Discrete modelling of continuous dynamic recrystallisation by modified Metropolis algorithm

Continuous dynamic recrystallisation (CDRX) is often the primary mechanism for microstructure evolution during severe plastic deformation (SPD) of polycrystalline metals. Its physically realistic simulation remains challenging for the existing modelling approaches based on continuum mathematics because they do not capture important local interactions between microstructure elements and spatial inhomogeneities in plastic strain. An effective discrete method for simulating CDRX is developed in this work. It employs algebraic topology, graph theory and statistical physics tools to represent an evolution of grain boundary networks as a sequence of conversions between low-angle grain boundaries (LAGBs) and high-angle grain boundaries (HAGBs) governed by the principle of minimal energy increase, similar to the well-known Ising model. The energy is minimised by a modified Metropolis algorithm. The model is used to predict the equilibrium fractions of HAGBs in several SPD-processed copper alloys. The analysis captures non-equilibrium features of the transitions from sub-grain structures to new HAGB-dominated grain structures and provides estimations of critical values for HAGB fractions and accumulated strain at these transitions

Triple junction disclinations in severely deformed Cu-0.4%Mg alloys

Stress fields arising from triple junction disclinations (TJDs) play a significant role in the microstructure evolution during the plastic deformation of metals. The calculation of TJD strengths from grain orientation data was developed by Bollmann more than 50 years ago, but so far applied only to collections of a few grains. Developed here is a new methodology for calculating TJD strengths and the associated stress fields in large polycrystalline assemblies using experimental electron back-scattered diffraction (EBSD) maps. The methodology combines Bollmann's approach with a representation of materials as cell complexes. It is computationally efficient and allows for obtaining the spatial distribution of TJD strengths from EBSD images containing thousands of grains. Analysed are the fraction, distribution, and strengths of TJDs within statistically representative microstructures of Cu-0.4%Mg alloy subjected to severe plastic deformation (SPD) by equal channel angular pressing. It is shown that the formation of low-angle grain boundaries (dislocation walls) during SPD leads to an increasing number of TJDs, whose spatial distribution is progressively more uniform and whose strength distribution remains nearly constant. This result suggests that the SPD reduces the internal stresses associated with disclinations in large regions of the material, as closely situated disclinations screen each other's fields. Regions with high local stresses can be expected between sparsely distributed TJDs with the highest strengths. The average distance between such TJDs could be considered as a natural length scale in a material

Research progress on intelligent optimization techniques for energy-efficient design of ship hull forms

The design optimization of ship hull form based on hydrodynamics theory and simulation-based design (SBD) technologies generally considers ship performance and energy efficiency performance as the design objective, which plays an important role in smart design and manufacturing of green ship. An optimal design of sustainable energy system requires multidisciplinary tools to build ships with the least resistance and energy consumption. Through a systematic approach, this paper presents the research progress of energy-efficient design of ship hull forms based on intelligent optimization techniques. We discuss different methods involved in the optimization procedure, especially the latest developments of intelligent optimization algorithms and surrogate models. Moreover, current development trends and technical challenges of multidisciplinary design optimization and surrogate-assisted evolutionary algorithms for ship design are further analyzed. We explore the gaps and potential future directions, so as to paving the way towards the design of the next generation of more energy-efficient ship hull form.Comment: 30 pages, 8 figure

MiR-103-3p promotes hepatic steatosis to aggravate nonalcoholic fatty liver disease by targeting of ACOX1

BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is a major risk factor for hepatocellular carcinoma, and alterations in miRNA expression are related to the development of NAFLD. However, the role of miRNAs in regulating the development of NAFLD is still poorly understood. METHODS: We used qRT-PCR to detect the level of miR-103-3p in both cell and mouse models of NAFLD. Biochemical assays, DCF-DA assays, Oil red O staining and HE staining were used to detect the role of miR-103-3p in NAFLD development. Target genes of miR-103-3p were predicted using the TargetScan database and verified by qRT-PCR, western blot and dual-luciferase assays. RESULTS: The expression of miR-103-3p increased in both NAFLD model cells and liver tissues from the NAFLD mouse model. Inhibition of miR-103-3p significantly alleviated the accumulation of lipid droplets in free fatty acid-treated L02 cells and liver tissues from mice with NAFLD. Inhibition of miR-103-3p reduced the contents of H CONCLUSIONS: These findings identified a negative regulatory mechanism between ACOX1 and miR-103-3p that promotes the pathogenesis of NAFLD and suggested that inhibition of miR-103-3p may be a potential treatment strategy for NAFLD

Robust Optical Data Encryption by Projection-Photoaligned Polymer-Stabilized-Liquid-Crystals

The emerging Internet of Things (IoTs) invokes increasing security demands that require robust encryption or anti-counterfeiting technologies. Albeit being acknowledged as efficacious solutions in processing elaborate graphical information via multiple degrees of freedom, optical data encryption and anti-counterfeiting techniques are typically inept in delivering satisfactory performance without compromising the desired ease-of-processibility or compatibility, thus leading to the exploration of novel materials and devices that are competent. Here, a robust optical data encryption technique is demonstrated utilizing polymer-stabilized-liquid-crystals (PSLCs) combined with projection photoalignment and photopatterning methods. The PSLCs possess implicit optical patterns encoded via photoalignment, as well as explicit geometries produced via photopatterning. Furthermore, the PSLCs demonstrate improved robustness against harsh chemical environments and thermal stability, and can be directly deployed onto various rigid and flexible substrates. Based on this, it is demonstrated that single PSLC is apt to carry intricate information, or serve as exclusive watermark with both implicit features and explicit geometries. Moreover, a novel, generalized design strategy is developed, for the first time, to encode intricate and exclusive information with enhanced security by spatially programming the photoalignment patterns of a pair of cascade PSLCs, which further illustrates the promising capabilies of PSLCs in optical data encryption and anti-counterfeiting

PALMD regulates aortic valve calcification via altered glycolysis and NF-κB-mediated inflammation

Recent genome-wide association and transcriptome-wide association studies have identified an association between the PALMD locus, encoding palmdelphin, a protein involved in myoblast differentiation, and calcific aortic valve disease (CAVD). Nevertheless, the function and underlying mechanisms of PALMD in CAVD remain unclear. We herein investigated whether and how PALMD affects the pathogenesis of CAVD using clinical samples from CAVD patients and a human valve interstitial cell (hVIC) in vitro calcification model. We showed that PALMD was upregulated in calcified regions of human aortic valves and calcified hVICs. Furthermore, silencing of PALMD reduced hVIC in vitro calcification, osteogenic differentiation, and apoptosis, whereas overexpression of PALMD had the opposite effect. RNA-Seq of PALMD-depleted hVICs revealed that silencing of PALMD reduced glycolysis and nuclear factor-κB (NF-κB)–mediated inflammation in hVICs and attenuated tumor necrosis factor α–induced monocyte adhesion to hVICs. Having established the role of PALMD in hVIC glycolysis, we examined whether glycolysis itself could regulate hVIC osteogenic differentiation and inflammation. Intriguingly, the inhibition of PFKFB3-mediated glycolysis significantly attenuated osteogenic differentiation and inflammation of hVICs. However, silencing of PFKFB3 inhibited PALMD-induced hVIC inflammation, but not osteogenic differentiation. Finally, we showed that the overexpression of PALMD enhanced hVIC osteogenic differentiation and inflammation, as opposed to glycolysis, through the activation of NF-κB. The present study demonstrates that the genome-wide association– and transcriptome-wide association–identified CAVD risk gene PALMD may promote CAVD development through regulation of glycolysis and NF-κB–mediated inflammation. We propose that targeting PALMD-mediated glycolysis may represent a novel therapeutic strategy for treating CAVD

Neratinib protects pancreatic beta cells in diabetes

The loss of functional insulin-producing β-cells is a hallmark of diabetes. Mammalian sterile 20-like kinase 1 (MST1) is a key regulator of pancreatic β-cell death and dysfunction; its deficiency restores functional β-cells and normoglycemia. The identification of MST1 inhibitors represents a promising approach for a β-cell-protective diabetes therapy. Here, we identify neratinib, an FDA-approved drug targeting HER2/EGFR dual kinases, as a potent MST1 inhibitor, which improves β-cell survival under multiple diabetogenic conditions in human islets and INS-1E cells. In a pre-clinical study, neratinib attenuates hyperglycemia and improves β-cell function, survival and β-cell mass in type 1 (streptozotocin) and type 2 (obese Leprdb/db) diabetic mouse models. In summary, neratinib is a previously unrecognized inhibitor of MST1 and represents a potential β-cell-protective drug with proof-of-concept in vitro in human islets and in vivo in rodent models of both type 1 and type 2 diabetes