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Search Results: 1 - 10 of 35061 matches for " Weimin Zhou "
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The Design and Improvement of a Software Project Management System Based on CMMI  [PDF]
Guoping Zhou, Weimin Shao
Intelligent Information Management (IIM) , 2012, DOI: 10.4236/iim.2012.46037
Abstract: The paper researched and analyzed the characteristics, deficiencies and reasons of a management system of a software enterprise project to design a software project management system based on CMMI 1.2, thus helping the enterprise to improve development and management efficiency of software project and reduce the risks and costs on project devel- opment. It studied CMMI model version 1.3 which is recently released by SEI, analyzed its characteristics and told the difference between version 1.2 and version 1.3. In addition, an improvement proposal and a solution of the software project management system were given from multiple perspectives.
Endovascular repair of a type B aortic dissection with a right-sided aortic arch: case report
Zhou Weimin
Journal of Cardiothoracic Surgery , 2013, DOI: 10.1186/1749-8090-8-18
Abstract: Right-sided aortic arch is a rare anomaly, and aortic dissection involving a right-sided aortic arch is extremely rare. We report the case of a 65-year-old man with a right-sided aortic arch and a right descending aortic dissection and a stent-graft was accurately deployed without perioperative complications. There were no any complaints and complications after 18 months follow-up. The CTA demonstrated that the false lumen was largely thrombosed only with a mild type II endoleak and a mild descending aortic expansion. We feel that endovascular repair is feasible to patient of type B aortic dissection with a right-sided aortic arch. However, long-term clinical efficacy and safety have yet to be confirmed.
A new theoretical approach to 1:1 electrolytes at low temperature
Weimin Zhou,Jerome K. Percus
Physics , 2004,
Abstract: A new theoretical approach to 1:1 electrolytes at low temperature is developed, RPM and SAPM are studied with this approach, and their critical points of first order phase transition are calculated. The result is in very good agreement with that of recent MC simulations, in particular it shows that, for SAPM, both the critical temperature and critical density decrease with the increase of size asymmetry.
Advances in Diagnosis and Treatment of Multiple Primary Lung Cancer
Wenxin LUO, Ping ZHOU, Weimin LI
- , 2015, DOI: : 10.3779/j.issn.1009-3419.2015.10.07
Abstract: Recently, the incidence and detection rates of multiple primary lung cancer (MPLC) are increasing. The diagnosis of MPLC depends mainly on the Martini-Melamed criterion and ACCP criterion at present, taking all features (histological, genetic, radiologic and clinical) into account. It may be easy to diagnose cases of MPLC that exhibit different histological types, but it is difficult to diagnose cases that exhibit similar histological type. DNA polity, gene mutations, microsatellite alteration and so on provide new methods for the accurate diagnosis of MPLC. They can evaluate the clonal relationship and help differential diagnosis between MPLC and metastasis. The first therapeutic choice for MPLC is curative operation. The surgical approach includes lobectomy, wedge resection and segmentectomy. For those which cannot be resected, we can synthesize chemotherapy, radiotherapy, stereotactic ablative radiotherapy (SABR), radiofrequency ablation (RFA), molecular targeted therapy, etc.
Effects of paclitaxel and gefitinib on the proliferation and cell cycle of human lung adenocarcinoma cell SPC-A1
Gang JIA,Weimin ZHANG,Juan ZHOU,Zhixia ZHOU
Chinese Journal of Lung Cancer , 2008,
Abstract: Background and objective Previous clinical trials showed that there was no clinical benefit in the treatment of advanced non-small cell lung cancer when chemotherapy combined with gefitinib. The present study aims to assess the sequential administration of paclitaxel and gefitinib on the cell proliferation of lung adenocarcinoma cell SPC-A1 and to explore its mechanism by observing their effects on the cell cycle. Methods The expression of EGFR mRNA and EGFR protein were examined by RT-PCR and western blotting respectively. MTT was used to measure the cell proliferation of SPC-A1 cells. Cell cycle was detected by flow cytometry. Results Both EGFR mRNA and EGFR protein were overexpressed in SPC-A1 cells. From 1×10-14 M to 1×10-6 M, both paclitaxel and gefitinib inhibited the cell proliferation of SPC-A1 cells in a dose-dependent and time-dependent manner in vitro. The effects of paclitaxel in combination with gefitinib on cell proliferation depended on the sequence. No significant additive effects on cell proliferation was found when they were used simultaneously or gefitinib was added before paclitaxel. However, sequential administration of gefitinib following paclitaxel can remarkably enhanced the effect of paclitaxel on the cell proliferation of SPC-A1 cells. Cell cycle studies showed that paclitaxel and gefitinib induced G2/M and G0/G1 arrest respectively. The G0/G1 arrest was observed when paclitaxel and gefitinib was used simultaneously or gefitinib was added before paclitaxel. In contrast, sequential administration of gefitinib following paclitaxel induced G2/M arrest. Conclusion Both paclitaxel and gefitinib inhibits the cell proliferation of SPC-A1 cells. The additive effects on cell proliferation are sequential-dependent. The concomitant and the sequential treatment of gefitinib followed by paclitaxel exert no significant additive effects on the cell proliferation and resulted in the accumulation of cells in G0/G1 phase, which may decrease the effectiveness of paclitaxel in subsequent cycles. The additive effected on the cell proliferation are observed only when gefitinib is sequentially administrated following paclitaxel, which results in the G2/M arrest. The increase in G2/M phase suggests that cell cycle effects might not explain the observed additive effects.
A Generalized Tanh-Function Type Method and the(G'/G) -Expansion Method for Solving  [PDF]
Weimin Zhang
Applied Mathematics (AM) , 2013, DOI: 10.4236/am.2013.410A1003
Abstract: In this paper a generalized tanh-function type method is proposed by using the idea of the transformed rational function method. We show that the (G'/G) -expansion method is a special case of the generalized tanh-function type method, so the (G'/G) -expansion method is considered as a special deformation application of the transformed rational function method. We demonstrate that all solutions obtained by the (G'/G) -expansion method were found by the generalized tanh-function type method. As applications, we consider mKdV equation. Compared with the (G'/G) -expansion method, the generalized tanh-function type method gives new and more abundant solutions.
The Analysis of Jackson’s Victory over the Second Bank of the United States  [PDF]
Weimin Liang
Modern Economy (ME) , 2018, DOI: 10.4236/me.2018.96073
Abstract: This article aims to analyze the reasons for the Jackson’s bank war over theSecond Bank of United States. It shows us a new perspective on the reason, which focuses on the different growth backgrounds of Jackson and Biddle. The President Jackson vetoed the bill for the postponement of the Second Bank of United States. And the different personality of Jackson and the Biddle, the president of the Second Bank of United States are important reasons for that. What’s more, the collapse of the Second Bank of United States prevented the financial power from being too concentrated, which did harm to the state power. The Jackson’s victory establishes the fundamental of Federal Reserve system, and gives the wall street spaces to flourish.
Pravastatin Prevents Aortic Atherosclerosis via Modulation of Signal Transduction and Activation of Transcription 3 (STAT3) to Attenuate Interleukin-6 (IL-6) Action in ApoE Knockout Mice
Xiaoxu Zhou,Dan Li,Wei Yan,Weimin Li
International Journal of Molecular Sciences , 2008, DOI: 10.3390/ijms9112253
Abstract: The purpose of this study was to determine whether pravastatin’s prevention of aortic atherosclerosis via attenuation of IL-6 action depends on modulation of STAT3 activity. Male apoE knockout (apoE-/-) mice fed on a diet containing 1.25% cholesterol (wt/wt) were divided into pravastatin group provided with pravastatin (80 mg kg-1 per day) and atherosclerosis group. After eight weeks, pravastatin significantly prevented atherosclerotic lesion and reduced levels of IL-6 in serum and lesion, and significantly decreased expressions of phosphorylated STAT3 (pSTAT3) and increased suppressor of cytokine signaling 3 (SOCS3) expressions in lesions. Our results suggested that pravastatin’s aortic atherosclerosis preventing action via attenuation of IL-6 action may partially depend on modulation of STAT3 activity.
The effect and mechanism of endothelin-1-induced intracellular free calcium in human lung adenocarcinoma cells SPC-A1
Juan ZHOU,Weimin ZHANG,Qianjun YE,Gang JIA
Chinese Journal of Lung Cancer , 2008,
Abstract: Background and objective Endothelin-1 (ET-1) is a potent mitogen involved in cell growth in human lung adenocarcinoma cells SPC-A1. The increase in intracellular free calcium ([Ca2+]i) plays a great role in this process. The aim of this study is to investigate the ET-1-induced [Ca2+]i responses in SPC-A1 cells and to explore its cellular mechanism. Methods [Ca2+]i was measured by Fura-2/AM fluorescent assay. Endothelin receptors antagonists, calcium channel blockers and intracellular signal transduction blockers were used to study the underlying mechanism of ET-1-induced [Ca2+]i responses in SPC-A1 cells. Results At the concentration of 1×10-15 mol/L-1×10-8 mol/L, ET-1 caused a dose-dependent increase of [Ca2+]i in SPC-A1 cells (P<0.05) in vitro. The ET-1-induced (1×10-10 mol/L) increase of [Ca2+]i was blocked by BQ123 at 1×10-7 mol/L (P<0.05), a highly selective endothelin receptor A (ETAR) antagonist, not by BQ788 at 10-7 mol/L (P>0.05), a highly selective endothelin receptor B (ETBR) antagonist. Depletion of extracellular Ca2+ with free Ca2+ solution and 0.1mmol/L ethyleneglycol bis (2-aminoethyl ether) tetraacetic acid (EGTA) or blockade of voltage dependent calcium channel with nifedipine at 1×10-6 mol/L significantly reduced the ET-1-induced increase of [Ca2+]i. The ET-1-induced (1×10-10 mol/L) increase of [Ca2+]i was also significantly attenuated by U73122 at 1×10-5 mol/L (P<0.05), a phospholipase C inhibitor, and by Ryanodine at 50×10-6 mol/L. However, Staurosporine (2×10-9 mol/L), a protein kinas C inhibitor, exerted no significant effect on the ET-1-induced (1×10-10 mol/L) increase of [Ca2+]i. Conclusion ET-1 elevates [Ca2+]i via activation of ETA receptor. Both phospholipase C/Ca2+ pathway and Ca2+ influx through voltage dependent Ca2+ channel activate by ETAR contribute to this process.
Nicotine Activates YAP1 through nAChRs Mediated Signaling in Esophageal Squamous Cell Cancer (ESCC)
Yue Zhao, Wei Zhou, Liyan Xue, Weimin Zhang, Qimin Zhan
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0090836
Abstract: Cigarette smoking is an established risk factor for esophageal cancers. Yes-associated protein 1 (YAP1), the key transcription factor of the mammalian Hippo pathway, has been reported to be an oncogenic factor for many cancers. In this study, we find nicotine administration can induce nuclear translocation and activation of YAP1 in ESCC. Consistently, we observed nuclear translocation and activation of YAP1 by knockdown of CHRNA3, which is a negative regulator of nicotine signaling in bronchial and esophageal cancer cells. Nicotine administration or CHRNA3 depletion substantially increased proliferation and migration in esophageal cancer cells. Interestingly, we find that YAP1 physically interacts with nAChRs, and nAChRs-signaling dissociates YAP1 from its negative regulatory complex composed with α-catenin, β-catenin and 14-3-3 in the cytoplasm, leading to upregulation and nuclear translocation of YAP1. This process likely requires PKC activation, as PKC specific inhibitor Enzastaurin can block nicotine induced YAP1 activation. In addition, we find nicotine signaling also inhibits the interaction of YAP1 with P63, which contributes to the inhibitory effect of nicotine on apoptosis. Using immunohistochemistry analysis we observed upregulation of YAP1 in a significant portion of esophageal cancer samples. Consistently, we have found a significant association between YAP1 upregulation and cigarette smoking in the clinical esophageal cancer samples. Together, these findings suggest that the nicotine activated nAChRs signaling pathway which further activates YAP1 plays an important role in the development of esophageal cancer, and this mechanism may be of a general significance for the carcinogenesis of smoking related cancers.
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