猪釉基质蛋白的提取及N末端氨基酸序列分析

目的：从猪牙胚提取釉基质蛋白并做氨基酸测序,为进一步研究釉基质蛋白诱导牙周组织再生的生物活性奠定基础。方法：选择乙酸提取法获得釉基质蛋白,采用ＳＤＳ－ＰＡＧＥ电泳和印迹膜测序法分析Ｎ末端氨基酸序列。结果：提取的釉基质蛋白分子量条带主要位于２０ＫＤａ以下,优势条带为２０ＫＤａ、１３ＫＤａ、５ＫＤａ。２０ＫＤａ、５ＫＤａ釉基质蛋白Ｎ末端前１０个氨基酸残基均为：Ｍｅｔ、Ｐｒｏ、Ｌｅｕ、Ｐｒｏ、Ｐｒｏ、Ｈｉｓ、Ｐｒｏ、Ｇｌｙ、Ｈｉｓ、Ｐｒｏ。结论：乙酸提取法可获得典型的釉原蛋白。印迹膜测序法简易、快速、敏感。     

猪釉基质蛋白对MC3T3-E1成骨细胞增殖分化的影响

目的：探索釉基质蛋白（ＥＭＰｓ）促进成骨细胞增殖分化的作用,为进一步研究提供基本数据。方法：选择ＭＣ３Ｔ３－ＥＩ成骨细胞株,利用体外细胞培养方法,分别加入不同浓度的ＥＭＰｓ α－ＭＥＭ培养液,于培养０、１、２、３、４、５、６ｄ进行细胞计数,采用ＳＡＳ软件对细胞计数数据作单因素方差分析。结果：ＥＭＰｓ各组细胞计数均高于阴性对照（Ｃ）组（Ｐ〈０．０１）。第２天,１００μｇ／ｍｌ ＥＭＰｓ组的细胞计数高     

猪釉基质蛋白的提取及N末端氨基酸序列分析

目的：从猪牙胚提取釉基质蛋白并做氨基酸测序,为进一步研究釉基质蛋白诱导牙周组织再生的生物活性奠定基础。方法：选择乙酸提取法获得釉基质蛋白,采用ＳＤＳ－ＰＡＧＥ电泳和印迹膜测序法分析Ｎ末端氨基酸序列。结果：提取的釉基质蛋白分子量条带主要位于２０ＫＤａ以下,优势条带为２０ＫＤａ、１３ＫＤａ、５ＫＤａ。２０ＫＤａ、５ＫＤａ釉基质蛋白Ｎ末端前１０个氨基酸残基均为：Ｍｅｔ、Ｐｒｏ、Ｌｅｕ、Ｐｒｏ、Ｐｒｏ、Ｈ     

8—甲氧基补骨脂素对粘液表皮样癌细胞的抑制作用

目的：研究８－甲氧基补骨脂素（８－ＭＯＰ）对粘液表皮样癌细胞（ＭＥＣ－１）的抑制作用。方法：应用常规ＭＴＴ法、细胞计数法和流式细胞术研究８－ＭＯＰ作用于粘液表皮样癌细胞的剂量－效应关系和时间－效应关系以及３０％抑制浓度的药物对细胞群体倍增时间和细胞周期的影响。结果：１）小剂量８－ＭＯＰ在短时间内对ＭＥＣ－１细胞没有抑制作用，当剂量大于２５ｍｇ／Ｌ时，药物的抑制作用呈剂量依赖性；作用时间在２４ｈ～７２ｈ之间时表现出时间依赖性关系；药物的抑制作用有延迟性。２）１２０ｈ作用组３０％抑制浓度ＩＣ３０＝３３．８６ｍｇ／Ｌ，５０％抑制浓度ＩＣ５０＝４５．３ｍｇ／Ｌ，ＲＡＡ值＝２．９。３）它阻止细胞进入Ｓ期完成细胞分裂。结论：ＭＥＣ－１细胞对８－ＭＯＰ较敏感，８－ＭＯＰ在人粘液表皮样癌的防治方面可能有一定意义。     

8—甲氧基补骨脂素对MEC—1细胞癌基因／抑癌基因表达的影响

目的：研究８－甲氧基补骨脂素对ＭＥＣ－１细胞部分基因表达的影响。方法：细胞贴壁后用３０％细胞生长抑制浓度的药物处理１２０ｈ，常规制备标本，ＡＢＣ法免疫组织化学染色。结果；药物处理后细胞Ｐ１６和ｎｍ２３－Ｈ１蛋白表达强度增强，而ＣＤＫ４和Ｈ－ｒａｓ蛋白表达强度减弱。结论：８－ＭＯＰ可以调节ＭＥＣ－１细胞部分基因的表达，从而可能影响细胞相关的生物学特性。     

稳定表达骨形成蛋白Ⅱ型突变受体的NIH3T3细胞的建立及鉴定

目的：建立稳定表达ＢＭＰｓⅡ型突变受体的ＮＩＨ３Ｔ３细胞株。方法：用ＦｕＧＥＮＥ６ Ｔｒａｎｓｆｅｃｔｉｏｎ Ｒｅａｇｅｎｔ Ｋｉｔ真核转染试剂盒将携带ＢＭＰｓⅡ型突变受体的ｃＤＮＡ的真核表达载体转染ＮＩＨ３Ｔ３细胞。结果：得到抗Ｇ－４１８的阳性细胞克隆转染细胞，ｎｅｏ基因原位杂交阳性。结论：成功建立了稳定表达ＢＭＰｓⅡ型突变受体的ＮＩＨ３Ｔ３细胞株。     

骨形成蛋白对牙周膜细胞增殖和碱性磷酸酶活性的影响

目的：了解骨形成蛋白（ＢＭＰ）剂量变化对人牙周膜细胞（ＰＤＬＣ）增殖和碱性磷酸酶（ＡＬＰａｓｅ）活性的影响。方法：应用细胞培养技术、噻唑盐比色测定（ＭＴＴ）和酶动力学方法。结果：ＢＭＰ作用后的实验组ＰＤＬＣ的增殖和ＡＬＰａｓｅ活性较对照组均有明显的升高；且有一个合适的剂量范围。ＰＤＬＣ的增殖和ＡＬＰａｓｅ活性受ＢＭＰ浓度梯度影响的变化幅度并不完全一致，表现在所需ＢＭＰ用量不同。结论：可以认为ＢＭＰ能够促进人ＰＤＬＣ的增殖和ＡＬＰａｓｅ活性功能，但各自的影响机制可能还有所差异。     

Ets—1在颌骨骨肉瘤中的表达

目的：分析Ｅｔｓ－１（Ｅ２６ ｔｒａｎｓｆｏｒｍａｔｉｏｎ－ｓｐｅｃｉｆｉｃ）在颌骨骨肉瘤的表达及意义。方法：采用免疫组织化学ＡＢＣ法检测Ｅｔｓ－１蛋白在２０例颌骨骨肉瘤和８例软骨瘤中的表达。结果：５５％（１１／２０）的骨肉瘤中Ｅｔｓ－１呈阳性表达，阳性表达率在各病理学分型间无显著性差异（Ｐ〉０．０５），而转移组明显高于未转移组（Ｐ〈０．０５）；１２．５％（１／８）的骨软骨瘤呈Ｅｔｓ－１阳性，与骨     

人成骨蛋白—1成熟肽基因5‘端的修饰及其在大肠杆菌中的表达

目的：对人成骨蛋白－１（ＯＰ－１）成熟肽基因进行修饰、克隆并在大肠杆菌中表达、检测，为ＯＰ－１的进一步纯化、复性、诱骨活性的研究以及未来的临床应用奠定基础。方法：在不改变氨基酸的前提下，用ＰＣＲ的方法对ＯＰ－１的成熟肽Ｎ端序列加以修饰，将编码成熟肽的ｃＤＮＡ３’端０．４２ｋｂ基因片段克隆于温控型大肠杆菌表达载体ｐＢＶ２２０，受控于ＰＬＰＲ启动子。重组子以大肠杆菌ＤＨ５α为宿主细胞进行温度诱导表达。用鼠抗牛天然ＢＭＰｓ单抗对表达产物进行ＥＬＩＳＡ检测和ＷｅｓｔｅｒｎＢｌｏｔｉｎｇ确证。结果：工程菌经４２℃、５ｈ诱导后，在ＳＤＳ－ＰＡＧＥ上出现一条新的蛋白带，分子量在１．６×１０４ｕ左右，约占菌体总蛋白的１９．８％。主要以包涵体形式存在的表达产物经初步纯化后，可获得纯度较高的重组人成骨蛋白－１成熟肽（ｒｈＯＰ－１）。表达产物的ＥＬＩＳＡ检测和ＷｅｓｔｅｒｎＢｌｏｔｎｇ确证确均呈阳性反应。结论：表达产物即为目的蛋白，使ｈＯＰ－１成熟肽基因５’端的修饰及其在大肠杆菌中的表达在国内第一次获得成功。     

釉基质蛋白对牙周膜细胞增殖和碱性磷酸酶活性的影响

目的：探讨釉基质蛋白对于牙周膜细胞增殖和碱性磷酸酶（ALP）活性的影响。方法：采用细胞培养技术,噻唑盐比色测定（MTT）法和酶动力学方法,观察釉基质蛋白对牙周膜细胞的作用。结果：釉基质蛋白组的牙周膜细胞,其增殖活性显著提高,以50mg/L浓度为最佳;其ALP活性也较对照组明显增加,以200mg/L浓度的效果最佳。具有一个合适的剂量范围。结论：釉基质蛋白可促进人牙周膜细胞的增殖和ALP活性。     

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.     

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.     

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。     

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