简介:摘要目的探讨针对产后出血(PPH)孕产妇,选择卡前列素氨丁三醇完成治疗后的临床效果表现。方法选取我院2011年12月—2013年12月PPH孕产妇120例,通过随机数表法将所有孕产妇分为C1组(观察组60例)以及C2组(对照组60例)。针对C2组PPH患者主要选择缩宫素进行治疗,针对C1组PPH患者主要选择卡前列素氨丁三醇进行治疗。对比C1组与C2组患者完成治疗后,在临床治疗效果、临床止血时间、患者产后2小时出血量以及临床出现不良反应的情况。结果C1组与C2组产后出血患者分别完成治疗后,在临床治疗总有效率方面,C1组PPH患者高于C2组患者明显(P<0.05)。在患者止血时间以及产后2小时出血量等方面,C1组PPH优于C2组患者明显(P<0.05)。结论针对PPH患者,选择卡前列素氨丁三醇对患者进行治疗,临床获得的止血效果显著,患者的出血量也表现为显著的缓解,临床应用意义显著。
简介:【摘要】目的:分析卡前列素氨丁三醇治疗产后出血的有效性。方法:设置研究时间段为2021.09-2022.09,选取此时我院收治的产后出血患者76例为研究对象,将其进行1-76号编号,前38号归入对比组并运用缩宫素治疗,后38号归入研究组并运用缩宫素与卡前列素氨丁三醇治疗。比较二组治疗后的产后出血量、止血时长、总有效性。结果:在治疗后,研究组的产后出血量少于对比组,且止血时间较短(P<0.05);研究组的总有效性高于对比组(P<0.05)。结论:在为产后出血患者治疗时,运用缩宫素与卡前列素氨丁三醇能够减少产后出血量,缩短止血时长,提高总有效性,值得借鉴。
简介:【摘要】目的:分析卡前列素氨丁三醇治疗产后出血的有效性。方法:设置研究时间段为2021.09-2022.09,选取此时我院收治的产后出血患者76例为研究对象,将其进行1-76号编号,前38号归入对比组并运用缩宫素治疗,后38号归入研究组并运用缩宫素与卡前列素氨丁三醇治疗。比较二组治疗后的产后出血量、止血时长、总有效性。结果:在治疗后,研究组的产后出血量少于对比组,且止血时间较短(P<0.05);研究组的总有效性高于对比组(P<0.05)。结论:在为产后出血患者治疗时,运用缩宫素与卡前列素氨丁三醇能够减少产后出血量,缩短止血时长,提高总有效性,值得借鉴。
简介:房间有大量的控制维持他们的完整并且阻止随机切换到另外一个一个生物状态。RafKinase禁止的蛋白质(RKIP),phosphatidylethanolamine绑定蛋白质(PEBP)的一个成员家庭,表明工作维持“yinyang”或生物系统的平衡的串联的调节的人的一个新类是代表性的。RKIP禁止地图kinase(Raf-MEK-ERK),表明串联的G联合蛋白质的受体(GPCR)kinase和NFkappaB。因为RKIP指向依赖于它磷酸化的状态的不同家族ases,RKIP也行动集成多重环境刺激开始的串音。RKIP的损失或弄空导致正常细胞的壅滞和罐头的混乱导致象癌症那样的chromosomal畸形和疾病状态。因为RKIP和PEBP家庭以前被考察了,这分析的目标是提供更改并且加亮一些RKIP的唯一的特征在细胞的发信号的过程的规定使它成为一个批评播放器。
简介:Humanrhodopsinkinase(RK)andacarboxylterminus-truncatedmutantRKlackingthelast59aminoacids(RKC)wereexpressedinhumanembryonickidney293cellstoinvestigatetheroleofthecarboxylterminusofRKinrecognitionandphosphorylationofrhodopsin.RKC,likethewild-typeRK,wasdetectedinbothplasmamembranesandcytosolicfractions.TheCterminaltruncatedrhodopsinkinasewasunabletophosphorylatephoto-activatedrhodopsin,butpossesseskinaseactivitysimilartothewild-typeRKinphosphorylationofsmallpeptidesubstrate.ItsuggeststhatthetruncationdidnotdisturbthegrossstructuresofRKcatalyticdomain.OurresultsalsoshowthatRKCfailedtotranslocatetophoto-activatedrodoutsegments.Takentogether,ourstudydemonstratethecarboxylterminusofRKisrequiredforphosphorylationofphoto-activatedrhodopsinandstronglyindicatethatcarboxyl-terminusofRKmaybeinvolvedininteractionwithphoto-activatedrhodopsin.
简介:AbstractBackground:Topoisomerase II alpha (TOP2A) has been reported to play a crucial role in the tumorigenesis of various cancer types. However, the biological role of TOP2A in gallbladder cancer (GBC) remains unknown. The current study aimed to explore the function and potential mechanism of TOP2A in GBC.Methods:Based on Gene Expression Profiling Interactive Analysis data, we found TOP2A was significantly up-regulated in GBC tissues and resulting in shorter overall survival. Quantitative real-time polymerase chain reaction and immunohistochemistry were conducted to detect the expression of TOP2A in 45 pairs of GBC tissues and adjacent non-tumor tissues. In vitro, cell proliferation, migration, and invasion ability were examined by cell counting kit-8 and transwell assay, respectively. Epithelial-mesenchymal transition (EMT) related and phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway-related markers were measured by Western blotting. Xenograft model assay was performed to evaluate the effect of TOP2A in vivo.Results:TOP2A was found up-regulated in GBC (tumor vs. normal, 12.62 vs. 0.34) and correlated with the late tumor node metastasis stage (P = 0.0032), present of lymph node metastasis (P = 0.0273), and poor prognosis in GBC patients (log-rank P = 0.028). In vitro and in vivo assays showed that knockdown of TOP2A notably inhibited cell proliferation, migration, invasion, EMT process, and tumor growth in GBC. In addition, TOP2A down-regulation significantly decreased the protein levels of phosphor (p)-PI3K, p-Akt, and p-mTOR.Conclusion:Our study demonstrates that TOP2A was overexpressed in GBC and associated with poor prognosis in GBC patients. TOP2A promotes GBC cell proliferation, migration, invasion, EMT process, and tumor growth through activating PI3K/Akt/mTOR signaling pathway, and may serve as a novel prognostic biomarker and therapeutic target for GBC.
简介:我公司单醇系统于1997年投产,其生产能力为3万吨/年,生产流程为:以煤为原料经煤气发生炉制得水煤气,水煤气经过栲胶脱硫,压缩机一、二段压缩至2.0MPa,进入变换、水洗脱碳、精脱硫工序,净化后的气体经压缩机三段压缩至5.0MP进入合成工序合成甲醇。其中,水洗气中总硫含量高达30mg/m^3,而单醇合成塔中铜系催化剂C302使用时要求总硫含量<0.1mg/m^3,否则很容易引起中毒,严重缩短催化剂的使用寿命。因此,微量硫的脱除成为单醇系统正常运行的关键问题。为此,我厂采用了湖北省化学研究所开发的JTL-1常温精脱硫工艺对水洗气进行处理,以保护甲醇合成催化剂,既可防止硫中毒,又可防止硫进入系统造成对设备的腐蚀。此工艺在我公司单醇系统投运三年多来的实践证明:该工艺脱硫效果好,运行稳定,出口总硫始终控制在0.1mg/m^3以下,为单醇系统的稳定、高产、长周期运行,延长甲醇合成催化剂的使用期奠定了重要的基础。