Finite element quantitative analysis and deep learning qualitative estimation in structural engineering

In the past two decades, finite element method (FEM) has been widely used to study mechanics of solids, fluid–structure interactions, and building construction strategies. FEM has been rapidly grown all over the world due to development of computer technology. Computer has much more powerful computing capability than humans. However, structural engineering education not only focused on teaching engineers to use FEM as computation tool, but also concentrated on cultivating engineers’ capability of experience-based qualitative analysis. In addition, artificial intelligence techniques have been rapidly developed in recent years. It is demonstrated that human experience-based capabilities might also be replaced by deep learning methods in various game-playing areas. Thus, this study aims at exploring what role artificial intelligence techniques will play in the futural structural analysis area. In this paper, several finite element analyses are carried out for three representative boundary value problems, such as tightly stretched wires under loading, soil seepage, and plane stress. Corresponding deep neural networks are trained using FEM simulation data to quickly and accurately predict results of relevant problems. It is indicated that to some extent artificial intelligence technique might replace human experience-based qualitative analysis as a surrogate of FEM

Escalation of Commiement in Software Projects: An Examination of Two Theories

Escalation of commitment is common in many software projects. It stands for the situation where managers decide to continue investing in or supporting a prior decision despite new evidence suggesting the original outcome expectation will be missed. Escalation of commitment is generally considered to be irrational. Past literature has proposed several theories to explain the behaviour. Two commonly used interpretations are self-justification and the framing effect. While both theories have been found effective in causing the escalation of commitment, their relative effect is less studied. The purpose of this study is to further investigate the primary factor that causes the escalation of commitment in software project related decisions. An experiment was designed to examine whether the escalation of commitment exists in different decision contingencies and which theories play a more important role in the escalation. One hundred and sixty two subjects participated in the experiment. The results indicate that both self-justification and problem framing have effects on commitment escalation in software projects but the effect of self-justification is stronger. Significant interaction effect is also found. A commitment is more likely to escalate if the problem is framed positively

On character table of Clifford groups

Based on a presentation of $\mathcal{C}_n$ and the help of [GAP], we construct the character table of the Clifford group $\mathcal{C}_n$ for $n=1,2,3$. As an application, we can efficiently decompose the (higher power of) tensor product of the matrix representation in those cases. Our results recover some known results in [HWW, WF] and reveal some new phenomena. We prove that the trivial character is the only linear character for $\mathcal{C}_n$ and hence $\mathcal{C}_n$ equals to its commutator subgroup when $n\geq 3$. A few conjectures about $\mathcal{C}_n$ for general $n$ are proposed.Comment: 13 pages; comments and suggestions are welcom

Motor neuron-derived Thsd7a is essential for zebrafish vascular development via the Notch-dll4 signaling pathway.

BackgroundDevelopment of neural and vascular systems displays astonishing similarities among vertebrates. This parallelism is under a precise control of complex guidance signals and neurovascular interactions. Previously, our group identified a highly conserved neural protein called thrombospondin type I domain containing 7A (THSD7A). Soluble THSD7A promoted and guided endothelial cell migration, tube formation and sprouting. In addition, we showed that thsd7a could be detected in the nervous system and was required for intersegmental vessels (ISV) patterning during zebrafish development. However, the exact origin of THSD7A and its effect on neurovascular interaction remains unclear.ResultsIn this study, we discovered that zebrafish thsd7a was expressed in the primary motor neurons. Knockdown of Thsd7a disrupted normal primary motor neuron formation and ISV sprouting in the Tg(kdr:EGFP/mnx1:TagRFP) double transgenic zebrafish. Interestingly, we found that Thsd7a morphants displayed distinct phenotypes that are very similar to the loss of Notch-delta like 4 (dll4) signaling. Transcript profiling further revealed that expression levels of notch1b and its downstream targets, vegfr2/3 and nrarpb, were down-regulated in the Thsd7a morphants. These data supported that zebrafish Thsd7a could regulate angiogenic sprouting via Notch-dll4 signaling during development.ConclusionsOur results suggested that motor neuron-derived Thsd7a plays a significant role in neurovascular interactions. Thsd7a could regulate ISV angiogenesis via Notch-dll4 signaling. Thus, Thsd7a is a potent angioneurin involved in the development of both neural and vascular systems

Antidepressant-Like Activity of the Ethanolic Extract from Uncaria lanosa Wallich var. appendiculata Ridsd in the Forced Swimming Test and in the Tail Suspension Test in Mice

This study investigated the antidepressant activity of ethanolic extract of U. lanosa Wallich var. appendiculata Ridsd (ULEtOH) for two-weeks administrations by using FST and TST on mice. In order to understand the probable mechanism of antidepressant-like activity of ULEtOH in FST and TST, the researchers measured the levels of monoamines and monoamine oxidase activities in mice brain, and combined the antidepressant drugs (fluoxetine, imipramine, maprotiline, clorgyline, bupropion and ketanserin). Lastly, the researchers analyzed the content of RHY in the ULEtOH. The results showed that ULEtOH exhibited antidepressant-like activity in FST and TST in mice. ULEtOH increased the levels of 5-HT and 5-HIAA in cortex, striatum, hippocampus, and hypothalamus, the levels of NE and MHPG in cortex and hippocampus, the level of NE in striatum, and the level of DOPAC in striatum. Two-week injection of IMI, CLO, FLU and KET enhanced the antidepressant-like activity of ULEtOH. ULEtOH inhibited the activity of MAO-A. The amount of RHY in ULEtOH was 17.12 mg/g extract. Our findings support the view that ULEtOH exerts antidepressant-like activity. The antidepressant-like mechanism of ULEtOH may be related to the increase in monoamines levels in the hippocampus, cortex, striatum, and hypothalamus of mice

Regulation of CLC-1 chloride channel biosynthesis by FKBP8 and Hsp90β.

Mutations in human CLC-1 chloride channel are associated with the skeletal muscle disorder myotonia congenita. The disease-causing mutant A531V manifests enhanced proteasomal degradation of CLC-1. We recently found that CLC-1 degradation is mediated by cullin 4 ubiquitin ligase complex. It is currently unclear how quality control and protein degradation systems coordinate with each other to process the biosynthesis of CLC-1. Herein we aim to ascertain the molecular nature of the protein quality control system for CLC-1. We identified three CLC-1-interacting proteins that are well-known heat shock protein 90 (Hsp90)-associated co-chaperones: FK506-binding protein 8 (FKBP8), activator of Hsp90 ATPase homolog 1 (Aha1), and Hsp70/Hsp90 organizing protein (HOP). These co-chaperones promote both the protein level and the functional expression of CLC-1 wild-type and A531V mutant. CLC-1 biosynthesis is also facilitated by the molecular chaperones Hsc70 and Hsp90β. The protein stability of CLC-1 is notably increased by FKBP8 and the Hsp90β inhibitor 17-allylamino-17-demethoxygeldanamycin (17-AAG) that substantially suppresses cullin 4 expression. We further confirmed that cullin 4 may interact with Hsp90β and FKBP8. Our data are consistent with the idea that FKBP8 and Hsp90β play an essential role in the late phase of CLC-1 quality control by dynamically coordinating protein folding and degradation