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排序方式: 共有3385条查询结果,搜索用时 125 毫秒
61.
Shuang Lu Hong Sun Kim Yubo Cao Karan Bedi Lili Zhao Ishwarya Venkata Narayanan Brian Magnuson Yumei Gu Jing Yang Zhujun Yi Sepideh Babaniamansour Sargis Shameon Chang Xu Michelle T. Paulsen Ping Qiu Sivakumar Jeyarajan Mats Ljungman Dafydd Thomas Yali Dou Howard Crawford Marina Pasca di Magliano Kai Ge Bo Yang Jiaqi Shi 《International journal of cancer. Journal international du cancer》2023,153(3):552-570
62.
Bin Dai Bai Ruan Juan Wu Jianlin Wang Runze Shang Wei Sun Xia Li Kefeng Dou Desheng Wang Yu Li 《International journal of clinical and experimental pathology》2014,7(9):5645-5654
Insulin-like growth factor binding protein-1 (IGFBP-1) plays an important role in the development and progression of cancer. However, the expression of IGFBP-1 remains equivocal, and little is known about its clinicopathological significance and prognostic value in hepatocellular carcinoma (HCC). In this study, we evaluated the expression of IGFBP-1 in 90 paired HCC tissues and adjacent non-cancerous liver tissues and analyzed its clinical and prognostic significance. The results showed that IGFBP-1 was detected in cytoplasm as well as cell nucleus, and down-regulated in HCC tissues compared to the adjacent non-cancerous liver tissues. The decreased expression of IGFBP-1 was correlated with tumor differentiation, liver cirrhosis, microvascular invasion or metastasis, TNM stage and poor survival. Moreover, low levels of IGFBP-1 may be an independent prognostic indicator for the survival of patients with HCC. We also evaluated its function by adding recombinant IGFBP-1 to the cultured HCC cell lines HepG2 and MHCC97-H. The result of the invasion chamber assay showed that IGFBP-1 could inhibit the invasion of HepG2 and MHCC97-H. MMP-9 secretion by these cells was significantly decreased when the cells were treated with IGFBP-1. Our results suggest that IGFBP-1 inhibits the invasion and metastasis of HCC cells and that IGFBP-1 may be useful as a valuable marker for the prognosis of patients with HCC. 相似文献
63.
目的研究KISS—1、VEGF—C在乳头状甲状腺癌组织中的表达情况,分析两者表达与乳头状甲状腺癌临床病理特征的关系以及两者的相关性。方法收集乳头状甲状腺癌组织病理标本48例及其正常甲状腺组织20例,采用免疫组织化学SP法检测KISS—1、VEGF—C在乳头状甲状腺癌组织中的表达情况,分析KISS—1、VEGF—C在乳头状甲状腺癌组织中阳性表达率与临床病理学特征之间的关系以及两者表达之间的相关性。结果KISS-1、VEGF—C在乳头状甲状腺癌组织和正常甲状腺组织中的阳性表达率之间具有显著性差异(P〈0.01)。KISS-1、VEGF—C在乳头状甲状腺癌组织中的阳性表达率与肿瘤大小、颈部淋巴结转移、临床分期相关且均有显著性差异(P〈0.05)。KISS-1和VEGF—C的表达与患者的性别、年龄均无关(P〉0.05);KISS-1与VEGF—C在乳头状甲状腺癌组织表达存在负相关关系(P〈0.05)。结论KISS—1、VEGF—C的表达水平与乳头状甲状腺癌有关,且与肿瘤大小、颈部淋巴结转移状况、临床分期相关,与患者性别、年龄无关。KISS-1在乳头状甲状腺癌组织的表达与VEGF—C呈负相关关系。KISS-1、VEGF—C联合检测可作为乳头状甲状腺癌恶性潜能的判断指标。 相似文献
64.
Pasha Apontes Zhongbo Liu Kai Su Outhiriaradjou Benard Dou Y. Youn Xisong Li Wei Li Raihan H. Mirza Claire C. Bastie Linda A. Jelicks Jeffrey E. Pessin Radhika H. Muzumdar Anthony A. Sauve Yuling Chi 《Diabetes》2014,63(11):3626-3636
Excessive dietary fat intake causes systemic metabolic toxicity, manifested in weight gain, hyperglycemia, and insulin resistance. In addition, carbohydrate utilization as a fuel is substantially inhibited. Correction or reversal of these effects during high-fat diet (HFD) intake is of exceptional interest in light of widespread occurrence of diet-associated metabolic disorders in global human populations. Here we report that mangiferin (MGF), a natural compound (the predominant constituent of Mangifera indica extract from the plant that produces mango), protected against HFD-induced weight gain, increased aerobic mitochondrial capacity and thermogenesis, and improved glucose and insulin profiles. To obtain mechanistic insight into the basis for these effects, we determined that mice exposed to an HFD combined with MGF exhibited a substantial shift in respiratory quotient from fatty acid toward carbohydrate utilization. MGF treatment significantly increased glucose oxidation in muscle of HFD-fed mice without changing fatty acid oxidation. These results indicate that MGF redirects fuel utilization toward carbohydrates. In cultured C2C12 myotubes, MGF increased glucose and pyruvate oxidation and ATP production without affecting fatty acid oxidation, confirming in vivo and ex vivo effects. Furthermore, MGF inhibited anaerobic metabolism of pyruvate to lactate but enhanced pyruvate oxidation. A key target of MGF appears to be pyruvate dehydrogenase, determined to be activated by MGF in a variety of assays. These findings underscore the therapeutic potential of activation of carbohydrate utilization in correction of metabolic syndrome and highlight the potential of MGF to serve as a model compound that can elicit fuel-switching effects. 相似文献
65.
66.
Hui Chen Guo-Hua Xie Wei-Wei Wang Xiang-Liang Yuan Wen-Ming Xing Hong-Jing Liu Jin Chen Min Dou Li-Song Shen 《Oncotarget》2015,6(24):20449-20465
Axon guidance protein Semaphorin 3E (Sema3E) promotes tumor metastasis and suppresses tumor cell death. Here, we demonstrated that Sema3E was decreased in gastric cancer. Its levels were inversely associated with tumor progression. Levels of Sema3E were associated with low p300 and high class I histone deacetylase (class I HDAC). Ectopic expression of Sema3E inhibited proliferation and colony formation of gastric cancer cell lines in vitro and xenografts in vivo. Sema3E overexpression inhibited migration and invasion of gastric cancer cells, which was associated with induction of E-cadherin and reduction of Akt and ERK1/2 phosphorylation. We suggest that silencing of Sema3E contributes to the pathogenesis of gastric cancer. 相似文献
67.
目的 旨在阐明吻内侧被盖核(rostromedial tegmental nucleus,RMTg)是否参与吗啡引起的大鼠睡眠障碍。方法 将雄性SD大鼠随机分为溶剂对照组和吗啡组,每组7只,对照溶剂为人工脑脊液(artificial cerebrospinal fluid,ACSF)。采用脑立体定位、核团微量注射和睡眠记录与解析等技术观察RMTg内给予吗啡对大鼠睡眠-觉醒周期的影响。结果 与对照组相比,双侧RMTg 给予吗啡(16 mmol/L,每侧0.5 μL)可以引起大鼠长达4 h的觉醒,期间非快动眼(non-rapid eye movement,NREM)睡眠深度降低、快动眼(REM)睡眠减少的现象与吗啡临床用药所引起的睡眠障碍的表现相一致。结论 RMTg参与吗啡引起的大鼠睡眠紊乱。 相似文献
68.
摘 要 目的: 本研究旨在建立肠肽胶囊的质量标准。方法: 采用薄层色谱法鉴别薏苡仁、蒲公英、白芷、厚朴,采用HPLC法测定三七中有效成分三七皂苷R1、人参皂苷Rg1和人参皂苷Rb1的含量。结果: 薄层鉴别斑点清晰,阴性对照无干扰;三七中有效成分三七皂苷R1、人参皂苷Rg1和人参皂苷Rb1分别在40~300 μg·mL-1、320 ~2 400 μg·mL-1、80~600 μg·mL-1范围内线性关系良好;平均加样回收率分别为99.76%、99.33%、99.48%,RSD分别为0.42%、0.48%、0.63%(n=9)。结论:该方法可用于肠肽胶囊的质量控制。 相似文献
69.
70.