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To synthesize lead-free primary explosives with good thermal stability, pyridine-2-carbohydrazide (2-PDCA) was used to prepare a novel energetic copper perchlorate complex (ECCs-1), which was structurally characterized by infrared spectroscopy, NMR, and elemental analysis. Its thermal decomposition properties were investigated by thermogravimetry and a synchrotron thermal analyzer, and the sensitivity was tested by the BAM method. The laser ignition experiment and the lead plate tests show that the ECCs-1 complex has a good detonation performance with a high thermal decomposition temperature (215.6 °C) and moderate sensitivity (impact sensitivity = 3 J and friction sensitivity = 5 N). [ABSTRACT FROM AUTHOR]

The curve-shaped Chaman transform fault between Pakistan and Afghanistan demarks the western boundary of the Indian plate, which is the locus of many catastrophic earthquakes, and this is poorly studied region to understand the earthquake/fault interaction and hazard assessment. Based on earthquake triggering theory, we investigate a sequence of earthquakes comprising five earthquakes that occurred in the Chaman Fault System since 1892. Our results elucidate that three out of four earthquakes are triggered by the preceding earthquakes. The 1935 earthquake of magnitude Mw 7.7 is somewhat an independent earthquake in this sequence, slightly influenced by the 1892 event. The 1935 earthquake significantly loaded either terminus of its rupture with positive stress, which later triggered the 1975 earthquake with 35% of its rupture length where ΔCFS is above triggering threshold value, and 1990 earthquake with 44% of its rupture length in positive stress lobe, on Ghazaband Fault, in the south lobe. Since the 1935 earthquake significantly increased the ΔCFS on either terminus of its rupture, the 2013 earthquake with magnitude Mw 7.7 occurred on Hoshab Fault in the positive stress zone with 23% of its rupture length where ΔCFS is positive. Moreover, the northern locked segment of CF, the southern segment of GBF, southeastern segment of HF and PAF demonstrate a high value of ΔCFS. It could trigger seismicity in these regions, thus requiring arrangements to mitigate any seismic hazards in future. [ABSTRACT FROM AUTHOR]

A highly active CuZn-SiO2 catalyst with excellent stability in hydrogenation of methyl acetate (MA) was fabricated by the hydrolysis precipitation (HP) method. The HP method caused notable high dispersion of both copper and zinc species due to the strong interaction between metal species and silica support caused by the pseudo-homogeneous reaction during the mixing process. According to the linear correlation between the TOF (Cu+) and Zn/Cu ratio, the Cu+ was considered the predominant active site, and the Cu+ site derived from the strong interaction between copper and zinc species has higher activity than those Cu+ species generated from copper phyllosilicate. Compared to the CuZnO/Al2O3 and Cu-SiO2 catalysts, the Cu9Zn1-SiO2 catalyst displayed the highest catalytic activity on account of the high dispersion of active species and the enhanced ability of Cu+ species on ester adsorption by stronger Cu-ZnO interaction. [ABSTRACT FROM AUTHOR]

Host-guest encapsulation of electron-rich naphthalene molecules into a weakly emissive porous metal-organic framework based on π-electron-deficient (π-acidic) naphthalene diimide tectons leads to orange-emissive crystals, which can be used to sense strongly basic organic amines in a fast response, high photostability, and tunable sensitivity. Moreover, such host-guest inclusion crystals are also a good photochromic probe for the detection of weakly basic N-methyl-2-pyrrolidone and N,N-dimethylformamide molecules. [ABSTRACT FROM AUTHOR]

The East Kunlun Fault zone, striking E-W to WNW-ESE, has been recognized as one of the largest and most active left-lateral strike-slip faults in the China continent. Presently, the Maqin-Maqu segment (MMS) is recognized as a seismic gap on the East Kunlun Fault. Since several highly populated counties are close to this region, understanding stress transfer and accumulation along this segment is important for hazard assessment along the MMS. In this study, we calculated the stress evolution along the MMS of the East Kunlun Fault zone during 1879-2008 by integrating coseismic effects, viscoelastic relaxation and tectonic loading. It is observed that the stress accumulation on the western part of the Maqin segment has been effected by the 1937 Tuosuo Lake earthquake, the stress on the eastern part of the Maqin segment. Also, the western part of theMaqu segment was relaxed by the 1947 Dari earthquake, and the stress loading on the eastern part of Maqu segment was increased by both the 1879 Wudu and 2008 Wenchuan earthquakes. It is observed that, compared to coseismic static stress changes, the post-seismic viscoelastic relaxation process has played a more important role on stress accumulation in theMaqu segment. The increased stress on theMaqin andMaqu segment is consistent with tectonic loading over 160 and 250 yr, respectively, which we expect will lead to future earthquakes and associated seismic hazard on these segments. [ABSTRACT FROM AUTHOR]

Voltage-gated sodium channels (VGSCs) are expressed not only in excitable cells but also in numerous metastatic cells, particularly in certain types of cancer cells. In some types of cancer, including prostate cancer, the expression of VGSCs is associated with cancer migration, invasion and metastasis in vivo. However, the detailed expression profiles of VGSC α subunits in normal human prostate, in prostatic hyperplasia and prostatic cancer remain controversial. In the present study, quantitative polymerase chain reaction was used to systematically detect all subtypes of VGSC α subunits in normal human prostate, benign prostatic hyperplasia (BPH) and prostate cancer cells. The expression profile of VGSC α subunits was observed to differ between these cell types. Nav1.5 was the major isoform expressed in normal human prostate tissue, while Nav1.5 and Nav1.2 were the predominant isoforms in BPH tissue. However, in PC-3 and LNCaP cells, two typical prostate cancer cell lines, Nav1.6 and Nav1.7 were abundantly expressed. By comparing the relative expression levels of Nav1.5, Nav1.6 and Nav1.7 in these cells, the mRNA levels of Nav1.6 and Nav1.7 were identified to be 6- to 27-fold higher in PC-3 and LNCaP cells than in either normal or BPH samples (P<0.05); however, Nav1.5 mRNA levels were relatively lower compared with those of Nav1.6 or Nav1.7 in all cells analyzed. To confirm whether Nav1.6 and Nav1.7 expression in cancer cells was functional, a patch-clamp technique was used to record whole-cell currents. A tetrodotoxin-sensitive sodium current was successfully recorded in PC-3 cells, but not in LNCaP cells. It was concluded that although all types of VGSC α subunits exhibited low expression levels in normal prostate and BPH cells, both Nav1.6 and Nav1.7 were significantly upregulated in the prostate cancer cell lines, suggesting these subtypes may be potential diagnostic markers and therapeutic targets for certain types of prostate cancer in humans. [ABSTRACT FROM AUTHOR]

Intramural hematoma (IMH) is a newly defined disease entity and the optimal management is still controversial as the disease shows varied clinical course. We present a case of type B IMH, initially presenting with paraplegia progressing to segmental aortic dissection (SAD) which the formed dissection displayed as a segmental distribution pattern. To our knowledge, it may become a new progression pattern of IMH progression. The SAD was successfully treated with both thoracic and abdominal endovascular aortic repair (TEVAR plus EVAR). In 1-year follow-up, the patient recovered almost completely with moderately neurological deficit and the blood pressure is in control. [ABSTRACT FROM AUTHOR]

Ethanol modified supercritical carbon dioxide (SC-CO2) extraction of flavonoids from Momordica charantia L. fruits and its antioxidant activity were performed. The influences of parameters such as temperature, extraction time and pressure on the yield of flavonoids were investigated. The antioxidant activities of flavonoids were assessed by means of 2,2-diphenyl-l-picrylhydrazyl (DPPH) radical-scavenging assay and β-carotene bleaching test. The experimental data obtained indicated that pressure, temperature and time had significant effect on the extraction yield. The optimum extraction conditions, determined by the 3D response surface and contour plots derived from the mathematical models, were as follows: extraction temperature 46 °C, pressure 33.4MPa, and extraction time 53.2 min. Under these conditions, the experimental value was 15.47 mg/g, which was well matched with value predicted by the model. The antioxidant activity of flavonoids obtained by ethanol modified SC-CO2 extraction method had higher antioxidant activity than the flavonoids extracted by conventional solvent extraction (CSE) method. The DPPH radical-scavenging ability of flavonoids obtained by ethanol modified SC-CO2 extraction method reached to 96.14 ± 1.02%, equivalent to the clearance rate of ascorbic acid at 1.2 mg/mL. Results indicated that ethanol modified SC-CO2 extraction was a suitable approach for the selective extraction of flavonoids from M. charantia L. [ABSTRACT FROM AUTHOR]

Heterogeneous surface expression of Thy-1 in fibroblasts modulates inflammation and may thereby modulate injury and repair. As a paradigm, patients with idiopathic pulmonary fibrosis, a disease with pathologic features of chronic inflammation, demonstrate an absence of Thy-1 immunoreactivity within areas of fibrotic activity (fibroblast foci) in contrast to the predominant Thy-1 expressing fibroblasts in the normal lung. Likewise, Thy-1 deficient mice display more severe lung fibrosis in response to an inflammatory injury than wildtype littermates. We investigated the role of Thy-1 in the response of fibroblasts to the pro-inflammatory cytokine TNF-α. Our study demonstrates distinct profiles of TNF-α-activated gene expression in Thy-1 positive (Thy-1+) and negative (Thy-1−) subsets of mouse embryonic fibroblasts (MEF). TNF-α induced a robust activation of MMP-9, ICAM-1, and the IL-8 promoter driven reporter in Thy-1− MEFs, in contrast to only a modest increase in Thy-1+ counterparts. Consistently, ectopic expression of Thy-1 in Thy-1− MEFs significantly attenuated TNF-α activated gene expression. Mechanistically, TNF-α activated Src family kinase (SFK) only in Thy-1− MEFs. Blockade of SFK activation abrogated TNF-α-activated gene expression in Thy-1− MEFs, whereas restoration of SFK activation rescued the TNF-α response in Thy-1+ MEFs. Our findings suggest that Thy-1 down-regulates TNF-α-activated gene expression via interfering with SFK- and NF-κB-mediated transactivation. The current study provides a novel mechanistic insight to the distinct roles of fibroblast Thy-1 subsets in inflammation. [ABSTRACT FROM AUTHOR]

Heterogeneous surface expression of Thy-1 in fibroblasts modulates inflammation and may thereby modulate injury and repair. As a paradigm, patients with idiopathic pulmonary fibrosis, a disease with pathologic features of chronic inflammation, demonstrate an absence of Thy-1 immunoreactivity within areas of fibrotic activity (fibroblast foci) in contrast to the predominant Thy-1 expressing fibroblasts in the normal lung. Likewise, Thy-1 deficient mice display more severe lung fibrosis in response to an inflammatory injury than wildtype littermates. We investigated the role of Thy-1 in the response of fibroblasts to the pro-inflammatory cytokine TNF-α. Our study demonstrates distinct profiles of TNF-α-activated gene expression in Thy-1 positive (Thy-1+) and negative (Thy-12) subsets of mouse embryonic fibroblasts (MEF). TNF-α induced a robust activation of MMP-9, ICAM-1, and the IL-8 promoter driven reporter in Thy-12 MEFs, in contrast to only a modest increase in Thy-1+ counterparts. Consistently, ectopic expression of Thy-1 in Thy-12 MEFs significantly attenuated TNF-αactivated gene expression. Mechanistically, TNF-α activated Src family kinase (SFK) only in Thy-12 MEFs. Blockade of SFK activation abrogated TNF-α-activated gene expression in Thy-12 MEFs, whereas restoration of SFK activation rescued the TNF-α response in Thy-1+ MEFs. Our findings suggest that Thy-1 down-regulates TNF-α-activated gene expression via interfering with SFK- and NF-κB-mediated transactivation. The current study provides a novel mechanistic insight to the distinct roles of fibroblast Thy-1 subsets in inflammation. [ABSTRACT FROM AUTHOR]

The effect of NO on CO oxidation was studied for Pt, Pd and PdAu catalysts. It was found that NO inhibits significantly the CO oxidation reactivity on both Pt and Pd catalysts. On PdAu catalyst, however, the presence of NO resulted in an enhancement of CO oxidation activity. In order to gain an atomistic understanding of this effect, density-function theory (DFT) calculations were performed on the adsorption and reaction properties of NO and CO on these metal surfaces. We have identified that the inhibition effects on Pt and Pd catalysts are due to stronger NO binding, and that the enhanced reactivity on PdAu is due to the reduced NO oxidation barrier on PdAu leading to NO2 formation. [ABSTRACT FROM AUTHOR]

In order to meet the double demands on the high temperature creep and the fatigue property, compound rolling is put forward in this study. This technique obtains dual microstructures of billet, fine microstructure on the surface and original state microstructure in the center, through localizing the plastic deformation on the surface layer and leaving little plastic deformation in the center. Based on the local load theory, a set of equipment for the compound rolling has been produced. In order to study the deformation regularity of the compound rolling, Q235 billets have been used and the flow net method for strain measurement has been employed. The deformation regularity difference between the compound rolling and the flat rolling has been investigated. In addition, the microstructural evolution after the compound rolling on the surface and in the center of the Q235 billet has been observed. The results indicate that the compound rolling technique will localize the plastic deformation on the surface of the billet but leave little plastic deformation in the center. [ABSTRACT FROM AUTHOR]

The aberrant expression of transforming growth factor (TGF)-β1 in the tumor microenvironment and fibrotic lesions plays a critical role in tumor progression and tissue fibrosis by inducing epithelial-mesenchymal transition (EMT). EMT promotes tumor cell motility and invasiveness. How EMT affects motility and invasion is not well understood. Here we report that HDAC6 is a novel modulator of TGF-β1-induced EMT. HDAC6 is a microtubule-associated deacetylase that predominantly deacetylates nonhistone proteins, including α-tubulin, and regulates cell motility. We showed that TGF-β1-induced EMT is accompanied by HDAC6-dependent deacetylation of α-tubulin. Importantly, inhibition of HDAC6 by small interfering RNA or the small molecule inhibitor tubacin attenuated the TGF-β1-induced EMT markers, such as the aberrant expression of epithelial and mesenchymal peptides, as well as the formation of stress fibers. Reduced expression of HDAC6 also impaired the activation of SMAD3 in response to TGF-β1. Conversely, inhibition of SMAD3 activation substantially impaired HDAC6-dependent deacetylation of α-tubulin as well as the expression of EMT markers. These findings reveal a novel function of HDAC6 in EMT by intercepting the TGF-β-SMAD3 signaling cascade. Our results identify HDAC6 as a critical regulator of EMT and a potential therapeutic target against pathological EMT, a key event for tumor progression and fibrogenesis. [ABSTRACT FROM AUTHOR]

The proinflammatory cytokine tumor necrosis factor-α (TNF-α) promotes tumor progression through activation of matrix metalloproteinase (MMP) activity. MMP-9 is a gelatinase secreted by both cancer cells and surrounding stromal cells, and it contributes to TNF-αstimulated tumor invasion and metastasis. Cyclin-dependent kinase 9 (CDK9), the catalytic component of positive transcription elongation factor-b, phosphorylates serine 2 residues in the C-terminal domain of RNA polymerase II for productive transcription elongation and is up-regulated upon exposure to various stresses. This study investigated roles of CDK9 in TNF-α-stimulated MMP-9 expression in human lung adenocarcinoma cells. CDK9 activity was inhibited using three different strategies, including the CDK9 pharmacological inhibitor 5,6-dichloro-1-β-D-ribofuranosylbenzimidazole (DRB), a dominant-negative CDK9, and a CDK9-specific small interfering RNA. All three approaches reduced TNF-α-mediated accumulation of MMP-9 in the conditioned media as demonstrated by gelatin zymography. In contrast, transforming growth factor-β1-induced accumulation of MMP-2 was unaffected by DRB. Expression of the MMP-9 gene was examined using reverse transcription real time PCR and using a transient transfection assay to evaluate MMP-9 promoter activity. DRB reduced the TNF-α-induced increase in MMP-9 mRNA levels but did not effect transforming growth factor-β1-induced MMP-2 mRNA expression. Consistently DRB and dominant-negative CDK9 completely abrogated TNF-α-stimulated human MMP-9 promoter activity. TNF-α did not regulate expression or localization of CDK9 or its regulatory partner Cyclin T. However, TNF-α stimulated CDK9 binding to Cyclin T and MMP-9 gene occupancy by both CDK9 and the serine 2-phosphorylated form of RNA polymerase II. Our findings indicate that CDK9 mediates TNF-α-induced MMP-9 transcription. Disruption of TNF-α signaling using CDK9 inhibitors could serve as a potential therapeutic strategy against tumor invasion and metastasis. [ABSTRACT FROM AUTHOR]

Intact pZ189 DNA was allowed to replicate in FL-FEN-1- cell line that was established in this laboratory in which the expression of FEN-1 gene was blocked by dexamethasone-inducible expression of antisense RNA to FEN-1. E. coli MBM7070 was transfected with the replicated plasmid, and those with mutations in the supF gene were identified. The frequency of mutants that did not contain recognizable changes in the electrophoretic mobility of the plasmid DNA was scored. The frequency of such mutants was 19.1 × 10-4 (34/17781), significantly higher than those of 2.9 × 10-4 (4/13668) and 3.0 × 10-4 (3/9857) in the corresponding controls, respectively. Sequence analysis of the supF genes of these mutants showed that all (37/37) the base substitutions occurred at C:G base pairs; 68% (23/37) of the base substitutions were base transversions, while 32% (12/37) were transitions. Approximately 76% (23/37) of these base substitutions occurred frequently at nine positions; two of these sites contain triple pyrimidine (T or C) repeat upstream to the mutated base; four of these sites consist of 5′-TTN1N2 and mutations occurred at N1 site sequence; another two sites have the characteristics of triple A flanked at both 5′ and 3′ side by TCT, with the base substitution occurring at C in the context sequence. These data suggested that these sites are the hot spot of mutagenesis in plasmid replicated in FEN-1-deficient cells. Besides the mutator phenotype of the FEN-1-deficient cell, it was also demonstrated that FEN-1-deficient cell exhibited an increased N-methyl-N′-nitro-N-nitrosoguanidine (MNNG) sensitive phenotype. [Copyright &y& Elsevier]

A human fibroblast cell line with conditional p53 expression displayed a p53-dependent increase in both the protein and mRNA levels of proliferating cell nuclear antigen (PCNA) after exposure to ionizing radiation (IR). The combination of p53 induction and IR cooperated to activate a transiently expressed human PCNA promoter-reporter gene via a p53-responsive element. Chromatin immunoprecipitation assays with antibodies specific for p53 or p300/CREB-binding protein revealed specific p53-dependent enrichment of PCNA promoter sequences in immunoprecipitates of sheared chromatin prepared from irradiated cells. Maximal and specific association of acetylated histone H4 with the PCNA promoter also depended on p53 induction and exposure to IR. These data demonstrate p53 binding to a target site in the PCNA promoter, recruitment of p300/CREB-binding protein, and localized acetylation of histone H4 in an IR-dependent manner. These molecular events are likely to play a role in mediating activation of PCNA gene expression by p53 during the cellular response to DNA damage. The analyses indicate that the combination of p53 induction and IR activate the PCNA gene via mechanisms similar to that of p21/wild-type p53-activated factor but to a lesser extent. This differential regulation of PCNA and p21/wild-type p53-activated factor may establish the proper ratio of the two proteins to coordinate DNA repair with cell cycle arrest. [ABSTRACT FROM AUTHOR]

The effective integration of nanomaterials with underlying current collectors is a key factor affecting the performance of nonenzymatic glucose sensors, where an inappropriate integration structure often leads to poor electron transport and instability. In this work, a seamless integrated electrode was constructed by the in situ immobilizing of a nickel-based metal-organic framework (Ni-MOF) on a three-dimensional (3D) conductive nickel foam (NF) for highly sensitive and durable glucose sensing. Facilitated by a rapid microwave-assisted reaction, a robust interfacial interaction between the Ni-MOF and the substrate was established through in situ conversion from nickel oxide (NiO). The fabricated Ni-MOF/NF electrode exhibits an excellent limit of detection (LOD) of 2.65 μM and an impressive sensitivity (14.31 mA cm-2 mM-1) within the linear range (4-576 μM), which is significantly boosted compared with that of an electrode prepared by a typical drop-casting method (3.56 mA cm-2 mM-1 in 4-1836 μM). Characterization and electrochemical tests reveal that this integrated structure on the one hand contributes to fast electron transport and thus has enhanced sensitivity and on the other hand leads to exceptional durability with its structural integrity maintained under bending, shaking, and ultrasonication. Moreover, this seamless integration method was also employed to immobilize the Ni-MOF converted from the pre-chemically deposited NiO layer on another type of substrate, 3D carbon paper (CP), demonstrating the versatility of this facile strategy in creating diverse electrochemical electrodes for applications beyond glucose sensing. [ABSTRACT FROM AUTHOR]

Metal-graphene contact is a key interface in graphene-based device applications, and it is known that two types of interfaces are formed between metal and graphene. In this paper, we apply first-principles calculations to twelve metal-graphene interfaces and investigate the detailed interface atomic and electronic structures of physisorption and chemisorption interfaces. For physisorption interfaces (Ag, Al, Cu, Cd, Ir, Pt, and Au), Fermi level pinning and Pauli-exclusion-induced energy-level shifts are shown to be two primary factors determining graphene's doping types and densities. For chemisorption interfaces (Ni, Co, Ru, Pd, and Ti), the combination of Pauli-exclusion-induced energy-level shifts and hybridized states' repulsive interactions lead to a band gap opening with metallic gap states. For practical applications, we show that external electric field can be used to modulate graphene's energy-levels and the corresponding control of doping or energy range of hybridization. [ABSTRACT FROM AUTHOR]

Aqueous well-dispersed and phase-pure anatase TiO2 truncated octahedron nanoplatelets (NPLs) were prepared via controlled hydrolysis of titanium tetrachloride (TiCl4) in ethylene glycol at 240 degC. Two shapes, square and hexagon, were observed by microscopy, exactly corresponding to the truncated octahedron NPLs. Ethylene glycol was found to produce water in situ that reacts with TiCl4 to produce TiO2 and HCl--the latter promoting TiO2 colloid peptization. TiO2 truncated octahedron NPLs are formed under the stabilizing action of ethylene glycol thermolysis derivatives, such as aldehydes. Crystal growth of the TiO2 NPLs was affected by the reaction temperature that determines the water production rate and HCl-assisted peptization. TGA and FT-IR results showed [?]1.2% ethylene glycol thermolysis derivatives are attached to the surface of the TiO2 NPLs, which prevents their agglomeration, hence making them easily dispersible in aqueous media. HR-TEM and SAED results showed that the TiO2 NPLs are well crystallized and that the SAED patterns of the single TiO2 NPL changes with its size and shape. XRD patterns showed that the TiO2 NPLs are phase-pure anatase and the percentage of the {101} plane in the TiO2 NPLs to be only 18%--a structural feature that renders the TiO2 NPLs with enhanced UV absorption and reactivity properties. [ABSTRACT FROM AUTHOR]

A fluidized bed coupled rotary reactor has been designed for coating on nanoparticles (NPs) via atomic layer deposition. It consists of five major parts: reaction chamber, dosing and fluidizing section, pumping section, rotary manipulator components, as well as a double-layer cartridge for the storage of particles. In the deposition procedure, continuous fluidization of particles enlarges and homogenizes the void fraction in the particle bed, while rotation enhances the gas-solid interactions to stabilize fluidization. The particle cartridge presented here enables both the fluidization and rotation acting on the particle bed, demonstrated by the analysis of pressure drop. Moreover, enlarged interstitials and intense gas-solid contact under sufficient fluidizing velocity and proper rotation speed facilitate the precursor delivery throughout the particle bed and consequently provide a fast coating process. The cartridge can ensure precursors flowing through the particle bed exclusively to achieve high utilization without static exposure operation. By optimizing superficial gas velocities and rotation speeds, minimum pulse time for complete coating has been shortened in experiment, and in situ mass spectrometry showed the precursor usage can reach 90%. Inductively coupled plasma-optical emission spectroscopy results suggested a saturated growth of nanoscale Al2O3 films on spherical SiO2 NPs. Finally, the uniformity and composition of the shells were characterized by high angle annular dark field-transmission electron microscopy and energy dispersive X-ray spectroscopy. [ABSTRACT FROM AUTHOR]

A systematic first-principles non-equilibrium Green's function study is conducted on the contact resistance between a series of metals (Au, Ag, Pt, Cu, Ni, and Pd) and graphene in the side contact geometry. Different factors such as the termination of the graphene edge, contact area, and point defect in contacted graphene are investigated. Notable differences are observed in structural configurations and electronic transport characteristics of these metal-graphene contacts, depending on the metal species and aforementioned influencing factors. It is found that the enhanced chemical reactivity of the graphene due to dangling bonds from either the unsaturated graphene edge or point defects strengthens the metal-graphene bonding, leading to a considerable contact resistance reduction for weakly interacting metals Au and Ag. For stronger interacting metals Pt and Cu, a slightly reduced contact resistance is found due to such influencing factors. However, the wetting metals Ni and Pd most strongly hybridize with graphene, exhibiting negligible dependence on the above influencing factors. This study provides guidance for the optimization of metal-graphene contacts at an atomic scale. [ABSTRACT FROM AUTHOR]

A systematic first-principles non-equilibrium Green's function study is conducted on the contact resistance between a series of metals (Au, Ag, Pt, Cu, Ni, and Pd) and graphene in the side contact geometry. Different factors such as the termination of the graphene edge, contact area, and point defect in contacted graphene are investigated. Notable differences are observed in structural configurations and electronic transport characteristics of these metal-graphene contacts, depending on the metal species and aforementioned influencing factors. It is found that the enhanced chemical reactivity of the graphene due to dangling bonds from either the unsaturated graphene edge or point defects strengthens the metal-graphene bonding, leading to a considerable contact resistance reduction for weakly interacting metals Au and Ag. For stronger interacting metals Pt and Cu, a slightly reduced contact resistance is found due to such influencing factors. However, the wetting metals Ni and Pd most strongly hybridize with graphene, exhibiting negligible dependence on the above influencing factors. This study provides guidance for the optimization of metal-graphene contacts at an atomic scale. [ABSTRACT FROM AUTHOR]

The impact of sulfur passivation on the structural and electronic properties of the HfO2/GaAs interface is investigated by density functional theory with a hybrid functional. The gap states at the HfO2/GaAs interface arise from three major contributions: Ga 3+ and partial oxidation, As-As dimers, and Ga dangling bonds. By introducing S atoms at the interface, the removal of the gap states within the lower half of the GaAs band gap is observed, while the gap states in the upper half are pushed upward by ∼0.15 eV. [ABSTRACT FROM AUTHOR]

In order to realize maneuver combat in the modern warfare, some special military vehicles require the ability of determining their position and orientation rapidly and accurately, and the position and orientation system should be highly autonomous and have strong anti-jamming capability. So a high-accuracy independent position and orientation method for vehicles that utilizes strapdown inertial navigation system/Doppler radar is presented in this article. Laser gyroscopes in strapdown inertial navigation system and Doppler radar are adopted to develop a dead-reckoning system for vehicles. Subsequently, the attitude, velocity,and position-updating algorithms of dead-reckoning system are designed. The error sources of dead-reckoning system are analyzed to establish the system error model, including the attitude error equations of the mathematical platform, velocity error equations, and position error equations. The errors of strapdown inertial navigation system and deadreckoning system are selected as system states of the integrated position and orientation method. The difference between the attitude output of strapdown inertial navigation system and that of dead-reckoning system, and the difference between the position output of strapdown inertial navigation system and that of dead-reckoning system are chosen as the measurements of integrated position and orientation. Then, Kalman filter is adopted to design the filtering algorithm of integrated position and orientation. In the end, the integrated position and orientation method is validated by simulation experiment and vehicular experiment. The experimental results show that strapdown inertial navigation system/Doppler radar integration can realize accurate positioning and orientation for a long time, and the accuracy of attitude/position integration mode is significantly higher than that of velocity/position integration mode. Therefore, the former integration mode is more suitable for accurate position and orientation for vehicles. [ABSTRACT FROM AUTHOR]

Structural colors are attracting considerable attention for their advantages of environmental friendliness and resistance to fading. However, the weak mechanical strength and intrinsic iridescent color restrict their widespread application. This article describes a SnO2 inverse opal composite film with low-angle-dependent structural color and enhanced mechanical strength. In the present study, a direct template method was used to prepare SnO2 inverse opals, which were then embedded in polydimethylsiloxane (PDMS). The structural colors of obtained composite films were low-angle-dependent due to light scattering and high effective refractive index. Meanwhile, because of the good physical strength of PDMS, structures of SnO2 inverse opals were provided with effective protection. No specific wavelength shift occurred during stretching, and exhibited excellent cycling stability. All these advantages indicated potential applications in packing and decorating materials. [ABSTRACT FROM AUTHOR]

At GMT time 13:19, August 8, 2017, an Ms7.0 earthquake struck the Jiuzhaigou region in Sichuan Province, China, causing severe damages and casualties. To investigate the source properties, seismogenic structures, and seismic hazards, we systematically analyzed the tectonic environment, crustal velocity structure in the source region, source parameters and rupture process, Coulomb failure stress changes, and 3-D features of the rupture plane of the Jiuzhaigou earthquake. Our results indicate the following: (1) The Jiuzhaigou earthquake occurred on an unmarked fault belonging to the transition zone of the east Kunlun fault system and is located northwest of the Huya fault. (2) Both the mainshock and aftershock rupture zones are located in a region where crustal seismic velocity changes dramatically. Southeast to the source region, shear wave velocity at the middle to lower crust is significantly low, but it rapidly increases northeastward and lies close to the background velocity across the rupture fault. (3) The aftershock zone is narrow and distributes along the northwest-southeast trend, and most aftershocks occur within a depth range of 5-20 km. (4) The focal mechanism of the Jiuzhaigou earthquake indicates a left-lateral strike-slip fault, with strike, dip, and rake angles of 152°, 74° and 8°, respectively. The hypocenter depth measures 20 km, whereas the centroid depth is about 6 km. The co-seismic rupture mainly concentrates at depths of 3-13 km, with a moment magnitude (Mw) of 6.5. (5) The co-seismic rupture also strengthens the Coulomb failure stress at the two ends of the rupture fault and the east segment of the Tazang fault. Aftershocks relocation results together with geological surveys indicate that the causative fault is a near vertical fault with notable spatial variations: dip angle varies within 66°-89° from northwest to southeast and the average dip angle measures ~84°. The results of this work are of fundamental importance for further studies on the source characteristics, tectonic environment, and seismic hazard evaluation of the Jiuzhaigou earthquake. [ABSTRACT FROM AUTHOR]

A spatial atomic layer deposition apparatus integrated with a modular injector and a linear motor has been designed. It consists of four parts: a precursor delivery manifold, a modular injector, a reaction zone, and a driving unit. An injector with multi-layer structured channels is designed to help improve precursor distribution homogeneity. During the back and forth movement of the substrate at high speed, the inertial impact caused by jerk and sudden changes of acceleration will degrade the film deposition quality. Such residual vibration caused by inertial impact will aggravate the fluctuation of the gap distance between the injector and the substrate in the deposition process. Thus, an S-curve motion profile is implemented to reduce the large inertial impact, and the maximum position error could be reduced by 84%. The microstructure of the film under the S-curve motion profile shows smaller root-mean-square and scanning voltage amplitude under an atomic force microscope, which verifies the effectiveness of the S-curve motion profile in reducing the residual vibration and stabilizing the gap distance between the injector and the substrate. The film deposition rate could reach 100 nm/min while maintaining good uniformity without obvious periodic patterns on the surface. [ABSTRACT FROM AUTHOR]

Myofibroblasts are important mediators of fibrogenesis; thus blocking fibroblast-to-myofibroblast differentiation (FMD) may be an effective strategy to treat pulmonary fibrosis (PF). Previously, we reported that histone deacetylase 4 (HDAC4) activity is necessary for transforming growth factor-β1 (TGF-β1)-induced human lung FMD. Here, we show that TGF-β1 increases NADPH oxidase 4 (NOX4) mRNA and protein expression in normal human lung fibroblasts (NHLFs) and causes nuclear export of HDAC4. Application of the NOX family inhibitor diphenyleneiodonium chloride reduces TGF-β1-induced HDAC4 nuclear export, expression of the myofibroblast marker α-smooth muscle actin (α-SMA), and α-SMA fiber formation. Inhibition of HDAC4 nucleus-to-cytoplasm translocation using leptomycin B (LMB) had little effect on α-SMA expression but blocked α-SMA fiber formation. A coimmunoprecipitation assay showed that HDAC4 associates with α-SMA. Moreover, LMB abolishes TGF-β1-induced α-SMA fiber formation and cell contraction. Relevant to human pulmonary fibrosis, idiopathic PF specimens showed significantly higher NOX4 RNA expression and scant HDAC4 staining within nuclei of fibroblast foci myofibroblasts. Taken together, these results indicate that reactive oxygen species promote TGF-β1-mediated myofibroblast differentiation and HDAC4 nuclear export. The physical association of HDAC4 with α-SMA suggests that HDAC4 has a role in regulating the α-SMA cytoskeleton arrangement. [ABSTRACT FROM AUTHOR]

Background: microRNAs are small noncoding RNAs that modulate a variety of cellular processes by regulating multiple targets, which can promote or inhibit the development of malignant behaviors. Accumulating evidence suggests that miR-675-5p plays important roles in human carcinogenesis. However, its precise biological role remains largely elusive. This study examined the role of miR-675-5p in non- small cell lung cancer (NSCLC). Methods: The expression of miR-675-5p was analyzed by real-time quantitative PCR (qRT-PCR). The effect of miR-675-5p on proliferation was evaluated through MTT and colony formation assays, and cell migration and invasion were evaluated through transwell assays. The expression of target proteins and downstream molecules was analyzed by western blotting and immunohistochemical staining. The luciferase reporter assay was used to assess the target genes of miR-675-5p in non-small cell lung cancer cells. Results: The expression levels of miR-675-5p in NSCLC tissues were significantly reduced compared to those in adjacent non-cancerous tissues (P < 0.001). The expression of miR-675-5p in patients with non-small cell lung cancer had a negative correlation with lymph node metastasis (P < 0.01) and TNM stage (P < 0.05). Down-regulation of miR-675-5p promoted cell growth, proliferation, colony formation, invasion and migration, and promoted the tumorigenicity graft growth of nude mice in vivo (P < 0.01); whereas up-regulation of miR-675-5p had the contrary effects. The luciferase reporter assay showed that GPR55 was a direct target gene of miR-675-5p. Overexpression of miR-675-5p can lead to the down-regulation of GPR55 and its signaling pathway, whereas the effect can be reversed by down-regulation of miR-675-5p expression. Conclusions: miR-675-5p functions as a novel tumor suppressor in NSCLC and the anti-oncogenic activity may involve its inhibition of the target gene GPR55. These findings suggest the possibility for miR-675-5p as a therapeutic target in NSCLC. [ABSTRACT FROM AUTHOR]

Long non-coding RNAs (lncRNAs) govern fundamental biochemical and cellular processes. lncRNA HOX transcript antisense RNA (HOTAIR) represses gene expression through recruitment of chromatin modifiers. The expression of HOTAIR is elevated in lung cancer and correlates with metastasis and poor prognosis. Moreover, HOTAIR promotes proliferation, survival, invasion, metastasis, and drug resistance in lung cancer cells. Here we review the molecular mechanisms underlying HOTAIR-mediated aggressive phenotypes of lung cancer. We also discuss HOTAIR's potential in diagnosis and treatment of lung cancer, as well as the challenges of exploiting HOTAIR for intervention of lung cancer. [ABSTRACT FROM AUTHOR]

MutS protein homolog 2 (MSH2) is a key DNA mismatch repair protein. It forms the MSH2-MSH6 (MutSα) and MSH2-MSH3 (MutSβ) heterodimers, which help to ensure genomic integrity. MutSα not only recognizes and repairs mismatched nucleotides but also recognizes DNA adducts induced by DNA-damaging agents, and triggers cell-cycle arrest and apoptosis. Loss or depletion of MutSα from cells leads to microsatellite instability (MSI) and resistance to DNA damage. Although the level of MutSα can be reduced by the ubiquitin-proteasome pathway, the detailed mechanisms of this regulation remain elusive. Here we report that histone deacetylase 6 (HDAC6) sequentially deacetylates and ubiquitinates MSH2, leading to MSH2 degradation. In addition, HDAC6 significantly reduces cellular sensitivity to DNA-damaging agents and decreases cellular DNA mismatch repair activities by downregulation of MSH2. Overall, these findings reveal a mechanism by which proper levels of MutSα are maintained. [ABSTRACT FROM AUTHOR]

Distinct from the common well faceted ZnO nanorods (R-ZnO), ZnO nanotetrapods (T-ZnO) exhibited a remarkable catalytic activity for the thermal decomposition of ammonium perchlorate (AP): the activation energy at high temperature decomposition (HTD) was significantly decreased to 111.9 kJ mol-1, much lower than 162.5 kJ mol-1 for pure AP and 156.9 kJ mol-1 for AP with R-ZnO. This was attributed to more abundant atomic steps on the surface of T-ZnO than that of R-ZnO, as evidenced by HRTEM and density function theory (DFT) calculations. It was shown that the initiation step of perchloric acid (PA) decomposition happened much faster on stepped T-ZnO edges, resulting in the formation of active oxygen atoms from HClO4. The formed oxygen atoms would subsequently react with NH3 to produce HNO, N2O and NO species, thus leading to an obvious decrease in the activation energy of AP decomposition. The proposed catalytic mechanism was further corroborated by the TG-IR spectroscopy results. Our work can provide atomic insights into the catalytic decomposition of AP on ZnO nanostructures. [ABSTRACT FROM AUTHOR]

Chronic obstructive pulmonary disease (COPD) involves aberrant airway inflammatory responses to cigarette smoke (CS) that are associated with epithelial cell dysfunction, cilia shortening, and mucociliary clearance disruption. Exposure to CS reduced cilia length and induced autophagy in vivo and in differentiated mouse tracheal epithelial cells (MTECs). Autophagy-impaired (Becn1+/- or Map1lc3B-/-) mice and MTECs resisted CS-induced cilia shortening. Furthermore, CS increased the autophagic turnover of ciliary proteins, indicating that autophagy may regulate cilia homeostasis. We identified cytosolic deacetylase HDAC6 as a critical regulator of autophagy-mediated cilia shortening during CS exposure. Mice bearing an X chromosome deletion of Hdac6 (Hdac6-/Y) and MTECs from these mice had reduced autophagy and were protected from CS-induced cilia shortening. Autophagy-impaired Becn1+/-, Map1lc3B-/-, and Hdac6-/Y mice or mice injected with an HDAC6 inhibitor were protected from CS-induced mucociliary clearance (MCC) disruption. MCC was preserved in mice given the chemical chaperone 4-phenylbutyric acid, but was disrupted in mice lacking the transcription factor NRF2, suggesting that oxidative stress and altered proteostasis contribute to the disruption of MCC. Analysis of human COPD specimens revealed epigenetic deregulation of HDAC6 by hypomethylation and increased protein expression in the airways. We conclude that an autophagy-dependent pathway regulates cilia length during CS exposure and has potential as a therapeutic target for COPD. [ABSTRACT FROM AUTHOR]

Background: The tumor microenvironment is a crucial determinant in tumor progression. Interstitial extracellular matrix (ECM), such as type I collagen (Col-1), is aberrantly enriched in the tumor microenvironment and promotes tumor progression. Long intergenic non-coding RNAs (lincRNA) are a new family of regulatory RNAs that modulate fundamental cellular processes via diverse mechanisms. Findings: We investigated whether the expression of lincRNAs was regulated by the tumor promoting Col-1. In a three-dimensional organotypic culture model using the reconstituted basement membrane ECM Matrigel (rBM 3-D), supplementation of Col-1 disrupted acini, a differentiation feature of well-differentiated lung adenocarcinoma cells, and concurrently induced the expression of a tumor-promoting lincRNA, HOX transcript antisense RNA (HOTAIR). Induction of HOTAIR by Col-1 was diminished by a neutralizing antibody against the Col-1 receptor α2β1 integrin. Col-1 activates the expression of a reporter gene controlled by the human HOTAIR promoter. Moreover the expression of HOTAIR and Col-1 was concurrently up-regulated in human non-small cell lung cancer. Conclusions: Our findings indicate that tumor-promoting Col-1 up-regulates the expression of HOTAIR in NSCLC cells. These initial results warrant further investigation of HOTAIR and other lincRNA genes in lung tumorigenesis. [ABSTRACT FROM AUTHOR]

A fribotic tumor microenvironment promotes progression of cancer. In this study, we utilize a reconstituted basement membrane mimics Matrigel based three-dimensional organotypic culture (rBM 3-D) to investigate the mechanisms that mediate the tumor promoting effects of the fibrogenic mediators TGF-β1 and type I collagen (Col-1) on lung adenocarcinoma cells. Similar to normal alveolar epithelial cells, the well-differentiated lung adenocarcinoma cells in rBM 3-D culture undergo acinar morphogeneis that features polarized epithelial cell spheres with a single central lumen. Either TGF-β1 or Col-1 modestly distorts acinar morphogenesis. On the other hand, TGF-β1 and Col-1 synergistically induce a transition from acinar morphology into stellate morphology that is characteristic of invasive and metastatic cancer cells. Inhibition of the Src kinase activity abrogates induction of stellate morphology, activation of Akt and mTOR, and the expression of tumor promoting genes by TGF-β1 and Col-1. To a similar extent, pharmacological inhibition of mTOR abrogates the cellular responses to TGF-β1 and Col-1. In summary, we demonstrate that TGF-β1 and Col-1 promote stellate morphogenesis of lung cancer cells. Our findings further suggest that the Src-Akt-mTOR axis mediates stellate morphogenesis. These findings also indicate that rBM 3-D culture can serve as an ideal platform for swift and cost-effective screening of therapeutic candidates at the interface of the tumor and its microenvironment. [ABSTRACT FROM AUTHOR]

The structural, energetic and electronic properties of carbon nanobuds (CNBs) with the smallest fullerene C20 covalently attached to the sidewall of singlewalled carbon nanotubes (SWNTs) are studied by first-principles calculations. Due to the high curvature of C20 and the resulting chemical activity, the binding between C20 and SWNTs is quite strong. Among different CNB configurations, bond cycloaddition is energetically most favorable. The activation barrier for C20-CNB formation is only one-fourth that of C60 and it would maintain good stability once formed. Our results also reveal that C20-CNB stability depends on the chirality of the SWNTs, and they exhibit tunable band gaps that can be modulated by the density of C20 attached to the SWNTs. [ABSTRACT FROM AUTHOR]

Human Cytomegalovirus (HCMV) is a ubiquitous herpesvirus that currently infects a large percentage of the world population. Although usually asymptomatic in healthy individuals, HCMV infection during pregnancy may cause spontaneous abortions, premature delivery, or permanent neurological disabilities in infants infected in utero. During infection, the virus exerts control over a multitude of host signaling pathways. Wnt/β-catenin signaling, an essential pathway involved in cell cycle control, differentiation, embryonic development, placentation and metastasis, is frequently dysregulated by viruses. How HCMV infection affects this critical pathway is not currently known. In this study, we demonstrate that HCMV dysregulates Wnt/β-catenin signaling in dermal fibroblasts and human placental extravillous trophoblasts. Infection inhibits Wnt-induced transcriptional activity of β-catenin and expression of β-catenin target genes in these cells. HCMV infection leads to β-catenin protein accumulation in a discrete juxtanuclear region. Levels of β-catenin in membrane-associated and cytosolic pools, as well as nuclear β-catenin, are reduced after infection; while transcription of the β-catenin gene is unchanged, suggesting enhanced degradation. Given the critical role of Wnt/β-catenin signaling in cellular processes, these findings represent a novel and important mechanism whereby HCMV disrupts normal cellular function. [ABSTRACT FROM AUTHOR]

Several studies have implicated gamma-herpesviruses, particularly Epstein-Barr virus (EBV), in the progression of idiopathic pulmonary fibrosis. The data presented here examine the possible role that EBV plays in the potentiation of this disease by evaluating the pulmonary response to expression of the EBV lytic transactivator protein Zta. Expression of Zta in the lungs of mice via adenovirus-mediated delivery (Adv-Zta) produced profibrogenic inflammation that appeared most pronounced by day 7 postexposure. Relative to mice exposed to control GFP-expressing adenovirus (Adv-GFP), mice exposed to Adv-Zta displayed evidence of lung injury and a large increase in inflammatory cells, predominantly neutrophils, recovered by bronchoalveolar lavage (BAL). Cytokine and mRNA profiling of the BAL fluid and cells recovered from Adv-Zta-treated mice revealed a Th2 and Th17 bias. mRNA profiles from Adv-Zta-infected lung epithelial cells revealed consistent induction of mRNAs encoding Th2 cytokines. Coexpression in transient assays of wild-type Zta, but not a DNA-binding-defective mutant Zta, activated expression of the IL-13 promoter in lung epithelial cells, and detection of IL-13 in Adv-Zta-treated mice correlated with expression of Zta. Induction of Th2 cytokines in Zta-expressing mice corresponded with alternative activation of macrophages. In cell culture and in mice, Zta repressed lung epithelial cell markers. Despite the profibrogenic character at day 7, the inflammation resolves by 28 days postexposure to Adv-Zta without evidence of fibrosis. These observations indicate that the EBV lytic transactivator protein Zta displays activity consistent with a pathogenic role in pulmonary fibrosis associated with herpesvirus infection. [ABSTRACT FROM AUTHOR]