PTEN抑癌基因对高转移性粘液表皮样癌细胞辐射敏感性的影响

目的:评价外源PTEN抑癌基因对人高转移性粘液表皮样癌细胞系M3SP2辐射敏感性的影响。方法:用汁质体介导法将PTEN抑癌基因导入M3SP2细胞系,以空载体转染细胞为对照,应用MTT比色实验和克隆形成实验测定两种癌细胞对~(60)Co-γ射线的敏感性。结果:与对照组比较,转染PTEN抑癌基因组的治疗指数为1.68,放射生物学参数SF_2减小49.6％,D_0减小41.7％,SER为1.72,DMF_(0.5)为1.65。结论:外源野生型PTEN抑癌基因能增强粘液表皮样癌细胞对γ-射线的敏感性。     

外源性PTEN基因诱导黏液表皮样癌细胞系凋亡的研究

目的：探讨转染外源性PTEN抑癌基因对黏液表皮样癌细胞系M3SP2的诱导凋亡作用。方法：用含野生型PTEN抑癌基因逆转录病毒载体转染高转移性涎腺黏液表皮样癌细胞系M3SP2,转染空载体亲本细胞为对照细胞。体外细胞凋亡采用苏木精-伊红染色、电镜、TUNEL染色和流式细胞仪检测,裸鼠移植瘤细胞凋亡应用苏木精-伊红染色形态学判定。Bc l-2、P53和H-ras蛋白表达用免疫组化染色检测。结果：试验细胞M3SP2-PTEN与对照细胞M3SP2-pBp比较,出现较多的典型的凋亡细胞特征。试验细胞和对照细胞凋亡率分别为7.5%-13.6%和1.2%-2.3%;裸鼠移植瘤M3SP2-PTEN组和M3SP2-pBp组的凋亡指数分别为17.4%和3.5%。免疫组化染色显示M3SP2-PTEN细胞与对照细胞比较,P53蛋白表达增强,Bc l-2和H-ras蛋白表达减弱。结论：外源性PTEN抑癌基因能显著诱导高转移性涎腺黏液表皮样癌细胞凋亡,并且与P53、Bc l-2和H-ras蛋白表达有一定关系。     

PTEN抑癌基因转染粘液表皮样癌细胞系M3SP2的建立和鉴定

目的：为了研究外源性基因PTEN对粘液表皮样癌细胞生物学行为的影响，建立稳定表达PTEN的粘液表皮样癌细胞系。方法：应用脂质体介导方法将野生型PTEN基因导入高转移性粘液表皮样癌细胞系M3SP2，嘌呤霉素筛选阳性克隆，用免疫印迹法和ABC免疫酶染色法检测转染细胞中PTEN蛋白的表达。结果：野生型PTEN基因成功地导入细胞M3SP2，转染细胞稳定表达PTEN蛋白，PTEN蛋白分布于细胞质。结论：M3SP2细胞能稳定表达外源性基因PTEN。     

PTEN基因对粘液表皮样癌细胞裸鼠移植瘤生长的抑制作用

目的研究外源野生型PTEN抑癌基因对人高转移性粘液表皮样癌细胞裸鼠移植瘤生长的抑制作用。方法取PTEN抑癌基因转染粘液表皮样癌细胞的M3SP2-PTEN及逆转录病毒空载体转染的对照细胞M3SP2-pBp,接种于裸鼠背部皮下,测定移植瘤生长曲线,并对移植瘤进行组织学观察。结果对照组移植瘤生长迅速,肿瘤体积倍增时间为32.68h。HE染色切片显示,细胞数量多、排列紧密,核分裂相较多见;而实验组M3SP2-PTEN细胞移植瘤生长比较缓慢,肿瘤体积倍增时间延长为36.58h,肿瘤结节体积明显小于对照组(P<0.01),抑瘤率达63.82%。HE染色切片显示,细胞排列比较松散,较多的细胞出现变性和坏死,部分细胞染色体边集并出现凋亡小体。结论外源野生型PTEN抑癌基因能够显著抑制人高转移性粘液表皮样癌细胞在裸鼠体内的生长,其作用机制与PTEN基因诱导癌细胞变性和凋亡有关。     

PTEN抑癌基因对高转移性黏液表皮样癌细胞系生物学行为的影响

目的　探讨外源野生型PTEN抑癌基因对人高转移性黏液表皮样癌细胞系M3SP2体外黏附、迁移和侵袭特性的影响。方法　用脂质体介导方法将PTEN抑癌基因导入M3SP2细胞系 (M3SP2 -PTEN细胞 ) ,转染空载体的细胞系作为对照(M3SP2 -pBp细胞 ) ,分别用四甲基偶氮唑蓝 (MTT)比色法、细胞迁移试验及细胞侵袭试验测定M3SP2 -PTEN细胞和M3SP2 -pBp细胞体外黏附、迁移和侵袭能力。结果　M3SP2 -PTEN细胞在Metrigel和Fn基质上黏附数量减少 ,与对照组比较差异有显著性 (P <0 0 1) ,黏附抑制率分别为 34 3%和 4 9 4 %。M3SP2 -PTEN细胞在Matrigel基质上迁移距离小 ,与对照组比较差异有显著性 (P <0 0 5 ) ,迁移抑制率为 2 6 0 %。M3SP2 -PTEN细胞体外侵袭细胞数量减少 ,与对照组比较差异有显著性 (P <0 0 1) ,侵袭抑制率为 31 4 %。结论　外源性PTEN抑癌基因对高转移性黏液表皮样癌细胞系M3SP2体外黏附、迁移和侵袭具有抑制作用。     

PTEN基因转染对粘液表皮样癌细胞系M_3SP_2增殖的抑制作用

目的:观察外源磷酸酶和张力蛋白同源物(PTEN)抑癌基因对高转移性粘液表皮样癌细胞系M3SP2体外生长的影响。方法:应用脂质体介导方法将野生型PTEN基因导入M3SP2细胞,通过活细胞观察、细胞生长曲线、分裂指数和克隆形成率了解细胞生长状态。结果:与亲本细胞比较,PTEN基因转染细胞数量减少、排列松散,部分细胞发生变性或崩解;细胞生长缓慢,分裂指数显著减至1612j(P<0101),细胞群体倍增时间明显延长(31174 h),细胞生长抑制率达57105%~71146%(P<01001);细胞克隆形成率为10140%~14193%,克隆形成抑制率高达65%~72% (P<0101)。结论:外源野生型PTEN抑癌基因能显著抑制高转移性粘液表皮样癌细胞系M3SP2体外增殖。     

外源性PTEN抑癌基因对高转移性黏液表皮样癌细胞系形态的影响

目的 :观察外源野生型PTEN基因对高转移性黏液表皮样癌细胞系形态的影响。方法 :应用倒置显微镜观察法、HE染色观察、扫描电镜及透射电镜观察法 ,比较野生型PTEN抑癌基因转染的黏液表皮样癌细胞M 3SP2 PTEN与对照的黏液表皮样癌细胞M 3SP2 pBp的形态学差异。 结果 :M 3SP2 pBp细胞体外生长活跃 ,细胞数量多 ,核分裂相多 ,细胞表面微绒毛丰富 ,细胞核切迹明显 ,细胞质中线粒体丰富 ;M 3SP2 PTEN细胞生长缓慢 ,分裂相很少 ,细胞数量少 ,部分细胞空泡变性 ,染色质凝集 ,细胞膜彭出 ,线粒体数量少并发生肿胀 ,较多的溶酶体融合。结论 :外源野生型PTEN基因的转染能导致体外培养的高转移性黏液表皮样癌细胞变性、坏死或凋亡。     

PTEN抑癌基因对黏液表皮样癌实验性裸鼠肺转移的抑制作用

目的　探讨外源野生型PTEN抑癌基因对人高转移性黏液表皮样癌M3SP2细胞系实验性裸鼠肺转移能力的影响。方法　用脂质体介导方法将PTEN抑癌基因导入M3SP2细胞系 (M3SP2 -PTEN细胞 ) ,转染空载体的细胞系作为对照M3SP2 -pBp细胞 ) ,应用裸鼠肺转移实验测定癌细胞的体内转移能力 ,并进行组织学观察。结果　对照组裸鼠肺转移结节数为 (2 4 0± 1.2 )个 ,组织学观察瘤细胞转移灶体积大 ,细胞生长活跃 ,可见较多核分裂。实验组裸鼠肺转移结节数量减少为 (8 5± 3 4 )个 ,转移抑制率为 6 5 6 % ;组织学观察可见转移灶数量少、体积小 ,并有较多的坏死和凋亡细胞。结论　转染野生型PTEN抑癌基因能降低人高转移性黏液表皮样癌细胞转移能力。     

PTEN抑癌基因对人黏液表皮样癌细胞系增殖和细胞周期的影响

目的：探讨外源性PTEN抑癌基因对唾液腺黏液表皮样癌细胞系增殖抑制的机制。方法：将含野生型PTEN抑癌基因cDNA重组反转录病毒表达质粒导入高转移性唾液腺黏液表皮样癌细胞系M3SP2,转染空载体细胞为对照。MTT比色法测定细胞增殖,流式细胞术测定细胞周期,免疫组化染色检测PCNA、EGFR、CDK4、P16INK4a和P57Kip2蛋白表达。采用SPSS11．0软件包进行统计学分析。结果：与对照细胞比较,PIEN基因转染癌细胞M3SP2-PTEN对表皮生长因子（EGF）介导的细胞增殖具有显著的抑制作用,癌细胞阻滞在G0／G1期,PCNA、EGFR、CDK4以及C—myc蛋白表达减弱,而P16INK4a和P57Kip2蛋白表达增强（P〈0．05）。结论：外源性PTEN基因具有抑制唾液腺黏液表样癌皮细胞系EGF介导的增殖作用,其作用机制与细胞周期进程受阻以及细胞周期调控分子有关。     

PTEN基因联合多西环素抑制黏液表皮样癌细胞系端粒酶活性的研究

目的探讨外源性PTEN抑癌基因联合多西环素对人黏液表皮样癌细胞系端粒酶活性的影响。方法用脂质体将野生型PTEN基因导入黏液表皮样癌细胞系,再用不同质量浓度的多西环素处理细胞,采用MTT比色法测定细胞存活,用端粒酶重复扩增法-酶联免疫吸附（TRAP-ELISA）测定细胞端粒酶活性。结果与对照细胞比较,野生型PTEN基因明显增加癌细胞对多西环素的敏感性,增敏比为1.65～4.75倍。PTEN基因转染或多西环素诱导癌细胞端粒酶活性明显下降（P＜0.05）,二者联合应用对癌细胞端粒酶活性抑制更为显著（P＜0.01）。结论PTEN抑癌基因联合多西环素对人黏液表皮样癌细胞系端粒酶活性具有显著的协同抑制效应。     

Evidence of the validity of a model of determinants of quality of restorative dental care

A model describing the relationship between self-reported quality of restorative dentistry and dentist characteristics for 119 Montana general dentists is presented. The best predictors formed a significant model explaining 22% of the variance of the quality measure. Results are contrasted with a previous estimation of the model for 102 Washington general practitioners. Evidence for the external validity of the model is presented.     

Experimental evidence of formation of imines in the course of reduction of hydrazones

The reduction of hydrazones is generally suggested to proceed through a reductive cleavage of the nitrogen–nitrogen bond followed by a reduction of the carbon–nitrogen bond. This sequence of reduction processes is here supported for fluorenone (V) and benzophenone (VI) hydrazones as well as by a comparison of the reduction of fluorenone and benzophenone hydrazonium ions (I,III) with corresponding imines (II,IV). Another proof of the presence of imines as intermediates is the splitting of four-electron waves of hydrazones V and VI and hydrazonium ions I and VIII into two waves at pH < 2. This has been interpreted as due to differences in slopes dE_1/2/dpH and pK_a-values of protonated hydrazine derivatives on one side and corresponding imines on the other. In this pH-range imines formed in reductions of VI and VIII are reduced in a single two-electron wave, those of I and V in two one-electron steps. Fluorenone imine (II) is sufficiently stable to allow recording of time-independent current–voltage curves between pH 6 and 11. In this pH-range the imine (II) is reduced in two one-electron steps. Benzophenone imine (IV) has been found stable between pH 4.6 and 12. At pH 4.6–8 the reduction of the imine IV takes place in a single two-electron step, at pH 8–12 in two one-electron steps. Final proof of the initial cleavage of the N–N bond is presented by comparison with the reduction of nitrones.     

不同剂型玻璃离子水门汀溶解性比较研究

目的:研究、比较不同剂型玻璃离子水门汀的溶解性和表面微观形态改变,为临床使用提供依据.方法:将3M树脂加强型玻璃离子水门汀(水粉剂型)、GC玻璃离子水门汀(水粉剂型)及GC玻璃离子水门汀(双糊剂型)分别在人工唾液中浸泡30 d,冷热循环15000次,烘干测重,比较前后质量变化,计算溶解率,并用扫描电镜观察表面微观改变.结果:不同剂型的玻璃离子水门汀溶解率由高到低分别为3M树脂加强型玻璃离子水门汀(水粉剂型)、GC玻璃离子水门汀(水粉剂型)、GC玻璃离子水门汀(双糊剂型).3种玻璃离子水门汀经浸泡溶解后,SEM扫描表面微观形态可观察到GE玻璃离子水门汀(双糊剂型)表面形态改变较少,其他2组玻璃离子水门汀表面微观改变较多.结论:双糊剂型玻璃离子水门汀理化性能及溶解率均低于传统水粉剂型,是未来临床修复治疗的的良好选择.     

Evaluation of efficacy of chemiluminescence for diagnosis of leukoplakia

ObjectiveLeukoplakia is the most common potentially malignant disorder preceding oral cancer. Chemiluminescence has been developed as an adjunct to conventional examination for the diagnosis of these potentially malignant disorders. This study was conducted to assess the efficacy of chemiluminescence in the diagnosis of leukoplakia and to compare the results with histopathological examination.Study designA total of 50 patients with leukoplakia were included from the outpatients attending the Department of Oral Medicine and Radiology, Dental Hospital, Bengaluru, Karnataka, India. These patients were subjected to conventional oral examination followed by chemiluminescent examination with Vizilite (Zila, Fort Collins, CO, USA) and biopsy for histopathological confirmation.ResultsThe sensitivity, specificity, positive predictive value, and negative predictive value of chemiluminescence were 93.75%, 55.56%, 78.95%, and 83.3%, respectively. The overall accuracy of chemiluminescence was 80%. A statistically significant association was observed between histopathology results and chemiluminescence results.ConclusionAlthough it is an easy, safe, minimal time consuming, and noninvasive technique, it has only adjunctive utility and it does not replace biopsy for the diagnosis of leukoplakia.     

颌骨动静脉畸形的栓塞治疗

目的：总结直接穿刺结合经血管内介入栓塞治疗颌骨动静脉静脉畸形的经验。方法：收治凳骨动静脉畸形患者6例,均进行了介入栓塞治疗。采用的栓塞材料为附凝血棉纤毛的螺圈,聚乙烯醇泡沫微粒和二氰基丙烯酸对丁酯。数字减影颈动脉造影在PHILIPSV300下完成。结果6例颌骨动静脉畸形患者中4,例急性出血得到了快速、有效控制,1例慢性渗血的右下 骨动静脉畸形患者,介入栓塞治疗,拔除松动的右下凳第一磨牙,有效地控制了出血,另1例伴局部软组织搏动性膨隆的上凳骨动静脉畸形患者,介入治疗后膨隆的搏动性得到明显改善,栓塞治疗后分别随访3－24个月,均未发现有口腔内渗血或出血。随访的X线片上,病灶区可见新骨形成。结论：局部穿刺结合经血管内介入栓塞治疗颌骨动静畸形是一种安全、有效的治疗方法。     

正畸患者切牙影像失真发生情况分析

目的研究正畸患者曲面体层片上的切牙影像失真发生情况，并分析其原因。 方法从中山大学附属口腔医院放射科影像数据库中选取500例正畸患者的曲面体层片和头影测量侧位片，所有曲面体层片均采用咬合杆投照，分别从切牙牙体影像放大、缩小、牙根变短、根尖模糊等评价指标分析上下颌切牙影像失真的发生情况，在头影测量侧位片上测量中切牙根尖-对颌切牙切缘的距离，探讨切牙影像失真发生的原因。采用SPSS 19.0统计软件对所得数据进行统计学检验。 结果500例患者中，切牙牙体影像正常者共417例，切牙牙体影像失真者共83例，影像失真发生率16.6%，其中切牙牙体影像放大17例、牙体影像缩小0例、牙根变短30例，牙根影像变短伴模糊36例。影像失真患者的根尖-切缘距离大于影像正常的患者，差异有统计学意义（F = 5 187.18，P = 0）；影像失真患者的覆盖值大于影像正常的患者，差异有统计学意义（F>477，P = 0）。 结论严重牙颌面畸形如反 、深覆盖是导致曲面体层片的切牙影像失真的主要原因之一。     

Design of clinical trials of traditional therapies of periodontitis

The present paper on the design of clinical trials of periodontal therapy first addresses the issue of the etiology of periodontal disease. It is suggested that most if not all forms of destructive periodontal disease are caused by microorganisms and that there are different forms of disease with different microbial etiologies. The progressive nature of destructive periodontal disease is subsequently discussed and it is emphasized that, in a given patient, periodontal sites which show signs of inflammation and attachment loss may not over a period of several months and years show further sign of attachment loss. The present methods of assessing periodontal disease do not allow us to discriminate between potentially active and inactive sites in untreated patients. The significance and variability of indicators of periodontal disease such as bleeding on probing, probing pocket depth and probing attachment level measurements are discussed. The errors inherent in the various measurements are analyzed and suggestions are presented describing how alterations in any of the above parameters could be identified and presented in a clinical trial. Of concern for the statistical analysis of clinical data of periodontal disease is the definition of the "experimental unit". For a number of years, the "experimental unit" in periodontal trials was the patient. It is clear, however, that different sites within the same individual show different patterns of disease progression and lesion morphology and often respond differently to periodontal therapy. Statistical analyses must consequently be designed which recognize differences in site-to-site infection and lesion morphology within a common host. Until such analyses are available, the investigator should be wary of pooling data within the same individual, since such pooling may obscure meaningful alternatives which may take place in individual periodontal sites. Some goals of periodontal therapy are subsequently identified. 4 goals are discussed more in detail, namely: to establish conditions which will allow the patient to maintain a dentition without further breakdown of the periodontium; to reduce pocket depth to establish an anatomy in the dentogingival region which with proper maintainance care will prevent the re-establishment of the subgingival infection; to gain attachment as a result of treatment; to assess the effect of a certain chemotherapeutic agent on periodontal disease.     

正常青年Monson球面半径的测量研究

目的测量正常青年Monson球面半径。方法选择60名(男30名,女30名)正常青年制取全口印模,应用立体摄影成像的原理与方法对Monson球面半径进行测量和统计学处理。结果Monson球面的半径平均为10.173 cm,大于理论值10.160 cm,差异有显著性(P<0.01);男、女性球面半径差异无显著性。结论本实验所得到的数据可作为全口义齿修复中记录颌位关系的一个参量。     

鼻测量法的进展

唇裂术后继发畸形是指唇裂修复术后,仍遗留或继发于手术操作和生长发育变化而表现出来的一类畸形[1]。包括唇畸形、鼻畸形和颌骨畸形。其修复较原发性唇裂修复更复杂,更灵活多变。而导致其修复复杂性的一个重要原因即是局部组织结构复杂变异和缺乏可靠的三维测量手段[2],鼻畸形     

口底癌34例临床分析

目的探讨口底癌的临床特性、治疗方法及预后。方法对我院自1992—2002年住院治疗的34例口底癌患者进行回顾性分析。结果34例口底癌患者中,男28例(82.4%),女6例(17.6%),男女比为4.7∶1,平均发病年龄58岁。发病部位:前口底22例(64.7%),后口底12例(35.3%)。淋巴结转移率41.2%。单纯手术组、化疗加手术组、放疗加手术组、化疗加手术加放疗组的5年生存率分别为45.5%、60.0%、50.0%、62.5%。结论口底癌以中老年患者好发,男性居多。易发生淋巴结转移,综合疗法疗效较好。