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Preterm Birth

截止至2002年5月,現有早產治療的臨床證據如下: (1) 高危早產:在一些國家實施的RCT發現,在降低早產危險方面,加強產前保健與普通產前保健沒有明顯差異.包括5個RCT的1個系統評價發現,對有宮頸改變的婦女行宮頸環扎術有不同的結果,沒有明確的結論.1個大樣本的RCT發現,孕9～29周宮頸功能可能不全的婦女進行預防性宮頸環扎手術與不環扎相比,能明顯降低早產(＜33孕周),但也會明顯增加產褥感染的危險.另外4篇較小樣本的RCT發現,孕10～30周、具各種早產高危因素的婦女,進行預防性宮頸環扎手術與不環扎相比,并不能降低早產(＜34孕周).1篇系統評價的2個RCT報告,對有宮頸改變的婦女進行環扎術有不同的結果,其中1個RCT發現其并不能明顯降低早產(＜34孕周),而另外1個較小樣本的RCT卻發現宮頸環扎手術加臥床休息與單純臥床休息比較,能明顯降低34周前的早產.沒有1個RCT證實行環扎術加臥床休息與單純臥床休息相比,能降低圍生兒死亡率. (2) 胎膜早破:1個系統評價發現,對胎膜早破的婦女,抗生素較安慰劑能明顯延長孕周、降低新生兒發病率的危險,如新生兒感染、出生后氧療、腦部超聲異常等.阿莫西林加克拉維酸治療與新生兒壞死性小腸結腸炎的發生率明顯增加有關.一個基于1個RCT的系統評價發現,沒有充足的證據證實羊膜腔灌注與不灌注比較能改善胎膜早破后的新生兒結局. (3) 先兆早產的治療:①β-腎上腺素興奮劑:1個系統評價發現,β-腎上腺素興奮劑與安慰劑或不治療相比,并不能明顯降低圍生兒死亡率、呼吸窘迫綜合征及低體重兒(＜2 500 g)發生率,且與與安慰劑或不治療相比,β-腎上腺素興奮劑增加孕母副反應,如胸痛、心悸、呼吸困難、震顫、惡心、嘔吐、頭痛、高血糖、低鉀血癥.②鈣離子通道拮抗劑: 沒有關于鈣離子通道拮抗劑與安慰劑比較的系統評價或RCT.1個系統評價發現,鈣離子通道抑制劑與其它保胎藥(主要是β-腎上腺受體興奮劑)比較,能顯著降低48 h內的早產分娩,減少因孕母副反應退出治療和新生兒發病率.③硫酸鎂:1個系統評價發現,硫酸鎂與安慰劑比較,并不能明顯降低孕36周前的早產率、圍生兒死亡率、呼吸窘迫綜合征的發生率.另一個系統評價發現,硫酸鎂和其他宮縮抑制劑(β-腎上腺素興奮劑、鈣離子通道拮抗劑、前列腺素合成抑制劑、硝化甘油、酒精和葡萄糖注射劑)比較,并不能明顯降低48 h內早產率(盡管結果沒有差異).④垂體受體拮抗劑(阿托西班):1個系統評價納入 2個RCT,對阿托西班和安慰劑治療早產進行比較有不同的結果.較大樣本的RCT發現,阿托西班較安慰劑能延長孕周,但阿托西班增加了孕28周以下的胎兒死亡率.另一個RCT發現,阿托西班增加了48 h內的早產.⑤前列腺素抑制劑(消炎痛):1個系統評價發現,消炎痛與安慰劑比較,能明顯降低孕37周前的48 h和7天的早產率的證據有限.然而,同時發現消炎痛與安慰劑或不治療相比,并不能明顯降低圍生兒死亡率、新生兒呼吸窘迫綜合征、肺支氣管發育不良、壞死性小腸結腸炎、新生兒敗血癥或低體重兒.但這個系統評價樣本太小,尚不能發現有臨床意義的差異. (4) 擇期或非擇期剖宮產對早產婦女治療效果:1個系統評價結果發現,擇期剖宮產較非擇期剖宮產會增加孕母的發病率,卻不能降低新生兒的發病率和死亡率.但尚不能證明此效果是否對新生兒有臨床意義. (5) 改善早產妊娠結局的干預措施:①對早產者采用皮質類固醇:1個系統評價認為,對可能發生早產的婦女使用皮質激素較安慰劑或不處理能明顯降低早產兒出生后呼吸窘迫綜合征、新生兒死亡率和顱內出血的發生.②促甲狀腺激素釋放激素在早產中的運用:1個系統評價發現,在早產的高危婦女中,促甲狀腺激素釋放激素和類固醇激素聯合應用與單用皮質類固醇激素比較,對新生兒結局的影響無明顯差異,但會明顯增加孕母和胎兒的不良反應.③抗生素:1個系統評價發現,抗生素與安慰劑比較,不能延長孕周、降低新生兒死亡率,但可降低孕母感染率.

Effect of MDL28170 on Neural Apoptosis after HypoxicIschemic Brain Damage in Neonatal Rats

摘要:目的:探討卡配因抑制劑3（MDL28170）對新生大鼠缺氧缺血性腦損傷(HIBD)神經細胞凋亡的影響。方法:建立新生SD大鼠HIBD模型,治療組于缺養缺血后即刻、2 h、4 h腹腔內注射MDL28170,對照組及手術組同時予生理鹽水。缺氧缺血后24 h用免疫組化方法觀察大腦皮質及海馬CA1區Caspase3 蛋白表達、TUNEL法檢測細胞凋亡,觀察組織病理改變并計算海馬神經元死亡數,透射電鏡觀察細胞超微結構。結果:缺氧缺血后24 h缺血側大腦皮質及海馬CA1區Caspase3和TUNEL陽性細胞數較對照組明顯增加,透射電鏡證實有凋亡細胞;MDL28170可減少陽性細胞數量,抑制神經元死亡,差異有顯著性(Plt;0.05)。結論:MDL28170可通過抑制神經凋亡而對新生大鼠HIBD具有一定保護作用。Abstract: Objective: To investigate the effect of (Calpain inhibitor3) MDL28170 on neural apoptosis in a neonatal model of hypoxicischemic brain damage (HIBD). Methods: A neonatal model of HIBD was established, 7dayold SD rats were divided into three groups. The treatment group received MDL28170(ip) at 0 h,2 h,4 h after HI, whereas the other two groups were administered normal saline simultaneously. The expression of caspase3 (by immunohistochemistry), neural apoptosis (by TUNEL) in cortex and hippocampus ipsilateral to the insult were observed 24 h after HI; hippocampal CA1 neural loss and electromicroscopic changes were assessed at the same time. Results: Apoptotic body was observed by electromicroscopy. Caspase3 positive cells and apoptotic cells increased significantly in the ipsilateral cortex and hippocampal CA1 region compared to the control, and MDL28170 reduced the number of positive cells, attenuated CA1 neural loss with significance (Plt;0.05). Conclusion: It is suggested that MDL28170 may protect the brain of neonatal rats after HIBD by suppressing neural apoptosis.

THE FUNCTION OF NITRIC OXIDE IN THE NECROSIS OF AVULSED SKIN FLAP IN DOMESTIC PIG

To investigate the function of nitric oxide (NO) and nitric oxide synthetase (NOS) inhibitor, N-nitro-L-arginine methyl ester (L-NAME), the skin avulsion model was made in the lower extremity of pig. The methods of measurement of size of the survived flap, weighing, immunocytochemistry and hybridization in situ were employed, so that the survival surface area of flaps, tissue wet/dry weight ratio, NO content in the serum, gene expression of NO and NOS content in the flap tissue were determined, respectively. The results showed that the early gene expression of NOS was increased as well as the NO content and tissue wet/dry weight ratio (P lt; 0.01). After L-NAME was applied introvenously, the NO content and tissue wet/dry weight ratio were decreased (P lt; 0.01), and the survival surface area of flaps was enlarged (P lt; 0.01). It could be concluded that the NO might play a role in the development of the pathological changes as early congestion, edema and secondary necrosis in the avulsed skin flaps. The early application of L-NAME could do some good to the avulsed skin flap and protect it from further necrosis owing to the presence of NO.

The Essential Points of Liver Transplantation in China

INFLUENCE OF HUMAN TISSUE FACTOR PATHWAY INHIBITOR GENE TRANSFECTION ON NEOINTIMAFORMATION IN VEIN GRAFTS

【Abstract】 Objective To reduce restenosis in vein grafts after coronary artery bypass grafting, to investigate theeffect of human tissue factor pathway inhibitor(TFPI) gene del ivery on neointima formation. Methods The eukaryotic expressed plasmid vector pCMV-(Kozak) TFPI was constructed. Forty-eight Japanese white rabbits were randomly divided into 3 groups with 16 rabbits in each group: TFPI group, empty plasmid control group and empty control group. Animal model of common carotid artery bypass grafting was constructed. Before anastomosis, vein endothel iocytes were transfected with cationic l iposome containing the plasmid pCMV- (Kozak) TFPI (400 μg) by pressurizing infusion (30 min) in TFPI group. In empty plasmid control group, vector pCMV- (Kozak) TFPI was replaced by empty plasmid pCMV (400 μg). In empty control group, those endothel iocytes were not interfered. After operation, vein grafts were harvested at 3 days for immunohistochemical, RTPCR and Western-blot analyses of exogenous gene expression and at 30 days for histopathology measurement of intimal areas, media areas and calculation of intimal/media areas ratio. Luminal diameter and vessel wall thickness were also measured byvessel Doppler ultrasonography and cellular category of neointima was analyzed by transmission electron microscope at 30 days after operation. Results Human TFPI mRNA and protein were detected in TFPI group. The mean luminal diameter of the TFPI group, empty plasmid control group and empty control group was (2.68 ± 0.32) mm, (2.41 ± 0.23) mm and (2.38 ± 0.21) mm respectively. There were statistically significant differences between TFPI group and control groups (P lt; 0.05). The vessel wall thickness of the TFPI group, empty plasmid control group and empty control group was (1.09 ± 0.11) mm, (1.28 ± 0.16) mm and (1.34 ± 0.14) mm respectively. There were statistically significant differences between TFPI group and other control groups (P lt; 0.01). The mean intimal areas, the ratio of the intimal/media areas of the TFPI group were (0.62 ± 0.05) mm2and 0.51 ± 0.08 respectively, which were reduced compared with those of the two control groups(P lt; 0.05). The mean media areas had no significant differences among three groups (P gt; 0.05). Through transmission electron microscope analyses, no smoothmuscle cells were seen in neointima of TFPI group in many visual fields, but smooth muscle cells were found in neointima of two control groups. Conclusion Human TFPI gene transfection reduced intimal thickness in vein grafts.

Effects of Recombinant Adenovirus-Mediated Overexpression of hTIMP-1 on Proliferation of Human Liver Cancer Cell Line HepG2 in Vitro

Objective　 To explore the effects of overexpression of human tissue inhibitors of metalloproteinase-1 (hTIMP-1) on proliferation of human liver cancer cell line HepG2 in vitro. Methods　A recombinant adenoviral vector containing full-length cDNA of hTIMP-1 was generated and transfected into HepG2. The viral titer was checked by measuring GFP, and the expression of hTIMP-1 in vitro was detected by the techniques of Western blot and semi-quantitative RT-PCR. The ultrastructure was observed by transmission electron microscope and the effects of overexpression of hTIMP-1 on proliferation of HepG2 in vitro was analyzed by MTT assay and growth curve. Results　The resultant AdhTIMP-1 was successfully constructed and the expression of hTIMP-1 was detected by Western blot and RT-PCR. The growth and proliferation of HepG2, which had been transfected with AdhTIMP-1,　 was significantly inhibited. Conclusion　The proliferation of HepG2 was markedly inhibited by recombinant adenovirus-mediated overexpression of hTIMP-1, which may pave the way for further application in liver gene therapy.

ACEI對心瓣膜置換術后患者s-ICAM-1、s—VCAM-1和v—WF含量的影響

目的 觀察血管緊張素轉化酶抑制劑（ACEI）對風濕性心臟病心瓣膜置換術后患者血漿中可溶性黏附分子含量和心功能的影響。方法 85例風濕性心臟瓣膜病患者行心瓣膜置換術后被分為雅施達組（28例）、卡托普利組（29例）和對照組（28例），分別給予雅施達、卡托普利和安慰劑治療。于手術后4周、8周抽血測定血漿中可溶性細胞間黏附分子-1（s—ICAM-1）、可溶性血管細胞問黏附分子-1（s—VCAM-1）和血管性血友病因子（v—WF）的含量，并同時測定心功能。結果 雅施達組和卡托普利組患者的s—ICAM-1、s—VCAM-1和v—WF濃度均低于對照組（P〈0．05），術后4周心功能恢復較對照組好（P〈0．05），但雅施達組和卡托普利組間比較差別無統計學意義（P〉0.05）。結論 ACEI能降低風濕性心臟病患者術后血漿中可溶性黏附分子水平，加強心瓣膜置換術后心臟功能恢復；而與ACEI的種類無明顯的關系。

RESEARCH ADVANCE OF ROLE OF INHIBITOR OF DIFFERENTIATION 2 IN SKELETAL MUSCLE REGENERATION

Objective To review researches of the role of inhibitorof differentiation 2(Id2) in skeletal muscle regeneration. Methods The latest original literature concerning Id2 and its role in skeletal muscle regeneration was extensively reviewed. Results Id2 could form heterodimers by combining with E protein to prevent myogenic regulatory factors (MRFs) forming heterodimers by combining with E protein, to inhibit the transcription activity of MRFs anddifferentiation of skeletal muscle cell. Conclusion Id2 plays an important role in skeletal muscle regeneration.

INHIBITOR OF NITRIC OXIDE SYNTHASE ON THE DENERVATED MUSCLE ATROPHY

Objective To study the effect of the competitive inhibitor of nitric oxide synthase NG-nitro-L-arginine methyl ester (LNAME) on thedenervated muscle atrophy. Methods A model of the denervated gastrocnemius atthe right lower limb was established in 36 SD adult rats. The rats were randomly divided into two groups: the L-NAMEgroup (Group A) and the control group(Group B). L-NAME 10 mg/ kg daily was injected into the denervated gastrocnemius inGroup A, and normal saline was injected into the denervated gastrocnemius in Group B. At 2, 4 and 8 weeks after operation, the rate of the muscle wet weight preservation, the cross section area of the myocyte, the protein amount, and the percentage of the apoptotic muscle cells were measured respectively and the ultramicrostructure of the myocyte was observed. Results At 2 and 4 weeks after operation, the rate of the muscle wet weight preservation, the cross section area of themyocyte, and the protein amount were significantly greater in Group A than in Group B; however, the percentage of the apoptotic muscle cells was significantly smaller in Group A than in Group B. The observation of the ultramicrostructure of themyocyte showed that an injection of L-NAME could protect the ultramicrostructure of themyocyte. At 8 weeks after operation, there was no significant difference between the two groups in the abovementioned parameters. Conclusion The nitric oxide synthase inhibition can delay the denervated muscle atrophy.

Suppressing Function of Breast Cancer Metastasis Suppressor 1 in Breast Cancer Metastasis

Objective　To review the recent studies on the suppressing function of breast cancer metastasis suppressor 1 (BRMS1) in breast cancer metastasis. Methods　The recent literatures on the mechanisms of BRMS1 in the breast cancer that were published in and abroad were reviewed and summarized. Results　BRMS1, similar to the other anti-metastasis genes, only suppresses the metastasis of breast cancer cells but has nothing to do with the growth of tumor. BRMS1 could suppress metastasis of tumor cells by reestablishing both the homospecific and the heterospecific gap junctional intercellular comminications (GJIC) and by altering the expressions of relevant metastasis genes in the breast cancer. Conclusion　Further studies on BRMS1 may be helpful to understand the metastasis of breast cancer, which may provide a new way for the diagnosis and treatment of breast cancer.