二硫代氨基甲酸吡咯烷诱导人肝癌细胞凋亡的铜离子依赖性机制

目的：测定二硫代氨基甲酸吡咯烷（PDTC）处理对人肝癌细胞Hep3B凋亡的诱导作用及Cu^2 对这种作用的影响。方法：运用细胞增殖力、膜损伤、DNA片断化、细胞周期DNA含量测定分析PDTC对人肝癌细胞株Hep3B细胞的增殖抑制及凋亡诱导作用及Cu^2 在其中发挥的作用。结果：PDTC处理后，细胞增殖能力显著下降。乳酸脱氢酶（LDH）分析显示细胞膜并没有被破坏，DNA凝胶电泳及细胞周期DNA含量测定发现明显的凋亡特征性DNA片断及亚G1峰，显示细胞增殖能力的降低源于细胞凋亡的发生。低浓度Cu^2 显著加强了PDTC的细胞增殖抑制及凋亡诱导作用，而Cu^2 络合剂Bathocuproine disulfonate(BCS)显著抑制PDTC的两种作用。结论：PDTC铜离子依赖性地抑制人肝癌细胞增殖并诱导细胞凋亡。     

波尔山羊重复超排效果的研究

对 2 0只波尔山羊实施两次超排处理。其结果如下 :1.第 1次超排处理时 2 0只供体羊全部发情并进行采卵 ,超排有效率为 10 0 % ;平均排卵数为 2 0 .2 5枚 /只 ,平均采集胚胎数 19.2 5枚 /只 ,平均采集可用胚胎数为 17.3枚 /只 ;第 2次超排处理时有 3只羊推迟发情 ,超排有效率为 85 % ;平均排卵数 19.2 9枚 /只 ,平均采集胚胎数 18.5 3枚 /只 ,平均采集可用胚胎数 17.35枚 /只 ;2 .两次超排所获得的平均可用胚胎数差异不显著(p >0 .0 5 )。     

Minactivin expression in human monocyte and macrophage populations

Adherent monolayer cultures of human blood monocytes, peritoneal macrophages, bone marrow macrophages, and colonic mucosa macrophages were examined for their ability to produce and secrete minactivin, a specific inactivator of urokinase-type plasminogen activator. All except colonic mucosa macrophages produced and secreted appreciable amounts of minactivin, but only blood monocytes were stimulated by muramyl dipeptide (adjuvant peptide) to increase production. The minactivin from each of these populations could be shown to preferentially inhibit urokinase-type plasminogen activator and not trypsin, plasmin, or "tissue"-type plasminogen activator (HPA66). A plasminogen-activating enzyme present in monocyte cultures appeared unaffected by the presence of minactivin and could be shown to be regulated independently by dexamethasone.     

Use of multiple T cell-directed intact ricin immunotoxins for autologous bone marrow transplantation

The monoclonal antibodies (MoAb) T101, G3.7, 35.1, and TA-1 were conjugated to intact ricin using a thioether linkage. These MoAb detect, respectively, the CD5[gp67], CD7[p41], CD2[p50], and [gp95, 170] determinants that are found in the vast majority of cases of T cell acute lymphocytic leukemia (T-ALL). The resulting immunotoxins (ITs) and an equimolar mixture of these ITs were evaluated as potential purgative reagents for autologous transplantation in T-ALL. Leukemic cell lines were used to compare the kinetics of protein synthesis inactivation mediated by each IT. The cells were treated with IT in the presence of lactose in order to block the native binding of ricin. The observed rates of protein synthesis inactivation correlated with target antigen expression detected by fluorescence-activated cell sorter analysis. Of the four ITs, T101-ricin (T101-R) exhibited the fastest rate of inactivation, followed in order by G3.7-ricin, TA-1-ricin, and 35.1-ricin. At concentrations greater than 300 ng/mL, a cocktail containing an equimolar amount of all four ITs (referred to as the four- IT cocktail) exhibited kinetics that were as fast or faster than those of T101-R. The long-term cytotoxic effects of individual ITs and the four-IT cocktail were evaluated using a sensitive clonogenic assay. Each IT was specifically cytotoxic and inhibited 1 to 4 logs of clonogenic leukemic cells at doses (300 to 600 ng/mL) that can be used clinically. The four-IT cocktail was highly cytotoxic; a concentration of 300 ng/mL inhibited greater than 4 logs of leukemic cells while sparing the majority of committed (CFU-GM, CFU-E) and pluripotent (CFU- GEMM) hematopoietic stem cells. The determination of both short-term kinetics of protein synthesis inactivation and longer-term inhibition of clonogenic growth allowed new insight into cell killing by IT. Our results suggest that ITs continue to act on clonogenic target cells for a period of three to five days. Interestingly, the four-IT cocktail was not as potent against clonogenic leukemic cells as T101-R alone, although it exhibited kinetics of protein synthesis inhibition that were as fast as those of T101-R alone. This finding suggests that internalized ITs may differ in the length of time they remain active within the cell. Our results also demonstrate the importance of using several different assays to evaluate IT reagents.     

中心静脉压联合全心舒张末容积指数指导感染性休克患者容量治疗的效果

目的 评价中心静脉压(CVP)联合全心舒张末容积指数(GEDVI)指导感染性休克患者容量治疗的效果.方法 感染性休克患者23例,性别不煨,年龄18～64岁,休克时间＜6h,急性生理和慢性健康状况评分13～31分,采用随机数字表法,将其随机分为2组:CVP指导容量治疗组(Ⅰ组,n=12)和CVP联合GEDVI指导容量治疗组(Ⅱ组,n=11).2组均静脉输注生理盐水和6％羟乙基淀粉200/0.5,晶体液和胶体液的比例为1∶(0.5 ～ 1.0),输注速率800～ 1600 ml/h,容量治疗过程中Ⅰ组维持CVP8～ 12mmHg;Ⅱ组维持CVP＞8 mm Hg和GEDVI 600 ～ 750 ml/m2.分别于容量治疗前及容量治疗开始后6h时采集动脉及中心静脉的血样,测定血乳酸浓度和中心静脉血氧饱和度(ScvO2),计算乳酸和ScvO2的变化率.结果 与Ⅰ组比较,Ⅱ组乳酸变化率升高(P＜0.05),ScvO2变化率差异无统计学意义(P＞0.05).结论 与CVP指导容量治疗比较,CVP联合GEDVI指导感染性休克患者容量治疗时可增加组织灌注,其效果较好.     

咪达唑仑复合氯胺酮应用于小儿基础麻醉的临床探讨

 目的 探讨应用咪达唑仑复合氯胺酮不同给药方法在小儿基础麻醉中的优化方案.方法 200例1～6岁,ASAⅠ～Ⅱ级患儿随机分成以下五组:A组为口服咪达唑仑0.7 mg/kg;B组为口服氯胺酮8 mg/kg;C组为肌注氯胺酮5mg/kg;D组为口服咪达唑仑0.5 mg/kg和氯胺酮4 mg/kg;E组为先口服咪达唑仑0.5 mg/kg,再肌注氯胺酮4 mg/kg.观察各组诱导结果及呼吸循环变化、不良反应.结果 ①A组与B组比较,A组起效更快(P<0.01),合作更好,不良反应较少;②A组、B组均比C组更合作,但不如C组起效更快;③D组和E组相比,患儿更合作,不良反应更少,但起效更慢,两组诱导效果无显著差异(P>0.05).结论 咪达唑仑复合氯胺酮优于单独给药,对循环呼吸影响小;口服给药可行性更佳.     

Off pump coronary artery bypass (OPCAB) in critical left mainstem stenosis—Our experience

Background Beating heart surgery has now become the commonest technique of doing Coronary Artery Bypass Graft Surgery (CABG) in our country. It is being used even in such high risk situations like diffuse coronary disease and Critical Left Main stem Stenosis (LMCS) with good results. The aim of this study is to retrospectively review our results in Off-Pump Coronary Artery Bypass Surgery (OPCAB) in patients with critical left main stem stenosis. Methods This study is a retrospective analysis of the data of patients who underwent primary coronary artery bypass surgery. During the period from April 2003 to September 2005 a total of 64 patients underwent OPCAB procedure for critical LMCS. During the same period 10 patients underwent CABG on Cardio Pulmonary Bypass (CPB). The age range was 36–77yrs. The sex distribution was M: F 53∶10. Ten patients were done as emergency. 2 of them were on Intra Aortic Balloon Pump (IABP) support preoperatively. 10 patients were high risk with a Euro score of ≥5. Results Left Internal Mammary Artery (LIMA) was used in 78% of cases. Average grafts per patient was 2.96. The median ventilation time was 5.91 hrs. New IABP insertion in postoperative period was required in 1 patient. One patient was reexplored for bleeding. There was one perioperative myocardial infarction. 57% of patients did not need any blood transfusion. There was no conversion to CPB. There was no operative mortality. Inotropes were used in ten cases. Conclusions OPCAB is a safe method of revascularization in patients with critical LMCS. Preoperative IABP is useful in patients with cardiogenic shock. However, there is a place for CPB in patients needing additional procedures like Mitral Valve repair (MV repair) or Dor's procedure or when the vessels are very diffusely diseased. Those patients who are unstable despite IABP support may be managed by Beating heart On Pump (BHOP) technique.     

健脾补肾方增加β-catenin、Runx2表达而促进骨质疏松性骨折愈合的疗效观察

目的研究健脾补肾方促进骨质疏松性骨折愈合的疗效机制,探讨"脾肾相关"、"先后天之本"中医理论在骨质疏松性骨折防治中的运用。方法建立去卵巢骨质疏松性骨折小鼠模型,随机分为7、14、28d 3个时间点,每个时间点分生理盐水、健脾补肾方2组。于骨折术后第2天给予相应药物灌胃治疗,分别于治疗3个时间点后处死小鼠,取材,进行影像学观察和病理组织学染色。结果 X-ray、Micro-CT结果显示,健脾补肾组7、14、28d均可促进骨痂形成及骨折愈合;Micro-CT定量分析显示,健脾补肾组7、14d骨痂BV/TV、Conn.D、mean/density of TV、mean/density of BV均明显高于生理盐水组(P0.05);有限元分析结果提示,健脾补肾组28d骨折部位刚度、弹性模量结果均高于生理盐水组(P0.05);HE染色、ABH/OG染色结果显示,健脾补肾方可以促进骨折部位早、中期膜内成骨和软骨内成骨,加速骨折愈合;免疫组化染色结果显示,健脾补肾方能增加骨痂部位β-catenin、Runx2的表达,促进骨折愈合。结论健脾补肾方可以促进骨质疏松性骨折的愈合,其机制可能与增加β-catenin、Runx2的表达相关。