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Decidual tissue is a very complex and highly concordant tiny environment between mother and embryo during pregnancy, which is constituted of the variety cells such as extravi11ous trophoblast,endometrium cells, bone marrow cells, decidua l microphage,T cells and a few B cells and so on.

正常蜕膜组织是母-胎界面间一个非常复杂而又高度协调的微环境,它由多种细胞如侵袭至蜕膜的绒毛外滋养细胞(extravi11ous trophoblast,EVT)、子宫内膜源性细胞(如上皮细胞和血管内皮细胞)、骨髓源性细胞(如大颗粒淋巴细胞、蜕膜巨噬细胞、T细胞和少许B细胞)构成,这些细胞以及由这些细胞、母体和胎儿所分泌到蜕膜的细胞因子共同形成了母-胎间信息交流的平台,并对胚胎滋养细胞"有控性"侵袭、子宫内膜的免疫容受性、蜕膜化和胎盘的形成进行精细的调控。

First we first establish the apoptosis of related protein glossary database, then downloads the neurodegenerative disorders of apoptosis related abstract from the on-line biomedicine literature , and searchesfor the protein information database of the neurodegenerative disorders of apoptosis related pathway, then uses the data mining technology,with apoptosis of protein related glossary database use already establishment. Automatically searches for the neurodegenerative disorders of apoptosis related protein by the program in the biomedicine literature abstract separately in,(1) a sentence,(2) two sentences,(3) aliterature, finding simultaneously appears protein-protein interation. And comparing to the neurodegenerative disorders of apoptosis related protein database, looking for their repetition. This result comparing to the known neurodegenerative disorders of apoptosis related pathway, thus looking for unestablished neurodegenerative disorders of apoptosis pathway.

首先我们先建立细胞凋亡讯息蛋白质相关词汇字库,再从线上生物医学文献下载神经退化性疾病细胞凋亡相关文献摘要,并且搜寻线上蛋白质资料库中神经退化性疾病之细胞凋亡讯息蛋白质传递路径,接著利用文献探勘技术,使用已建立之细胞凋亡讯息蛋白质相关词汇字库,以程式自动在生物医学文献摘要中搜寻神经退化性疾病细胞凋亡相关蛋白质分别在,(1)一个句子、(2)二个句子、(3)一篇文献,中同时出现的两两蛋白质关系,再与已知线上神经退化性疾病细胞凋亡讯息传递路径资料库的蛋白质两两关系做比较,找出两者重复建立的部分,把这个结果与线上已知之细胞凋亡讯息传递路径资料库蛋白质关系作比较,由此找出尚未建立之细胞凋亡讯息传递路径图。

Results: Tyroserleutide can significantly increase the life span of H22 tumor-bearing mice by 50-70% in dosages of 20ug/kg/d-80ug/kg/d,specially the high dosage of 80ug/ml can significantly increase the life span by 69.24%; Tyroserleutide can inhibit the growth of transplanted hepatocellular tumor BEL-7402 in nude mice,the rate of tumor inhibition was25-50% in dosages of 40-320ug/ml ,the inhibition rate of 160ng/ml was 44.03%; Tyroserleutide could inhibit the growth of H22 and BEL-7402 tumor in a dose-dependent manner. Simultaneously, tumoricidal activity of tyroserleutide against BEL-7402 cell line in vitro was observed hinger when compared with the control group(P.05).The inhibition effect of 72hrs was higher than 24hrs,48hrs,96hrs.And specially the high dosage of 160ug/ml can significantly inhibit growth of tumor cell by 19.36%. Tyroserleutide can activated PEM and marked enhance cytotoxicity andphagocytosis functions in vitro and in vivo. The OD values of cytotoxicity were observed hinger when compared with the control group(P.05).The cytotoxicity of macrophages activated by tyroserleutide against BEL-7402 and B16-F10 was 35.58%,61.2% in vitro and21.39%,47.63% in vivo. The cytotoxicity rate of nude mice PEM was 32.86%,73.07% in vivo. Furthermore, tyroserleutide alone could stimulated the production of IL-1B TNF- a and NO by M . Tyroserleutide and LPS could synergistically activated M producing more cytotoxicity effectors. Conclusion: Tyroserleutide had inhibition functions against hepatoma carcinoma .Its possible mechanisms were related to the affect that Tyroserleutide could inhibit tumor cell directively and induce tumor cells apoptosis or death effectively.

结果:酪丝亮肽能显著延长腹水型肝癌H_(22)小鼠的生存时间,给药剂量为80μg/kg/d时疗效最显著,达到69.24%,在20μg/kg/d-80μg/kg/d剂量范围内生命延长率为50-70%,给药剂量与荷瘤鼠生存时间呈现一定量效关系;酪丝亮肽能显著抑制人肝癌BEL-7402移植瘤裸鼠的肿瘤生长,给药剂量为160μg/kg/d时疗效最显著,抑制率为44.03%,并且在40-320μg/kg/d剂量范围内抑制率为25-50%,给药剂量与肿瘤抑制率呈现一定量效关系;酪丝亮肽体外对人肝癌BEL-7402细胞生长有一定的抑制作用,在作用72hrs时各浓度酪丝亮肽对肿瘤细胞的抑制作用较24hrs、48hrs、96hrs明显,其中浓度为100μg/ml时抑制率达19.36%;酪丝亮肽体内外均能增强小鼠腹腔巨噬细胞对肿瘤细胞的杀伤:体外作用中巨噬细胞对BEL-7402、B16-F10的杀伤功能明显增强,与效应细胞对照组相比有显著性差异(P<0.05)杀伤率分别达到35.58%、61.2%;体内作用中巨噬细胞对BEL-7402、B16-F10的杀伤功能明显增强,与生理盐水对照组相比有显著性差异(P 。05),杀伤率分别达到21.39%、47.63%;裸鼠腹腔巨噬细胞经酪丝亮肤作用后对BEL一7402、B 16一F10杀伤功能明显增强,与生理盐水对照组相比有显著性差异(P.05),最高杀伤率分别达到32.86%、73.07%;酪丝亮肤能增强单核巨噬细胞系统的吞噬功能,吞噬指数与生理盐水组比较有显著性差异(P.05);酪丝亮肤体外作用能促进小鼠腹腔巨噬细胞分泌合成细胞毒效应分子IL一lp、TNF一Q和NO,与效应细胞对照组相比有显著性差异(P.05);酪丝亮肤体内作用能促进小鼠腹腔巨噬细胞分泌合成细胞毒效应分子IL一lp、TNF一Q和NO,与生理盐水对照组相比有显著性差异(P.05);酪丝亮肤能促进鼠巨噬细胞株R戌W264.7分泌合成IL一1p和NO,IL一1日、NO水平分别在酪丝亮肤作用24hrs、12hrs时达到高峰,酪丝亮肤单独应用能提高巨噬细胞的分泌合成功能,而且酪丝亮肤能与LPS协同作用刺激巨噬细胞的细胞毒效应分子分泌合成。

TyPe II collagen induced arthritisln the rat ank1e joint andoVathumin as antigen induced arthritis WA in the rabbit knee joint wereestab1ish2 Qualitative evaluation of me in skin, muscle, synovium, cedilagearound joint and blood was performed by OMA3 The CIA rats were treated on day 7 after hind paw swelling and erythemaAnimals were injected intravenously with ase at a dose of 10mg/kg,tWenty minuots 1ater, one ankle of the rats random1y assigned was exPosedlaser irradiation at l00J/cm fOr l000 seconds, and another ankle wasM grouP wihout laser The other two groups is unmanipulatedcontrol group and untreated CIA group Bimaleolar ankle widthmeasuremellts were taken in all animals every tWo days using amicrometer The histopathology of the ank1e Joint was assessed at day 21after disease onset4 The pro1iferating cell nuclear antigen WCNA of CIA treated by PDT andthe HMME group without laser was doterdrined by immunohistochemiStry5 The AfA rabbits were treated on day 7 after knee swelling and erythemaThe theraPy invo1ved lntravenous injection of l0mg/kg HMME, fOl1owedby 20 minues period in dim light, and transdermal light treatment with\l00 J/cm2 fOr l000 seconds The inner sides of the treated Anees wereirradiated at first, and then the outer side did 24 hours later, the synovialtissue of the Anees joint were removed and in situ cel1 aPoptosis wasdetCCted With tednal deoxync1eotidyl transferase-mediated dUTP nickend labelingR6suIt8:l The pathologic changes of CIA and AIA include subsynovial inflammation,opovial hyPerplasia, pannus formation, cartilage and bone destructionresemble RA.2 The studies demonstrated that there are different uptake of HMME withinskin, muscle, synovium, cartilage and b1ood, and the synovium cou1draPidly uPtake more ase than skin and cartilage at the firSt 30 minuesaller intravenous injection of HMME3 The bimaleolar anke width had no different among PDT treated group,H group withollt 1aser and untreated CIA group But hlstologicalevaluation showed statiStical1y significallt reductions in synovialhyperplasia, pannus formation and cart1lage reosion, bone destruction andtotal score in PDT treated group4 Image analysis showed that the ratlo bforeen the areas of the coufltedobect to that of the entire area in PDTtreated grOup is lower than that in conirol group, but the integrated oPticaldensity had no different between the two groups5 Imape analysis showed that the ratio between the area of the countedobject to that of the e

治疗组在大鼠出现踝关节红肿后1周,炎症达到高峰时进行PDT治疗。随机治疗大鼠一侧的踝关节,另。2。一一侧作单纯HMME 对照。治疗方法是大鼠麻醉后尾静脉注入 HMME10ngkg,20分钟后踝关节照光,激光波长627.sum,功率密度 100mwcm',照射时间1000秒,能量密度100)/。治疗后避光喂养72 小时。隔日一次测量大鼠的踝关节左右横径,治疗后两周取关节进行病理d 观察。 4。大鼠CIA模型用上述方法进行PDT治疗后,治疗组和单纯HMME 组用兔疫组化SP法检测石蜡切片的核增殖抗原。 5。兔AIA模型在关节炎出现第七天进行PDT治疗,随机治疗一侧膝关节,另一侧作自身对照。兔耳静脉注入I'arrainrelomg/Kg,20分钟后,膝关节用金蒸气激光照射,激光能量密度100)儿旷。24 /J'时后取膝关节滑膜作病理检查,并用脱氧核昔酸末端转移酶介导的缺口末端标记法原位检测凋亡细胞。结果: 1。模型观察:CIA大鼠炎症高峰期滑膜下炎细胞浸润明显,滑膜细胞明显增殖,炎症达到高峰后二周,血管缀形成,并侵蚀和破坏软骨和骨, CIA模型病理改变与人类RA相似。兔AIA模型膝关节滑膜病理可见滑膜细胞增生,滑膜下炎细胞浸润,也与人类RA滑膜改变相似。 2。关节周围组织中光敏剂含量的测定结果表明,各组织对HMME 的吸收速度和吸收量不同,荧光值一时间曲线不同,滑膜组织比皮肤和软骨对 HMME的吸收多,在 2 0分钟时即有明显差异。 3.PDT对CIA模型的治疗结果表明:PDT治疗后关节炎组、单纯 HMME组和治疗组踝关节左右横径统计学检验差异没有显著性,但病理评分PDT治疗组滑膜增生、血管资形成及软骨破坏、骨破坏和总分比关节炎对照组和HMME对照组好,统计学检验差异有显著性。。3_军医进修学院硕士学位论文中文摘要 4.PDT治疗组PCNA阳性细胞较对照组少,图像分析结果表明面密度(阳性染色的面积总和与统计视野面积的比值)治疗组小于对照组,统计学检验差异有显著性。。 5.PDT治疗组凋亡阳性细胞较对照组明显增多,图像分析结果单位视野内阳性细胞数和面密度PDT治疗组高于对照组,统计学检验差异有显著性。凋亡细胞核直径PDT治疗组较小,与对照组相比,统计学检验差异有显著性。结论:二。CIA、AIA的病理改变类似人类RA,可作为研究RA病因、发病机制、检查及治疗方法的模型。 2。各组织对HMME的吸收速度和吸收量不同,滑膜组织比皮。

Furthermore, preliminary work also performed to examine whether PI3K/AKT signal transduction pathway was activated in the process of refractory leukemia development. Materials and methods An immortalized human bone marrow stromal cell line, HS-5, was introduced to establish a bi-phase culture system for the cultivation of B-lineage precursor leukemia cells. ELISA and RT-PCR were used to investigate the expression of VEGF and its receptors in the leukemia cell lines and primary childhood leukemia cells in different treated groups. Flow cytometory method and immunofluorescent staining were employed to examine the apoptosis signals both in the VP16 treated and untreated leukemia cells. Western blot was utilized to explore the PI3K/AKT activated status in the drug induced or uninduced leukemia cells and lymphocytes from healthy donors.

材料和方法使用来源于人类骨髓基质细胞的细胞株HS-5作为滋养层细胞进行急性淋巴细胞性白血病细胞的体外培养,通过细胞生物学和免疫学方法评估培养体系并鉴定出难治性白血病细胞克隆;以ELISA和RT-PCR方法检测急性白血病细胞株和患儿白血病细胞VEGF及其受体的表达,了解不同治疗阶段VEGF及其受体的表达状况,并结合临床指标进行分析,明确VEGF及其受体在白血病发生过程中的作用;流式细胞仪和免疫荧光染色法对正常健康儿童、初发白血病患儿、复发白血病患儿及缓解后患儿进行凋亡因子检测和分析,初步阐明难治性白血病抗凋亡形成的原因;蛋白印记分析检测PI3K/AKT信号传导通路在健康儿童、初发白血病和复发白血病患儿的表达,初步了解难治性白血病形成的分子生物学机制。

The histopathologic changes included lymphocyte and monocyte infiltration,hyperplasia of synovial cells and small vessels,interstitial fibrosis,hyaline degeneration and cartilaginous metaplasia.The immunohistochemical observations showed that the high expressions of IL-1 and IL-6 were significantly different between the pathologic plicae and the control groups(P<0.01).The positive expressions of IL-1 and IL-6 were the synovial cells and monocyt-lymph cells in the pathologic synovial plicae.The positive expressions of MMP-1 and TIMP-1 have significant difference between the experiment and control group(P<0.01,P<0.05).The expression of MMP-1 was positive in synovial lining cell,monocyte,fibroblast,endothelial cell in small vessel and chondrocyte.The TIMP-1 expression was detected in the synovial lining cells and a small quantity fibroblast.

结果 正常滑膜皱襞和病理性滑膜皱襞在滑膜细胞增生及小血管增生、间质纤维化及玻璃样变、软骨化生组织学改变方面,差异均有显著性(P<0.01);IL-1、IL-6在病理性滑膜皱襞内的增生滑膜细胞、单核及淋巴细胞和在正常滑膜皱襞内的表达差异均有显著性(P<0.01); MMP-1、TIMP-1在病理性滑膜皱襞和正常皱襞内的阳性表达,差异具有显著性(P<0.01,P<0.05),MMP-1在增生滑膜衬里层细胞、单核和纤维母细胞、血管内皮细胞和软骨化生的软骨细胞呈阳性表达;TIMP-1只在滑膜衬里层细胞和少量纤维母细胞有表达。

Results were shown as followings:(1) Sodium selenite at 0~2.5 μmol/L significantly increased the antioxidative capacity of L-02 cells without having remarkable impact on SMMC-7721 cells;(2) Sodium selenite at concentrations above significantly increased telomerase activity, hTERT gene expression and telomere length of L-02 cells without significant impact on SMMC-7721 cells;(3) Sodium selenite at higher concentrations (larger than 5 μmol/L) resulted in peroxidation of L-02 cells, while scutellarin significantly counteracted its effect;(4) Selenium-rich amino acids from silkworm pupas in the range of 0.5~2.5 μmol/L Se significantly inhibited SMMC-7721 cell growth, induced apoptosis and cell cycle change, and the generation of reactive oxygen species. In contrast, sodium selenite and selenomethionine only had weak impact on them at the same concentrations;(5) A new selenium-containing protein was found from selenium-rich silkworm pupas, which is worthy to be study further;(6) An expression vector containing ansense RNA of hTERT gene were constructed and used to transfect SMMC-7721 cells. They were observed to inhibit hepatoma cells.

结果如下:(1)0~2.5μmol/L亚硒酸钠显著性增强L-02细胞的抗氧化能力;而对SMMC-7721细胞的作用不显著;(2)该浓度硒显著性提高L-02细胞端粒酶活性、增强hTERT基因表达和延长细胞端粒长度;而对SMMC-7721细胞的作用均不显著;(3)高浓度硒(5μmol/L以上)显著性抑制L-02细胞生长、致细胞过氧化,灯盏花素能拮抗硒所致过氧化、降低硒毒性;(4)0.5~2.5μmol/L富硒蚕蛹氨基酸显著性抑制肝癌细胞SMMC-7721生长、导致细胞凋亡和周期改变、诱导细胞产生活性氧,同浓度亚硒酸钠和硒代蛋氨酸对其抑制不显著;(5)富硒蚕蛹蛋白经分离纯化和鉴定后发现存在一新含硒蛋白,其结构和功能有待研究;(6)通过已有的含hTERT基因质粒,成功构建hTERT反义RNA表达质粒,转染SMMC-7721细胞后对其生长具有抑制作用。

Monocyte-platelet aggregates remained elevated for 30 min after stress in the emotion trigger group.

心理应激组在应激过后30分钟单核细胞性血小板的聚集仍在增加。

Relationship between hepatitis B virus covalently closed circular DNA and HBx protein expression in hepatocellular carcinoma and its significance.

乙型肝炎病毒cccDNA与HBx蛋白在肝细胞性肝癌中表达的关系及意义。

AIM: To explore relationship of hepatitis B virus covalently closed circular DNA expression to the expression of HBx protein within hepatocellular carcinoma and to investigate their significance.

目的: 探讨肝细胞性肝癌中乙型肝炎病毒cccDNA与HBx蛋白表达的关系及其意义。

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