High-fidelity Modeling of Multilayer Building Process in Electron Beam Powder Bed Fusion:Build-quality Prediction and Formation-Mechanism Investigation

High-fidelity simulations of powder bed fusion(PBF)additive manufacturing have made significant progress over the past decade.In this study,an efficient two-dimensional frame was developed for simulating the electron beam PBF process with hundreds of tracks for the direct prediction of the build quality.The applicable parameter range of the developed model was determined by comparing the heat transfer with that in three-dimensional cases.Subsequently,powder deposition and selective melting were coupled for a continuous simulation of the multilayer process.Three powder deposition models were utilized to generate random powder particles,and their effects on the packing structure and the resultant simulated build quality were investigated.The predicted build quality was validated using experimental results from independent studies.By reproducing the building process,the defect development mechanism in a multilayer process was revealed for the coalescence behaviors of randomly distributed powder particles,which also confirmed the importance of simulation at the high-fidelity powder scale.The effects of key process parameters during multilayer and multi-track processes on the build quality were systematically investigated.In particular,the formation statuses of all tracks during the simulated building process were recorded and analyzed statistically,which provided crucial information on the printing process for understanding the building mechanism or performing uncertainty analysis.

Dysfunction of PLA2G6 and CYP2C44-associated network signals imminent carcinogenesis from chronic inflammation to hepatocellular carcinoma

很少长期的发炎怎么贡献 hepatocellular 癌(HCC ) 的前进被知道，特别癌症的开始。揭开从长期的发炎的批评转变到在网络水平的 HCC 和分子的机制，我们用我们的动态网络 biomarker (DNB ) 分析了土拨鼠肝炎 virus/c-myc 鼠标和匹配年龄的 wt-C57BL/6 鼠标的时间系列 proteomic 数据模型。DNB 分析显示在转基因的老鼠的出生以后的第 5 月是癌症开始的批评时期，就在批评转变前，它与临床的症状一致。同时，联系 DNB 的网络在批评转变前后显示出蛋白质表示和 coexpression 层次的激烈的倒置。DNB， PLA2G6 和 CYP2C44 的二个成员，与他们的联系差别一起表示了蛋白质，被发现导致 arachidonic 酸新陈代谢的机能障碍，进一步通过短暂受体潜力隧道的煽动性的调停人规定激活煽动性的回答，并且最后导致肝 detoxification 和恶意的转变的缺陷到癌症。作为一个 c-Myc 目标， PLA2G6 断然在表示与 c-Myc 相关，显示出从减少到在 carcinogenesis 期间增加的一个趋势，与在批评转变的最小的点或付小费给的点。相应 PLA2G6 和 c-Myc 的如此的趋势也在人的 hepatocarcinogenesis 期间被观察，与在高级 dysplastic 小瘤(就在 carcinogenesis 前的一个阶段) 的最小的点。我们的学习暗示 PLA2G6 可能在 hepatocarcinogenesis 期间作为象著名 c-Myc 一样的 oncogene 工作，当 PLA2G6 和 c-Myc 的 downregulation 能是显示逼近的 carcinogenesis 的一个警告信号时。