抑制...

KIR bind corresponding HLA-Ⅰmay hame four results followed:1、When inhibitory KIR bind HLA-Ⅰand there has no activatory KIR bind it,cell isn\'t dissolve because inhibitory signal access was done;2、When activatory KIR bind corresponding HLA-Ⅰand there has no inhibitory KIR bind it,form activate signal,lead cell dissolve.3、If activatory or inhibitory receptor both bind HLA-Ⅰ,both signal access is make done,when activatory signal play the main role,NK cell still actived,lead target cell dissolve.4、If activatory or inhibitory receptor both bind HLA-Ⅰ,both signal access is make done,when inhibitory signal play the main role,or both signal access don\'t play,NK cell do not make effect.this is NK cell recognice nomal tissue.

与活化型KIR受体相比，抑制型KIR受体与HLA-Ⅰ类抗原结合的亲和性更强，当抑制型和活化型KIR受体识别和结合同一HLA-Ⅰ类抗原分子时，以抑制作用为主。KIR与相应HLA-Ⅰ结合后可能产生以下4种情况：①当抑制型KIR与HLA-Ⅰ结合而无活化型KIR与HLA-Ⅰ相互作用时，因抑制信号通路启动而不产生细胞溶解；②当活化型KIR与靶细胞表面的相应HLA-Ⅰ结合同时无抑制型KIR与HLA-Ⅰ的相互作用时，形成刺激信号通路，导致靶细胞溶解。

Immunohistochemical localization of inhibin α-subunit in normal mature rats was carried out by using Strept Avidin-Biotin-Peroxidase Complex .The results showed that there was positive immunoreactivity of the McAb to inhibinα-subunit in heart ,kidney , spleen , lymph ,adrenal gland and pancreas cells. It indicated that inhibinα-subunit existed in the above tissues , But no positive sites were seen in hypothalamus, pituitary, lung and liver, that means they have no inhibinα-subunit. Compared with the ovariectomized rats, the hypothalamus and pituitary of the rats injected with inhibin-α fragment（1～32）showed an positive reaction, suggesting that inhibin α-subunit could pass through the blood-brain barrier .

用链霉亲和素-生物素-过氧化物酶(Strept Avidin-Biotin-Peroxidase Complex， SABC)免疫组织化学方法，以抑制素α亚基单克隆抗体对正常雌性性成熟大鼠各组织的抑制素α亚基进行定位观察，结果显示：⑴大鼠心脏、肾、脾、淋巴、肾上腺、胰腺均呈阳性反应，表明存在抑制素α亚基；下丘脑、垂体、肝脏和肺组织呈阴性反应，表明其不存在抑制素α亚基；⑵与去卵巢大鼠相比，外源注射抑制素α（1～32）片段的大鼠其下丘脑和垂体出现阳性反应，说明抑制素α亚基能通过血脑屏障。

Analysis of nuclear extracts of human cells has indicated a similar excision repair mechanism for nick-directed mismatch correction in higher cells, and several reconstituted systems that rely on purified human proteins have been described, such as hMutSα、hMutSβ、hMutLα. Recently, scientists discovered that nickel could be inhibitors of DNA repair. Nickel can greatly enhance the mutagenicity and genotoxicity of compounds in cigarette by inhibiting the nucleotide excision repair pathway in human cells. We have confirmed that nickel could inhibit MMR of E. coli and human and presumed that nickel inhibited repair before MutH incision of the MMR in E. coli. However, there is no evidence of mechanism of nickel inhibiting MMR in human cells.

镍是存在於香菸中的微量金属，近年来有学者发现镍是DNA修复反应的抑制剂，长期抽烟的人会容易因为香菸中化合物攻击DNA而引起突变，进而引起肺癌，而镍会抑制核苷酸移除修复系统（nucleotide excision repair；NER），所以使得体内的DNA损伤无法修复；过去实验室已经证实大肠杆菌的核酸配对错误修复系统会受到镍等重金属的抑制，并且推测出镍的抑制反应是抑制在修复反应的上游nicking的步骤；另外，也证实了人类的核酸配对错误修复系统也会受到镍的抑制，然而还没研究证实会抑制在核酸配对错误修复反应的哪个步骤。

Results: Of 59 superficial bladder cancer samples, sensitivity tests were successfully performed in 45 samples, and the others failed, the successful rate was 76.3%.Diversity of inhibiting rates of antitumor drugs was observed in samples from different individuals. Except MTX in stage of G1 and G3, no correlation has been found between the phenotype of sensitivity assay and the pathological grade and stage. Sensitivity and mean inhibiting rates of antitumor drugs in the primary group were notedly higher than that in the recurrent group.The combination of two therapy agents, which have different mechanisms or different cell-cycle targets, showed significantly more sensitivity and higer mean inhibiting rates than single one in superficial bladder cancer in different individuals.

结果：14例失败，45例获得成功，总体可评价率为76.3％，不同抗癌药物对不同个体膀胱癌的抑制率存在明显差异；除MTX对膀胱癌G1和G3级平均抑制率差异有统计学意义外，其它抗癌药物对不同个体膀胱癌细胞的平均抑制率与膀胱癌的病理分级、分期均无关；抗癌药物对初发膀胱癌的敏感率和平均抑制率均高于复发膀胱癌；两种不同作用机制的抗癌药物联合应用对不同个体膀胱癌细胞的敏感率和平均抑制率均高于单一药物，二者敏感率和平均抑制率差异有统计学意义。

AIM: To isolate bioactive secondary metabolites from the fruits of Schisandra rebriflora Rehd. et. Wils and study their effects on HIV-1 infectivity. METHODS: Inhibition of syncytia formation, HIV-1 reverse transcriptase and protease, protection of HIV-1 infected cells, level of HIV-1 p24 antigen,blockage of fusion were detected. RESULTS: A lignan compound, named rubrifloralignan A, was first isolated as a natural product with modest inhibition effects on syncytium formation and HIV- 1 replication and could protect HIV-1 infected cells with weak inhibition effects on fusion and RT, but it showed no effects on the replication of HIV-1 chronic H9 and PR. CONCLUSION: Rubrifloralignan A is an efficient anti-HIV-1 product with effect on early stage of HIV-1 replication.

目的：从红花五味子果实中寻找活性代谢产物，研究其抗HIV—1活性和作用机制方法：通过合胞体抑制、HIV-1感染细胞保护、HIV—1p24抗原测定、融合阻断、逆转录酶和蛋白酶活性分析等实验，检测分离化合物的抗HIV—1活性并探讨其作用机制一结果：红花五味子甲素能够抑制病毒诱导的合胞体形成，保护病毒感染细胞，抑制病毒在细胞内的复制对HIV-1感染细胞与正常CD4^＋细胞间的融合，逆转录酶活性有一定的抑制作用但是红花五味子甲素不抑制病毒在慢性感染细胞中的复制，也不抑制蛋白酶的活性、结论：首次从天然产物中分离得到红花五味子甲素，它对HIV—1病毒复制早期具有抑制作用

Studies also indicated that genistein exsists not only in soybeans but also in many kinds of plants such as vegetables and fruits.As a potential anticancer agent, the actional mechanisms of genistein mainly includes as follows:First, genistein can depress the activity of protein tyrosine kinase and transduction pathways for the phosphorylation of receptors and mitosis signal. So genistein can lead to cells' proliferation depressed. Second, genistein has minimal effects of phytoestrogens. It can be combined with estrogen receptor and improve the synthesis of cellular sex hormone binding glulobin, and improve the activity of UDP-glucuronyl transferase. Through these pathways, it can inhibit the cell activity of breast cancer and prostate cancer.

作为一个很有潜力的抗肿瘤物质，三羟异黄酮的作用机制主要包括：①抑制蛋白酪氨酸激酶活性，可阻抑PTK引起的受体磷酸化和有丝分裂的信号传递，导致癌细胞增殖受抑；②弱雌激素作用：可通过与体内雌激素受体结合，并可增加细胞内性激素结合球蛋白的合成，增加UDP-葡糖醛酸转移酶的活性等途径抑制乳腺癌和前列腺癌细胞活性；③拓扑酶Ⅰ和Ⅱ抑制剂，抑制细胞活性；④上调细胞周期性负性调节因子P21WAF1/CIP1的表达，使之负性调节因子作用增强；⑤可阻止胰岛素样生长因子-Ⅰ、肝细胞生长因子和神经生长因子的作用而抑制肿瘤生长；⑥其他：抗氧化作用、抑制热休克蛋白、诱导细胞凋亡、抑制新生血管生成和抑制多种耐药相关蛋白等。

Dialectic retinopathy,the most common microvascular complication of diabetes is the leading cause of blindness.Many drugs have been used to prevent the development of it.The primary drug treatment includes the intensive control of blood glucose,blood pressure and the reducing ofblood-fat. The directed against drug treatment includes advanced glycation end products inhibitor, vascular endothelial growth factor inhibitor,inhibitive factor promoter,supplement of inosital, aldose reductase , protein kinase C inhibitors, GH inhibitors,improvement of retinal microcirculation, DAG-PKC inhibitor, ginkgo blibe extract, antioxidant.

糖尿病视网膜病变是最常见的糖尿病微血管病变，目前有很多致力于延缓糖尿病视网膜病变的药物研究，包括严格控制血糖、血压，降低血脂的基础药物治疗，以及蛋白非酶糖基化终末产物抑制剂、血管内皮生长因子抑制剂和抑制因子促进剂、肌醇的补充及醛糖还原酶抑制剂的应用，及蛋白激酶C抑制剂、生长激素抑制素、改善视网膜微循环药物、DAG-PKC抑制剂、银杏叶提取物、抗氧化剂等针对性药物的应用。

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。

RESULTS:(1) ET-1 could increase total protein production, surface area, ERKs activity and ［Ca2+］i in cultured cardiomyocyte in dose-dependent manner at concentrations ranging from 10-9 to 10-7 mol/L. And this effect could be abolished by BQ123, an antagonist of ETA receptor, partly inhibited by PTX, but not by BQ788, an antagonist of ETB receptor.（2）The activation of ERKs and the increase of ［Ca2+］i induced by ET-1 were obviously inhibited by PD98059, a selective ERKs kinase inhibitor, and nifedipine, a calcium channel blocker, respectively. Both antagonists partially inhibited ET-1-stimulated cardiomyocyte hypertrophic response.(3) Staurosporine, a selective PKC inhibitor, could inhibit ET-1-stimulated cardiomyocyte hypertrophic response and increase of ［Ca2+］i, but not affect the activation of ERKs.

结果： ①ET-1浓度依赖性增加新生大鼠心肌细胞蛋白质含量和心肌细胞表面积、ERKs活性及［Ca2+］i浓度，以上作用可被ETA受体拮抗剂BQ123所完全抑制，被百日咳毒素部分抑制，而ETB受体拮抗剂BQ788则无效；②ERKs激酶特异性抑制剂PD98059可完全抑制ET-1激活ERKs的作用，钙通道拮抗剂硝苯地平可明显抑制ET-1介导的［Ca2+］i浓度增加，但二者皆仅部分抑制ET-1介导的心肌细胞肥大反应；③蛋白激酶C选择性抑制剂staurosporine并不能明显抑制ET-1介导的ERKs激活，但可抑制ET-1介导的的［Ca2+］i浓度增加及心肌细胞肥大反应。

Results After suppression of1mg dexamethasone,the plasma cortisol of all patients with Cushing's syndrome were more than1.8μg/dl,and94.6%patients'more than5μg/dl.Several kinds of diagnostic standards were good when used for2mg dexamethasone suppression test in Cushing's syndrome,a-mong them,the standard for urine free cortisol after suppression should be adjusted to50%of the contrast and the as-sayed data should in normal limits.Low dose dexamethasone suppression tests were not satisfied when used among the patients with some situations needed to differentiate with Cushing's syndrome.Suppressed by8mg dexamethasone could direct the diagnose of Cushing's disease（97.0%）,though17.7%of this kind of patients could not be sup-pressed;it was not suppressed in other etiological diseases（93.4%）Conclusion The results of dexamethasone sup-pression tests were match the clinical examination.

结果 所有库欣综合征病人在1mg地塞米松抑制后血皮质醇大于1.8μg/dl，94.6%的病人大于5μg/dl；2mg地塞米松抑制后多种诊断标准在库欣综合征病人中均较好，其中尿游离皮质醇抑制后诊断标准应调整为对照值的50%并在正常范围内；小剂量地塞米松抑制试验对类库欣情况鉴别均较差；8mg地塞米松试验能抑制的病人基本可诊断为库欣病（准确性97.0%），但有17.7%的病人不抑制，其他病因的库欣综合征基本不抑制（准确性93.4%）。

The labia have now been sutured together almost completely.The drains and the Foley catheter come out at the top.

此刻阴唇已经几乎完全的缝在一起了，排除多余淤血体液的管子和Foley导管从顶端冒出来。

To get the business done, I suggest we split the difference in price.

为了做成这笔生意，我建议我们在价格上大家各让一半。