临床胃粘膜活检及胃癌手术标本纤维连结蛋白的定位观察

采用免疫组化及免疫电镜技术对临床胃粘膜活检及胃癌手术标本进行了纤维连结蛋白(FN)的定位观察。结果,FN见于胃粘膜上皮细胞和部分癌细胞内以及各种基底膜、间质中。肠化及异型增生上皮细胞FN染色增强,胃癌细胞和其基膜FN减少缺失且与癌细胞分化程度相关,胃癌间质FN丰富,尤其以癌浸润前缘明显。本文着重讨论了胃癌FN改变与癌细胞生物学特性的关系。     

三维斑点追踪技术预测急性心肌梗死患者近期急性心衰风险的研究

目的:分析三维斑点追踪技术预测急性心肌梗死(AMI)患者近期发生急性心衰的诊断价值。方法:选取医院诊治的155例AMI患者,均予抗血小板聚集、改善心肌供血等对症治疗,并对患者出院后进行为期3个月的随访,除3例患者失联外,将剩余152例患者纳入随访结果研究。将152例患者中出现急性心力衰竭的43例患者纳入心衰组,未出现心力衰竭的109例患者纳入无心衰组。比较两组患者的年龄、性别等一般资料,并对患者N-末端脑钠肽前体(NT-pro BNP)、超敏C反应蛋白(hs-CRP)、肌钙蛋白I(cTnI)等临床常用指标及三维斑点相关指标进行比较。结果:心衰组患者的年龄、NT-proBNP、hs-CRP、c Tn I及左室收缩末期容积指数(LVESVI)均明显高于无心衰组,差异有统计学意义(t=2.279,t=3.385,t=2.212,t=2.943,t=2.289;P<0.05),射血分数(EF)、左室整体径向应变(GRS)、整体圆周应变(GCS)、整体纵向应变(GLS)及整体面积应变(GAS)明显低于无心衰组,差异有统计学意义(t=6.606,t=2.804,t=2.945,t=7.226,t=2.687;P<0.05);而两组患者的性别、合并高血压等一般资料及肾小球滤过率(e GFR)、LVEDVI等指标间差异均无统计学意义;多因素logistic分析提示,NT-pro BNP、LVESVI是影响急性心衰的独立危险因素(OR=1.002,OR=1.118;P<0.05),EF、GLS则是其独立保护因素(OR=0.795,OR=0.452;P<0.05);受试者工作特征(ROC)曲线提示GLS预测急性心衰的ROC曲线下面积(AUC)为0.881,显著高于NT-pro BNP、LVESVI及EF(Z=2.751,Z=3.107,Z=2.895;P<0.05),其诊断的最佳截点<13.42%,此时其灵敏度为95.3%,特异度为67.9%。结论:三维斑点追踪技术可以对急性AMI患者近期发生急性心衰进行有效地预测,具有较高的灵敏性及诊断效能,可以应用于急性AMI患者心衰的早期预测。     

义眼台取出的原因分析

目的分析义眼台取出的原因。方法回顾本科2001年9月至2004年8月期间收治的义眼台取出22例。结果义眼台暴露20例，义眼台感染10例，无纤维血管化4例。结论义眼台暴露，感染及无纤维血管化等是义眼台取出的常见原因。     

Flk-1特异性蛋白激酶抑制剂SU5416阻断小鼠Lewis肿瘤新生血管形成并延长生存期

Objective:To reveal the mechanism and effect of SU5416 in the treatment of mouse Lewis cancer in vivo.Methods:Lewis cell was transplanted into groin of C57/B6 mouse by subcutaneous injection,then SU5416 was administrated intraperitoneally to investigate the impact of SU5416 on tumor angiogenesis and growth in vivo.32 mice were treated with SU5416 at two different doses every day until the end-point.As a control,8 mice received no treatment and 8 mice were treated with vehicle (DMSO) only after implantation.Results:Median survival in the treated group was statistically longer compared to that in the control groups (P＜0.05) and no significant systemic adverse was observed.Histological analysis of the treated tumors showed an increase in necroses and reduced in angiogenesis compared to the control tumors.Furthermore,the percent of apoptotic cells increased in the treated tumors by FCM,the expressions of VEGF and KDR had no change after SU5416 administration by western blot,Conclusion:SU5416 may be useful therapeutics drug that specifically inhibits the enzymatic activity of KDR kinase and could down regulate the tumor angiogenesis.     

Flk-1特异性蛋白激酶抑制剂SU5416阻断小鼠Lewis肿瘤新生血管形成并延长生存期

Objective  To reveal the mechanism and effect of SU5416 in the treatment of mouse Lewis cancer in vivo. Methods  Lewis cell was transplanted into groin of C57/B6 mouse by subcutaneous injection, then SU5416 was administrated intraperitoneally to investigate the impact of SU5416 on tumor angiogenesis and growth in vivo. 32 mice were treated with SU5416 at two different doses every day until the end-point. As a control, 8 mice received no treatment and 8 mice were treated with vehicle (DMSO) only after implantation. Results  Median survival in the treated group was statistically longer compared to that in the control groups (P < 0.05) and no significant systemic adverse was observed. Histological analysis of the treated tumors showed an increase in necroses and reduced in angiogenesis compared to the control tumors. Furthermore, the percent of apoptotic cells increased in the treated tumors by FCM, the expressions of VEGF and KDR had no change after SU5416 administration by western blot. Conclusion  SU5416 may be useful therapeutics drug that specifically inhibits the enzymatic activity of KDR kinase and could down regulate the tumor angiogenesis. Supported by a grant from the National Key Project of Scientific and Technical Supporting Programs funded by Ministry of Science & Technology of China (No. 2006BAI02A05).     

63例老年眼附属器淋巴组织增生性疾病临床及病理分类研究

目的分析老年眼附属器淋巴组织增生性疾病的临床特点及病理分类。方法回顾性分析60岁以上眼附属器淋巴组织增生性疾病63例患者的临床、病理资料,并予以分类。结果63例眼附属器淋巴组织增生性疾病中反应性淋巴组织增生7例（11.1%）,不典型淋巴组织增生5例（7.9%）,淋巴瘤51例（81.0%）,各类型病变临床特征相似;51例眼附属器淋巴瘤中,有45例为黏膜相关淋巴组织边缘带B细胞淋巴瘤（MALT-EMZL）。结论老年眼附属器淋巴组织增生性疾病临床表现无特异性,大多数为低度恶性的淋巴瘤,病理检查是分类与鉴别诊断的主要依据,免疫组织化学技术能进一步明确诊断。     

拉米夫定治疗HBV DNA阳性慢性重型乙型肝炎疗效分析

目的为了阻断HBV诱导的免疫性肝损伤、提高慢性重型肝炎患者的存活率,我们采用拉米夫定治疗血清HBV DNA阳性的慢性重型乙型肝炎患者,观察治疗效果与不良反应发生情况。方法 106例慢性重型乙型肝炎患者,入院时血清HBVDNA阳性而其它肝炎病毒血清学指标阴性,并排除妊娠性和酒精性肝病。随机分为A、B两组,A组在护肝、促进肝细胞再生、降酶、利胆等一般综合疗法的基础上加服拉米夫定100mg,每晚1次,不再使用其它抗病毒药物;B组仅采用一般综合疗法。两组患者住院日均大于30d,观察疗程均为1年,治疗中肝功能恢复后又出现异常者为肝炎再活动。所有病例入院时、入院后每月定期采血用ELISA法检测HBVM,荧光定量PCR法检测HBV DNA;同时观察血清总胆红素、血常规及甲胎蛋白等指标。结果 A组患者存活率为67.9％(36/53),与B组(49.1％,26/53)比较具有显著性差异(P<0.05)。存活患者中,A组HBeAg、HBV DNA阳性率分别为25.0％(9/36)、5.6％(2/36),B组分别为61.5％(16/26)、84.6％(22/26),两组差异有高度显著性(P均<0.01);A组血清HBV DNA阳性者的HBVDNA平均含量(103.8±126.0 copy/μl)也显著低于B组(5 196.4±2 353.8 copy/μl)(P<0.01),两者与入院时(3 944.7±859.6 copy/μl)比较,差异均有高度显著性(P<0.01)。A组TBiL复常时间(98.5±21.3d)比B组(124.7±32.0d)明显缩短(P<0.01),1年后肝炎再活动率(13.9％,5/36)明显低于B组(65.4％,17/26)(P<0.01)。A组中仅个别患者出现轻度腹泻,未见血常规和甲胎蛋白检测异常。结论拉米夫定能够抑制HBV DNA合成,减少新表达的靶抗原量,使炎症反应逐渐缓解。本研究发现,应用拉米夫定治疗血清HBV DNA阳性的慢性重型乙型肝炎,可促使HBeAg和HBV DNA转阴,且血清HBV DNA未转阴者的HBV DNA平均含量也显著低于对照病例与自身治疗前水平,说明患者体内HBV DNA的复制受到抑制。相反,对照病例经一般综合治疗后血清HBV DNA阳性者的HBV DNA平均含量不仅明显高于拉米夫定治疗患者,还明显高于自身治疗前水平,表明未采用拉米夫定治疗患者体内仍存在HBV DNA大量复制。我们还观察到经拉米夫定治疗后,患者TBiL复常时间明显缩短,肝炎再活动率也明显降低,说明拉米夫定能够促进肝功能的恢复、减少肝炎的复发。此外,拉米夫定副作用少见,对造血系统和肝细胞增生无明显抑制作用。上述机制可能与本研究中采用拉米夫定治疗时患者生存率较高有关。本研究证明:拉米夫定是治疗慢性重型乙型肝炎、抗HBV的安全有效药物。     

无症状HBsAg携带者血游离HBV-DNA动态变化的流行病学意义

本文对65例无症状HBsAg携带者(ASC)的血清乙型肝炎病毒脱氧核糖核酸(HBV-DNA)进行了1~2年随访观察,并对不同HBV-DNA动态变化类型ASC的e抗原、DNA多聚酶(DNAP)、乙肝病毒表面抗原多聚白蛋白受体(HBsAg-PHSA-R)等乙肝病毒(HBV)复制标志及肝功能作了检查和比较,对部分ASC的家庭成员HBV感染情况作了调查。结果表明,在ASC中存在着传染性强的HBV-DNA持续阳性者27例(41.54%)、传染性弱的HBV-DNA持续阴性者21例(32.31%)、HBV-DNA阳转阴10例(15.38%)和阴转阳7例(10.77%)。其在流行病学上具有不同的意义。     

32例恶性淋巴瘤尸检资料分析

32例恶性淋巴瘤尸检资料按新标准重新分类,初步发现淋巴母细胞性恶性程度较高。25%病例合并白血病、其中3例曾经放射治疗。提出瘤组织所以容易沿淋巴组织扩散,可能与某些肿瘤性淋巴细胞仍具有再循环和归巢等特性有关。合并症最多的是感染和出血。全身衰竭是死亡常见原因。     

Interpretation of liver stiffness measurement‐based approach for the monitoring of hepatitis B patients with antiviral therapy: A 2‐year prospective study

Liver biopsy is not routinely performed in treated chronic hepatitis B. Liver stiffness measurement has been validated for noninvasive liver fibrosis assessment in pretreatment chronic hepatitis B but has not been assessed for fibrosis monitoring during antiviral therapy. Liver stiffness was systemically monitored by Fibroscan^® every 6 months in a cohort of patients with hepatitis B receiving antiviral therapy and compared with liver biopsies at baseline and week 104. A total of 534 hepatitis B e antigen‐positive treatment‐naive patients receiving telbivudine‐based therapy with qualified liver stiffness measurement at baseline and week 104 were analyzed, 164 of which had adequate paired liver biopsies. Liver stiffness decreased rapidly (?2.2 kP a/24 weeks) in parallel with alanine aminotransferase (ALT ) from 8.6 (2.6‐49.5) kP a at baseline to 6.1 (2.2‐37.4) kP a at week 24. Interestingly, liver stiffness decreased slowly (?0.3 kP a/24 weeks) but continually from week 24 to week 104 (6.1 vs 5.3 kP a, P  <  .001) while ALT levels remained stable within the normal range. More importantly, liver stiffness declined significantly irrespective of baseline ALT levels and liver necroinflammation grades. From baseline to week 104, the proportion of patients with no or mild fibrosis (Ishak, 0‐2) increased from 74.4% (122/164) to 93.9% (154/164). Multivariate analysis revealed that percentage decline of 52‐week liver stiffness from baseline was independently associated with 104‐week liver fibrosis regression (odds ratio, 3.742; P  =  .016). Early decline of 52‐week liver stiffness from baseline may reflect the remission of both liver inflammation and fibrosis and was predictive of 104‐week fibrosis regression in treated patients with chronic hepatitis B.