologically active cytokines by normal cells after in vivo gene transfer.     

Participation of CD45, NKR-P1A and ANK61 antigen in rat hepatic NK cell (pit cell)mediated target cell cytotoxicity

AIM Several triggering receptors have been described to be involved in natural killer (NK) cellmediated target cytotoxicity. In these studies, NK cells derived from blood or spleen were used. Pit cells are liver-specific NK cells that possess a higher level of natural cytotoxicity and a different morphology when compared to blood NK cells. The aim of this study was to characterize the role of the NK-triggering molecules NKR-P1A, ANK61 antigen, and CD45 in pit cell-mediated killing of target cells. METHODS 51 Cr-release and DNA fragmentation were used to quantify target cell lysis and apoptosis, respectively. RESULTS Flow cytometric analysis showed that pit cells expressed CD45, NKR-P1A, and ANK61 antigen. Treatment of pit cells with monoclonal antibody ( mAb ) to CD45 ( ANK74 ) not only inhibited CC531s or YAC-1 target lysis but also apoptosis induced by pit cells. The mAbs to NKRP1A (3.2.3) and ANK61 antigen (ANK61) had no effect on pit cell-mediated CC531s or YAC-1 target cytolysis or apoptosis, while they did increase the Fcγ receptor positive (FcγR+) P815 cytolysis and apoptosis. This enhanced cytotoxicity could he inhibited by 3,4-dichloroisocoumarin, an inhibitor of granzymes. CONCLUSION These results indicate that CD45 participates in pit cell-mediated CC531s and YAC-1 target cytolysis and apoptosis. NKR-P1A and ANK61 antigen on pit cells function as activation structures against FcγR+ P815 cells, which was mediated by the perforin/granzyme pathway.     

A method for simultaneous study of the karyotype, morphology, and immunologic phenotype of mitotic cells in hematologic malignancies

A major problem in the cytogenetic analysis of hematologic neoplasms has been an inability to identify the cell from which the chromosomes were obtained. We describe a procedure that allows simultaneous analysis of karyotype and cell cytology in mitotic cells. The method differs from conventional cytogenetic analysis in that after mild hypotonic treatment, the cells are cytocentrifuged onto glass slides. In mitotic cells, this procedure often results in adequate spread of the chromosomes within the intact cell membrane. The cytoplasmic structure also remains intact, so that cytologic preparations are of good quality. Morphologic and immunologic identification of mitotic cells can be done using routine hematologic stains, such as Giemsa or Sudan black B, and various antisera using immunofluorescence techniques. The chromosomes can be simultaneously analyzed either without banding on slides stained with Giemsa or with Q-banding on slides stained with immunofluorescence techniques. Identification of numerical and structural karyotype aberrations thus is possible in morphologically identified cells.