细胞发生

At early stage of cancer cell formation, provoked autophagy help to eliminate damaged cell organelle、and degrade the noxious substance in endochylema(eg: peroxidate)as well, pretect normal cells from cancerization.Autophagy level modulation might be cooperation or rivalry with chemotherapy to cancer cells compares to single use of chemotherapy drugs, apoptosis rate of cancer cells fluctuates with autophagy level.

癌细胞形成早期刺激自噬能够清除受损细胞器，分解细胞内过多的有害物质，阻止正常细胞向癌细胞转化，调控自噬的表达和化疗药物联合对肿瘤细胞的生长有协同或拮抗作用，表现为与单纯用化疗药物相比，调控自噬表达后肿瘤细胞的凋亡率发生了变化。

Three categories of cytokines, including Thl/Th2 cytokines, chemokines and adipocytokines, are involved in the physiopathological process of NASH. In order to elucidate the significances of cytokines in the pathogenesis, serological diagnosis, and treatment efficacy evaluation of HASH, we reviewed the documents on the relationship between cytokines and non-alcoholic steatohepatitis.

参与NASH病理生理过程的细胞因子归纳起来有3类，即Th1、Th2细胞因子和趋化因子及脂肪细胞因子，本文了回顾3类细胞因子与NASH发生、发展关系的最新研究进展，从而阐明细胞因子在NASH发病机制、血清学诊断和治疗效果评价等方面的意义。

Three categories of cytokines, including Th1/Th2 cytokines, chemokines and adipocytokines, are involved in the physiopathological process of NASH. In order to elucidate the significances of cytokines in the pathogenesis, serological diagnosis, and treatment efficacy evaluation of HASH, we reviewed the documents on the relationship between cytokines and non-alcoholic steatohepatitis.

参与NASH病理生理过程的细胞因子归纳起来有3类，即Th1、Th2细胞因子和趋化因子及脂肪细胞因子，本文了回顾3类细胞因子与NASH发生、发展关系的最新研究进展，从而阐明细胞因子在NASH发病机制、血清学诊断和治疗效果评价等方面的意义。

Examination the cell shape and pseudopodia with confocal laser scanning microscopy, scanning electron microscopy, and atomic force microscopy, we found that cell spreading well on nanogrooved substrates and their body was more flat and slim; meanwhile, on plain substrates, cells were mostly round.

纳米沟槽能很好地促进细胞贴壁黏附、铺展、生长和增殖，并影响细胞的周期；纳米沟槽诱导细胞骨架发生重组，肌动蛋白骨架沿着纳米沟槽的方向取向排列；纳米沟槽影响细胞伪足形成的方式和形成与细胞中的位置。

While the tissue spaces surrounding a few blood vessels wasAl and Fg positive,no Al or Fg positive cells were observed.In antemortem injurygroup,diffuse subarachnoid hemorrhage,cerebral edema,swelling or pyknotic neu-rons could be observed.The axons showed irregular swelling and disconnection at1～3h,marked swelling and disconnection at 6h,and retraction ball at 15h whichwas more remarkable at 24h after injury.The space between myelin sheaths andaxons was increased at 3～6h after injury.Tortuous and wavelike myelin sheathswhich adhered on axons incompletely,or even peeled off could be found from 15hto 24h after injury.Perinuclear lysis of Nissl bodies began at 24h after injury.Thenumber of GFAP positive cells in cerebrum and brain-stem increased significantlyfollowed by decrease,and then increased again,but the time courses of the changesin different areas of brain were not same.Al and Fg positive neural cells,mainlysurrounded blood vessels,with diffuse or peripherally distributed positive matter incytoplasm could be observed at 0.5h after injury.The number of Al or Fg positivecells and the intensity of immunoreaction increased with the time of injury.The areaof SYN positivity in medulla oblongata and pons decreased notably 3～6h afterinjury,then return to normal levels and continued to 24h after injury.

生前损伤组，可见广泛蛛网膜下腔出血，脑组织水肿，神经细胞肿胀，晚期神经元固缩；伤后1～3h见部分神经轴突不规则增粗、断裂，伤后6h断端膨大，伤后15h可见收缩球，至伤后24h更为明显；伤后3～6h可见部分神经髓鞘与轴突之间的间隙增宽，伤后15h髓鞘明显曲折，不完全附着在轴突两侧，甚至剥脱，持续到伤后24h；核周尼氏体减少在伤后24h才开始出现；同一部位的GFAP阳性细胞数目随损伤时间发生改变，先增多（最早在伤后0.5h），达到高峰后减少，其后又有增多趋势，但不同部位的GFAP阳性细胞数目增减的时间过程不尽相同，同时，大脑中的GFAP阳性细胞数目也有改变；伤后0.5h，可在脑干组织中见到Al和Fg阳性神经细胞，主要位于血管周围，阳性物在胞浆中呈弥散性分布，但部分细胞的阳性物仅分布于靠近胞膜的胞浆中而呈环状，随损伤时间延长，阳性细胞数目增多，反应强度增加；伤后3～6h，延髓及桥脑中的SYN阳性物面积减少，其后恢复到正常水平，并持续到伤后24h。

When cells undergo programmed cell death, cell corpses adopt a refractile and disc like structure. Using this morphological change as a cell death marker, we analyzed the death of the first 13 cells in the AB cell lineage of wild type and cnx-1; crt-1 mutant embryos.

进一步以4D摄影分析线虫AB世系细胞中最早死亡的13颗细胞之相对死亡时间和细胞尸体持续的时间长短的结果则显示，此死亡细胞数量提高的现象应是源於吞噬步骤发生问题而非细胞死亡执行上的问题。

If GVHD occurred, GCV would be administered in order to kill TK〓T lymphocytes selectedly and to control GVHD, while preserving therapeutic effects of T lymphocytes.

将TK基因体外转染供者T细胞成为TK〓T细胞，然后和CD34〓细胞混合移植，一旦发生GVHD，则给予特异性药物丙氧鸟苷治疗，选择性杀死引起GVHD的TK〓T细胞，使GVHD得到控制，同时又可保留T细胞的治疗作用。

Reactive oxygen species causing DNA oxidative damage comes from two kinds of ways:one is from cellular normal physiological metabolism;the other is from outer environment.Redox-sensitive green fluorescent protein was expressed in Saccharomyces cerevisiae.Recombinant cells were evaluated in monitoring the changes in the redox state of living cells when challenged with toxicologically relevant metal ions NaAsO_2 or Pb(NO_3)_2 by measuring emission intensity at 510 nm with a Hitachi F6500 fluorescence spectrophotometer,roGFP expressed in yeast responded not only to typical membrane-permeant oxidants H_2O_2 and reductants DTT,but also to toxicological metal ion-induced intracellular redox changes in a dose-dependent manner.Moreover,exposure of yeast cells to NaAsO_2 or Pb(NO_3)_2 at concentrations that induced redox changes reported by roGFP caused up to 2～3 fold increases in DNA mutation frequency.This mutagenic effect was largely caused by oxidative stress since blocking the production of hydryl radicals with thiourea significantly reduced the mutation rate as well as delayed the cell death.

本文将对氧化还原状态变化敏感的绿色荧光蛋白roGFP1-R12，在酵母细胞中实现了多拷贝强表达；荧光扫描经强氧化剂H_2O_2和还原剂DTT以及环境中重金属NaAsO_2或Pb(NO_3)_2处理后的酵母细胞悬液，测定510 nm处的荧光发射强度结果显示，表达的绿色荧光蛋白对氧化还原水平敏感，且在510 nm处的荧光强度与一定的重金属浓度呈正相关，即roGFP1-R12在510nm处的荧光发射值随重金属浓度的增高而增强，从而说明重金属对细胞的毒性在一定程度上很可能是通过破坏细胞内的氧化还原平衡发生作用；同时通过该绿色荧光蛋白对胞内氧化还原状态变化的响应情况可以来实时检测环境中的重金属；遗传学的点突变频率及致死率实验数据表明，重金属能导致菌体的点突变频率和致死率升高，且活性氧的清除剂巯基脲能明显降低这种点突变和致死率，说明由重金属引发的这种点突变和致死效应在很大程度上是依赖于重金属对细胞诱导产生的氧化胁迫。

In summary, the BRD7 gene acted as a candidate of tumor suppressor gene with NPC. The overexpression of BRD7 can partly reverse malignant phenotype of NPC cell line. The suppression effect of BRD7 on NPC tumorigenesis my be achieved by recognizing acetylated histone peptide through their motif-bromodomain, then modulating gene transcription by taking part in histone acetylating and chromosome remodeling, finally influencing signal-transduction pathways.

综上所述，BRD7基因作为一个重要的鼻咽癌抑瘤基因侯选者，在鼻咽癌细胞中的过表达后，可导致鼻咽癌细胞 HNE蛋白质表达谱发生改变，逆转其恶性表型，其作用机理可能是：BRD7基因通过其功能域彭聪硕士学位论文10Bromodomain与乙酚化的组蛋白特异性结合，参于染色体的乙酚化，染色质的组装，从而影响基因转录的调控，最终影响细胞内的信号传导通路并实现对细胞周期的调控，从而发挥抑制鼻咽癌细胞生长的作用。

As exposed to optics microscope and inverted microscope,compared to control,SW480 cells with Giemsa staining that treated with the H2RA(cimetidine、nizatidine) took on malignance declining as crimpled firstly,cellular bulk and heteromorphism dimimished,the amount of rounded cell manifolded,nucleolus bulk lessened,dyeing thin,the amount of nucleolus decreased,partial cell organs manifest side-gathering phenomenon on chromatin,and the link between SW480 cell is loosened , subsequently partial rounded cell is floated.When the H2RA(cimetidine 40μM、nizatidine 20μM) against SW480 cells after 3 day,SW480 cells change roundly,nucleolus smashed,shrinking nucleolus came into being,and part of those not adhibited cell wall.

在光镜和倒置相差显微镜下，与对照组相比，经姬姆萨染色观察，西咪替丁、尼扎替丁处理的SW480细胞，先发生皱缩，体积变小，异形性减少，细胞变圆数目增多，细胞核变小，染色变淡，核仁数量减少，部分可见染色质边集现象；细胞间连接疏松，随后部分变圆细胞浮起。40μM西咪替丁及20μM尼扎替丁连续处理3天后，SW480细胞全部变圆，细胞核碎裂，固缩微核形成，部分不再贴壁。

Do you know, i need you to come back

你知道吗，我需要你回来

Yang yinshu、Wang xiangsheng、Li decang,The first discovery of haemaphysalis conicinna.

1〕 杨银书，王祥生，李德昌。安徽省首次发现嗜群血蜱。