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BMK can suppress HL-60 the growth and the induction cell perishes, the caspase-3 activation poisonously participated in the East Asian pliers scorpion to induce the process which the HL-60 cell weakly perished.

BMK能抑制HL-60的生长和诱导细胞亡,caspase-3活化参与了东亚钳蝎毒诱导HL-60细胞凋亡的过程。

Expression of CD44V6 can be an early biological indicator of precarcinomatous epithelial cells. Gastric mucosa intestinal metaplasia can induce the expression of CD44V6, moreover, Hp infection can promote it.

CD44V6的表达可能是上皮细胞癌前病变出现的早期生物学信号,肠上皮化生细胞可能诱导CD44V6的表达,而Hp感染则有促进这种诱导表达的作用。

The median BP wasdetermined preinduction and for 0–5 and 5–10 minpostinduction of anesthesia.

平均血压采用麻醉诱导前和诱导后0–5分钟、5–10分钟的血压。

When compared with preinduction values, there were significantpostinduction changes in multiple variables of the HF QRS inmany leads studied that were within previously described normallimits.

诱导前比较,诱导后多导联 HF QRS 的多个变量有显著变化。

METHODS: Femur and tibia were obtained from Wistar rats for primary culture of BMSCs. MSCs at passage 15-20 were firstly incubated in preinduction medium, for 24 hours, and then incubated in induction medium containing α-MEM, 2% dimethyl sulfoxide and 200 μmol/L butylated hydroxyanisole.

取Wistar大鼠股骨和胫骨,进行骨髓间充质干细胞原代培养,传至第15~20代融合状态的间充质干细胞置于预诱导培养基中培养24 h后,换用诱导培养基。

Propofol were used by target controlled infusion method in all patients during induction.The changes of MAP、HR were recorded at preinduction、 preintubation、intubation and post-intubation 1,3,5 minuters.

观察诱导前、气管插管前、插管时及插管后1、3、5min等6个时点的血流动力学参数值变化,并记录各组气管插管诱导应用异丙酚的总量。

RESULTS: HIF-1α positively expressed at stratum neuroepitheliale retinae and purpurogenous membrane in the embryonic phase. Additionally, HIF-1α still positively expressed at stratum neuroepitheliale retinae and purpurogenous membrane, especially in ganglionic cells and inner plexiform layer, in early development.

结果:胚胎期视网膜神经上皮层及色素上皮层均有低氧诱导因子1α阳性表达,生后发育早期视网膜神经上皮层及色素上皮层也可见低氧诱导因子1α阳性表达,以神经节细胞、内网层更明显,随着发育进展,其阳性表达主要位于视网膜节细胞层。

RESULTS: After differentiation of human adherent myoblasts by neural induction medium, no cells with a neural cell morphology (ie., small, refractile cell body with dendritic cell extensions) were seen. All remaining myoblasts cultured with neural induction medium, myoblasts with proliferation medium and myotubes with differentiation medium containing 20 mL/L HS were positive for β Tubulin Ⅲ. C2C12 myoblasts were negative for β Tubulin Ⅲ. In contrast, all the above cells were negative for the markers Neurofilament Mr 68×103 and GFAP.

结果:用诱导分化液作用后,未见小的、伴有突起的放射状形态的神经细胞;抗β Tubulin Ⅲ对经神经元胶质细胞诱导分化液作用后的人成肌细胞、增殖培养液培养后的各代人成肌细胞及仅含20 mL/L HS分化液分化形成的肌管细胞染色均为阳性; C2C12细胞β Tubulin Ⅲ抗体染色阴性;上述所有细胞抗Neurofilament Mr 68×103和抗GFAP染色均为阴性。

The expression of AT2R gene can be regulated efficiently in vivo by local delivery of MSC with dual-stable expression of AT2R gene, thus reduces the formation of intimal hyperplasia.④AT2R gene can influence the expression of ECM and significantly promote the cellular apoptosis in the injury rat carotid artery.⑤These data demonstrate the clinical potential of AT2R regulatable expression to prevent restenosis after PCI.

研究结论:(1)与VSMC直接接触可以诱导MSC向血管成分细胞分化;(2)构建的Dox-on可调控的MSC细胞株诱导活性可靠,使外源AT2R基因的表达处于有效的主动控制下;(3)局部导入MSC不影响球囊损伤后大鼠颈动脉新生内膜增生;(4)由MSC介导的AT2R可调控表达受到Dox的良好调控,可有效抑制球囊损伤后大鼠颈动脉新生内膜增生;(5)AT2R影响血管损伤后修复时ECM成分的表达,并促进细胞凋亡的发生,可能是AT2R介导抑制新生内膜形成的机制。

TUNEL method was used to detected the apoptosis in the artery. Results:①The MSC cocultured with VSMC expressed smooth muscle a-actin, calponin and CD31, no cells positive for calponin and CD31 were detected in the control group; and a lot of filaments were observed in the co-cultured MSC by electron microscopy.②We gain dual-stable expression of AT2R gene medicated by doxycycline regulatable system of mesenchymal stem cells.

单独培养及VSMC条件培养液培养的MSC仅SM-α-actin表达阳性;(2)Dox-on系统由四个质粒组成:调节质粒pUHD17-1 hyg,荧光报告质粒pUHC 13-3,筛选质粒pSV2neo以及含目的基因AT2R的应答质粒pUHD10-3/AT2R,以上质粒经鉴定均与其背景资料相符合,可用于实现目的基因片段在靶细胞中可调控表达研究;(3)本实验通过连续两个回合的转染及抗生素压力筛选,经Dox诱导表达后获取出低背景、高诱导表达AT2R基因的克隆。

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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)。

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然而,要让一个真正的引用,你需要提供详细的个人和财务信息。