阿尔茨海默病患者脑白质损害与认知功能的关系

目的用磁共振扩散张量成像(DTI)研究阿尔茨海默病(AD)患者脑白质损害的特点及其与认知功能改变的相关性。方法对16例AD患者和12名年龄及性别相当的健康老年人行DTI、T1液体衰减反转恢复序列(FLAIR)及T2-FLAIR检查,测量胼胝体膝部和压部、内囊前肢和后肢、额颞顶枕叶白质的部分各向异性分数值(FA)和平均弥散度(MD),分析FA、MD值与简易精神状态量表(MMSE)评分之间的相关关系。结果AD患者胼胝体压部、额叶、顶叶、颞叶FA值分别为0.602±0.043、0.270±0.034、0.294±0.043、0.302±0.032,与健康老人组相比显著下降(P<0.05),且与MMSE评分呈正相关关系,而内囊前后肢、枕叶、胼胝体膝部的FA值则无明显变化(P>0.05);胼胝体压部、顶叶白质的MD值分别为(0.918±0.029)、(0.826±0.015)×10-9m2/s,与健康老人组相比显著升高(P<0.01),且与MMSE评分呈负相关,而内囊前后肢、额叶、颞叶、枕叶和胼胝体膝部的MD值则无明显变化(P>0.05)。结论AD患者表现为脑白质的选择性损害,且损害程度与认知功能密切相关;这种选择性损害反映了AD病理机制中皮质-皮质及皮质-皮质下联系的丢失;DTI技术可以用来监测疾病的进展情况及评价AD治疗药物的临床疗效。     

正常小肠螺旋CT三期扫描技术和方法研究

目的探索正常小肠螺旋CT三期扫描技术和方法的最佳合理配伍关系。方法 80例正常小肠患者 ,随机分为两组 ,按两种配对参数各自进行螺旋CT三期扫描 ,通过双盲法分别选择确定两组显示良好影像质量小肠CT片 ,其中甲组 36例 ,乙组2 5例 ,两组经X2 检验 ,其P 相似文献   

大鼠脑组织单胺类递质及其代谢产物的检测方法研究

目的 :研究大鼠脑组织中单胺类递质及其代谢产物的高效液相反相离子对色谱测定法。方法 :采用LiChrosorbC18,10 μm色谱柱 ,流动相为甲醇 :水 (4 0 :60 ) ,含 0 .0 2 8g LEDTANa2 ,0 .15g LSDS ,0 .2ml LH2 SO4(pH 2 .5～ 3 ) ,荧光检测波长 :λEX=2 85 ,λEM=3 3 3。结果 :对 87只大鼠脑组织中 4种单胺类递质及其代谢产物的含量进行了同时测定 ,高香草酸 (HVA) 2 .5 0～ 40 .0 μg ml、去甲肾上腺素 (NE) 0 .0 1～ 0 .5 0 μg ml、多巴胺 (DA)0 .0 5～ 1.0 0 μg ml、5 羟色胺 (5 HT) 0 .0 2 5～ 0 .5 0 μg ml,峰面积与其含量呈良好的线性关系。 结论 :该法操作简便、快速、准确 ,为组织中单胺类递质及其代谢产物检测的一种理想方法 ,并适用于临床相关研究。     

阿奇霉素治疗脑梗死后不明原因长期发热的研究

目的研究阿奇霉素对脑梗死后不明原因长期发热的疗效。方法用免疫荧光法测定不明原因长期发热脑梗死患者112例的血清抗肺炎衣原体抗体,患者随机分为2组并分别给予阿奇霉素和新青霉素加入生理盐水中静脉滴注10d,每日观察比较2组患者的病情。结果所有病例抗肺炎衣原体IgM抗体滴度均≥1∶16;阿奇霉素组显效率为92.86%,高于新青霉素组的44.64%,差异有统计学意义(P<0.01)。结论长期发热的脑梗死患者肺炎衣原体的感染率高,用阿奇霉素治疗效果好。     

鼻咽癌CT灌注成像及其生物学相关性研究

目的研究鼻咽癌CT灌注值与肿瘤微血管密度（MVD）、肿瘤分期的关系，探讨多层螺旋CT灌注成像对鼻咽癌的临床应用价值。方法49例鼻咽部CT灌注检查中，鼻咽癌组30例，鼻咽癌放疗后组14例，正常鼻咽部5例，测量鼻咽癌和鼻咽黏膜位置的血流量（BF）、最大强化指数（PEI）、峰值到达时间（TTP）及血容量（BV）作为灌注指标，其中16例鼻咽癌活检组织行免疫组织化学CD34单抗染色后，Weidner方法计数MVD。各组灌注值比较行方差分析，CT灌注值、肿瘤分期与MVD之间行Spearman等级相关分析。结果49例中1例鼻咽癌灌注检查失败。鼻咽癌组（29例）肿瘤CT灌注值BF为（48．6±16．9）ml·100g^-1·min^-1，PEI为（32．3±7．9）HU，TTP为（17．5±4．9）s，BV为（12．8±4．4）ml·100g^-1；正常对照组（5例）BF、PEI、TTP、BV值分别为（15．9±5．9）ml·100g^-1·min^-1、（12.6±1．3）HU、（22．6±6．9）s、（3．5±0．5）ml·100g^-1；鼻咽癌放疗后组（14例）BF、PEI、TTP、BV值分别为（25．2±7．0）ml·100g^-1·min^-1、（19．8±5．9）HU、（22．6±4．3）s、（6．1±2．4）ml·100g^-1，三组各灌注值差异有统计学意义（P值均〈0．01）；相关分析显示，鼻咽癌组（29例）中TNM分期（其中Ⅰ期3例，Ⅱ期9例，Ⅲ期10例，Ⅳ期7例）与PEI和BV存在相关性（r值分别为0．48和0．50），与BF和TTP无明显相关性（r值分别为0．23和0．22）；16例鼻咽癌MVD为（30．8±12．6）个／高倍镜视野，与其BF（51．4±17．0）ml·100g^-1·min^-1、PEI（33．2±9．6）HU和TTP（16．3±4．1）8存在相关性（r值分别为0．85、0．60和0．78），与BV（13．2±5．6）ml·100g^-1弱相关（r=0．48）。结论鼻咽癌有着特征的CT灌注表现，多层螺旋CT灌注成像的灌注值可以反映鼻咽癌微血管密度特征，PEI和BV值与鼻咽癌的TNM分期存在一定的相关性。     

Pathogenesis of congenital pyrimidine 5′ -nucleotidase | deficiency: A study on relationship among erythrocyte morphology, enzyme protein content and activity

Objective: To further explore the mechanism of congenital pyrimidine 5'-nucleotidase I deficiency. Methods; The samples were collected from the family members of a patient with P5'N- I deficiency. The enzyme activities were measured by UMP method and the enzyme proteins were quantified by ELISA while the morphology of peripheral blood cells was observed. Results: The enzyme contents reduced as their enzyme activities decreased in the family especially in four members. There was a significant positive correlation(r =0. 955) between the activity and the content of P 5'N- I . The count of the stippling cell was varied in the family. Conclusion.- One of the reasons for congenital P5' N- I deficiency might be the deficiency in the enzyme content. The morphology of peripheral blood erythrocyte may be an assistant diagnotic index. The P5'N- I activities and contents were measured simultaneously may be a effective method in clinic diagnosis.     

组织扩张术皮肤胶原的代谢改变

目的：研究常规扩张（ＩＴＥ）和持续快速扩张（ＣＴＥ）对皮肤胶原代谢的影响。方法用白色小家猪制作组织扩张术动物模型，用Ｇｏｒｄｅｌａｄｚｅ法测定血清和扩张组织的羟脯氨酸（ＨＰ）含量，藻酸盐印模材膜片法测量标记区面积；光镜测量真皮厚度。结果：ＩＴＥ组血清ＨＰ含量升高，０．８倍，ＣＴＥ组升高１．２倍，ＩＴＥ和ＣＴＥ组皮肤含量与正常皮肤相同，组织中ＨＰ总量均明显升高，持续扩张皮瓣组（ＣＴＥＦ）术后４ｗｋ皮     

nm23基因在前列腺癌中的表达与癌转移的关系

应用ＬＳＡＢ免疫组织化学染色方法，研究转移抑制基因ｎｍ２３表达产物二磷酸核苷激酶（ＮＤＰＫ）在前列腺癌中的表达及其意义。结果表明，ＮＤＰＫ／ｎｍ２３在前列腺癌中有较高的表达，阳性率为５００％（２０／４０）。无前列腺癌转移者其阳性率为６６７％（１２／１８），有前列腺癌转移者其阳性率为３６４％（８／２２），两者比较差异有显著性（Ｐ＜００５），并与前列腺癌分化程度和临床分期有显著相关。因此，ｎｍ２３基因可能在前列腺癌形成及转移过程中起不同的调节作用，其表达程度与前列腺癌转移呈负相关，有可能成为评价前列腺癌病人预后的一项新指标。     

Overexpression/amplification of HER-2/neu is uncommon in hepatocellular carcinoma

BACKGROUND： Hepatocellular carcinoma （HCC） is one of the most prevalent fatal cancers in the world. Despite advances in early diagnosis and improvements in surgical techniques, the survival of patients with HCC even after resection is poor because of the high incidence of recurrences. Therefore, the identification of prognostic factors may be helpful in the development of new treatment protocols. AIMS： To investigate HER-2/neu status in HCC by immunohistochemistry （IHC） and fluorescence in situ hybridisation （FISH）, and to explore the possibility of using trastuzumab in the treatment of HCC. METH ODS： Eight hundred and sixty eight surgical samples from patients with primary HCC were examined for their HER-2/neu status. IHC for HER-2/neu was performed with the HercepTest kit; FISH analysis was performed with the PathVysion HER-2 DNA probe kit. The correlations between HER-2/neu overexpression and clinicopathological characteristics were analysed statistically. RESULTS： HER-2/neu overexpression was detected in 21 （2.42%） of the 868 primary HCCs. Only one specimen showed HER-2/neu gene amplification by FISH. No significant associations were found between HER-2/neu overexpression and the clinicopathological parameters. CONCLUSIONS： There is a low frequency of HER-2/neu overexpression/amplification in HCC. There appears to be no role for HER-2/neu as a prognostic marker and no benefit of anti-HER-2/neu trastuzumab treatment in patients with HCC.     

The upregulation of glial glutamate transporter-1 participates in the induction of brain ischemic tolerance in rats.

Glial glutamate transporter-1 (GLT-1) plays an essential role in removing glutamate from the extracellular space and maintaining the glutamate below neurotoxic level in the brain. To explore whether GLT-1 plays a role in the acquisition of brain ischemic tolerance (BIT) induced by cerebral ischemic preconditioning (CIP), the present study was undertaken to observe in vivo changes in the expression of GLT-1 and glial fibrillary acidic protein (GFAP) in the CA1 hippocampus during the induction of BIT, and the effect of dihydrokainate (DHK), an inhibitor of GLT-1, on the acquisition of BIT in rats. Immunohistochemistry for GFAP showed that the processes of astrocytes were prolonged after a CIP 2 days before the lethal ischemic insult, which could protect pyramidal neurons in the CA1 hippocampus against delayed neuronal death induced normally by lethal ischemic insult. The prolonged processes extended into the area between the pyramidal neurons and tightly surrounded them. These changes made the pyramidal layer look like a 'shape grid'. Simultaneously, the prolonged and extended processes showed a great deal of GLT-1. Western blotting analysis showed significant upregulation of GLT-1 expression after the CIP, especially when it was administered 2 days before the subsequent lethal ischemic insult. Neuropathological evaluation by thionin staining showed that DHK dose-dependently blocked the protective role of CIP against delayed neuronal death induced normally by lethal brain ischemia. It might be concluded that the surrounding of pyramidal neurons by astrocytes and upregulation of GLT-1 induced by CIP played an important role in the acquisition of the BIT induced by CIP.