积分加权法评价磷化学烧伤实验病理的意义与应用

目的：积分加权法在病理组织学检查中的应用，方法：在常规病理描述基础上，采用积分加权法将病理结果予以定量，综合评价致伤后实验动物的主要脏器，结果：实验动物同等面积的磷酸烧伤各脏器积分降低，钙治疗后则显著改善，均与其它方面报道的资料一致，结论：积分加以数值使各脏器损伤程度一目了然，对不同脏器间的损伤情况有可比性，从而有助于了解主要受损脏器与总体的关系以及药物的治疗效果。     

基于直方图拟合的MRI图像水平集分割

利用混合高斯模型对MRI图像直方图进行分析,将拟合获得的特征参数作为水平集曲线进化的约束条件,对医学图像进行分割。分割中采用的自适应Level Set方法,能够自适应地确定曲线进化方向（扩张或收缩）,而不必在分割之前指定其进化方向,减少了人工干预;同时也克服了传统测地活动轮廓线（GAC）方法对图像梯度信息的过分依赖,以及由于对图像进行大尺度高斯平滑处理造成边缘点移动、定位准确度下降的缺陷。分别对MRI仿真和真实图像进行了实验,MRI仿真实验的分割敏感性、专一性和总体性能指标分别达到了94.72%、97.52%和97.22%。分割结果的定量分析和定性分析表明算法的有效性以及较高的分割准确度。     

几丁糖预防屈肌腱粘连的临床效果

目的：观察几丁糖预防肌腱粘连的临床效果。方法：对Ⅱ区肌腱损伤４８例７２条肌腱断裂行一期修复,术中采用改良Ｋｅｓｓｌｅｒ法缝合肌腱,在肌腱鞘管内注入２％医用几丁糖０．５￣１．０ｍｌ,缝合皮肤。     

急性心肌缺血时锌铜含量的变化及影响

目的　探讨急性心肌缺血时锌铜含量的变化及影响。方法　分别测定急性心肌缺血家兔局部心肌、心血、外周血及 15 0例急性心肌缺血病人血清中锌铜含量 ,并与对照组比较。腹腔给予急性心肌缺血家兔补充锌铜溶液 ,观察给予前后ECG变化。结果　家兔随心肌缺血时间延长 ,锌铜含量在局部心肌中逐渐减少 ,心血及外周血中逐渐增加 ,与对照组比差异显著 (P <0 .0 5 ) ;急性心肌缺血病人血清锌铜含量明显降低 (P <0 .0 1) ;家兔腹腔给予锌铜溶液心肌缺血及心律失常明显好转。结论　急性心肌缺血早期锌铜含量变化能引起心电活动的改变 ,可能是猝死的原因之一。补充锌铜对纠正心律失常及心肌缺血有一定作用。     

单肺通气时肺内分流与PETCO2的相关性研究

目的：研究单肺通气时PETCO2和Qs/Qt之间的关系。方法：选择28例择期开胸手术的患者分别于TLV 20min、OLV 5min、15min、30min、60min测动脉血和混合静脉血气并同时记录PETCO2,计算Qs/Qt,进行统计学处理。结果：OLV时不同时段PETCO2、PaCO2、Qs/Qt比TLV时增大(P＜0.05),TLV时PETCO2与Qs/Qt不相关(r=-0.0230,P=0.9077)。OLV时PETCO2与Qs/Qt相关(r=0.4739,P=0.00001),其直线回归方程为y=3.4862+0.0147x(y=PETCO2,x=Qs/Qt)。结论：OLV时PETCO2与Qs/Qt呈直线相关,PETCO2随Qs/Qt增加而增大。     

英汉颜色词差异浅探

英、汉语分属两种不同的语系 ,受语言与文化特殊性的影响 ,人们对色彩的感受和赋予颜色词的意义也各不相同。翻译时 ,不可望文生义 ,“对号入座” ,必须在充分了解中西方文化差异的基础上 ,准确把握颜色词所处的语境 ,力求做到信、达、雅     

癫痫大鼠脑组织内免疫反应特点研究

目的研究脑“免疫特免性”与癫痫发病的关系。方法用免疫细胞化学法观察IgG免疫反应阳性(IgG-IR)细胞在两种不同处理程序的正常成年、癫痫及尼莫地平作用下癫痫大鼠脑组织内分布情况。结果灌注大鼠,除癫痫组个别脑片散在弱IgG-IR细胞外,其余均阴性;未灌注大鼠,各组脑片均散布IgG-IR细胞;癫痫大鼠脑组织IgG-IR细胞分布较正常组增多(p<0.01);尼莫地平作用下癫痫大鼠脑组织内IgG-IR细胞分布与正常组比较无显著差异。结论脑“免疫特免性”在癫痫发病中具有一定意义。     

血清总胆汁酸测定在肝脏疾病中的临床价值

目的 为探讨血清总胆汁酸测定对肝病的诊断意义。方法 采用酶耦联比色法检测１１９例各种肝病患者血清总胆汁酸水平。结果 显示急性为、慢性肝炎、重型肝炎、肝硬化、肝癌及脂肪肝患者血清胆汁酸水平均明显高于正常对照组。肝硬化患者血清总胆汁酸异常率为９４．３％,高于其它肝功能指标异常率,且与血清白蛋白呈负相关。结论提示血清总胆汁酸是一项较灵敏的肝功能指标,尤其是在肝功能常规指标改变不明显时,对各种肝病特别 硬     

QT Dispersion Level and Its Clinical Significance.in Dilated Cardiomyopathy

［1］Richardson CP, Mckenna RM, Bristow CM, et al.Report of the 1995 Word Health Organization/International Society and Federation of Cardiology Task Force on the definition and classification of cardiomyopathies. Circulation, 1996,93: 841 ［2］Barr CS, Naas A, Freeman M, et al. QT dispersion and sudden unexpected death in chronic heart failure. Lancet, 1994,343:327 ［3］Martin AB, Garson A, Perry JC, et al. Prolonged QT interval in hypertropic and dilated cardiomyopathy in children. Am Heart J, 1994,127(1):64 ［4］Pye M, Quinn AC, Cobble SM. QT dispersion: a non-invasive marker of susceptibility to arrhythmia in patients with sustained ventricular arrhythmias?Br Heart J, 1994,71(5):51 ［5］Berger RD, Kasper EK, Baughman KL, et al. Beat to beat QT interval variability: novel evidence for repolarization lability in ischemic and non ischemic dilated cardiomyopathy. Circulation, 1997, 96 (5):1557 ［6］Wolfram G, Ulrike S, Volker M, et al. QT dispersion and arrhythmic events in idiopathic dilated cardiomyopathy. Am J Cardiol, 1997,78: 458 ［7］Fei L, Goldman JH, Prasal K, et al. QT dispersion and RR variations on 12-lead ECGs in patients with congestive heart failure secondary to idiopathic dilated cardiomyopathy. Eur Heart J, 1996,17: 258 ［8］Pan YZ, Guo NS, Xing ZF, et al. The relation between QT dispersion and ventricular arrhythmia of dilated cardiomyopathy. Chin J Inter Medi, 1996,35(11):73 ［9］Galinier M, Vialette JC, Fourcade J, et al. QT interval dispersion as a predictor of arrhythmic events in congestive heart failure. Importance of aetiology. Eur Heart J, 1998,19(7) :1054     

Inhibition of telomerase activity correlates with a decrease in the RNA component of telomerase during differentiation

In most normal somatic cells the telomeres of human chromosomes shorten with each cell division because of low expression or lack of telomerase activity. Telomerase, a ribonucleoprotein that synthesizes telomeric DNA onto chromosomal ends, is reactivated or upregulated in tumor cells and maintains the stability of telomere length. We previously showed that treatment of HL60 leukemia cells with differentiation-inducing agents resulted in inhibition of telomerase activity. In the present study, we found that the decrease in telomerase activity did not temporally correlate with the expression of a differentiation marker, CD11b, on the cell surface. Mixing of protein extracts from telomerase-negative differentiated HL60 cells with those from parental HL60 cells did not result in inhibition of telomerase activity, suggesting that a diffusible cellular telomerase inhibitor was not produced in the differentiated cells. However, a decrease in telomerase activity correlated with a selective decrease of telomerase RNA expression, a decrease in the levels of total cellular RNA, and an increase in cells at G(0) phase.