Incentive effect of structural tax reduction policy on consumption upgrading and high-tech industry

China is implementing a structural tax reduction policy to upgrade the structure of household consumption and promote the development of high-tech industry. This article constructs a heterogeneous NK-DSGE (New Keynesian - Dynamic Stochastic General Equilibrium) model to study the effects of tax reduction policies on consumption upgrading and the development of high-tech industry. The tax categories involved in this model are divided into demand-side tax and supply-side tax. We build two indexes to measure the consumption structure and the development of high-tech industry. It is found that reducing high-tech enterprise income tax would upgrade the consumption structure and promote the development of high-tech industries in the short term. Reducing low-tech enterprise income tax would achieve similar effects in the medium and long term. Moreover, tax such as consumption tax, labour income tax and capital income tax reduction policies can upgrade the consumption structure and promote the development of high-tech industry in the long term. Finally, this article finds that when the elasticity of labour substitution is smaller, reducing high-tech enterprise income tax is more effective

A compendium of genetic regulatory effects across pig tissues

The Farm Animal Genotype-Tissue Expression (FarmGTEx) project has been established to develop a public resource of genetic regulatory variants in livestock, which is essential for linking genetic polymorphisms to variation in phenotypes, helping fundamental biological discovery and exploitation in animal breeding and human biomedicine. Here we show results from the pilot phase of PigGTEx by processing 5,457 RNA-sequencing and 1,602 whole-genome sequencing samples passing quality control from pigs. We build a pig genotype imputation panel and associate millions of genetic variants with five types of transcriptomic phenotypes in 34 tissues. We evaluate tissue specificity of regulatory effects and elucidate molecular mechanisms of their action using multi-omics data. Leveraging this resource, we decipher regulatory mechanisms underlying 207 pig complex phenotypes and demonstrate the similarity of pigs to humans in gene expression and the genetic regulation behind complex phenotypes, supporting the importance of pigs as a human biomedical model.</p

Quantitative characterization of helium in the ITER-like co-deposition layer by laser-induced breakdown spectroscopy

As a product of the D-T burning plasma in tokamak fusion reactors, helium (He) ash would be retained in plasma-facing components like the first wall and divertor, harming the stable operation of burning plasma. The quantitative monitoring of He retention is critical for He removal in these regions. Laser-induced breakdown spectroscopy (LIBS) is a promising technique for this task due to its remote, in-situ, online, and all-element monitoring capabilities. In this work, the LIBS method was employed to quantitatively determine He retention in ITER-like wall material under a vacuum. The characteristic line of He I at 587.56 nm was clearly observed in the collected emission spectrum of the laser-induced plasma, and it was used for the subsequent quantitative analysis. The parameters of LIBS, i.e., the laser fluence and the gate delay of the spectrometer, were optimized to obtain He lines with high signal-to-noise ratios. The absolute concentration of He retained in the ITER-like co-deposition layer was measured by thermal desorption mass spectrometry (TDS) for calibration. The calibration curve exhibited a highly linear relationship between the LIBS intensity of the He I at 587.56 nm line and the He concentration in the co-deposition layer with a fitting coefficient R2 of 0.995. The limit of detection for He areal density using the current LIBS approach with the optimized parameters is achieved to be 1.8 × 1020 He/m2

BRMS1 suppresses glioma progression by regulating invasion, migration and adhesion of glioma cells.

Breast cancer metastasis suppressor 1 (BRMS1) is a metastasis suppressor gene in several solid tumors. However, the expression and function of BRMS1 in glioma have not been reported. In this study, we investigated whether BRMS1 play a role in glioma pathogenesis. Using the tissue microarray technology, we found that BRMS1 expression is significantly decreased in glioma compared with tumor adjacent normal brain tissue (P<0.01, χ(2) test) and reduced BRMS1 staining is associated with WHO stages (P<0.05, χ(2) test). We also found that BRMS1 was significantly downregulated in glioma cell lines compared to normal human astrocytes (P<0.01, χ(2) test). Furthermore, we demonstrated that BRMS1 overexpression inhibited glioma cell invasion by suppressing uPA, NF-κB, MMP-2 expression and MMP-2 enzyme activity. Moreover, our data showed that overexpression of BRMS1 inhibited glioma cell migration and adhesion capacity compared with the control group through the Src-FAK pathway. Taken together, this study suggested that BRMS1 has a role in glioma development and progression by regulating invasion, migration and adhesion activities of cancer cells

BRMS1staining and clinicopathological characteristics of 192 glioma patients.

<p>*χ² test.</p

Overexpression of BRMS1 inhibits glioma cells adhesion ability.

<p><b>A, B</b> Cell attachment assay after BRMS1 overexpression in U251 and U87 cells. The graph shows the percentage of attached cells compared with the control group. <b>C</b> Western blot analysis of the relative protein levels of Src and FAK in BRMS1 overexpression and control group for both U251 and U87 cell lines. <b>D</b> Quantitative analysis of relative protein level of Src and FAK in glioma U251 and U87 cells. All experiments were carried out in triplicate. Data are shown as mean ± SD. *<i>P</i><0.05, **<i>P</i><0.01.</p

Representative images show BRMS1 immunohistochemical staining.

<p><b>A</b> Positive BRMS1 staining in normal brain tissue (NB); <b>B</b> Positive BRMS1 staining in adjacent normal brain tissue (AB); <b>C</b> Negative BRMS1 staining in benign tumor (BT); <b>D</b> Negative BRMS1 staining in malignant tumor (MT); <b>E</b> A significant difference in BRMS1 staining was observed between normal brain tissue and glioma tissue (GT) (<i>P</i><0.01, χ² test) and between tumor adjacent normal brain tissue and glioma tumor (<i>P</i><0.01, χ² test). <b>F</b> Whole-cell protein extracts were further prepared from four paired tumor adjacent normal glioma tissues and glioma tissues. The BRMS1 protein level was determined by Western blot analysis. <b>G</b> Western blot analysis of BRMS1 expression in normal human astrocytes NHA and glioma cell lines, including SHG44, C6, U251, T98G, U87. <b>H</b> BRMS1 staining was dramatically decreased in malignant tumor compared with benign tumor (<i>P</i><0.05). All experiments were carried out in triplicate. Data are shown as mean ± SD. *<i>P</i><0.05, **<i>P</i><0.01, ***<i>P</i><0.001. Original magnification (<b>A–D</b>) ×40.</p

Overexpression of BRMS1 inhibits glioma cell migration.

<p><b>A, B</b> Wound-healing assay was done on monolayers of U251and U87 glioma cells after 24 hour of transfection. The photographs were taken at 0 and 24 hours after wounds were made. <b>C, D</b> Cell migration assay was performed after overexpression of BRMS1 in glioma U251 and U87 cells. The graph shows the percentage of cells migrated in 5 fields of view compared with the control group. All experiments were carried out in triplicate. Data are shown as mean ± SD. **<i>P</i><0.01; ***<i>P</i><0.001.</p

Overexpression of BRMS1 suppresses cell invasion but not cell proliferation in glioma cells.

<p><b>A</b> Twenty-four hours after transfection, the expression of BRMS1 in U251 and U87 glioma cells was evaluated by western blot. <b>B, C</b> CCK-8 cell proliferation assay was performed after BRMS1 overexpression in U251 and U87cells. <b>D, E</b> Matrigel cell invasion assay was performed after the overexpression of BRMS1 in U251 and U87 cells. The graph shows the percentage of cells invaded in 5 fields of view compared with the control group. <b>F</b> BRMS1 inhibits MMP-2 activity in U251 and U87 cells by zymography. <b>G</b> Western blot analysis of the relative protein levels of MMP-2, uPA and NF-κB in BRMS1 overexpression and control group of U251 and U87 cells. <b>H</b> Quantitative analysis of relative protein level of MMP-2, uPA, p27 and NF-κB in glioma U251 and U87 cells. All experiments were carried out in triplicate. Data are shown as mean ± SD. *<i>P</i><0.05, **<i>P</i><0.01.</p

MicroRNA-21 Regulates PI3K/Akt/mTOR Signaling by Targeting TGFβI during Skeletal Muscle Development in Pigs

<div><p>MicroRNAs (miRNAs), which are short (22–24 base pairs), non-coding RNAs, play critical roles in myogenesis. Using Solexa deep sequencing, we detected the expression levels of 229 and 209 miRNAs in swine skeletal muscle at 90 days post-coitus (E90) and 100 days postnatal (D100), respectively. A total of 138 miRNAs were up-regulated on E90, and 31 were up-regulated on D100. Of these, 9 miRNAs were selected for the validation of the small RNA libraries by quantitative RT-PCR (RT-qPCR). We found that miRNA-21 was down-regulated by 17-fold on D100 (P<0.001). Bioinformatics analysis suggested that the transforming growth factor beta-induced (TGFβI) gene was a potential target of miRNA-21. Both dual luciferase reporter assays and western blotting demonstrated that the TGFβI gene was regulated by miRNA-21. Co-expression analysis revealed that the mRNA expression levels of miRNA-21 and TGFβI were negatively correlated (r = -0.421, P = 0.026) in skeletal muscle during the 28 developmental stages. Our results revealed that more miRNAs are expressed in prenatal than in postnatal skeletal muscle. The miRNA-21 is a novel myogenic miRNA that is involved in skeletal muscle development and regulates PI3K/Akt/mTOR signaling by targeting the TGFβI gene.</p></div