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1.
目的:探讨人胃癌细胞中乙酰肝素酶(HPSE)调控的差异蛋白和信号通路,为以HPSE为靶点防治胃癌提供依据。方法:利用siRNA干扰技术,在乙酰肝素酶(HPSE)基因高表达的SGC7901细胞中转入干扰HPSE的慢病毒载体(LV-HPSE-RNAi),通过嘌呤霉素筛选出稳定株,利用qPCR和Western blot分别检测HPSE mRNA和蛋白表达;利用细胞划痕实验和Transwell侵袭实验测定细胞的迁移和侵袭能力;利用同位素标记的相对和绝对定量(iTRAQ)联合二维液相色谱串联质谱(2DLC-MS/MS)技术筛查差异蛋白,并进行生物信息学分析,对差异蛋白PKCa应用Western blot进一步验证。结果:人胃癌SGC7901细胞和沉默HPSE表达的ZSGC7901细胞对比检测出98个差异蛋白,并且富集在157条信号通路上。与肿瘤发生发展关系密切的有6条:细胞外基质和受体相互作用、局灶性黏附、PI3K-Akt信号通路、癌途径、癌中microRNAs、Wnt信号通路。且上调的FAK、ITGA、PKCa等蛋白和下调的PKA、CDK6等蛋白在通路中处于重要的位置。Western blot结果证明PKCa在沉默HPSE的ZSGC7901细胞中表现为上调,差异具有统计学意义(P<0.05),与蛋白质组学筛选结果一致。结论:HPSE在人胃癌细胞中调控的蛋白,参与细胞重要生物学过程、参与重要分子功能及重要信号途径,有望可以成为防治胃癌的新靶点。  相似文献   
2.
Background: Hepatocellular carcinoma (HCC) develops most often in a background of chronic inflammatory liver injury from viral infection or alcohol use. Most HCCs are diagnosed at a stage at which surgical resection is not feasible. Even in patients receiving surgery rates of recurrence and metastasis remain high. There are few effective HCC therapies and hence a need for novel, rational approaches to treatment. Platelet derived growth factor receptor-α (PDGFR-α) is involved in tumor angiogenesis and maintenance of the tumor microenvironment and has been implicated in development and metastasis of HCC. Objective: To examine PDGFR-α as a target for therapy of HCC and explore opportunities and strategies for PDGFR-α inhibition. Methods: A review of relevant literature. Results/conclusions: Targeted inhibition of PDGFR-α is a rational strategy for prevention and therapy of HCC.  相似文献   
3.
Objective An organic layer prepared from the cortex of Morus alba (Moraceae) was studied in order to identify the active compounds for heparinase. Methods Bioassay-guided fractionation resulted in the isolation of sanggenon G. Results The compound showed inhibitory activity with IC50 of 3.7 μmol/L on heparinase in vitro as well as 24 μmol/L in invasion assay using MDA-MB231 cells. Sanggenon G also had the moderate cytotoxicity at SW 620 (colon) and ACHN (kidney) cancer cell lines with IC50 of 10.96 and 13.44 μmol/L, respectively. Conclusion This is the first time that prenylated flavonoid sanggenon G is described as heparinase inhibitor. Besides, this flavonoid would be expected to be a metastasis inhibitor of cancer cells and also a valuable reagent to explore the mechanism of heparinase/heparanase-mediated metastasis.  相似文献   
4.
Heparin therapy for preeclampsia has been reported frequently.1-3 Most of the authors used heparin to prevent thrombosis and achieved good results. But its mechanism is not clear.4 Here we describe a case of severe early-onset preeclampsia complicated with hypercoagulable state, fetal growth restriction, and twin-twin transfusion syndrome, that responded well to heparin.  相似文献   
5.
Flow cytometry, singlet platelet counting, and optical aggregation have been used to monitor clopidogrel and glycoprotein IIb/IIIa (GPIIb/IIIa) platelet antagonists. Optical aggregation is considered the gold standard, but neither it nor flow cytometry is convenient in larger-scale clinical studies or point-of-care systems. Singlet platelet counting, a point-of-care assay correlated with optical platelet aggregation, only provides a measurement of platelet function at a single point in time. The Thrombelastograph is used to assay whole blood for thrombin-generated maximal clot-shear elasticity, referred to as the maximal amplitude (MA). Although platelet dysfunction, thrombocytopenia, and the in vitro effect of strong inhibitors such as IIb/IIIa antagonists can be observed, with thrombin generation milder platelet inhibitors cannot be assessed. We modified the Thromboelastograph assay, using reptilase and factor XIIIa, to form a clot, without thrombin generation, in heparinized whole blood. The resulting clot MA is dependent on added platelet agonists such as ADP or arachidonic acid, is sensitive to platelet antagonists, and provides a continuous measure of platelet function more analogous and better correlated with optical aggregation. This novel modification of the Thromboelastograph assay should prove to be a useful point-of-care whole-blood assay with which to monitor the effects of GPIIb/IIIa, ADP, and thromboxane A(2)-receptor-inhibiting drugs in patients.  相似文献   
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7.
Eosinophils localize to and release their granule proteins in close association with nerves in patients with asthma and rhinitis. These conditions are associated with increased neural function. In this study the effect of the individual granule proteins on cholinergic neurotransmitter expression was investigated. Eosinophil peroxidase (EPO) upregulated choline acetyltransferase (ChAT) and vesicular acetylcholine transporter (VAChT) gene expression. Fluorescently labeled EPO was seen to bind to the IMR-32 cell surface. Both Poly-l-Glutamate (PLG) and Heparinase-1 reversed the up-regulatory effect of EPO on ChAT and VAChT expression and prevented EPO adhesion to the cell surface. Poly-l-arginine (PLA) had no effect on expression of either gene, suggesting that charge is necessary but insufficient to alter gene expression. EPO induced its effects via the activation of NF-κB. MEK inhibition led to reversal of all up-regulatory effects of EPO. These data indicate a preferential role of EPO signaling via a specific surface receptor that leads to neural plasticity.  相似文献   
8.
肿瘤转移是一个复杂的过程,而针对转移治疗一直是研究的热点.低分子肝素通过抑制肝素酶对基底膜的降解、降低血液黏稠度等作用,对肿瘤细胞转移有明显的干预作用.本文就低分子肝素(LMWH)对肿瘤转移过程影响和作用机制做一综述,讨论其抗肿瘤转移的临床应用价值.  相似文献   
9.
目的探讨检测胃癌腹膜转移的方法。方法收集50例胃癌患者及8例胃良性病变患者的腹腔冲洗液。采用流式细胞术(FCM)检测胃癌患者术中腹腔冲洗液肝素酶(HPA)和存活素(Survivin)的表达情况,并采用薄层液基细胞制片术进行腹腔冲洗液细胞学(PLC)检查。结果 50例胃癌患者腹腔冲洗液中HPA阳性表达为52.0%(26/50);Survivin阳性表达率58.0%(29/50),HPA和Survivin联合检测阳性率为68.0%(34/50),两者阳性率皆高于PLC 22.0%的阳性率(P<0.01);HPA的阳性率与浸润深度、组织分化程度以及TNM分期呈正相关;Survivin的阳性率与肿瘤浸润深度、组织分化程度、淋巴结转移及TNM分期呈正相关。8例良性病变患者腹腔冲洗液中HPA和Survivin无阳性表达。结论 (1)腹腔冲洗液HPA和Survivin的检测可作为判断肿瘤恶性程度和预后的一项指标。(2)FCM方法检测腹腔冲洗液HPA和Survivin可能成为临床预测胃癌腹膜转移的一种方法。  相似文献   
10.
Abstract In a previous paper, we demonstrated that deep hypothermia in dogs provokes a release of a heparin-like factor. In the present study, we investigated some properties of this anticoagulant activity and compared it with exogenous heparin activity. The endogenous anticoagulant inhibited factors IIa and Xa; it was hydrolysed by heparinase and was AT III dependent. However, it differed from heparin in so far as it was adsorbed on cation exchange gel at neutral pH, its inhibition was decreased in the presence of neuraminidase, and it could not be neutralized with Polybrene or protamine. A release of heparan sulphate is suggested but remains to be demonstrated.  相似文献   
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