细胞发生的

Can accelerate the bone marrow cell from G1 phase into S phase when we measure it's Cell cycle, it make S phase rate was increased .thus it promoted DNA synthesize and repaired. Mice irradiated at dose of 5.5 Gy gamma-irradiation showed timed-related decreases and restores in peripheral blood picture at day 1 through day 21, the counts of WBC of these group had taken drug has various degree to increase than irradiation control group in day 1. Grugs failed to protected the peripheral blood cell at lowest point, but seems promote their rescovery.9803 treated group was distinct. At 7days after mice were radiated in 3.5 Gy. we observed drug can Significantly hold back the decreased number of hematopoietic progenitors colony forming radiation induced. These findings indicated 9803 have a certain radioprotective activity against gammer irradiation in mice.

给药组的 CFU-S 数量较照射对照组明显增加，3.5Gy 照后第七天观察给药9803组对小鼠骨髓造血组细胞集落生成能力的影响，给药组的造血祖细胞集落的形成能力强于照射对照组，并且9803组明显优于523组。5.5Gy 照射引起的小鼠的外周血细胞数量的降低以 WBC 发生最早，照后24小时给药组的 WBC 数量均比照射对照组有不同程度的升高，以9803各给药组最为明显，药物未能使照射引起的外周血细胞最低值升高，而有降低的趋势，但给药对照射后期外周血象的总体恢复有较好的促进作用。7.5Gy 照射后第七天测定小鼠骨髓细胞周期的测定中发现9803具有促进骨髓细胞由 G1期进入 S 期的效应，致使 G0/G1期细胞显著减少， S 期细胞比率显著增加，这利于促进 DNA 合成修复，即促进骨髓细胞增殖，骨髓细胞 DNA 含量给药组显著高于照射对照组。

The backbone of sugar residues chain in LBP-4a were contained l-6 indican bond according to periodate oxidation and the results of -elimination reaction indicated that the chain of polysaccharides and protein were connected by O-linked chemical bond.

腑实验证明用含有LBP一4 50 mg一1、100 mg·L-l、200mg.L'，和400mg·L-l的培养液培养人肝癌细胞邻Y一7703可显著抑制其增殖；细胞形态学观察发现LBP一4可诱导那Y一7703细胞发生凋亡，使细胞凋亡指数显著提高。

TJU103 combined with CTLA4-Ig could induce tolerance of donor CD4〓 T-cell to the given antigen, and the tolerance could be transferred by the anergic CD4〓 T-cell and supernatants.

TJU103联合CTLA4-Ig应用，能够调节Th细胞分化，诱导Th细胞发生免疫偏离，使辅助性T细胞更多地向Th2细胞方向分化，有利于免疫耐受的形成。

mitochondrial dnais the only inheritant substance except for the nuclear dna in a euˉkaryon cell,which is related to the oxidative phosphorylation of a cell.mitochondrial dna is the important target of carcinogens and is vulnerable because of its structure and function.the mutation of mtdna could reduce the nomal respitation and release large quantities of ros,whichincrease the danger of cancer happening.so,mtdna has been thought to be involved in carcinogenesis and recently more and more studies in this aspect have comeout.in this paˉper,we review the researches for relationship among mtdna mutation and tumors in digestion system,woman system,head and neck,urinary systemand blood system.

线粒体dna（mitochondrial dna，mt dna）是真核细胞中唯一存在的独立于核dna之外的遗传物质，与细胞的氧化磷酸化功能密切相关。mtdna自身的结构和功能特点决定了它是致癌物作用的重要靶点，易受致癌因素的损伤而发生突变。mtdna的突变可削弱正常的呼吸功能，释放高水平的活性氧，进而增加肿瘤发生的危险性，所以mtdna被认为与肿瘤发生有密切关系。近年来，这方面的研究越来越多，本文现就mtdna突变与消化系统肿瘤、妇科肿瘤、头颈部肿瘤、泌尿系统肿瘤等实体瘤以及血液系统恶性肿瘤之间的关系作一简单的综述。

Result 1 Magnetic nanoparticles, magnetic nanoparticles modified with antisense oligodeoxynucleotide of human telomerase reverse transcriptase induced HL-60 tumor cells to apoptosis, we could see typical morphologic change of apoptosis cells: karyopyknosis, chromation"s condensing and aggregation in nuclear, forming crescent-shaped or annulus structures to lean on edge of cell nucleus"s membrane and posing apoptosis body by Atomic Force Microscope, Fluorescence microscope, transmission electron Microscope 2 There was a significant difference compared with control group(p.01), inhibition ratio had significant positive correlation with medication dosage and time ;during 0.8-8μM dosage amplitude, inhibition ratio accrescenced by dosages increasing. However, the inhibition ratio would decrease when dosage over 8-80μM.

结果 1 磁性纳米粒子、修饰有端粒酶反义寡核苷酸的磁性纳米粒子诱导HL-60细胞发生凋亡，原子力显微镜、光学显微镜、荧光显微镜和透射电镜下均观察到HL-60细胞呈现典型的凋亡细胞的形态变化：细胞核固缩，核内染色质浓缩、凝聚、形成新月形或环状结构紧靠在细胞核膜边缘，并形成凋亡小体。2 磁性纳米粒子、修饰有端粒酶反义寡聚脱氧核苷酸的磁性纳米粒子对HL-60肿瘤细胞的生长和增殖有明显的抑制作用，与对照组相比有显著性差异(p＜0.01)，在剂量为0.8-8μmol／L范围内，抑制率随剂量的增加而增加，当剂量超过8μmol／L时，抑制率反而下降；3 磁性纳米粒子、修饰有端粒酶反义寡聚脱氧核苷酸的磁性纳米粒子可增强p53基因的表达活性，引起DNA降解损伤，反向调节细胞周期活动，促使细胞从G0期进入G1期，抑制肿瘤细胞的生长。4 修饰有端粒酶反义寡聚脱氧核苷酸的量子点能通过内吞作用进入HL-60肿瘤细胞的细胞核，可以在细胞内进行定位和促进HL-60肿瘤细胞的凋亡。

Affect on the liver pathological state after XIEZHIPING treated: the golden hamster hepatic tissue morphous structure of normal control was normal, which had regular hepatic lobules and no lipid droplet;that of model control manifested diffuse heavy adipose degeneration and heavy ballooning degeneration with inflammatory cell infiltrate which mainly composed of lympholeukocyte;that of high dose group showed midrange ballooning degeneration with chronic inflammatory cell infiltrate which mainly composed of lympholeukocyte and plasmocyte;that of media dose group indicated slight focus ballooning degeneration with a small quantity normal hepatic cells in some locals;that of low dose group appeared midrange adipose degeneration with a few lympholeukocyte cell infiltrate in the parts of central veins and port area.

泻脂平治疗后对肝脏病理状况的影响：空白对照组金黄地鼠的肝组织形态结构正常，肝小叶规则，无脂滴发现；模型对照组肝脏弥漫性重度脂肪变性，发生重度气球样变，伴见以淋巴细胞为主的慢性炎性细胞浸润；泻脂平高剂量组肝细胞呈现中度气球样变，伴见以淋巴细胞、浆细胞为主的慢性炎性细胞浸润；中剂量组肝细胞轻度灶性气球样变，局部可见少量正常肝细胞；低剂量组肝细胞呈中度脂肪变性，可见中央静脉及汇管区些许淋巴细胞浸润。

Affect on the liver pathological state afterXIEZHIPING treated: the golden hamster hepatic tissue morphous structureof normal control was normal, which had regular hepatic lobules and nolipid droplet: that of model control manifested diffuse heavy adiposedegeneration and heavy ballooning degeneration with inflammatory cell infiltrate which mainly composed of lympholeukocyte; that of high dosegroup showed midrange ballooning degeneration with chronic inflammatorycell infiltrate which mainly composed of lympholeukocyte and plasmocyte;that of media dose group indicated slight focus ballooning degenerationwith a small quantity normal hepatic cells in some locals; that of lowdose group appeared midrange adipose degeneration with a fewlympholeukocyte cell infiltrate in the parts of central veins and portarea.

泻脂平治疗后对肝脏病理状况的影响：空白对照组金黄地鼠的肝组织形态结构正常，肝小叶规则，无脂滴发现；模型对照组肝脏弥漫性重度脂肪变性，发生重度气球样变，伴见以淋巴细胞为主的慢性炎性细胞浸润；泻脂平高剂量组肝细胞呈现中度气球样变，伴见以淋巴细胞、浆细胞为主的慢性炎性细胞浸润；中剂量组肝细胞轻度灶性气球样变，局部可见少量正常肝细胞；低剂量组肝细胞呈中度脂肪变性，可见中央静脉及汇管区些许淋巴细胞浸润。

Both Fas and NO can lead chondrocyte apoptosis respectively and cause articular cartilage destruction. IGF-Ⅰ, TGF-β, bFGF, BMP and other growth factors are polypeptide agents that can influence cell activity by signal convection. They can accelerate chondrocyte proliferation and proteoglycan synthesis, play the local regulation action on formation and plerosis of bone and cartilage tissue by autocrine or paracrine. They have the ability to induce cartilage formation. Some investigations showed that growth factors can influence chondrocyte metabolism, synthesis of specific Ⅱ type collagen and proteoglycan by co-operation and inhibition. 1. 3 Situation of OA therapeutics The therapeutic methods of OA mainly comprised non-drug treatment, drug treatment, operation treatment, tissue and genetic engineering, et al. Drug treatment is the chief method among them.

若其活性发生改变，则将导致关节软骨基质成分的丢失和进行性破坏；软骨细胞凋亡与OA的发病密切相关，Fas与NO可各自独立介导软骨细胞凋亡，造成关节软骨破坏；IGF-Ⅰ、TGF-β、bFGF、BMP等生长因子是一组通过细胞间信号传递影响细胞活动的多肽因子，具有促进细胞生长、增殖与合成等作用，可通过自分泌或旁分泌方式对骨和软骨的形成和修复起局部调节作用，可促进软骨细胞增殖、分化与蛋白多糖的合成，具有较强的诱导软骨形成的能力，研究表明多种生长因子相互促进、相互抑制，以协同或拮抗方式影响软骨细胞代谢，影响软骨细胞特异性Ⅱ型胶原和蛋白多糖的合成分泌。

ANP and CX43 began to express at 2nd week after induction and increased gradually,about 60% of the resulting myogenic cells were positive at 4th week after induction ,they were negative for uninduced cells.hMSCs'surface antigen profiles obtained by Flow Cytometry were negative for CD31\CD34\CD45 before and after induction,but CD90 expressed higher after induction while was weak positive before induction(P.05). Apotosis index was correlated with the cultural time after induction,The apoptosis rate of induced hMSCs was remarkably higher than control group(P.01),and the variation between groups was notable(P.05),the cell cycle analysis showed that the percentages of G_0/G_1phases were reduced significantly after induction. The expresstion levels ofβ-MHC and CTNT mRNA were undetectable before induction,began to increase at 1st、4th week after induction,reached the peak at 6th week and decreased after that,the expression of Bcl-2 and Bax mRNA varied regularly after treated with 5-azacytidine. hMSCs'resting membrane potential、range and rate of depolarization were heightened gradually after being induced.

结果：hMSCs诱导前为纺锤形，诱导后第2天部分细胞即开始发生形变，呈球形或短棒状，1周后胞浆中颗粒增多，约20～30%细胞边缘呈毛刷样变化；hMSCs表面抗原CD31、CD34、CD45在诱导前后差异无统计学意义，CD90未诱导时表达呈弱阳性，诱导后明显增高(P.05)；ANP和CX43在诱导前无表达，诱导后第2周开始表达且表达随时间逐渐增强，但CX43在诱导后第5周表达量开始降低。hMSCs诱导后凋亡指数随诱导后培养时间增加，低浓度诱导组低于标准浓度诱导组，组间差异有统计学意义(P.05)，G_0/G_1期细胞比例诱导后较对照组显著减少(P.05)；β-MHC和CTNT基因分别在诱导后第1周和第4周时表达开始增强，在第6周时均达到高峰，第8周时表达开始衰减，Bcl-2、Bax基因表达呈时间依赖性变化，hMSCs经诱导后随心肌样细胞特征的表达膜静息电位、去极化幅值和去极化速率逐渐增高。

Additionally XBP1 mRNA which functioned as centrally regulating molecule during ER stress was spliced partially,while it was completely spliced in positive control cells and unspliced in H7721.These results gave the proof that blocking expression of GnT-V caused H7721"s ER stress and response was more weak than that caused by DTT. It may be the chronic process.Additionally,previous studies reported that the ds-RNA may activate the kinase PKR which phosphorylated eIF2 α and inhibited synthesis of proteins.In this paper the antisense cDNA of GnT-V was integrated with GnT-V-AS/H7721"s gene and functioned through the binding of antisense RNA and mRNA of GnT-V.Additionally,the integration of GnT-V cDNA in genome also may be a non-specific factor.

对这三种ER stress关键分子的检测发现：和阴性细胞相比较，实验细胞中BIP的表达无论是蛋白水平还是转录水平都有明显的上调，但上调程度都要低于DTT处理的ER stress阳性细胞；XBP-1 mRNA在实验细胞中部分被剪接，在阳性细胞中XBP-1 mRNA完全被剪接，而在阴性细胞中其以非剪接形态存在；此外和DTT处理的ER stress阳性细胞相似，实验细胞中的PERK发生磷酸化，表明ER stress过程中通过磷酸化eIF2α抑制蛋白合成机制的活化，这和芯片所检测到的GnT-V-AS／H7721细胞蛋白合成系统水平下调相一致。

Breath, muscle contraction of the buttocks; arch body, as far as possible to hold his head, right leg straight towards the ceiling (peg-leg knee in order to avoid muscle tension).

呼气，收缩臀部肌肉；拱起身体，尽量抬起头来，右腿伸直朝向天花板（膝微屈，以避免肌肉紧张）。

The cost of moving grain food products was unchanged from May, but year over year are up 8%.

粮食产品的运输费用与5月份相比没有变化，但却比去年同期高8％。