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Long non-coding metastasis-associated lung adenocarcinoma transcript (lnc-Malat1) emerges as a novel regulator in skeletal muscle development, while its function and the related mechanism is not fully revealed yet. In this study, knockdown of lnc-Malat1 by siRNA significantly inhibited the expression of myoblast marker genes (MyHC , MyoD , and MyoG) and slow muscle fiber marker genes (MyHC I), together with repressed expression of mitochondria-related genes COX5A , ACADM , CPTA1 , FABP3 , and NDUFA1. Overexpression of lnc-Malat1 exerted an opposite effect, promoting myoblast differentiation and slow muscle fiber formation. Dual luciferase reporter assay revealed a direct interaction between lnc-Malat1 and miR-129-5p, and overexpression of lnc-Malat1 significantly inhibited miR-129-5p expression, thereby elevating the expression of Mef2a , miR-129-5p target protein. In addition, enforced expression of lnc-Malat1 restored the inhibitory effect of miR-129-5p on myoblast differentiation and MyHC I expression. Taken together, our results suggest that lnc-Malat1 promotes myoblast differentiation, and maintains the slow muscle fiber phenotype via adsorbing miR-129-5p. [Display omitted] [ABSTRACT FROM AUTHOR]

Abstract: A new bridge-building technique was used for facilitating H spillover on metal doped adsorbents for hydrogen storage at room temperature. By preadsorbing of CH4 on Pt/AX-21 (superactivated carbon), the adsorbed amount of hydrogen increased by ∼100% at 1 atm and 25 °C, attributed to the adsorbed CH4 serving as bridges for spillover. We conclude that the Benson–Boudart method can provide a good assessment for the dispersion of metals supported on Al2O3 (and zeolites). For carbon and SiO2 supports, even with pure H2, spillover leads to overestimates of dispersion, and any small amounts of gaseous impurities could lead to much greater overestimates. [Copyright &y& Elsevier]

Ventricular septal defect (VSD) is the most common congenital heart malformation in children. This study aimed to investigate potential pathogenic genes associated with Tibetan familial VSD. Whole genomic DNA was extracted from eight Tibetan children with VSD and their healthy parents (a total of 16 individuals). Whole-exome sequencing was performed using the Illumina HiSeq platform. After filtration, detection, and annotation, single nucleotide variations and insertion-deletion markers were examined. Comparative evaluations using the Sorting Intolerant from Tolerant, PolyPhen V2, Mutation Taster, and Combined Annotation Dependent Depletion databases were conducted to predict harmful mutant genes associated with the etiology of Tibetan familial VSD. A total of six missense mutations in genetic disease-causing genes associated with the development of Tibetan familial VSD were identified: activin A receptor type II-like 1 (c.652 C > T: p.R218 W), ATPase cation transporting 13A2 (c.1363 C > T: p.R455 W), endoplasmic reticulum aminopeptidase 1 (c.481 G > A: p.G161 R), MRI1 (c.629 G > A: p.R210Q), tumor necrosis factor receptor-associated protein 1 (c.224 G > A: p.R75H), and FBN2 (c.2260 G > A: p.G754S). The Human Gene Mutation Database confirmed activin A receptor type II-like 1, MRI1 , and tumor necrosis factor receptor-associated protein 1 as pathogenic mutations, while FBN2 was classified as a probable pathogenic mutation. This novel study directly screens genetic variations associated with Tibetan familial VSD using whole-exome sequencing, providing new insights into the pathogenesis of VSD. [ABSTRACT FROM AUTHOR]

• The fiber can realize strict dual-mode operation (HE 11 mode and HE 21 mode) and reduce mode coupling. • Effective area of fundamental mode is up to 1423.972 μm2 by optimizing structural parameters, which can reduce nonlinear effect in the fiber and increase transmission capacity. • Bending loss of the fiber is less than 10-4dB/m at R > 0.26 m, which can be used for FTTH. • The fiber has potential in large number of high power optical fiber devices. In this paper, a multi-core fiber with 22 air holes and 15 conventional cores is proposed. The fiber can realize dual-mode operation of fundamental mode HE 11 and second-order mode HE 21 under certain conditions. The relationship between performance of the fiber and the structural parameters that include core pitch, refractive index difference between core and cladding, and fiber core radius is investigated systematically. By adjusting the above parameters, the effective area of fundamental mode can be up to 1423.972 µm2 and keep a low bending loss at 1550 nm. Due to its flexibility of the structure, the proposed fiber is significant for theoretical research and practical manufacturing. [ABSTRACT FROM AUTHOR]

Inherently coupled flow and geomechanics processes in fractured shale media have implications for shale gas production. The system involves highly complex geo-textures comprised of a heterogeneous anisotropic fracture network spatially embedded in an ultra-tight matrix. In addition, nonlinearities due to viscous flow, diffusion, and desorption in the matrix and high velocity gas flow in the fractures complicates the transport. In this paper, we develop a multiscale model reduction approach to couple gas flow and geomechanics in fractured shale media. A Discrete Fracture Model (DFM) is used to treat the complex network of fractures on a fine grid. The coupled flow and geomechanics equations are solved using a fixed stress-splitting scheme by solving the pressure equation using a continuous Galerkin method and the displacement equation using an interior penalty discontinuous Galerkin method. We develop a coarse grid approximation and coupling using the Generalized Multiscale Finite Element Method (GMsFEM). GMsFEM constructs the multiscale basis functions in a systematic way to capture the fracture networks and their interactions with the shale matrix. Numerical results and an error analysis is provided showing that the proposed approach accurately captures the coupled process using a few multiscale basis functions, i.e. a small fraction of the degrees of freedom of the fine-scale problem. [ABSTRACT FROM AUTHOR]