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991.
Yoshimasa Nobeyama Yoshinori Umezawa Hidemi Nakagawa 《Experimental dermatology》2017,26(11):1068-1074
Analysis of psoriatic parakeratotic cells is helpful for understanding the pathogenesis of psoriasis. Methylation analysis can be performed on psoriatic scales, but it is unclear whether genes can be silenced by DNA methylation in psoriatic stratum corneum. The present study was conducted to detect genes silenced in psoriatic stratum corneum. Methylation array analysis with 485 577 probes, quantitative real‐time methylation‐specific PCR (RT‐MSP) and bisulphite sequencing were performed for 30 psoriatic scale samples, 6 fully developed psoriatic skin samples and 12 normal skin samples. Immunohistochemical staining of HOXA5 was performed for 29 psoriatic epidermal samples and 13 normal epidermal samples. The genome‐wide methylation array detected two CpG sites within CpG islands (CGIs) located in promoter regions of HOXA5 and LIAS that had methylation levels of >0.6 in at least one of the three psoriatic scale samples and of <0.2 in all three normal skin tissue samples (methylation rate range, 0.0‐1.0). RT‐MSP for HOXA5CGI, in which the primers were successfully developed, revealed that the average methylation level of 27 psoriasis scales (60.2%) is significantly higher than that of 9 normal skin samples (34.6%) (P=.013). Immunohistochemical staining revealed that HOXA5 protein was not expressed in the stratum corneum of fully developed psoriatic epidermis, but the protein was expressed in the stratum corneum of incompletely developed epidermis and normal epidermis. In conclusion, HOXA5 can be silenced in the stratum corneum of psoriasis. The silenced gene was identified by non‐invasive methylation analysis of psoriatic scales. 相似文献
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目的本研究旨在探讨microRNA-9-3(miR-9-3)在慢性淋巴细胞性白血病骨髓细胞中的甲基化异常及其意义。方法采用甲基化特异性聚合酶链反应(MSP)技术检测8例正常骨髓组织、78例新确诊的慢性淋巴细胞性白血病患者和7种白血病细胞株甲基化水平。结果正常对照组miR-9-3呈未甲基化状态;7种白血病细胞株中有5种呈未甲基化状态(71.4%);78例慢性淋巴细胞性白血病患者中65例呈miR-9-3甲基化,MSP阳性率为83%。5-氮杂-2'-脱氧胞苷(5-Aza Dc)处理白血病细胞株后I83-E95和WAC3CD5+细胞株miR-9-3呈未甲基化状态。结论慢性淋巴细胞性白血病患者存在miR-9-3表达受抑,可能与其基因甲基化异常有关。而miR-9-3甲基化在激活慢性淋巴细胞性白血病患者NF-κB1信号通路的作用值得进一步研究。 相似文献
995.
������a����־Զb 《中国实用口腔科杂志》2017,10(8):493-496
??Objective To study the role of the CCR5 antagonists Maraviroc in the migration??chemotaxis??invasion and proliferation of human salivary adenoid cystic carcinoma. Methods Scratches??migration??invasion and MTT assays were performed to detect the migration??chemotaxis??invasion and proliferation of SACC-83 and SACC-LM in vitro. Results Compared with control group, the experimental group which was pretreated by CCR5 inhibitor Maraviroc had lower recuperability in cell scratch model. The number of cells which were blocked by inhibitor decreased significantly on the lower surface of the filters which were fixed in methanol in migration and invasion assays. And proliferation experiment results show that the multiplication capacity of SACC-83 and SACC-LM were obviously inhibited by Maraviroc. Conclusion Maraviroc may be a kind of new targeted anti-tumor drugs and small-molecule antagonists of CCR5 could inhibit the development of salivary gland adenoid cystic carcinoma. 相似文献
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Lluis Asmarats François Dagenais Elisabeth Bédard Sergio Pasian Rebecca T. Hahn José L. Navia Josep Rodés-Cabau 《The Canadian journal of cardiology》2018,34(10):1370.e5-1370.e7
Despite the growing evidence with emerging transcatheter tricuspid valve repair therapies, the experience with transcatheter tricuspid valve replacement remains sparse. We describe a case of severe tricuspid regurgitation in a 79-year-old patient deemed unsuitable for isolated tricuspid valve surgery, successfully treated with a 40-mm self-expandable NaviGate (NaviGate Cardiac Structures, Inc, Lake Forest, CA) valved stent via a transatrial approach, with excellent result and hemodynamic performance at 4 months. 相似文献
1000.
Jane L Roberts Laurence Booth Adam Conley Nichola Cruickshanks Mark Malkin Rakesh C Kukreja Steven Grant Andrew Poklepovic Paul Dent 《Cancer biology & therapy》2014,15(6):758-767
We determined whether clinically relevant phosphodiesterase 5 (PDE5) inhibitors interacted with clinically relevant chemotherapies to kill medulloblastoma cells. In medulloblastoma cells PDE5 inhibitors interacted in a greater than additive fashion with vincristine/etoposide/cisplatin to cause cell death. Knockdown of PDE5 expression recapitulated the combination effects of PDE5 inhibitor drugs with chemotherapy drugs. Expression of dominant negative caspase 9 did not significantly inhibit chemotherapy lethality but did significantly reduce enhanced killing in combination with the PDE5 inhibitor sildenafil. Overexpression of BCL-XL and c-FLIP-s suppressed individual and combination drug toxicities. Knockdown of CD95 or FADD suppressed drug combination toxicity. Treatment with PDE5 inhibitors and chemotherapy drugs promoted autophagy which was maximal at ~12 h post-treatment, and in a cell type-dependent manner knockdown of Beclin1 or ATG5 either suppressed or enhanced drug combination lethality. PDE5 inhibitors enhanced the induction of chemotherapy-induced DNA damage in a nitric oxide synthase-dependent fashion. In conclusion, our data demonstrate that the combination of PDE5 inhibitors with standard of care chemotherapy agents for medulloblastoma represents a possible novel modality for future treatment of this disease. 相似文献