Simulation of Piezoelectric Laminated Smart Structure under Strong Electric Field

Applying strong electric field on piezoelectric actuators, on one hand very significant electroelastic material nonlinear effects will occur, on the other hand piezo plates and shells may undergo large displacements and rotations. In order to give a precise prediction of piezolaminated smart structures under large electric field, this paper develops a finite element (FE) model accounting for both electroelastic material nonlinearity and geometric nonlinearity with large rotations based on the first order shear deformation (FSOD) hypothesis. The proposed FE model is applied to analyze a piezolaminated semicircular shell structure

New fault tolerance method for open-phase PMSM

Once the motor stator winding is opened, balanced three-phase windings turn into unbalanced two-phases windings. Unfortunately, by conducting Clarke and Park transformation for open-phase PMSM, complete decoupling of the torque and flux cannot achieve. To maintain the rated torque, the two remained phase currents have to be modified as sinusoidal currents with 60◦ phase difference (not 120◦). As a result, the current controller design becomes complicated. In order to solve this problem, a new fault tolerance method for the open-phase PMSM is proposed in this paper. It is designed based on a novel reference frame transformation. Through proposed frame transformation, the modified sinusoidal time-varying current commands are turned into dc variables in the redefined synchronous rotating frame. Hence, the design of the open-phase PMSM current controller can be simplified. This method can deal with different phase open fault and different current control mode (id = 0 or id 6= 0 mode). In addition, considering that the neutral current ripple at usual switching frequencies may be very high, an optimal additional inductance that inserted into the neutral wire is designed. With the designed additional inductance, complete decoupling can be achieved. Experimental results confirm that the reliability and the performance of the PMSM drive can be improved distinctly with the proposed open-phase fault tolerance strategy

Application of the Local Fractional Series Expansion Method and the Variational Iteration Method to the Helmholtz Equation Involving Local Fractional Derivative Operators

We investigate solutions of the Helmholtz equation involving local fractional derivative operators. We make use of the series expansion method and the variational iteration method, which are based upon the local fractional derivative operators. The nondifferentiable solution of the problem is obtained by using these methods

Localization of heme biosynthesis in the diatom Phaeodactylum tricornutum and differential expression of multi-copy enzymes

Heme is essential for all organisms. The composition and location of the pathway for heme biosynthesis, have been influenced by past endosymbiotic events and organelle evolution in eukaryotes. Endosymbioses led to temporary redundancy of the enzymes and the genes involved. Genes were transferred to the nucleus from different endosymbiotic partners, and their multiple copies were either lost or retained, resulting in a mosaic pathway. This mosaic is particularly complex in organisms with eukaryote-derived plastids, such as diatoms. The plastids of diatoms are clearly derived from red algae. However, it is not entirely clear whether they were acquired directly from a red algal ancestor or indirectly in higher-order endosymbioses. In the diatom Phaeodactylum tricornutum, most enzymes of the pathway are present in a single copy, but three, glutamyl-tRNA synthetase (GluRS), uroporphyrinogen decarboxylase (UROD) and coproporphyrinogen oxidase (CPOX), are encoded in multiple copies. These are not direct paralogs resulting from gene duplication within the lineage but were acquired horizontally during the plastid endosymbioses. While some iso-enzymes originate from the host cell, others originate either from the genome of the cyanobacterial ancestor of all plastids or from the nuclear genome of the eukaryotic ancestor of the diatom complex plastid, a rhodophyte or an alga containing rhodophyte-derived plastids, a situation known as pseudoparalogy. Using green fluorescent protein-tagged expression and immunogold labeling, we experimentally localized all enzymes of the pathway in P. tricornutum, and confirmed their localization in the plastid, with a few possible exceptions. Our meta-analyses of transcription data showed that the pseudoparalogs are differentially expressed in response to nitrate starvation, blue light, high light, high CO2, and the cell cycle. Taken together, our findings emphasize that the evolution of complex plastids via endosymbiosis has a direct impact not only on the genetics but also on the physiology of resulting organisms

Using diatom and apicomplexan models to study the heme pathway of Chromera velia

Heme biosynthesis is essential for almost all living organisms. Despite its conserved function, the pathway’s enzymes can be located in a remarkable diversity of cellular compartments in different organisms. This location does not always reflect their evolutionary origins, as might be expected from the history of their acquisition through endosymbiosis. Instead, the final subcellular localization of the enzyme reflects multiple factors, including evolutionary origin, demand for the product, availability of the substrate, and mechanism of pathway regulation. The biosynthesis of heme in the apicomonad Chromera velia follows a chimeric pathway combining heme elements from the ancient algal symbiont and the host. Computational analyses using different algorithms predict complex targeting patterns, placing enzymes in the mitochondrion, plastid, endoplasmic reticulum, or the cytoplasm. We employed heterologous reporter gene expression in the apicomplexan parasite Toxoplasma gondii and the diatom Phaeodactylum tricornutum to experimentally test these predictions. 5-aminolevulinate synthase was located in the mitochondria in both transfection systems. In T. gondii, the two 5-aminolevulinate dehydratases were located in the cytosol, uroporphyrinogen synthase in the mitochondrion, and the two ferrochelatases in the plastid. In P. tricornutum, all remaining enzymes, from ALA-dehydratase to ferrochelatase, were placed either in the endoplasmic reticulum or in the periplastidial space

β‐catenin deficiency in hepatocytes aggravates hepatocarcinogenesis driven by oncogenic β‐catenin and MET

Both activating and inactivating mutations in catenin β1 (ctnnb1), which encodes β-catenin, have been implicated in liver tumorigenesis in humans and mice, although the underlying mechanisms are not fully understood. Herein, we show that deletion of endogenous β-catenin in hepatocytes aggravated hepatocellular carcinoma (HCC) development driven by an oncogenic version of β-catenin (CAT) in combination with the hepatocyte growth factor receptor MET proto-oncogene receptor tyrosine kinase (MET). Although the mitogenic signaling and cell cycle progression was modestly impaired after CAT/MET transfection, the β-catenin-deficient livers displayed changes in transcriptomes, increased DNA damage response, expanded Sox9+ cells, and up-regulation of protumorigenic cytokines, including interleukin-6 and transforming growth factor β1. These events eventually exacerbated CAT/MET-driven hepatocarcinogenesis in β-catenin-deficient livers, featured by up-regulation of extracellular signal-regulated kinase (Erk), protein kinase B (Akt), and Wnt/β-catenin signaling and cyclin D1 expression. The resultant mouse tumors showed similar transcriptomes to human HCC samples with concomitant CTNNB1 mutations and MET overexpression.ConclusionThese data argue that while dominantly activating mutants of β-catenin are oncogenic, inhibiting the oncogenic signaling pathway generates a pro-oncogenic microenvironment that may facilitate HCC recurrence following a targeted therapy of the primary tumor. An effective therapeutic strategy must require disruption of the oncogenic signaling in tumor cells and suppression of the secondary tumor-promoting stromal effects in the liver microenvironment. (Hepatology 2018;67:1807-1822)

A laser-engraved wearable sensor for sensitive detection of uric acid and tyrosine in sweat

Wearable sweat sensors have the potential to provide continuous measurements of useful biomarkers. However, current sensors cannot accurately detect low analyte concentrations, lack multimodal sensing or are difficult to fabricate at large scale. We report an entirely laser-engraved sensor for simultaneous sweat sampling, chemical sensing and vital-sign monitoring. We demonstrate continuous detection of temperature, respiration rate and low concentrations of uric acid and tyrosine, analytes associated with diseases such as gout and metabolic disorders. We test the performance of the device in both physically trained and untrained subjects under exercise and after a protein-rich diet. We also evaluate its utility for gout monitoring in patients and healthy controls through a purine-rich meal challenge. Levels of uric acid in sweat were higher in patients with gout than in healthy individuals, and a similar trend was observed in serum

Liquid biopsy-based single-cell metabolic phenotyping of lung cancer patients for informative diagnostics.

Accurate prediction of chemo- or targeted therapy responses for patients with similar driver oncogenes through a simple and least-invasive assay represents an unmet need in the clinical diagnosis of non-small cell lung cancer. Using a single-cell on-chip metabolic cytometry and fluorescent metabolic probes, we show metabolic phenotyping on the rare disseminated tumor cells in pleural effusions across a panel of 32 lung adenocarcinoma patients. Our results reveal extensive metabolic heterogeneity of tumor cells that differentially engage in glycolysis and mitochondrial oxidation. The cell number ratio of the two metabolic phenotypes is found to be predictive for patient therapy response, physiological performance, and survival. Transcriptome analysis reveals that the glycolytic phenotype is associated with mesenchymal-like cell state with elevated expression of the resistant-leading receptor tyrosine kinase AXL and immune checkpoint ligands. Drug targeting AXL induces a significant cell killing in the glycolytic cells without affecting the cells with active mitochondrial oxidation