目的 了解細胞增殖標記物微小染色體支持蛋白2（minichromosome maintenance protein 2，MCM2）在大腸腫瘤診斷中的應用現(xiàn)狀。 方法復習國內(nèi)、外的文獻并加以綜述。結(jié)果 MCM2在腫瘤研究中可作為評估其細胞分化發(fā)育異常和突變的指標，細致地分析MCM2在不同大腸細胞突變階段的表達有助于早期監(jiān)測大腸細胞的突變。結(jié)論MCM2作為一個相對敏感而特異性的細胞增殖標記物，有望為早期臨床檢測大腸癌提供一種新的指標，從而有助于早期診斷大腸癌，提高患者的治愈率。
目的 探討雙水平氣道正壓通氣( BiPAP) 呼吸機加平臺呼氣閥( PEV) 聯(lián)合呼吸興奮劑治療慢性阻塞性肺疾病急性加重( AECOPD) 合并肺性腦病的療效。方法 70 例AECOPD 合并肺性腦病的患者隨機分為治療組和對照組。兩組均予以抗感染、解痙平喘、止咳祛痰等常規(guī)治療, 根據(jù)痰培養(yǎng)及藥敏結(jié)果應用敏感抗生素, 并使用BiPAP 呼吸機治療。治療組在此基礎上加PEV, 并加用納洛酮和尼可剎米靜滴治療( 療程3 d) 。觀察兩組神志轉(zhuǎn)清時間、生命體征、動脈血氣、APACHEⅡ評分及不良反應。結(jié)果 治療組與對照組相比, 治療后心率、呼吸頻率、PaCO2 及APACHEⅡ評分均明顯下降, 神志轉(zhuǎn)清時間縮短, PaO2 、SaO2 、pH 值及格拉斯哥昏迷評分明顯上升, 差異均具有統(tǒng)計學意義( P lt;0. 01) 。治療組2 例因療效不佳行氣管插管機械通氣, 死亡1 例。對照組5 例因療效不佳行氣管插管機械通氣, 死亡2 例。結(jié)論 早期使用BiPAP 呼吸機加PEV 聯(lián)合呼吸興奮劑治療AECOPD合并肺性腦病患者, 能明顯改善癥狀, 縮短神志轉(zhuǎn)清時間, 減少氣管插管, 迅速糾正低氧血癥和CO2 潴留, 療效顯著。
【摘要】 目的 探討微弧氧化（microarc oxidation，MAO）結(jié)合應用于純鈦種植體表面處理的可行性?！》椒ā「鶕?jù)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(yǎng)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?！〗Y(jié)果 掃描電鏡顯示成骨細胞在C組鈦片上細胞黏附情況優(yōu)于A、B組；MTT法及ALP活性檢測示培養(yǎng)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(tǒng)計學意義（Plt;0.05）?！〗Y(jié)論 MAO結(jié)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(jié)直腸腺瘤-癌序列中的表達變化及其相關性?！》椒ā?006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(jié)直腸腺瘤、72例結(jié)直腸癌中Livin及Caspase-3的表達情況?！〗Y(jié)果 結(jié)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(nèi)絨毛狀腺瘤與管狀腺瘤相比較，Livin蛋白表達率差異有統(tǒng)計學意義（Plt;0.05）。結(jié)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(nèi)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(tǒng)計學意義（Pgt;0.05）。Livin表達與Caspase-3表達呈負相關（Plt;0.05）。 結(jié)論 凋亡抑制蛋白Livin參與了大腸腫瘤的發(fā)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(jié)腸癌發(fā)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.
目的探討人急性胰腺炎早期外周血單核細胞(peripheral blood monocytes,PBMCs)表面Toll樣受體4(Toll like receptor 4,TLR4)表達變化。方法發(fā)病24 h內(nèi)入院的早期急性胰腺炎患者30例，采集入院當天及第3、7 d外周血及20名正常志愿者外周血，分離單核細胞。用流式細胞儀檢測單核細胞表面TLR4、CD14表達變化情況。同時檢測血清腫瘤壞死因子-α（tumor necrosis factor alpha,TNF-α）、白細胞介素6（interleukin 6,IL-6）等指標，研究它們之間的相關性。結(jié)果急性胰腺炎患者PBMCs表面TLR4發(fā)病后表達上調(diào)， 1周左右恢復正常。TNF-α的變化與TLR4變化一致。結(jié)論人急性胰腺炎早期可能通過先天性免疫門戶蛋白TLR4激活單核巨噬細胞系統(tǒng)導致TNF-α等促炎細胞因子的產(chǎn)生和釋放。