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| 1 | 超声速边界层内小激波的数值模拟(英文)显示文摘本文通过有限差分计算求解了NS方程,对超声速二维平板边界层的非线性稳定性问题进行了模拟。流场的来流马赫数为4.5。平板从尖前缘开始,流场在前缘处产生一道前缘激波。数值计算模拟了边界层对成倍频关系的双频扰动波的吸收问题。通过计算发现,在一定频率下边界层内可出现小激波。计算给出了小激波的发展过程。 | Shen Qing Zhang Hanxin Yuan Xiangjiang (China Aerodynamics Research and Development Center,Sichuan Mianyang 621000) | 2000 | 空气动力学学报2000，18，z1： | 2 |
| 2 | A characteristic based shock-capturing scheme for hyperbolic problems显示文摘 | TU Guohuai YUAN Xiangjiang | 2007 | Jour nal of Computational Physics2007，225，2： | 1 |
| 3 | A triple-combination nanotechnology platform based on multifunctional RNA hydrogel for lung cancer therapy显示文摘Conventional cancer combination therapy usually involves systemic delivery of anticancer drugs which may lead to the destruction of normal cells and physiological toxicity due to the lack of targeting ability and toxicity of drug carriers. In the present study, a triple combination nanosystem of gene therapy, chemotherapy and phototherapy delivered by multifunctional RNA nanohydrogels(RNA NHs) was established. By taking the advantages of DNA nanotechnology and rolling circle transcription(RCT), three lung cancer inhibitor microRNA(let-7 a, microRNA 34 a, microRNA 145) hairpins were integrated in one RNA NH nanoparticle, leading to the simultaneous silencing of three targeted m RNAs. Meanwhile, RNA NH carried doxorubicin(DOX, a chemotherapy drug) as well as 5,10,15,20-tetrakis(1-methylpyridinium-4-yl) porphyrin(TMPyP4, a photosensitizer) and delivered these drugs to cancer cells. It was demonstrated that lung cancer inhibitor microRNAs integrated in RNA NHs, DOX and TMPyP4 could play a synergistic anti-cancer role in multi-drug resistance cancer cells. Under the action of aptamer sequence S6 that was modified with cholesterol, the resulting RNA NHs were condensed to feasible size without the assistance of polyelectrolyte condensation reagents and showed cancer-specific cellular targeting. Subsequently, thousands of copies of miRNA together with chemotherapy drug as well as photosensitizer were delivered to cancer cells specifically, and an ideal synergistic treatment effect was achieved in vivo, thus playing a combined role of gene therapy, chemotherapy and phototherapy. Through this study, it can be concluded that the triple combination therapy nanosystem can overcome the multidrug resistance caused by the malfunction of genes in chemotherapy and shows a great potential in the field of multifunctional synergistic cancer treatment. | Junwei Li Dandan Yuan Xiangjiang Zheng Xinyue Zhang Xuemei Li Shusheng Zhang | 2020 | Science China Chemistry2020，63，4： | 1 |
| 4 | miR-139-5p mediates the palmitate-induced inhibition of insulin secretion by targeting neuronal pentraxin 1 in INS-1 cells显示文摘High fatty acid reduces insulin secretion in pancreatic β-cells and miR-139-5p is increased in diabetic pancreatic tissues and induces islet β-cell apoptosis.However,to date,there is no study exploring whether or not miR-139-5p is involved in high fatty acid-induced insulin secretion.In the present study,INS-1 cells were exposed to different concentrations(0.1,0.2,and 0.4 mM)of palmi-tate for different time periods(12,24,and 48 h).The expression levels of miR-139-5p and neuronal pentraxin 1(NPTX1)were evaluated by real-time PCR and western blot analysis.The regulation of NPTX1 by miR-139-5p was examined by luciferase assay.Cell transfection was conducted using Lipo8000 or Lipofectamine RNAiMAX.Potassium or glucose-stimulated insulin secretion levels were used to verify the function of miR-139-5p or NPTX1 in insulin secretion.Insulin secretion levels were detected by radioimmunoassay.We found that miR-139-5p was increased in INS-1 cells stimulated with palmitate.In addition,miR-139-5p was also elevated in islets of high-fat diet-fed mice and db/db mice compared to those in islets of normal diet-fed mice and wild-type mice.Knockdown of miR-139-5p could reverse high fatty acid-induced insulin secretion defects in INS-1 cells.Furthermore,we demonstrated that NPTX1 is a target of miR-139-5p.miR-139-5p mediated palmitate-induced insulin secretion defects by targeting NPTX1.Moreover,palmitate treatment declined the expression of NPTX1 and the NPTX1 expression was also decreased in islets of high-fat diet-fed mice and db/db mice.Impaired NPTX1 expression is involved in fatty acid-induced insulin secretion defects.Collectively,our results illustrate that the induction of β-cell insulin secretion defects by fatty acids is mediated,at least in part,by miR-139-5p via downregulation of NPTX1 expression. | Kai Zhang Yijian Zhang Cheng Chen Yuexing Yuan Xiaotian Jiang Xiangjiang Yuan Yao Wang | 2021 | Acta Biochimica et Biophysica Sinica2021，53，8： | 0 |
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