腰椎滑脱后路矫形固定的疗效评定

目的通过对腰椎滑脱症手术治疗的长期随访分析,比较不同术式治疗效果。方法通过对1986年-2000年收治的腰椎滑脱患者临床资料及功能进行分析。结果60例患者分别采用Luque术式、Steffee术式、RF-Ⅱ、RF-Ⅱ加BAK术式,随访3～8年,其矫正率分别为42%、67%、95%、97%。结论手术器械矫正加融合对腰椎滑脱的疗效是肯定的,尤以BAK的应用可进一步维持滑脱的矫正,减少远期并发症。     

肝脏移植术后肺部感染病原体调查及危险因素分析

目的　总结肝移植术后肺部感染的病原体分布特点并探讨其危险因素。方法　对我院1999年 11月至 2 0 0 3年 6月间的 130例肝脏移植进行前瞻性调查 ,统计其发病率、病死率 ,描述其时间分布、病原学分布 ,利用非条件Logistic回归方程筛选术后肺部感染危险因素。结果　肝移植术后肺部感染发病率为 32 .31% ,病死率为 35 .71%。 78.5 7%的肺部感染发生在术后第一周。革兰氏阴性菌是最常见肺部感染病原体且多高度耐药。肝移植术后肺部感染危险因素包括 :术后使用呼吸机≥ 2d、长时间手术、纤支镜检查或治疗、术前大量腹水、术后气管切开、术后肾功能异常、术后肺水肿、术后长时间留置胃管、术中长时间低血压。结论　肝移植术后肺部感染多发生在移植术后早期 ,具有高发病率、病死率高的特点。病原体多为具耐药性的革兰氏阴性菌。围手术期多方面因素均可能成为肺部感染的诱因 ,其防治工作必须贯穿整个围手术期     

大鼠移植胰腺冷缺血再灌注后细胞凋亡的变化

目的　探讨移植胰腺冷缺血再灌注后胰腺细胞凋亡的变化过程。方法　 6 5只SD大鼠随机分成 7组 :假手术组 ,冷缺血 2h组 ,冷缺血 2h再灌注 1、3、6、9、12h组。通过HE染色后光镜及电镜观察各组的胰腺组织的病理变化 ;采用脱氧核糖核苷酸末端转移酶介导的缺口末端标记法(TUNEL)检测凋亡细胞的分布及计数。结果　胰腺移植后早期即可观察到细胞凋亡的典型改变 ,胰腺冷缺血再灌注后发生凋亡的高峰期为再灌注后 3h[AI为 (9.4 6± 2 .91) % ,P <0 .0 1) ,再灌注 6h较 3小时细胞凋亡有所减少 [AI为 (5 .74± 1.6 6 ) % ,P <0 .0 1],再灌注 9h及 12h细胞凋亡进一步减少 [AI分别为 (3.6 0± 1.6 4 ) %及 (3.2 6± 1.35 ) % ,P <0 .0 5 ]。结论　细胞凋亡是胰腺移植后的早期事件 ,移植胰腺冷缺血再灌注后早期主要的死亡方式是凋亡 ;移植胰腺冷缺血再灌注后的凋亡高峰发生在再灌注后 3h。     

内镜标本端粒酶定量检测对良恶性梗阻性黄疸的诊断价值

目的　为探讨胆胰系统恶性肿瘤组织与端粒酶表达的关系 ,并在术前找出一种简便、安全、快速的早期诊断及鉴别良、恶性梗阻性黄疸的方法。方法　对梗阻性黄疸病例于术前行内镜逆行胰胆管造影 (ERCP)检查 ,于造影前抽取胆汁或胰液、部分病例取活检组织 ,并于开腹手术当中再次切取癌组织标本 ,所有标本进行端粒酶活性的定量检测 ,所得数据进行统计学处理。结果　 (1)恶性梗阻性黄疸组织标本中端粒酶表达阳性率为 87 5 0 % (2 8/ 32 ) ,良性梗阻性黄疸组织标本中端粒酶表达阳性率为 3 33% (1/ 30 ) ;(2 )恶性梗阻性黄疸体液标本中端粒酶表达阳性率为 71 88% (2 3/ 32 ) ,良性梗阻性黄疸体液标本中端粒酶表达阳性率为 3 33% (1/ 30 ) ,恶性梗阻性黄疸内镜下钳取的活检组织 ,其端粒酶阳性率为 83 33% (10 / 12 )。结论　在术前通过十二指肠镜采集患者的胆汁和胰液 ,并钳取活检组织 ,分别进行端粒酶活性的定量检测 ,这是一种简便、安全、快速的早期诊断及鉴别良、恶性梗阻性黄疸的方法。     

肝移植术后早期脂肪乳剂支持治疗对移植肝功能影响的临床研究

目的　研究含脂肪乳剂的肠外营养 (TPN)对肝移植受体肝脏功能的影响。方法　选择2 0 0 1年 9月～ 2 0 0 4年 6月期间在我所肝移植中心住院行肝移植手术治疗的患者 ,取符合标准的 30例作为研究对象 ,随机分组 ,进行前瞻性的临床研究。肝移植术后 6h开始给予单糖或脂肪乳剂和单糖联合功能的TPN(分别为Glu对照组和MCT/LCT组 ) ,TPN期为 7d ,期间严格禁食。于TPN后第 1、4、7、10、30、90及 180天收集标本 ,检测血ALT、AST、GGT、TBil及DBil。结果　TPN支持后MCT/LCT和Glu组ALT、AST、GGT、TBil及DBil水平均呈现下降趋势 ,与单糖组相比 ,脂肪乳组降低迅速。结论　含脂肪乳的TPN较单糖TPN更有利于促进移植肝早期功能恢复     

Abnormalities in myelopoietic regulatory interactions with acidic isoferritins and lactoferrin in mice infected with Friend virus complex: association with altered expression of Ia antigens on effector and responding cells

The regulation of myelopoiesis was evaluated in B6D2F1 mice inoculated with Friend virus complex (spleen focus-forming virus plus helper virus) or helper virus alone by analyzing acidic isoferritin (AIF) and lactoferrin (LF) interactions with target cells. Under normal conditions, AIF suppresses colony and cluster formation by an Ia- antigen-positive cycling subpopulation of mouse granulocyte-macrophage progenitor cells (CFU-GM). Under the same conditions, the release of AIF-inhibitory activity and granulocyte-macrophage colony stimulatory factors (GM-CSF) from an Ia-antigen-positive subpopulation of monocytes and macrophages is suppressed by LF. Within one to two days after inoculation in vivo with Friend virus complex or helper virus, mouse CFU-GM become insensitive in vitro to suppression by purified human AIF as well as crude mouse AIF, and by four days, bone marrow, spleen, and thymus cells of these mice release much greater quantities of AIF- inhibitory activity than the cells from mice injected with control medium. The Friend virus complex itself has no influence in vitro on CFU-GM from normal mice. In addition, the release of AIF-inhibitory activity from bone marrow, spleen, and resident peritoneal cells and the release of GM-CSF from resident peritoneal cells of mice infected with Friend virus complex are not suppressed by LF. The inability of AIF to suppress colony formation by bone marrow and spleen CFU-GM from mice infected with Friend virus complex is associated with the loss of Ia (I-A subregion) antigens from CFU-GM, even though CFU-GM are in cycle. The nonresponsiveness of bone marrow, spleen, and peritoneal cells from these mice to LF suppression of AIF release and the inability of LF to influence GM-CSF release from peritoneal cells is associated with loss of Ia antigens from these cells. The above abnormalities are similar to the defects noted using cells from patients with leukemia. These results suggest that mice infected with Friend virus complex can serve as a model for investigating abnormalities in cell regulation and their relationships to disease progression.     

Constitutive production of leukemia differentiation, colony- stimulating, erythroid burst-promoting, and pluripoietic factors by a human hepatoma cell line: characterization of the leukemia differentiation factor

Conditioned medium (CM) obtained from a human hepatoma cell line, SK- HEP-1, contains colony-stimulating factors (CSFs) active on murine and human bone marrow-derived granulocyte and macrophage colony-forming units (CFU-GM) and a factor capable of inducing granulocyte-macrophage differentiation (GM-DF) of murine myelomonocytic leukemic cells WEHI- 3B(D+) and human promyelocytic leukemic cells HL-60 when assayed in semisolid agar cultures. The human active granulocyte-macrophage colony- stimulating factor (GM-CSF) for day 7 CFU-GM and the GM-DF for WEHI- 3B(D+) and for HL-60 are not separable by acrylamide agarose column chromatography, eluting at an apparent molecular weight between 20,000 and 35,000 daltons, or by isoelectric focusing (isoelectric point, pH 5.4). In addition, SK-HEP-1 CM contains erythroid burst-promoting activity (BPA) and a factor that promotes the growth of human mixed colonies. SK-HEP-1 cells, which grow as an adherent monolayer, appear not to be endothelial or monocytic in origin since by immunofluorescent staining they are negative for Ia (HLA-DR), monocyte antigen 1 and 2, lysozyme, and factor VIII-related antigen. Positive immunofluorescent staining for keratin and fibronectin suggests the possibility that SK- HEP-1 is an epithelial cell line. Constitutive production of GM-DF as well as other hematopoietic activities including GM-CSF, erythroid BPA, and an activity that promotes the growth of human mixed colony progenitors by a human epithelial tumor cell line, SK-HEP-1, suggests that this cell line is a valuable resource for both large-scale production of these factors and the cloning of the gene(s) that code for these regulators.     

Comparative influences of phytohemagglutinin-stimulated leukocyte conditioned medium, hemin, prostaglandin E, and low oxygen tension on colony formation by erythroid progenitor cells in normal human bone marrow

The comparative influences of phytohemagglutinin-stimulated leukocyte conditioned medium (PHALCM), hemin, prostaglandin E1 (PGE1), and growth of cells at low oxygen tension (5% O2) were evaluated for their capacity to enhance colony formation in vitro from normal human bone marrow erythroid progenitor cells (BFU-E). Each treatment enhanced colony formation by itself, and the combinations of treatments resulted in an additive enhancing effect on erythroid colony formation. Removal of T-lymphocytes from the bone marrow sample ablated the enhancing activity of PGE1, but did not influence the enhancing activities of PHALCM, hemin, and growth at low oxygen tension. The results suggest that the mechanisms of action of these various erythroid colony-enhancing effects may be different.     

CT增强静脉期直方图分析在甲状腺癌诊断和分型中的应用价值

目的:探讨基于增强CT静脉期的直方图参数在诊断甲状腺癌(TC)及预测其病理分型中的应用价值.方法:将2017年4月-2021年4月在我院经手术或穿刺活检病理证实的103例甲状腺结节患者作为研究对象,包括良性结节82个、恶性结节37个(分化型24例,非分化型13例).所有患者术前行颈部和上胸部CT平扫和双期(动脉期和静脉...