【摘要】 目的 探討微弧氧化（microarc oxidation，MAO）結合應用于純鈦種植體表面處理的可行性。 方法 根據對純鈦鈦片處理的不同將實驗分為對照組（A組，不作處理）、MAO組（B組，純鈦片上進行MAO處理）及MAO加Ⅰ型膠原組（C組，純鈦片上MAO處理后吸附Ⅰ型膠原）。將成骨細胞培養于各組鈦片上，通過掃描電鏡、MTT法檢測不同時間點各組鈦片表面的細胞生長及增殖情況，并檢測堿性磷酸酶（alkaline phosphatase，ALP）活性。 結果 掃描電鏡顯示成骨細胞在C組鈦片上細胞黏附情況優于A、B組；MTT法及ALP活性檢測示培養3、6 d，成骨細胞在C組鈦片上的增殖及ALP活性與A、B組比較差異均有統計學意義（Plt;0.05）。 結論 MAO結合Ⅰ型膠原處理的鈦片可更有效提高成骨細胞表面附著、增殖，且具有較高的ALP活性。【Abstract】 Objective To study the feasibility of applying microarc oxidation (MAO) with collagen Ⅰ in surface modification of pure titanium. Methods According to different processing methods, the pure titanium was divided into three groups: the control group (without surface modification, group A), MAO group (with microarc oxidation applied in pure titanium surface modification, group B), MAO+Ⅰ group (with microarc oxidation and collagen Ⅰ applied in pure titanium treatment, group C). Osteoblasts were cultured on the surface of titanium in each group, and the cell proliferation in each group was detected at different time points by scanning electron microscopy and MTT method. Moreover, the activity of alkaline phosphatase (ALP) was also detected. Results Scanning electron microscopy showed that adhesion of osteoblasts for group C was better than group A and group B. MTT method and ALP activity detection indicated that there was a significant difference between group C and group A, B in cell proliferation and ALP activity on the third and sixth day of cultivation (Plt;0.05). Conclusion MAO with collagen Ⅰ applied in surface modification of pure titanium may increase osteoblast attachment, and promote its proliferation and ALP activity.
【摘要】 目的 探討凋亡抑制蛋白Livin與凋亡蛋白Caspase-3在結直腸腺瘤-癌序列中的表達變化及其相關性。 方法 2006年7月—2009年12月，采用免疫組織化學染色鏈霉菌抗生物素蛋白-過氧化物酶鏈接法streptavidin-peroxidese，SP）法檢測18例正常黏膜、84例結直腸腺瘤、72例結直腸癌中Livin及Caspase-3的表達情況。 結果 結直腸腺瘤組織中Livin蛋白的陽性表達率明顯高于正常黏膜組織（Plt;0.05），而低于腺癌組（Plt;0.05）；腺瘤組內絨毛狀腺瘤與管狀腺瘤相比較，Livin蛋白表達率差異有統計學意義（Plt;0.05）。結直腸腺瘤組織中Caspase-3的陽性表達率明顯高于正常黏膜組織（Plt;0.05）；而腺瘤組織與癌組織之間Caspase-3陽性表達率差異（Plt;0.05）；腺瘤組內絨毛狀腺瘤與管狀腺瘤相比較，Caspase-3蛋白陽性表達率差異無統計學意義（Pgt;0.05）。Livin表達與Caspase-3表達呈負相關（Plt;0.05）。 結論 凋亡抑制蛋白Livin參與了大腸腫瘤的發生，且在大腸腺瘤-腺癌階段起到了重要作用；凋亡抑制蛋白Livin與Caspase-3表達呈負相關，抑制Caspase-3蛋白的活性可能是Livin促進結腸癌發生的途徑之一。【Abstract】 Objective To investigate the expression of Livin and Caspase-3 among colorectal adenoma-carcinoma sequence, and to identify the relationship between Livin and Caspase-3 expression in colorectal adenoma-carcinoma sequence. Methods Formalin-fixed paraffin embedded colorectal tissues from 174 patients, including 84 adenomas, 72 carcinomas, and 18 normal mucosa, were examined for expression of Livin and Caspase-3 by streptavidin-peroxidase (SP) immunohistochemistry between July 2006 and December 2009. Results The positive rates of Livin protein expression in colorectal adenoma was significantly higher than that in normal mucosa (Plt;0.05), but lower than that in adenocarcinoma (Plt;0.05); the expression of Livin in tubular adenoma was significantly higher than that in villous adenoma (Plt;0.05). The positive rates of Caspase-3 protein expression in colorectal adenoma were significantly higher than that in normal mucosa and carcinoma (Plt;0.05), and the difference in positive rate of Caspase-3 expression was not significant between the villous adenoma and tubular adenoma (Pgt;0.05). Livin expression had negative correlation with the Caspase-3 expression (Pgt;0.05). Conclusion The difference in expression of Livin between adenoma and adenocarcinoma indicates the potential value of it in carcinogenesis of colorectal cancer, which suggestes that suppressing Caspase-3 protein activity is one of the channels by which livin promotes colorectal carcinogenesis.
