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实施独立计量分区(district metered area,DMA)是辅助供水管网管理和漏损识别的重要手段.图划分算法是进行DMA分区的方法之一,常规图划分算法应用中,存在解空间受限、分区后原水流状态易发生较大改变、形成较多串联分区(对流量计算不利)的缺点.在常规图划分算法基础上进行了改进:粗化阶段按照特定规则匹配、合并非输水干管两端的节点,形成简化的管网拓扑结构;分区阶段得到管网初步分区方案;细化阶段提出基于贪心算法、枚举算法、蒙特卡洛算法的分区调整方法,结合改进的仪表安置方法、水力模拟、优劣解距离法(technique for order preference by similarity to an ideal solution,TOPSIS),对分区方案进行调整.将该方法应用于YX市供水管网,成功进行了分区. 相似文献
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Dr. Yahu A. Liu Dr. Qihui Jin Qiang Ding Dr. Xueshi Hao Tingting Mo Shanshan Yan Dr. Yefen Zou Dr. Zhihong Huang Xiaoyue Zhang Wenqi Gao Dr. Tom Y.-H. Wu Chun Li Dr. Badry Bursalaya Dr. Michael Di Donato Dr. You-Qing Zhang Lisa Deaton Dr. Weijun Shen Dr. Brandon Taylor Anwesh Kamireddy Dr. George Harb Dr. Jing Li Dr. Yong Jia Dr. Andrew M. Schumacher Dr. Bryan Laffitte Dr. Richard Glynne Dr. Shifeng Pan Dr. Peter McNamara Dr. Valentina Molteni Dr. Jon Loren 《ChemMedChem》2020,15(16):1562-1570
Loss of β-cell mass and function can lead to insufficient insulin levels and ultimately to hyperglycemia and diabetes mellitus. The mainstream treatment approach involves regulation of insulin levels; however, approaches intended to increase β-cell mass are less developed. Promoting β-cell proliferation with low-molecular-weight inhibitors of dual-specificity tyrosine-regulated kinase 1A (DYRK1A) offers the potential to treat diabetes with oral therapies by restoring β-cell mass, insulin content and glycemic control. GNF4877, a potent dual inhibitor of DYRK1A and glycogen synthase kinase 3β (GSK3β) was previously reported to induce primary human β-cell proliferation in vitro and in vivo. Herein, we describe the lead optimization that lead to the identification of GNF4877 from an aminopyrazine hit identified in a phenotypic high-throughput screening campaign measuring β-cell proliferation. 相似文献
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CMP系统技术与市场 总被引:3,自引:1,他引:2
葛劢冲 《电子工业专用设备》2003,32(1):17-24
概述了CMP系统技术的发展历史、发展趋势以及在IC生产中的重要性,介绍了国外CMP设备主要制造厂家的设备型号和性能及CMP设备市场分布和需求,阐述了CMP系统技术的基础研究、关键技术和国内研究概况。 相似文献
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J. B. Quinn G. E. Schumacher L. W. Schultheis 《Journal of Failure Analysis and Prevention》2004,4(1):41-46
Several days after heart surgery, a patient discovered his upper right canine tooth had broken at the root. Such tooth damage,
recognized post-operatively, is usually assumed to be caused by blunt mechanical force from an instrument used by the anesthesiologist
during placement of a breathing tube at the start of surgery.
In this case, the patient had saved the crown portion of the broken tooth, and it was possible to examine the root fracture
characteristics. The curvature and direction of the crack path and natural tooth situation suggested that failure could be
described through a cantilever beam model. This was confirmed when a whole extracted sample tooth was embedded and broken
by a measured force in a manner consistent with the model. The resulting fracture surface matched that of the patient’s broken
canine tooth. However, the high load and force direction necessary to fracture the root was inconsistent with forces applied
during the anesthesia procedure. The failure analysis and further investigation indicated tooth clenching on the breathing
tube during recovery was the likely cause of fracture.
This paper presents an alternate explanation for intubation-related dental injury, demonstrates the practicality of fractographic
analysis of biological materials, and introduces a methodology for simulating in vitro tooth settings for mechanical testing. 相似文献
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KJ Shon M Grilley R Jacobsen GE Cartier C Hopkins WR Gray M Watkins DR Hillyard J Rivier J Torres D Yoshikami BM Olivera 《Canadian Metallurgical Quarterly》1997,36(31):9581-9587
A paralytic peptide, psi-conotoxin Piiie has been purified and characterized from Conus purpurascens venom. Electrophysiological studies indicate that the peptide inhibits the nicotinic acetylcholine receptor (nAChR). However, the peptide does not block the binding of alpha-bungarotoxin, a competitive nAChR antagonist. Thus, psi-conotoxin Piiie appears to inhibit the receptor at a site other than the acetylcholine-binding site. As ascertained by sequence analysis, mass spectrometry, and chemical synthesis, the peptide has the following covalent structure: HOOCCLYGKCRRYOGCSSASCCQR* (O = 4-trans hydroxyproline; * indicates an amidated C-terminus). The disulfide connectivity of the toxin is unrelated to the alpha- or the alphaA-conotoxins, the Conus peptide families that are competitive inhibitors of the nAChR, but shows homology to the mu-conotoxins (which are Na+ channel blockers). 相似文献