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排序方式: 共有10000条查询结果,搜索用时 203 毫秒
991.
Ha-Soon Choi Paul V. Rucker Zhicheng Wang Yi Fan Pamela Albaugh Greg Chopiuk Francois Gessier Fangxian Sun Francisco Adrian Guoxun Liu Tami Hood Nanxin Li Yong Jia Jianwei Che Susan McCormack Allen Li Jie Li Auzon Steffy AnneMarie Culazzo Celine Tompkins Van Phung Andreas Kreusch Min Lu Bin Hu Apurva Chaudhary Mahavir Prashad Tove Tuntland Bo Liu Jennifer Harris H. Martin Seidel Jon Loren Valentina Molteni 《ACS medicinal chemistry letters》2015,6(5):562-567
992.
Bryce A. Harrison Zheng Y. Almstead Hugh Burgoon Michael Gardyan Nicole C. Goodwin Jason Healy Ying Liu Ross Mabon Brett Marinelli Lakshman Samala Yulian Zhang Terry R. Stouch N. Andrew Whitlock Suma Gopinathan Beth McKnight Shuli Wang Nita Patel Alan G. E. Wilson Brian D. Hamman DennisS. Rice David B. Rawlins 《ACS medicinal chemistry letters》2015,6(1):84-88
993.
994.
Christopher N. Johnson Christophe Adelinet Valerio Berdini Lijs Beke Pascal Bonnet Dirk Brehmer Frederick Calo Joseph E. Coyle Phillip J. Day Martyn Frederickson Eddy J. E. Freyne Ron A. H. J. Gilissen Christopher C. F. Hamlett Steven Howard Lieven Meerpoel Laurence Mevellec Rachel McMenamin Elisabeth Pasquier Sahil Patel DavidC. Rees Joannes T. M. Linders 《ACS medicinal chemistry letters》2015,6(1):31-36
995.
目的分析对接蛋白3(DOK3)和蛋白酪氨酸激酶7(PTK7)在不同级别结肠腺瘤组织中的表达情况,探讨其在结肠癌的发生、发展机制中的作用。方法收集2015-01~2018-12广西壮族自治区南溪山医院经病理科确诊的结肠腺瘤伴低级别异型增生(LGD)标本22例,结肠腺瘤伴高级别异型增生(HGD)标本23例,结肠癌标本22例,瘤旁非肿瘤黏膜组织标本20例。采用免疫组织化学染色法检测不同类型标本DOK3和PTK7的表达情况。结果DOK3和PTK7均主要表达于腺上皮的胞浆和胞膜。瘤旁非肿瘤黏膜和LGD组织的DOK3高表达率均显著高于HGD和结肠癌组织(P<0.05);HGD组织的DOK3高表达率也显著高于结肠癌组织(P<0.05)。结肠癌和HGD组织的PTK7高表达率均显著高于瘤旁非肿瘤黏膜和LGD组织(P<0.05);结肠癌组织的PTK7高表达率也显著高于HGD组织(P<0.05)。结论DOK3可能是作为抑癌因子,而PTK7作为促癌因子参与结肠癌的发生、发展。 相似文献
996.
Maxim Cherneha Johannes Korth Meike Kaulfuß Mirko Trilling Marek Widera Hana Rohn Sebastian Dolff Nina Babel Andr Hoerning Andreas Kribben Oliver Witzke 《Viruses》2021,13(3)
Reactivations of BK polyoma virus (BKPyV) and human cytomegalovirus (HCMV) frequently cause life- and graft-threatening complications after renal transplantation. Both viruses are dependent on the mTOR pathway for replication. In this study we investigated the association of viral replication with mTOR activity in peripheral lymphocytes of renal transplant recipients. A flow-cytometry based assay for the measurement of Thr389 p70S6k phosphorylation, a surrogate marker of the mTOR pathway was established. Forty-eight adult renal transplant recipients were recruited to measure p70S6k activity in their peripheral blood mononuclear cells. This data set in conjunction with information concerning previous replication of BKPyV and HCMV was examined for correlations. Episodes of BKPyV replication were significantly associated with increased p70S6k phosphorylation in CD4+ T lymphocytes (p = 0.0002) and CD19+ B lymphocytes (p = 0.0073). HCMV infection of patients with a high-risk HCMV constellation of donor and recipient (D+/R−) was associated with increased p70S6k phosphorylation in CD19+ B lymphocytes (p = 0.0325). These associations were found to be independent of the trough levels of the immunosuppressive drugs. Conclusion: P70S6k phosphorylation in peripheral lymphocytes is associated with BKPyV reactivations and to a lesser extent with HCMV infections in renal transplant recipients. 相似文献
997.
Guilherme Piovezani Ramos Konstantinos A. Papadakis 《Mayo Clinic proceedings. Mayo Clinic》2019,94(1):155-165
Inflammatory bowel diseases (IBDs), represented by Crohn disease and ulcerative colitis, are associated with major morbidity in Western countries and with increasing incidence in the developing world. Although analysis of the genome of patients with IBD, especially through genome-wide association studies, has unraveled multiple pathways involved in IBD pathogenesis, only part of IBD heritability has been explained by genetic studies. This finding has revealed that environmental factors also play a major role in promoting intestinal inflammation, mostly through their effects in the composition of the microbiome. However, in order for microbial dysbiosis to result in uncontrolled intestinal inflammation, the intestinal barrier formed by intestinal epithelial cells and the innate immune system should also be compromised. Finally, activation of the immune system depends on the working balance between effector and regulatory cells present in the intestinal mucosa, which have also been found to be dysregulated in this patient population. Therefore, IBD pathogenesis is a result of the interplay of genetic susceptibility and environmental impact on the microbiome that through a weakened intestinal barrier will lead to inappropriate intestinal immune activation. In this article, we will review the mechanisms proposed to cause IBD from the genetic, environmental, intestinal barrier, and immunologic perspectives. 相似文献
998.
High glucose-induced mesangial cell altered contractility: role of the polyol pathway 总被引:2,自引:0,他引:2
B. Derylo T. Babazono E. Glogowski J. Kapor-Drezgic T. Hohman C. Whiteside 《Diabetologia》1998,41(5):507-515
Summary Glomerular mesangial cells cultured in high glucose conditions display impaired contractile responsiveness. It was postulated
that glucose metabolism through the polyol pathway leads to altered mesangial cell contractility involving protein kinase
C. Rat mesangial cells were growth-arrested for 24 h with 0.5 % fetal bovine serum in either normal (5.6 mmol/l) or high (30
mmol/l) glucose concentrations or high glucose plus the aldose reductase inhibitor, ARI-509 (100 μmol/l). The reduction of
cell planar surface area (contraction) in response to endothelin-1 (0.1 μmol/l), or to phorbol 12-myristate 13-acetate (50
pmol/l), was studied by videomicroscopy. In response to endothelin-1, mesangial cells in normal glucose contracted to 52 ±
3 % of initial planar area. In high glucose, the significantly (p < 0.05) smaller cell size and no contractile responsiveness to endothelin-1 were normalized with ARI-509. Membrane-associated
diacylglycerol, measured by a kinase specific 32P-phosphorylation assay, in high glucose was unchanged after 3 h, but significantly increased (p < 0.05) after 24 h which was normalized with ARI-509. Protein kinase C activity, measured by in situ 32P-phosphorylation of the epidermal growth factor receptor substrate was: increased by 32 % at 3 h of high glucose, unchanged
by ARI-509; and decreased significantly (p < 0.05) at 24 h compared to cells in normal glucose, normalized by ARI-509. Total cellular protein kinase C-alpha, -delta
and -epsilon, analysed by immunoblotting, were unchanged in high glucose at 24 h. Only protein kinase C-epsilon content was
reduced by ARI-509 in both normal and high glucose. Therefore, high glucose-induced loss of mesangial cell contractility,
diacylglycerol accumulation and altered protein kinase C activity are mediated through activation of the polyol-pathway, although
no specific relationship between elevated diacylglycerol and protein kinase C activity was observed. In high glucose, altered
protein kinase C function, or another mechanism related to the polyol pathway, contribute to loss of mesangial cell contractile
responsiveness. [Diabetologia (1998) 41: 507–515]
Received: 18 July 1997 and in final revised form: 17 January 1998 相似文献
999.
A study of 102 patients consecutively admitted to a coronary care unit (CCU) investigated the clinical usefulness of three different immunoenzymometrical CKMB methods: NovoClone CK-MB, ICON QSR CKMB and IMx CK-MB. Blood samples were drawn on admission and then every 6 h for 48 h. The three different methods correlated very well (r = 0.93-0.96). With discrimination levels of 10 micrograms.l-1 for NovoClone CK-MB and 5 micrograms.l-1 for the other two methods, a sensitivity of 1.0 and a still acceptable specificity (> 0.81) were achieved. In the group of patients (n = 53) with suspicion of acute myocardial infarction (AMI) but with no standard criteria for AMI, 14 patients were identified with small but significant increase of serum CKMB (mass concentration) and an increased CKMB (mass concentration)/CK ratio. During a 4 year follow-up nine out of these 14 patients died within 2 years, the majority being coronary deaths, as compared to only two out of the remaining 39 non-AMI patients with suspicion of AMI but with normal CKMB values (chi 2 = 18.47, P < 0.001). The finding of such a high mortality rate among patients with increased CKMB (mass concentration) has an important prognostic value even in patients without standard criteria for AMI. 相似文献
1000.
BACKGROUND & AIMS: Epidermal growth factor receptor (EGFR) activation, which plays an important role in regulating intestinal ion transport, can alleviate clinical symptoms such as diarrhea in patients with ulcerative colitis and promote mucosal restitution in animal models of colitis. Here, we investigate whether EGFR can regulate colonic ion transport in the setting of colitis. METHODS: Distal colon from control mice and mice with colitis was retained for immunohistochemistry or mounted in Ussing chambers. Ion transport responses across the tissues to the calcium agonist carbachol and the adenosine 3',5'-cyclic monophosphate agonist forskolin were measured with or without epidermal growth factor (EGF) pretreatment. RESULTS: EGF pretreatment of normal colonic mucosa inhibited ion transport responses to carbachol and forskolin but potentiated the reduced ion transport responses seen in dextran sulfate sodium (DSS)-treated and mdr1a knockout mouse colon. Ion substitution studies and the sodium transport inhibitor amiloride showed that sodium movement primarily accounted for the potentiating effect of EGF in DSS-treated tissues, despite decreased sodium channel expression. EGF potentiation of transport responses in DSS-treated colon was completely blocked by the cytoskeletal disruptor cytochalasin D and the phosphatidylinositol 3-kinase inhibitor wortmannin, whereas the novel and conventional protein kinase C isoform inhibitor G?6850 and the extracellular signal-regulated kinase inhibitor PD98059 partially reduced EGF effects. EGFR epithelial distribution and transforming growth factor alpha expression were also altered in DSS-treated tissues. CONCLUSIONS: Chronic inflammation uncovers a potentiating effect of EGFR activation on epithelial electrogenic sodium absorption that would be expected to ameliorate diarrheal symptoms associated with colitis. 相似文献