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321.
周晓 《井冈山大学学报(自然科学版)》2014,(3):98-100
目的通过比较孕晚期凶险型前置胎盘孕妇和正常妊娠孕妇血清中肌酸激酶的差异,探讨其用于凶险型前置胎盘合并胎盘植入产前诊断的价值。方法回顾性分析2012年6月至2013年6月江西省妇幼保健院凶险型前置胎盘单胎孕妇92例,其中合并胎盘植入者38例,归入凶险型前置胎盘合并胎盘植入组,其余54例归入未合并胎盘植入组,再随机抽取同期分娩的既往有剖宫产史,本次为正常妊娠的孕妇50例作为对照组,比较三组孕妇血清肌酸激酶水平的差异。结果凶险型前置胎盘合并胎盘植入组CK数值为(128.6±19.8)U/L,未合并胎盘植入组为(67.7±21.2)U/L,单纯剖宫产史组为(65.1±20.3)U/L。凶险型前置胎盘合并胎盘植入时,孕妇血清肌酸激酶水平明显升高,差异具有统计学意义。而在中央型前置胎盘、部分型前置胎盘和边缘型前置胎盘中,肌酸激酶分别为(80.3±38.2)U/L、(77.1±36.0)U/L、(79.6±29.7)U/L,三者差异无统计学意义。结论孕妇血清肌酸激酶的测定对凶险型前置胎盘合并胎盘植入的产前预测有价值,与前置胎盘的类型无关。 相似文献
322.
为研究大分子拥挤试剂对蛋白质折叠过程的影响作用及其机制提供有价值的依据,在大分子拥挤环境下进行了人肌肌酸激酶的折叠动力学研究,发现质量浓度高的大分子拥挤试剂(ρ=200 g·L-1的BSA、 Dextran 70与Ficoll 70)通过增进部分折叠中间体的错误聚集,使酶的复性产率显著降低.相对质量浓度较低的大分子拥挤试剂(ρ≤100 g·L-1)对酶的复性产率影响不大,但对酶复性的动力学过程有较大影响,一方面可使无活性单体的二聚化变为复性速率最慢的限速步骤,另一方面又加快了二聚化的折叠中间体到天然构象的复性过程. 相似文献
323.
Qi Zhang Fangyan Dai Min Zhang Peirong Hu Qiang Fu Yuxin Fan Long Yu Shouyuan Zhao 《科学通报(英文版)》1999,44(9):778-778
A novel full-length cDNA encoding a putative serine/threonine kinase has been isolated from a human testis cDNA library. A
nucleotide sequence of 1225 bp length has been determined containing an open reading frame of 1 044 nucleotides (encoding
348 amino acids). In view of its degree of homology to members of the Ser/Thr protein kinase family and the closest relationship
toMus musculus STK-1, the predicted product was designated by the name of HUMSTK-1. Its mRNA is present in large amounts in thymus, and
small amounts in testis, small intestine and colon. 相似文献
324.
观察趋化素诱导成骨细胞代谢过程中的影响,探讨内质网应激反应在此过程中的机制。将成骨细胞随机分组,给予不同浓度的趋化素(Chemerin)进行诱导,观察成骨细胞活力变化;ELISA法测定细胞趋化蛋白1(MCP-1)、E选择素(E-selection)变化;Western blot法检测成骨细胞黏附分子1(ICAM-1)、需肌醇跨膜激酶/核酸内切酶1(inositol-requiring transmembrane kinase/endonuclease 1,IRE1)、葡萄糖调节蛋白78(Glucose-regulated protein 78,GRP78)的表达情况。通过研究发现Chemerin对成骨细胞活力未见明显影响;与正常对照组相比,Chemerin呈浓度依赖性上调MCP-1、E-selection、ICAM-1等炎症因子的表达(P0.05),上调内质网应激反应相关指标IRE1、GRP78的表达(P0.05);其中,1×10-5mol/L组Chemerin作用最为显著。研究结果表明趋化素可诱导成骨细胞的凋亡过程,在成骨细胞的代谢中发挥重要作用,此过程可能和内质网应激反应相关。 相似文献
325.
S. K. Grant 《Cellular and molecular life sciences : CMLS》2009,66(7):1163-1177
Protein kinase inhibitors represent an important and still emerging class of targeted therapeutic agents. Drug discovery and
development strategies have explored numerous approaches to target the inhibition of protein kinase signaling. This review
will highlight some of the strategies that have led to the successful clinical development of therapeutic protein kinase inhibitors,
particularly as anticancer drugs. Some notable advances have been made in the development of novel protein and oligonucleotide-based
biologics that target growth factor or receptor tyrosine kinases. Also, advances have been made in the rational design of
small-molecule inhibitors that target unique kinase conformational forms and binding sites, and have specific kinase selectivity
profiles. A review will also be given of some of the potential clinical toxicities and adverse side-effects associated with
these kinase-targeted drugs. Therapeutic protein kinase inhibitors have been highly beneficial to cancer patients and offer
the promise of future therapies for other diseases as well.
Received 02 September 2008; received after revision 13 October 2008; accepted 15 October 2008 相似文献
326.
Mitogenic signals stimulate cell division by activating cyclin/cyclin-dependent kinase (CDK) complexes. Their timely regulation
ensures proper cell cycle progression. It is therefore not surprising that cyclin/CDK complexes are integrators of multiple
signals from both the extracellular environment and intracellular cues. Important regulators of cyclin/CDKs are the CDK inhibitors
that have attracted attention due to their association with disease. p27KIP1 is a CDK inhibitor that controls CDK activity throughout the cell cycle. As a CDK inhibitor, p27KIP1 has tumor suppressor activity. Besides CDKs, p27KIP1 regulates additional cellular processes, including cell motility, some of which seem to mediate oncogenic activities of p27KIP1. These activities of p27KIP1 are regulated through multiple phosphorylation sites, targeted by several signal transduction pathways. Understanding functions
and regulation of p27KIP1 will be important to determine which isoform of p27KIP1 has anti- or pro-tumorigenic activities. Such knowledge might be of prognostic value and may offer novel therapeutic windows.
Received 26 May 2008; accepted 17 June 2008 相似文献
327.
The serine/threonine kinase glycogen synthase kinase-3 (GSK-3) was initially identified as a key regulator of insulin-dependent
glycogen synthesis. GSK-3 was subsequently shown to function in a wide range of cellular processes including differentiation,
growth, motility and apoptosis. Aberrant regulation of GSK-3 has been implicated in a range of human pathologies including
Alzheimer’s disease, non-insulin-dependent diabetes mellitus (NIDDM) and cancer. As a consequence, the regulation of GSK-3
and the therapeutic potential of GSK-3 inhibitors have become key areas of investigation. This review will focus on the mechanisms
of GSK-3 regulation, with emphasis on modulation by upstream signals, control of substrate specificity and GSK-3 localisation.
The details of these mechanisms will be discussed in the context of specific signalling pathways.
Received 30 January 2007; received after revision 5 March 2007; accepted 16 April 2007 相似文献
328.
Isakovic A Harhaji L Stevanovic D Markovic Z Sumarac-Dumanovic M Starcevic V Micic D Trajkovic V 《Cellular and molecular life sciences : CMLS》2007,64(10):1290-1302
The present study reports for the first time a dual antiglioma effect of the well-known antidiabetic drug metformin. In low-density
cultures of the C6 rat glioma cell line, metformin blocked the cell cycle progression in G0/G1 phase without inducing significant cell death. In confluent C6 cultures, on the other hand, metformin caused massive induction
of caspase-dependent apoptosis associated with c-Jun N-terminal kinase (JNK) activation, mitochondrial depolarization and
oxidative stress. Metformin-triggered apoptosis was completely prevented by agents that block mitochondrial permeability transition
(cyclosporin A) and oxygen radical production (N-acetylcisteine), while the inhibitors of JNK activation (SP600125) or glycolysis
(sodium fluoride, iodoacetate) provided partial protection. The antiglioma effect of metformin was reduced by compound C,
an inhibitor of AMP-activated protein kinase (AMPK), and was mimicked by the AMPK agonist AICAR. Similar effects were observed
in the human glioma cell line U251, while rat primary astrocytes were completely resistant to the antiproliferative and proapoptotic
action of metformin.
Received 14 February 2007; received after revision 26 March 2007; accepted 3 April 2007 相似文献
329.
Tauopathies are a group of neurodegenerative diseases characterised by intracellular deposits of the microtubule-associated
protein tau. The most typical example of a tauopathy is Alzheimer’s disease. The importance of tau in neuronal dysfunction
and degeneration has been demonstrated by the discovery of dominant mutations in the MAPT gene, encoding tau, in some rare dementias. Recent developments have shed light on the significance of tau phosphorylation
and aggregation in pathogenesis. Furthermore, emerging evidence reveals the central role played by tau pre-mRNA processing
in tauopathies. The present review focuses on the current understanding of tau-dependent pathogenic mechanisms and how realistic
therapies for tauopathies can be developed.
Received 3 December 2006; received after revision 23 February 2007; accepted 20 March 2007 相似文献
330.
Decoding the Hedgehog signal in animal development 总被引:4,自引:0,他引:4
The Hedgehog (Hh) family of secreted proteins plays essential roles in a myriad of developmental processes via a complex signaling
cascade conserved in species ranging from insects to mammals. In many developmental contexts, Hh acts as long-range morphogen
to control distinct cellular outcomes as a function of its concentration. Here we review the current understanding of the
Hh signaling mechanisms that govern the establishment of the Hh gradient and the transduction of the Hh signal with an emphasis
on the intracellular signaling cascade from the receptor to the nuclear effector. We discuss how graded Hh signals are transduced
to govern distinct developmental outcomes.
Received 28 October 2005; received after revision 6 February 2006; accepted 15 February 2006 相似文献