MR ventilation-perfusion imaging of human lung using oxygen-enhanced and arterial spin labeling techniques.

Magnetic resonance ventilation-perfusion (V/Q) imaging has been demonstrated using oxygen and arterial spin labeling techniques. Inhaled oxygen is used as a paramagnetic contrast agent in ventilation imaging using a multiple inversion recovery (MIR) approach. Pulmonary perfusion imaging is conducted using a flow-sensitive alternating inversion recovery with an extra radiofrequency pulse (FAIRER) technique. A half Fourier single-short turbo spin echo (HASTE) sequence is used for data acquisition in both techniques. V/Q imaging was performed in ten of the twenty volunteers, while either ventilation or perfusion was imaged in the other ten. This V/Q imaging scheme is completely noninvasive, does not involve ionized radiation, and shows promising potential for clinical use in the diagnosis of lung diseases such as pulmonary embolism.     

lncRNA MIR4435-2HG的表达水平及甲基化状态与脑胶质瘤病理分级的关系

目的 探讨长链非编码RNA MIR4435-2HG的表达水平及甲基化状态与脑胶质瘤病理分级的关系.方法 选取2019年1～12月手术切除的脑胶质瘤组织110例和颅脑损伤内减压术中切除正常脑组织20例(对照组).采用实时荧光定量PCR和甲基化特异性PCR检测组织和血清MIR4435-2HG水平及甲基化状态.结果 110例...     

Eriodictyol inhibits high glucose‐induced extracellular matrix accumulation,oxidative stress,and inflammation in human glomerular mesangial cells

Diabetic nephropathy (DN) is one of the major complications of diabetes mellitus. The progression of DN has been found to be associated with high glucose (HG)‐induced oxidative stress and inflammation in diabetes mellitus. Eriodictyol is a flavonoid that possesses antioxidant and anti‐inflammatory effects. However, the effect of eriodictyol on DN remains unknown. In the present study, we evaluated the role of eriodictyol in mesangial cells (MCs) in response to HG condition. The results showed that eriodictyol repressed cell proliferation of HG‐stimulated MCs. Treatment with eriodictyol attenuated oxidative stress, which was evidenced by increased superoxide dismutase activity as well as decreased production of reactive oxygen species (ROS) and malondialdehyde. Besides, eriodictyol suppressed the expressions of two NADPH oxidase (NOX) isoforms, NOX2 and NOX4, which are responsible for the generation of ROS. Eriodictyol suppressed the production of extracellular matrix proteins including fibronectin and Collagen IV, as well as the secretion of inflammatory cytokines including TNF‐α, IL‐1β, and IL‐6 in HG‐induced MCs. Moreover, the HG‐induced activation of Akt/NF‐κB pathway was mitigated by eriodictyol. In conclusion, eriodictyol protected MCs from HG stimulation though inhibition of Akt/NF‐κB pathway.     

Hepatic stellate cell-released CXCL1 aggravates HCC malignant behaviors through the MIR4435-2HG/miR-506-3p/TGFB1 axis

Hepatic stellate cell (HSC) activation is a critical event in the development of hepatic fibrosis and hepatocellular carcinoma (HCC). By the release of soluble cytokines, chemokines, and chemotaxis, HSCs affect HCC cell phenotypes through a complex tumor microenvironment. In this study, weighted gene co-expression network analysis (WGCNA) was used to identify the TGF-β signaling pathway as a key signaling pathway in Hep3B cells cultured in HSC conditioned medium. MIR4435-2HG is a hub lncRNA associated with the TGF-β signaling pathway and HSC activation. HSC-condition medium (CM) culture induced HCC cell malignant behaviors, which were partially reversed by MIR4435-2HG silencing. miR-506-3p directly bound to MIR4435-2HG and the 3′UTR of TGFB1. Similarly, overexpression of miR-506-3p also attenuated HSC-CM-induced malignant behavior of HCC cells. In HSC-CM cultured HCC cells, the effects of MIR4435-2HG knockdown on TGFB1 expression and HCC cell phenotypes were partially reversed by miR-506-3p inhibition. HSCs affected HCC cell phenotypes by releasing CXCL1. In an orthotopic xenotransplanted tumor model of HCC cells plus HSCs in mice, CXCR2 knockdown in HCC cells significantly inhibited tumorigenesis, which was partially reversed by MIR4435-2HG overexpression in HCC cells. In HCC tissue samples, the levels of CXCL1, TGF-β1, and MIR4435-2HG were upregulated, while miR-506-3p expression was downregulated. In conclusion, HSC-released CXCL1 aggravated HCC cell malignant behaviors through the MIR4435-2HG/miR-506-3p/TGFB1 axis. In addition to CXCL1, the MIR4435-2HG/miR-506-3p/TGFB1 axis might also be the underlying target for HCC therapy.     

人LncRNA MIR31HG基因稳定转染PC9细胞系的构建及其对细胞增殖和迁移的影响

目的：检测过表达人MIR31HG基因对PC9细胞增殖和迁移的影响,阐明促癌基因MIR31HG的作用机制。方法：通过RT-PCR法扩增长链非编码RNA（LncRNA）MIR31HG全长序列,分子克隆至pcDNA3.1（-）真核表达载体,将pcDNA3.1-MIR31HG过表达质粒和对照质粒pcDNA3.1分别转染人肺癌PC9细胞。采用酶切鉴定法检测MIR31HG过表达载体的构建情况。通过G418药物筛选建立稳定过表达MIR31HG的PC9细胞系（PC9-pcDNA3.1-MIR31HG,稳定转染组）和对照细胞系（PC9-pcDNA3.1,空载体组）。采用RT-PCR法检测稳定转染细胞系中MIR31HG基因表达水平,采用CCK-8法和划痕愈合实验检测PC9细胞增殖活性和迁移能力。结果：琼脂糖凝胶电泳,成功扩增得到了MIR31HG的特异基因片段;MIR31HG真核表达载体经双酶切后分别产生目的基因和载体2个片段。RT-PCR法检测,稳定转染组细胞中MIR31HG mRNA表达水平明显高于空载体组（P<0.05）。CCK-8检测,在培养24、36和48h时,稳定转染组细胞增殖活性明显高于空载体组（P<0.01）。划痕愈合实验,在培养48h时,稳定转染组细胞划痕愈合率明显高于空载体组（P<0.05）。结论：成功构建了人LncRNA MIR31HG基因的真核过表达载体和过表达MIR31HG的稳定转染PC9细胞系,且MIR31HG过表达能够促进肺癌PC9细胞增殖和迁移。