前哨淋巴结活检术应用于外阴癌的初步研究

目的 探讨前哨淋巴结活检术(SLNB)应用于外阴癌的可行性.方法 选择2004年10月-2008年4月间于中国医学科学院肿瘤医院接受手术治疗、术中采用SLNB的外阴癌患者21例,其中处于研究前期(即2005年5月前)的11例患者采用染料法识别前哨淋巴结(SLN)、处于研究后期的10例患者采用核素-染料联合法识别SLN,术后行常规病理检查.以病理检查结果为金标准,观察SLNB的检测效果;并观察与SLNB相关的并发症的发生情况.结果 21例患者中,20例(95%)检出SLN,其中8例为单侧腹股沟、12例为双侧腹股沟.20例SLN阳性患者共检出83枚SLN,每例患者平均检出4.2枚(1～9枚),每侧腹股沟平均2.6枚(1～6枚).其中,染料法每例患者平均检出4.4枚、每侧腹股沟平均2.5枚,核素-染料联合法每例患者平均检出3.9枚、每侧腹股沟平均2.7枚,分别比较,差异均无统计学意义(t=0.459,P=0.652;t=-0.421,P=0.717).20例SLN阳性患者腹股沟浅组淋巴结中均检出SLN,其中1例双侧腹股沟深组淋巴结中也检出SLN.20例SLN阳性的患者中,8例(10侧腹股沟)术后病理检查显示腹股沟淋巴结转移,其中7例患者(9侧腹股沟)的转移淋巴结中均包括有SLN、1例(1侧腹股沟)出现假阴性.以SLN识别预测同侧腹股沟淋巴结转移的假阴性率为10%(1/10),阴性预测值为96%(22/23).未发现与SLNB相关的损伤及不良反应.结论 SLNB应用于外阴癌安全、可行,以SLN预测同侧腹股沟淋巴结转移具有较高准确性.     

人工心脏起搏器的植换

探讨人工心脏起搏器植换方式选择。方法：起搏器植换２２例，其中，能源耗竭１４例，感知和起搏功能障碍４例，囊袋感染破溃致ＰＭ外露４例。非感染者起搏阈值，〈２．５Ｖ，行原位植换：ＰＴ值〉３．０Ｖ或有感染者，更换全套起搏系统。结果：非感染的１８例中，１０例ＰＴ〈２．５Ｖ，实行原位植换；８例ＰＴ值〉３．０Ｖ和其余４例有感染者，植入新的起搏系统。     

Carotid stenosis in lacunar stroke.

The prevalence of extracranial carotid stenosis in patients with a clinical syndrome of lacunar stroke has not been extensively studied using noninvasive methods. We performed carotid duplex sonography on 168 patients referred to the neurosonology laboratory with a diagnosis of ischemic stroke. Strokes were independently classified as lacunar or nonlacunar hemispheric infarction without knowledge of the ultrasound results. We excluded patients with infarcts that were clearly vertebrobasilar, presumed to be cardioembolic, or had occurred greater than 1 year earlier, and patients for whom classification of the nature and location of the event was not possible. Fifty-five patients had lacunar and 54 had nonlacunar stroke. No differences in age, sex, distribution, or prevalence of hypertension, diabetes, prior ischemia, or Hispanic surname existed between the two groups. Tobacco use was more frequent in the nonlacunar group (p less than 0.01). The prevalence of important extracranial carotid stenosis (greater than or equal to 50% diameter reduction) in the lacunar stroke group was 13% (seven of 55) in the ipsilateral and 4% (two of 55) in the contralateral carotid artery. Of the 54 patients with nonlacunar hemispheric stroke, 41% (22) had ipsilateral (p less than 0.01) and 26% (14) had contralateral (p less than 0.01) carotid stenosis. This study suggests that important carotid stenosis is infrequent among patients presenting with a clinical syndrome of lacunar stroke. These data impact on decisions regarding cerebrovascular work-up in such patients.     

Relationships between Activators and Inhibitors of Plasminogen, and the Progression of Small Abdominal Aortic Aneurysms

OBJECTIVE: plasmin is a common activator of the known proteolytic systems involved in the aneurysmal degradation, and is reported to be associated with the expansion of abdominal aortic aneurysms (AAA). The aim of this study was to study the activating pathways of plasminogen as predictors of the progression of AAA. MATERIALS AND METHODS: one hundred and twelve of 122 male patients with a small AAA (def.: +3cm) were interviewed, examined, had blood samples taken at diagnosis, and scanned annually for 1-5 years (mean 3.5 years), and referred for surgery if the AAA exceeded 5cm in diameter.A random sample of 70 of the 112 cases had plasma levels of urokinase-like-plasminogen activator (uPA), tissue-type-plasminogen activator (tPA), plasminogen-activator-inhibitor-1 (PAI-1), macrophage inhibiting factor (MIF), tumour-growth-factor-beta1 (TGF-beta1), homocysteine, and serum levels of IgA-antibodies against Chlamydia pneumoniae (IgA-CP) and Cotinine (a nicotine metabolite) measured. Spearmans correlation analysis was used for statistics. RESULTS: the annual expansion rate correlated positively with tPA, IgA-CP and S-Cotinine; r =0.37 (p=0.002), 0.29 (p=0.006) and 0.24 (p=0.038), while PAI1, uPA, TGF-beta1, homocysteine, and MIF did not. S-Cotinine did also correlate positively with tPA, r=0.24 (p=0.049). CONCLUSION: the aortic matrix degradation in AAA may be partly caused by an activation of plasminogen by tPA, but apparently not by uPA, which usually dominates matrix degradation. Smoking seems to be a factor for this pathway, while the pathways of IgA-CP and MIF, a new marker of aneurysmal progression, seem different. The latter observations suggest that other proteolytic pathways are involved in the aortic wall degradation in AAA.     

视盘血管炎——关于混合型的研讨

对６０例（６３眼）视盘血管炎的临床分型进行了探讨，结果表明，除分为Ⅰ、Ⅱ两型外，尚存在混合型，当视盘睫状血管炎性病变波及中央静脉，或两个血管系统同时受炎症侵犯时，即可再现混合型的临床表现，视盘明显水肿，视网膜静脉迂张，散在渗出，出血，动脉狭细。眼底荧光血管造影可见视盘荧光早期充盈明显迟缓，后期渗漏面积〉２．０ＰＤ，视网膜循环时间延长，混合型兼有Ⅰ，Ⅱ两型的临床特征，应作为一个独立类型存在，同时观察     

聚合酶链反应诊断单纯疱疹病毒性脑炎

用聚合酶链反应（ＰＣＲ）扩增患者脑脊液（ＣｈＦ）中病毒特异性ＤＮＡ可早期快速诊断单纯疱疹病毒性脑炎（ＨＳＥ）。１９例临床确诊的病毒性脑炎患者，经ＰＣＲ在ＣＳＦ中检出单纯疱疹病毒（ＨＳＶ）１３例，全部阳性标本均经分子杂交证实为ＨＳＶ－ＤＮＡ，而１４例其他神经疾病（ＯＮＤ）对照组均为阴性，显示了这一方法的特异性。其中７例病毒性脑炎ＣＳＦ标本分别用ＰＣＲ分子杂交和病毒分离等三种方法检测ＨＳＶ；显示ＰＣＲ最为敏感。表明ＰＣＲ技术的广泛应用将提高ＨＳＥ的早期诊断水平，指导临床正确治疗。     

刮治＋自体骨移植术治疗牙源性角化囊肿（附14例报告）

本文总结了１４例应用刮治和自体骨移植术治疗大型牙源性角化囊肿的方法，１４例植骨均成活，４例术后囊肿复发，再次手术，指出：与骨断切除治疗大型角化囊肿的方法比较，此法最大的优点是有利于保持患者面容和咀嚼功能，并对大型角化囊肿的手术原则，自体骨移植问题及手术注意事项进行了讨论。     

UVB radiation induces phosphorylation of the epidermal growth factor receptor, decreases EGF binding and blocks EGF induction of ornithine decarboxylase gene expression in SV40-transformed human keratinocytes

Abstract We previously demonstrated that epidermal growth factor (EGF) induces a several-fold increase in ornithine decarboxylase (ODC) activity and the steady-state level of ODC mRNA in cultured SV40-transformed human keratinocytes (1). Pretreatment of cell cultures with ultraviolet B (UVB) radiation resulted in a reduction of EGF-induced ODC activity. To determine whether UVB inhibits the accumulation of ODC mRNA by EGF, cells were pretreated with 20 mJ/cm² UVB or sham-irradiated and then incubated with 100 ng/ml EGF. Northern blot analysis revealed that UVB irradiation entirely blocked the EGF induction of ODC mRNA. Since the binding of EGF to its plasma membrane receptor is the first step in initiating a biological response, the effect of UVB on EGF binding was evaluated. UVB treatment of cultured keratinocytes resulted in an immediate and dose-dependent reduction of EGF binding. Scatchard analysis revealed thai the reduction of EGF binding was due to a 52% decrease in the number of available receptors, from 6.2 × 10⁴/cell to 3.0 × 10⁴/cell. However, UVB decreased the EGF-binding affinity very little (Kd = 0.60 nM in control and Kd=0.75 nM in UVB-treated Z114 cells). In addition, UVB did not alter the rate of EGF internalization. These data suggest that UVB blocks the signal transduction pathway of EGF that is involved in regulation of ODC gene expression. Immunoblot analysis of extracts from irradiated cells showed that UVB induced tyro-sine phosphorylation of EGFR and that the quantity of EGFR protein was unaffected by UVB treatment. Phosphorylation of EGFR may be responsible for decreased binding of EGF to its receptor.