192Ir 血管内照射防止兔球囊血管成形术后再狭窄

目的本研究旨在检验192Ir血管内照射对兔球囊血管成形术后再狭窄的作用。方法建立兔髂动脉粥样硬化模型，对病变血管行球囊成形术，同时随机分为对照组，10?Gy照射组和18?Gy照射组。以导管导入192Ir放射性导丝对照射组动物的扩张处进行血管内照射。4周后处死动物，取出血管标本，进行病理组织学分析。结果 18?Gy照射组终管腔面积较对照组及10?Gy照射组大(P<0.05)，18?Gy照射组内膜面积较小(P<0.05)。结论本动物实验提示192Ir血管内照射可防止球囊血管成形术后再狭窄，其效果与照射剂量相关，其机制涉及抑制新生内膜增殖。

人类细胞和组织Ki-67基因exon 13的转录和表达

目的研究Ki-67基因在人类正常和异常细胞的mRNA 转录和翻译，了解其在肿瘤细胞增殖中的作用。方法以PCR扩增Ki-67基因的exon 13、codon 2的cDNA片断 (435?bp)，地高辛标计转录合成mRNA探针，原位杂交结合MIB-1免疫组化分析Ki-67基因的第13外显子（exon 13)在Hela细胞、结肠癌细胞、扁桃体和胰腺癌石蜡切片中的转录及翻译。结果应用地高辛标记的mRNA原位杂交技术可成功地在Hela 细胞、结肠癌细胞、扁桃体和胰腺癌的石腊切片检测到Ki-67 mRNA信号，结肠癌和胰腺癌细胞均存在Ki-67基因的exon 13 mRNA的过度转录，并且exon 13的转录与MIB-1所测Ki-67蛋白相一致。结论本研究首次在人类组织和细胞中，应用原位杂交和免疫组化研究Ki-67基因外旋子13的转录和翻译，研究发现结肠癌和胰腺癌Ki-67基因的exon 13的过度转录，并与其蛋白水平高度相关，提示该此基因表达异常，尤其是exon 13,在恶性肿瘤的发生和发展可能起一定作用。

Objective　To study the clinical characteristics of 2952 patients with epilepsy who had received drug treatment from the neurology outpatient clinics of eight major hospitals in Hong Kong.Methods　Retrospective review of outpatient records.Results　1601 (54.3%) males and 1351 (45.7%) females with a median age of 35.8 years (range, 10-94.8) were studied. Seizure types included generalized tonic-clonic in 80.7% of patients, complex partial in 28.3%, simple partial in 14.4%, atypical absence in 2.6% and myoclonic in 1.4%, and 30.4% of patients had more than one seizure type. EEG, CT brain, MRI brain and neuropsychological evaluation were obtained in 81.2%, 61.7%, 17.0% and 2.2% of patients, respectively. The etiology of epilepsy was cryptogenic in 59.9%, symptomatic in 35.1% and idiopathic in 3.9%; the commonest were intracranial infection, cerebral vascular disease, cranial trauma and perinatal insult. Phenytoin, carbamazepine and valproate were the most frequently used drugs and 25.9% of patients were taking more than two drugs. 48.3% of patients had active seizures in the past six months and 26.4% were considered to have unsatisfactory control of their epilepsy. Medical refractoriness of epilepsy was associated with a history of perinatal insult, intracranial infection, congenital brain malformation, intracranial neoplasm, cerebral vascular disease, hippocampal sclerosis, mental retardation and a history of status epilepticus (P<0.05). Conclusion　In this local cohort of adult patients with epilepsy under specialist care, there were a considerable number of patients falling into the category of cryptogenic epilepsy. Risk factors associated with medical refractoriness are similar to previous studies.

应用差异显示技术从高低转移癌系克隆出肿瘤转移相关基因G3BP

目的克隆肿瘤转移相关基因。方法应用倍比稀释法对人肺巨细胞癌PG进行单细胞克隆，并应用裸鼠异种接种及自发性转移体内实验对各亚系的转移潜能进行鉴定。以具有不同转移潜能的癌细胞亚系为研究对象，应用mRNA差异显示技术克隆差异片段, sanger双脱氧末端终止法测序及自动双向测序获得其碱基序列, 与GenBank数据库进行同源性比较。在两组具有不同转移潜能的癌细胞亚系（人肺癌，前列腺癌）中Northern杂交验证表达差异。结果两个具有不同转移潜能的亚系BE1和LH7，在完全相同的遗传背景下，亚系BE1在裸鼠体内100%成瘤，100%转移；亚系LH7在裸鼠体内100%成瘤，无一例转移。二者转移表型的显著差异必然反映了转移相关基因表达与调控的差异。因此该系统是mRNA差异显示的良好模型。应用mRNA差异显示技术克隆差异片段, 一个849?bp片段在高转移亚系BE1中低表达，而在不转移亚系LH7高表达，二者差异显著，在重复实验中得到了验证。成功的回收该片段，连接入pGEM-T载体，经sanger双脱氧末端终止法测序及自动双向测序获得其碱基序列,经GenBank Blastn检索，与G3BP（U32519）同源性高达99%。Northern杂交显示G3BP在LH7高表达（约3.3?kb），而在BE1中低表达，验证了差异显示的结果，排除了假阳性的可能性。为了进一步探讨这一规律,我们引入了另一组来自人前列腺癌PC-3M的具有不同转移潜能的亚系(我室建立)：亚系1E8在裸鼠体内转移率100%，亚系2B4在裸鼠体内转移率0。Northern杂交显示G3BP在高转移亚系1E8中表达显著低于不转移亚系2B4，符合上述规律,即G3BP的表达降低与高转移潜能具有相关性。G3BP由法国Rhone-Poulenc Rorer实验室于1996年克隆，在血清刺激的而非静止状态的中国仓鼠肺成纤维细胞中，G3BP与GAP-SH3功能区牢固结合， G3BP 具有DNA/RNA解旋能力以及内源性核糖核酸酶（RNase）活性，G3BP可在多个位点断裂c-myc mRNA的3’非编码区，导致c-myc mRNA的降解。通过G3BP 将RNA的稳定性与上游Ras信号传导通路联系起来，为我们勾划出一个新的Ras信号传导通路:Ras可能通过GAP和G3BP控制新合成的mRNA的稳定性来传导信号。基于其所处的关键位置，G3BP已引起广泛的关注。结论 G3BP在高低转移癌系中的表达具有显著差异，G3BP的表达降低与高转移潜能具有相关性，提示G3BP可能参与肿瘤的转移过程，为G3BP功能的研究提供了新的线索。

脂肪组织源性肿瘤与抑癌基因p53关系的研究

目的从蛋白表达及基因水平探讨脂肪组织源性肿瘤与p53基因的关系。方法 LSAB免疫组化法, PCR-SSCP及DNA序列分析方法。 结果 p53蛋白只在脂肪肉瘤中表达，阳性率为48.08%(25/52)。不同类型脂肪肉瘤，分化良好者阳性率30.00%(9/30),低于分化较低者(P<0.005)．p53第6、7、8外显子PCR-SSCP分析，2例多形性脂肪肉瘤出现异常泳动带。DNA序列分析证实1例第8外显子第268位编码区出现错义突变(AACATC),另1例第6外显子第221位编码区出现可疑杂合同义突变(GAGGAA)。结论 p53蛋白与脂肪肉瘤的形成及分化和恶性程度有关。p53蛋白表达可作为判断脂肪肉瘤分化程度及恶性程度参考指标之一。脂肪肉瘤中p53 基因第6、8外显子分别存在点突变。

肝移植后乙肝复发的预防和治疗

目的探讨原位肝移植治疗乙型肝炎相关疾病的效果及Lamivudine在防治肝移植后乙肝复发中的作用。方法 10例患者接受了原位肝移植，其中9例男性为乙肝患者，1例女性为肝癌患者，术前无乙肝感染。9例乙肝患者中，6例并有不同程度的肝性脑病，1例并肝肾综合征，1例并上消化道大出血。9例乙肝中，7例服用Lamivudine预防术后乙肝复发。结果 8例存活2-12个月，2例死亡。存活的8例中，7例为乙肝患者，仅1例术后6个月出现HBsAg(+)，但全部均肝功能良好；另1例为肝癌患者，术后6个月出现乙肝。死亡的2例中，1例为术后乙肝复发暴发性肝功能衰竭所致，另1例死于术后多器官功能衰竭。结论原位肝移植加Lamivudine是治疗乙肝和肝细胞癌病例的有效方法。Lamivudine在观察期内可预防乙肝移植后乙肝复发。

大鼠慢性阻塞性肺疾病模型气道和肺组织M受体水平及溴化异丙托品的影响

目的观察大鼠慢性阻塞性肺疾病（COPD）模型气道和肺组织M受体水平，以及吸入溴化异丙托品对M受体的影响及其规律。方法通过长期吸入高浓度SO2气体的方法（250?ppm, 5?h/d, 5?d/wk, 共7?wk）建立COPD模型, 大鼠在密闭箱内吸入雾化的0.025%溴化异丙托品溶液10?ml（2次/d, 20?min/次），采用放射配基结合法，分别测定正常大鼠、吸入和未吸入异丙托品大鼠气道和肺组织的M受体。结果支气管肺病理学及肺功能检查显示，大鼠长期吸入高浓度SO2气体可引起与人类COPD相似的病理生理改变。COPD大鼠气道和肺组织M受体的密度（0.038±0.011?pmol/mg蛋白质）及亲和力（Kd, 23±11?pmol/L）与正常大鼠相比（分别为0.030±0.008，29±19）无明显变化（P>0.05）。吸入异丙托品30天后，气道和肺组织M受体密度显著升高(P<0.05)，停药6天后，M受体的密度恢复正常。 结论长期吸入高浓度SO2可制备与人类COPD病理生理改变相似的大鼠模型。COPD大鼠气道和肺组织M受体的数量及功能无异常改变，但长期应用异丙托品可使M受体上调。

甲型流感病毒H9N2亚型毒株血凝素基因特性的研究

目的了解人甲型流感病毒H9N2亚型毒株的来源及从分子生物学角度来弄清不同宿主来源的H9N2亚型毒株间相互关系。方法病毒在鸡胚中传代，从收获的尿囊液中提取病毒粒RNA，通过逆转录合成cDNA。cDNA通过PCR进行扩增，接着PCR产物用纯化试剂盒进行纯化。而后，RNA序列测定是采用双脱氧链末端终止和克隆法。后用MegAlign（1.03版）和Editseq（3.69版）软件进行种系发生学分析。结果从中国所分离出的H9N2亚型毒株。它们的HA1与HA2间裂解部位的氨基酸序列均为R-S-S-R，除一株鸽病毒其HA蛋白分子上仅含7个潜在的糖基化位点外,而其余的均含8个。6株H9N2毒株HA蛋白分子上氨基酸序列有2-16个不同，这些不同分布在24个不同的位点上。近来在中国同时流行着多种HA基因系的H9N2亚型毒株。结论人甲型流感病毒H9N2亚型毒株可能性大来自鸡的H9N2毒株，而不是来源于鸽的H9N2毒株。但，H9N2毒株是否具有人传人能力，至今仍不清楚。在中国同时流行着多种HA基因系的H9N2毒株。

涎腺淋巴瘤临床与病理研究

目的探讨涎腺粘膜淋巴瘤的病理诊断特征及发病机理。方法分析临床资料，利用HE染色，白细胞共同抗原、CD20、CD45RO、上皮膜抗原的SP法免疫组化及电镜观察32例涎腺粘膜淋巴瘤。结果男性27例，女性5例，平均年龄54.76岁，其中腮腺17例，颌下腺15例。涎腺粘膜淋巴瘤是由弥漫性中心细胞样(CCL)细胞组成，并有“淋巴上皮病变”。免疫组化：CCL细胞CD20阳性、CD45RO阴性。电镜下瘤细胞圆形，高核浆比，胞浆内少量溶酶体和免疫球蛋白的颗粒，无胞质丝，无细胞外基膜，无细胞间连接。随访:存活5年以上者9例，3～4年者5例，不足1年6例，3例死亡。结论大多数涎腺粘膜淋巴瘤为低度恶性，瘤细胞有“回归"现象，治疗以手术加化疗为主，少数可转变为高度恶性，预后差。自身免疫性疾病和/或感染可导致机体产生获得性涎腺粘膜淋巴瘤，并在持续性刺激下发展为涎腺肌上皮炎，进而转变为涎腺粘膜淋巴瘤。

氧化砷通过线粒体跨膜电位下降与激活Caspase-3诱导多发性骨髓瘤细胞凋亡

目的探讨氧化砷(As2O3)是否诱导多发性骨髓瘤细胞凋亡与其可能机制。方法以两株多发性骨髓瘤细胞系RPMI8226和U266为体外模型。以细胞形态学观察、流式细胞仪检测亚G1期细胞含量以及DNA凝胶电泳判定细胞凋亡。通过检测胞内Rhodamine123染色强度来判定线粒体跨膜电位。通过Western印迹分析蛋白表达。结果 0.1-0.5?μmol/L As2O3抑制RPMI8226与U266细胞系生长，2.0?μmol/L As2O3诱导两株细胞凋亡，而1.0?μmol/L As2O3抑制细胞生长同时也诱导部分细胞凋亡。As2O3诱导的细胞凋亡伴随线粒体跨膜电位下降与细胞凋亡，而二巯基苏糖醇(二巯基还原剂)则部分抑制以上效应。虽然全反式维甲酸(ATRA)诱导RPMI8226细胞凋亡，但是它与As2O3无协同效应。结论不同深度As2O3可抑制多发性骨髓瘤细胞生长与诱导细胞凋亡。线粒体是As2O3诱导细胞凋亡的重要且共同的“靶子”。

螺旋CT仿真喉镜、三维重建和多平面重组在喉及下咽癌的临床应用价值

目的探讨螺旋CT仿真喉镜(CTVL)、三维重建(3D)和多平面重组(MPR)在喉及下咽癌的临床应用价值。方法 22例喉及下咽癌患者进行轴位螺旋CT扫描，同时做MPR、3D和CTVL成像，并与纤维喉镜、手术所见对照分析。结果螺旋CT轴位结合MPR图像对术前肿瘤分期和诊断颈部淋巴结转移的准确性都是95%；23%的病例MPR显示肿瘤侵犯的范围优于轴位，3D重建可立体显示肿瘤的侵犯范围及其与血管、气管的关系；头端CTVL显示喉及下咽部腔内病变的部位、大小及侵犯范围与纤维喉镜所见相似，3例从足侧观察肿瘤与声带和前联合的关系弥补了纤维喉镜的不足。结论螺旋CT轴位图像能很好地显示喉及下咽癌的部位、大小及其侵犯范围，MPR和3D重建是轴位图像的有力补充，CTVL能清楚显示喉及下咽部的腔内结构，是纤维喉镜的很好补充手段。

不稳定型心绞痛的择时冠状动脉内支架治疗

目的观察紧急支架术治疗不稳定型心绞痛（UAP）的疗效和安全性，并与延迟支架术治疗作比较。方法 55例UAP患者随机于入院后48小时内（29例；早期介入组）或7-10天后（26例；延迟介入组）行冠状动脉造影及支架术。观察两组手术成功率、心绞痛缓解时间、住院时间和30天总心脏事件发生率。结果两组的临床特征和冠状动脉病变严重性相似。早期介入组中手术成功率与延迟介入组无显著差异（93%和96%），但早期介入组心绞痛缓解时间（4.4±3.1天）和住院时间（8.8±3.2天）较延迟介入组（5.7±2.9天和13.5±3.1天，P均<0.05）明显缩短。早期介入组30天总心脏事件发生率较延迟介入组明显减低（0%和19.2%，P<0.05）。结论不稳定型心绞痛时，早期冠状动脉内支架术治疗安全、有效。

99mTc-RBC连续减影显像诊断胃肠出血的临床价值

目的 99m Tc-RBC连续减影显像为早期诊断胃肠出血提供了新的手段。本文评价其临床应用价值。 方法用数字Υ相机对90例疑诊胃肠出血患者行99m Tc体内标记红细胞胃肠出血显像。每帧5分钟，连续采集60分钟，得到12帧常规非减影图像（CNS）。12帧动态图像用计算机以t+5分钟为时间轴作连续减影处理，得到11帧减影图像（SSS）。若早期显像结果为阴性或怀疑有再出血时行3、6或24小时延迟显像。结果 90例疑诊胃肠出血患者中，62例确诊为活动性胃肠出血。图像以30分钟、60分钟以及24小时内三个时间段进行分析。SSS的灵敏度分别为87%（30分钟）和92.8%（60分钟），明显高于CNS的56.4%（30分钟）和63.9%（60分钟）。24小时延迟显像CNS的灵敏度增至85.4%。两种方法的特异性之间无明显差异。62例确诊病人中42例经手术明确出血部位。SSS的定位诊断符合率为92.8，明显高于CNS的73.8%。结论 99mTc-RBC连续减影显像是一种早期诊断胃肠出血的有效方法，较之常规非减影显像能够更早期、更准确地对微量胃肠出血作出定性定位诊断。

双功能逆转录病毒载体介导耐药基因转染人脐血CD34+细胞能增强联合化疗抗性

目的为探讨转染醛脱氢酶基因（ALDH1）和多药耐药基因 (MDR1)的人脐血CD34+细胞能否同吮增强对活性环磷酰胺（4-HC）和P-gp转运泵靶药的抗性。方法构建了同时含ALDH1和MDR1双耐药基因的逆转录病毒表达质粒G1Na-ALDH1-IRES-MDR1，经LipofectAMINE介导转染GP+E86和PA317包装细胞，采用含长春新碱（VCR）和4-HC的培养基克隆选择后，收集重组病毒上清于单向型与双嗜型包装细胞行乒乓交互感染，获得PA317重组病毒生产细胞（高滴度达5.6×105?CFU/ml），将含ALDH1和MDR1耐药基因重组病毒上清在细胞生长因子刺激下重复感染人脐血CD34+细胞。结果经PCR,RT-PCR, Southern blot, Northern blot, FACS和MTT方法检测显示外源ALDH1与MDR1基因已经整合入转染靶细胞中基因组并获得有效表达，同时传递不同的耐药表型。经耐药基因修饰的脐血CD34+细胞对4-HC和P-gp转运泵靶药同时产生抗性，其IC50值分别比未转染细胞高4倍（4-HC）, 5.5倍(柔红霉素-DNR)和7.2倍(VCR)。结论双功能逆转录病毒载体介导两种不同耐药基因转染人脐血CD34+细胞能增强联合化疗抗性，本基因转移系统的建立为开展肿瘤基因治疗的临床研究奠定了实验基础。

抗人血小板Tetraspanin (CD9)单克隆抗体以不依赖Fc受体的方式激活血小板整合素αⅡbβ3

目的研究2种抗人血小板tetraspanin单克隆抗体HI117和SJ9A4引起的血小板整合素活化及其机制。方法用125 Ⅰ标记的人纤维蛋白原，测定HI117和SJ9A4引起的纤维蛋白原与人血小板的特异的结合，表明这2种单抗激活血小板整合素αⅡbβ3。结果 HI117和SJ9A4(10?μg/ml和20?μg/ml)引起纤维蛋白原与人血小板特异的结合，表明这2种单抗引起血小板整合素αⅡbβ3激活，进一步研究表明这种激活不依赖血小板Fc受体，而且HI117和SJ9A4引起的血小板整合素αⅡbβ3激活可由于以Sphingosine、Aspirin、αβ、rase和成PGI2预处理血小板而被抑制。结论抗人血小板tetraspanin (CD9)单克隆抗体HI117和SJ9A4能引起血小板整合素αⅡbβ3激活且不依赖Fc受体，3种信号途径即血栓烷，分泌ADP和CAMP途径可能涉及这一过程，蛋白激酶C激活可能是这3个途径的共同步骤。

CYP11B2基因在肝脏的表达及安体舒通对肝纤维化大鼠的治疗作用

目的业已证明，醛固酮可以促进纤维化的形成，血管、脑及肝脏等肾上腺外组织能够合成醛固酮。本实验意在研究醛固酮合成酶基因—CYP11B2在正常与肝纤维化大鼠肝组织中的表达，评价安体舒通的治疗作用。方法取雄性Wistar大鼠160只，体重250克左右，随机分为4组，每组40只。模型组：CCl4油0.25?ml/100?mg皮下注射，每周三次；安体舒通组：CCl4 油注射的同时予以安体舒通20?mg*kg-1*d-1灌胃，1次/日；马洛替酯组：CCl4油注射的同时予以马洛替酯50?mg*kg-1*d-1灌胃，1次/日；对照组：橄榄油皮下注射。于第2、4、6、8和10周宰杀动物，光镜及电镜下动态观察组织学改变，图像分析仪测量胶原面积。RT-PCR和原位杂交检测CYP11B2在正常及纤维化大鼠肝脏的表达。结果原位杂交及RT-PCR显示CYP11B2表达定位于肝星形细胞胞浆，在纤维化形成时表达增强。第四、六周，安体舒通组肝纤维化分级、胶原面积低于模型组（P<0.05），安体舒通组与马洛替酯组无明显差异（P>0.05）。第八、十周，安体舒通组肝纤维化分级,胶原面积高于马洛替酯组（P<0.05）。安体舒通组与模型组相比差异无显著意义（P>0.05）。结论 CYP11B2在纤维化肝脏的星形细胞中表达增强。安体舒通对早期肝纤维化具有一定的治疗作用。

全仅式维甲酸(ATRA)和三氧化二砷(As2O3)对APL细胞组织因子表达的影响

目的探讨全反式维甲酸（ATRA）和三氧化二砷（As2O3）在体内外对急性早幼粒细胞性白血病（APL）细胞组织因子（TF）表达的影响。方法利用复钙时间测定、ELISA和RT-PCR等方法，分别检测了ATRA和As2O3治疗前后APL患者骨髓单个核细胞的促凝活性、TF抗原及其mRNA的转录水平，同时还检测了使用ATRA和As2O3处理APL细胞株NB4细胞和NB4-R1细胞以及转染PML-RARa融合基因的U937细胞的促凝活性、TF抗原及其mRNA的转录水平。结果 ATRA和As2O3在体内和体外均可以时间依赖的方式下调NB4细胞的促凝活性、TF抗原水平以及TF mRNA的转录。转染PML-RARa融合基因的U937细胞与仅转染逆病毒载体的U937细胞相比，其TF表达水平显著升高；使用ATRA或As2O3分别处理转染PML-RARa和转染逆病毒载体的U937细胞，其TF抗原水平均显著降低。结论 ATRA和As2O3均可下调APL细胞TF的表达并降低其PCA，As2O3在诱导APL细胞凋亡的同时有可能通过下调APL细胞TF的表达而改善APL患者与DIC相关的出血症状。结果还提示APL细胞染色体易位产生的融合蛋白PML-RARa可能对TF的异常表达有一定的影响，而ATRA和As2O3对TF的下调作用可能不依赖于对融合蛋白PML-RARa的降解。

树突状细胞和巨噬细胞对外源性抗原内吞路径的比较研究

目的观察并比较小鼠树突状细胞(DC)和巨噬细胞对外源性抗原的内吞路径的差异。方法将小鼠骨髓DC和腹腔巨噬细胞与辣根过氧化物酶(HRP)-5 nm胶体金共孵育10分钟后再培养0～120分钟，进行酸性磷酸酶细胞化学反应和组织相容性抗原(MHC)Ⅱ免疫胶体金标记，后在电镜下观察5 nm胶体金的细胞内运行路径。结果 DC内吞HRP-5 nm胶体金10分钟后再培养30分钟，大部分5 nm胶体金进入MHC Ⅱ隔室(MⅡC)中，只有极少数酸性磷酸酶阳性的溶酶体内含少量5 nm胶体金。而与DC显著不同的是巨噬细胞摄入的大部分5 nm胶体金进入了溶酶体，还有部分5 nm胶体金进入MⅡC中。内吞后再培养60分钟，DC内仍有许多5 nm胶体金，而巨噬细胞内已很少见到5 nm胶体金。结论同一种外源性抗原被DC和巨噬细胞内吞后，在这两类细胞中的运行路径明显不同。内吞后30分钟，巨噬细胞摄入的大部分抗原进入溶酶体，而DC则将大部分抗原送入MⅡC，这可能与DC独特的抗原提呈功能有关。另外，巨噬细胞对抗原的清除能力比DC强得多。

声门上型喉癌颈淋巴结隐匿性转移的病理特点

目的探讨声门上型喉癌颈淋巴结隐匿性转移的病理特点和规律，帮助临床治疗。方法对100例临床N0的声门上型喉癌患者和颈廓清标本（153侧）进行连续切片，光镜观察。结果隐匿性转移率为38%。发现转移淋巴结51个:Ⅰ区1个（2％）、Ⅱ区37个（73％）、Ⅲ区12个（23％）、Ⅳ区1个（2％）。转移淋巴结的长径0.5-2.6?cm，平均为1.1?cm。51个淋巴结中，癌早期21个（41％)、癌长期18个（35％）、癌满期7个（14 ％）、破膜期5个（10％）。结论声门上型喉癌颈淋巴结的隐匿性转移率高，早期不易诊断，应积极行选择性颈廓清术。

Objective　To investigate the prevalence of significant enterococcal isolates from urine and determine what factors are associated with the increased prevalence, with particular reference to antibiotic susceptibilities. Methods　Retrospective analysis over an 8-year period of hospital laboratory records of urinary isolates of enterococci was done. Species were identified via colony morphology, growth in 6.5% sodium chloride and their ability to hydrolyze esculin in the presence of 40% bile salts. Susceptibility testing via the disc diffusion technique with 9 commonly used antibiotics was also done as defined by the National Committee for Clinical Laboratory Standards.Results　From 39?881 urine specimens, 9116 (22.9%) were culture positive. Of this 9116, 1001 (11.0%) were enterococci, the 4th most common urinary isolate. E. coli was the most common (36.2%). Most enterococci were from pediatric patients (28.4%) and the urology unit (24.5%). All enterococci were fully sensitive to ampicillin and augmentin (amoxicillin-clavulanic acid). Sensitivity to gentamicin decreased significantly from 79% in 1990 to 58% in 1997 (P<0.005). Sensitivity to the cephalosporins and nitrofuratoin were relatively stable, but sensitivity to nalidixic acid varied. No resistance to vancomycin was detected during the study, and no cases of bacteremia complicated bacteriuria were seen.Conclusion　Isolation of enterococci was relatively stable during the 8-year period, and all isolates were fully sensitive to the older β-lactams, ampicillin, cefaclor and augmentin, but displayed varying degrees of multi-resistance to other commonly used urinary agents such as nalidixic acid and co-trimoxazole (trimethoprim-sulfamethoxazole). Because of the emergence of multi-resistant enterococci in many countries, and the high cost of drugs in our society, it is imperative that vigilance be maintained in monitoring enterococcal infections in hospitals.

Subfertility can be caused by acquired or genetic factors. Y chromosome microdeletion is one of the genetic factors associating with male infertility.1 Azoospermia factors (AZFa, AZFb and AZFc) have been mapped to different subregions in Yq11.2 So far, two gene families, RNA-binding motif (RBM) and deleted in azoospermia (DAZ) from interval 6, were proposed as candidate spermatogenesis genes for AZF.3,4 Recent studies demonstrated that microdeletions were detected at a frequency of 5% to 18% in the AZF region of oligospermic and azoospermic men.5-7 With the development of assisted reproductive technologies, particularly intracytoplasmic sperm injection (ICSI), these men can now father a child and the genetic abnormalities in defective spermatozoa could be transmitted to future offspring. To examine the possible transmission of the Y-chromosome microdeletion to the offspring via ICSI treatment, we performed both cytogenetic and molecular analyses of the Y chromosome on both an infertile patient with Y chromosome microdeletion and his offspring.

Purpose and Methods　Open-heart surgery with the use of cardiopulmonary bypass (CPB) is associated with an inflammatory cascade which contributes to the development of postoperative complications including multiple organ failure. To provide an update on the subject, we briefly review the recent English-language literature.Results　During CPB, various factors have been recognized to induce a complex inflammatory response. Based on an enhanced understanding of the underlying mechanisms, therapeutic strategies have been developed to reduce this inflammatory reaction and its subsequent damaging effects. Off-pump coronary artery bypass grafting may result in less inflammatory injury as compared with the conventional maneuver, which can in turn, diminish the incidence of cardiac, renal, or neurological dysfunction. It is also clear that improving the biocompatibility of CPB materials can lead to a better patient recovery. Inasmuch as the pathophysiology involved appears to be multifactorial, it is unlikely that a single intervention could achieve the desired goal. Both pharmacologic strategies, such as steroid pretreatment, and modification of mechanical devices, such as the use of heparin-coated CPB circuits, could have important clinical implications. The balance between pro- and anti-inflammatory responses may be crucial in limiting the extent of inflammatory injury. Conclusions　To date, the concept of organ protection should no longer be limited to the individual organ. Instead, investigations must be extended to focus on a systemic level.

Purpose　To investigate the role of cationic antimicrobial protein of Mr 37?kDa (CAP37) a neutrophil-derived inflammatory mediator on endothelial cell function.Data sources　Endothelial cells used in this study were obtained from human lung microvessels and rat aorta. The latter was a kind gift of Dr. Paula Grammas. The mono-mac 6 cell line used in this study was the generous gift of Dr. H.W. Loms Ziegler-Heitbrock.Study selection and data extraction　Endothelial cell proteins kinase C activity was determined by measuring calcium- and phospholipid-dependent phosphorylation of histone. Endothelial cell migration was determined using CostarTM Transwell apparatus. Cell surface expression of adhesion molecules, ICAM-1 and PECAM-1 was determined using flow cytometry. RT-PCR was used to amplify the CAP37 from endothelial cells treated with LPS.Results　We demonstrated that CAP37 which was originally identified as having potent antimicrobial activity and chemotactic activity for monocytes was capable of modulating endothelial cell functions. CAP37 activated endothelial cell protein kinase C in a dose- and time-dependent fashion. Importantly CAP37 increased the adhesive properties of the endothelium for monocytes. CAP37 upregulated the well known adhesion molecules, ICAM-1 and PECAM-1 in a dose- and time- dependent manner. In addition, CAP37 promoted endothelial cell migration. Further investigations indicated that CAP37 was induced in endothelial cells in response to pro-inflammatory cytokines such as tumor necrosis factor-α and interleukin-1α as well as inflammatory mediators such as lipopolysaccharide. Unstimulated endothelial cells did not constitutively express CAP37. The cDNA sequence of endothelial CAP37 was determined and found to be highly homologous to the sequence obtained for neutrophil-derived CAP37.Conclusions　Our studies strongly suggest that CAP37 plays a pivotal role in monocyte-endothelial interactions and the transmigration of monocytes from the vasculature into extravascular tissues.

Chinese Medical Journal (CMJ) and its electronic version are published monthly by the Chinese Medical Association and distributed worldwide. Manuscripts are welcome from any part of the world and should be sent to the Editorial Office, Chinese Medical Journal, Chinese Medical Association, 42 Dongsi Xidajie, Beijing 100710, China.Manuscripts. Manuscripts are received with the understanding that they have not previously been published in English and are not under simultaneous consideration for another publication and electronic medium. A complete report following presentation or publication of preliminary findings elsewhere (e.g., in an abstract) can be considered. A covering letter and an introduction letter from author's institution are needed. For multicenter clinical trial, at least one person's name must accompany a group name-e.g., Zhu Wenling, for the Collaborative Study Group on Thrombolysis with China-made Recombinant Streptokinase. All persons who meet the criteria for authorship as stated in the Uniform Requirements for Manuscripts Submitted to Biomedical Journals are listed as authors who must make substantial contributions to: ① conception and design, or analysis and interpretation of data; ② the drafting of the article or critical revision for important intellectual content; and ③ the final approval of the version to be published. All three conditions must all be met.