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Porcine reproductive and respiratory syndrome virus (PRRSV) infection inhibits swine leukocyte antigen class I (SLA-I) expression in pigs, resulting in inefficient antigen presentation and subsequent low levels of cellular PRRSV-specific immunity as well as persistent viremia. We previously observed that the non-structural protein 4 (nsp4) of PRRSV contributed to inhibition of the β2-microglobulin (β2M) and SLA-I expression in cells. Here, we constructed a series of nsp4 mutants with different combination of amino acid mutations to attenuate the inhibitory effect of nsp4 on β2M and SLA-I expression. Almost all nsp4 mutants exogenously expressed in cells showed an attenuated effect on inhibition of β2M and SLA-I expression, but the recombinant PRRSV harboring these nsp4 mutants failed to be rescued with exception of the rPRRSV-nsp4-mut10 harboring three amino acid mutations. However, infection of rPRRSV-nsp4-mut10 not only enhanced β2M and SLA-I expression in both cells and pigs but also promoted the DCs to active the CD3+CD8+T lymphocytes more efficiently, as compared with its parental PRRSV (rPRRVS-nsp4-wt). These data suggested that the inhibition of nsp4-mediated β2M downregulation improved β2M/SLA-I expression in pigs. • The Nsp4 gene of PRRSV on virus level inhibit the expression of β2M/SLA-I gene in pigs in this research filed. • The three amino acid sites of Nsp4 gene we have screened play a key role in inhibition of the expression of β2M/SLA-I gene in pigs. • The rPRRSV-nsp4-mut10 can induce more expression of β2M/SLA-I which accelerates the clearance of PRRSV in pigs. [ABSTRACT FROM AUTHOR]

Shear horizontal (SH) waves are widely used in the non-destructive evaluation and structural health monitoring fields. Conventional periodic permanent magnet electromagnetic acoustic transducers (PPM EMAT) can generate a single SH wave mode, which propagates in both forward and backward directions. Generation in a single direction is usually preferred to ease signal interpretation and increase inspection reliability. Recently, we have proved that a single, either fundamental or high-order, SH wave mode can be unidirectionally generated using a dual PPM EMAT, with carefully designed driving signals. Distinct SH modes present different applicability due to their particular response to features in the structure, such as defects. Hence, unidirectional generation of two different SH modes simultaneously with a dual-array transducer is investigated in this paper. The selectivity of wave modes and the selectivity of the propagation direction are studied by combining pure wave mode excitability with the superposition of optimal excitation signals for unidirectional generation, addressed in the frequency–wavenumber domain. Excitation signals for optimal and simultaneous generation of the SH0 and SH1 modes propagating in the same direction or in opposite directions have been designed. Experiments on an aluminium plate have demonstrated that the two wave modes can be effectively simultaneously generated with only one dual-array transducer and the propagation direction of each wave mode can be flexibly controlled using the designed excitation signals. • A single dual-array transducer excites distinct unidirectional waves simultaneously. • Pure wave excitation and direction are addressed in the frequency–wavenumber domain. • Superposition of optimal excitation signals ensures simultaneous wave generation. • A dual PPM-EMAT simultaneously generated SH0 and SH1 modes in distinct directions. • The generation direction of each wave mode can be conveniently controlled. [ABSTRACT FROM AUTHOR]

Array transducers are commonly used to generate several types of waves, such as ultrasonic guided waves. They consist of a series of periodic wave source elements, and thus define a nominal or dominant wavelength of generated waves. A common approach to generating waves in a single direction is to use two identical wave sources, or two arrays of sources forming a dual-array transducer, that are separated by a quarter wavelength. Then, one source is activated a quarter of a time period after the other. In this way, constructive interference arises in one direction, whilst destructive interference arises in the opposite direction, making the total wave source unidirectional. This principle assumes that the frequency content of the generated wave is monochromatic. When there is some frequency bandwidth to the wave generated, such as with finite-length pulses, one cannot satisfy simultaneously constructive and destructive interference in opposite directions with dual-array transducers. For a non-dispersive wave mode, ideal destructive interference for pulsed waveform is obtained if one of the sources is inverted relative to the other, so that, in theory, complete cancellation can be achieved. Moreover, most guided wave modes are dispersive, meaning that, different frequencies propagate at different phase speeds. This limits the amount of wave cancellation in one direction and constructive interference in the other. Here, we describe the operation of the dual-array transducer in the frequency–wavenumber domain and use it to propose two new excitation methods, based on a frequency-dependent phase-shift strategy, that is designed through the dispersion relationship of the wave mode of interest. These provide ideal constructive or destructive interferences for dispersive waves, and achieve optimal unidirectional generation behaviour for dispersive wave modes. The new methods were experimentally assessed with shear horizontal ultrasonic waves, generated by a dual periodic permanent magnet electromagnet acoustic transducer. The optimal excitation signal yielded up to 30 dB unidirectionality, when generating the dispersive SH1 wave mode in an aluminium plate. • Unidirectional wave generation is addressed in the frequency–wavenumber domain. • Usual time-delay excitation methods were proved not appropriate for dispersive waves. • We propose a method that optimally generates dispersive waves unidirectionally. • A dual PPM-EMAT was used to generate shear horizontal waves in a single direction. • About 30 dB unidirectionality was achieved for the dispersive SH1 mode experimentally. [ABSTRACT FROM AUTHOR]

A new ternary phosphidopolysilicate (IV), KSi2P3, has been synthesized by high temperature solid state reaction. The compound crystallizes in a new structure type in the monoclinic space group C2/c with a=10.1327(5)Å, b=10.1382(5)Å, c=21.1181(10)Å, β=96.88(0)°, and Z=8. In the structure, all SiP4 tetrahedra are connected with each other by corner-sharing P atoms to form layers, which are stacked along c direction and separated by K+ cations. The two-dimensional structure of KSi2P3 contrasts with those of the two known members in the ternary A/Si/P (A=alkali metal) system, namely Na5SiP3 (zero-dimensional) and K2SiP2 (one-dimensional), which contains less amount of Si. The band gap deduced from UV–vis–IR diffuse reflectance spectrum is 1.72eV. [ABSTRACT FROM AUTHOR]

Urbanization has been considered a driver of PM 2.5 pollution and the attributed health burden. This study systematically measured the spatiotemporal and urban-rural heterogeneity of PM 2.5 -attributed health burden drivers, including income, population, baseline mortality rate, and PM 2.5 level. The results reveal the significantly positive contribution of disposable income and the periodical and urban-rural differentiation of population contribution to PM 2.5 -attributed health burden. The difference in driver performance due to socioeconomic development and urbanization stages might be an important determinant for different or even opposite results of previous studies. Policymaking for mitigating PM 2.5 -attributed health risk could incorporate the re-assessment and driver determination for PM 2.5 -attributed health burden into the construction and development plan from the overall urbanization perspective. The urbanization-perspective driver decomposition could be synergized with the flow analysis, equality evaluation, and policy benefit estimation to achieve further direction-determining and quantitative assessment of the urban-rural PM 2.5 health risk management strategies. • We decomposed the urbanization drivers of PM 2.5 health burden in China 2008–2021. • Drivers were determined as population, baseline mortality rate, income, and PM 2.5. • New driver disposable income showed significant driving influence. • Urban-rural heterogeneity of the drivers was presented during urbanization. [ABSTRACT FROM AUTHOR]

Highlights: [•] miR-30a represses Eya2 expression by binding to the 3′-untranslated region of Eya2. [•] The miR-30a/EYA2 axis regulates breast cancer cell proliferation and migration. [•] The miR-30a/EYA2 axis modulates G1/S cell cycle progression. [•] The miR-30a/EYA2 axis is dysregulated in breast cancer patients. [ABSTRACT FROM AUTHOR]

Abstract: A new series of transition-metal rare-earth chalcogenides, Ln 3FeGaQ7 (Ln=Nd, Sm, Gd, Dy, Q=S; Ln=Nd, Gd, Dy, Q=Se), have been synthesized by solid state reactions. They are isostructural and crystallize in the space group P63. They adopt a three-dimensional framework composed of LnQ7 monocapped trigonal prisms with the interesting [FeS3]4− chains and isolated GaQ4 tetrahedra lying in two sets of channels in the framework. Magnetic susceptibility measurements on Ln 3FeGaQ7 (Ln=Gd, Dy; Q=S, Se) indicate that they are paramagnetic and obey the Curie–Weiss law. Based on the diffuse reflectance spectra, Ln 3FeGaQ7 (Ln=Gd, Dy; Q=S, Se) should have band gaps smaller than 0.5eV. Electronic conductivity measurement on Dy3FeGaSe7 demonstrates semiconducting behavior with σ 300=0.124S/cm. The first-principles calculations were also performed to study the electronic structures of these compounds. [Copyright &y& Elsevier]

Abstract: HCV and HBV are the major causes of chronic liver diseases worldwide. Patients with both viruse’s co-infection tend to develop severer liver diseases and are at high risk of liver-related death. NS5A protein of HCV plays key roles in HCV replication and inhibition of host immune responses. In this study, we described the establishment of HepG2-derived cell line that stably expresses NS5A protein and the application of a cellular system for HBV replication based on a recombinant adenovirus carrying HBV genome. Our results demonstrated that NS5A enhances the expression of S and E proteins of HBV, as well as the synthesis of viral DNA. Moreover, we showed that NS5A assists HBV to escape interferon responses. These data suggested that NS5A of HCV may employ multiple strategies contributing to the enhancement of HBV replication and interferon resistance during the co-infection of HCV and HBV. [Copyright &y& Elsevier]

In this study, ordered mesoporous nanosheet SAPO-11 molecular sieves were synthesized using uncalcined SBA-15 molecular sieves as a Si source. The effects of different Si sources on the structure and properties of SAPO-11 molecular sieves were examined, and their growth mechanism was elucidated. An electrostatically polarized region was formed between a P123 template (triblock copolymer) contained in uncalcined SBA-15 and two-dimensional channels of SBA-15 molecular sieves. When AlO 2 − and PO 2 + species diffused into this region, its electrostatic polarization promoted the preferential growth of SAPO-11 molecular sieves along the c -axis, which contained a large number of exposed catalytically active sites with acidic properties. During the isomerization of long-chain alkanes, the synthesized sieves exhibited high isomerization activity and selectivity. When the conversion rate of n -dodecane reached 87.96%, the yield of i -dodecane was 68.08%, and the yield of multi-branched i -dodecane was 31.65%. Mechanism illustration of ordered mesoporous SAPO-11 with nanosheets morphology. [Display omitted] • Ordered mesoporous nanosheet SAPO-11 sieves are synthesized from uncalcined SBA-15. • A preferential growth mechanism of nanosheet SAPO-11 sieves is proposed. • Ordered mesoporous nanosheet SAPO-11 sieves expose more pore active sites. • Hydroisomerization of long-chain n -alkanes is investigated. [ABSTRACT FROM AUTHOR]

Abstract: The overexpression of osteopontin is associated with various inflammatory liver diseases. Interestingly, each of these diseases is also associated with IL-17 expression. Therefore, we sought to determine whether there is any mechanistic link between osteopontin and IL-17. Herein we show that IL-17 and osteopontin levels were significantly increased in patients with chronic hepatitis B. We found that IL-17 and osteopontin levels increased similarly in mice with concanavalin A-induced hepatitis. Both osteopontin- and IL-17-deficient mice were resistant to concanavalin A-induced hepatic injury. In addition, osteopontin markedly induced IL-17 expression by leukocytes (from humans and mice). This effect could be blocked by a specific antibody against osteopontin. β3 integrin (one of the osteopontin receptors) was critically involved in the induction of IL-17 production by osteopontin. Osteopontin-induced IL-17 expression was mediated through the p38, JNK, and NF-κB pathways. These findings suggest that osteopontin regulates IL-17 production during the pathogenesis of hepatitis and provide new evidence for the critical roles of osteopontin and IL-17 in hepatitis. [Copyright &y& Elsevier]

Abstract: Hepatitis C virus (HCV) causes chronic hepatitis, which often results in the development of liver cirrhosis and hepatocellular carcinoma (HCC) worldwide. In this study, we demonstrated that the non-structural protein NS3 of HCV enhances cyclooxygenase-2 (COX-2) gene promoter activity, COX-2 mRNA expression, COX-2 protein production, and prostaglandin E2 (PGE2) release in HepG2 cells in a concentration-dependent fashion. We also showed that transcription factor NF-κB is required for the activation of COX-2 regulated by NS3. In addition, multiple signaling pathways are involved cooperatively in the expression of COX-2 activated by the viral protein in a calcium-independent manner, which requires signaling components including JNK, ERK, and PKD2. A thorough investigation of mechanism involved in the activation of COX-2 regulated by HCV would provide insights into our understanding the processes of liver inflammatory response and hepatocellular carcinoma development caused by the viral infection and also into the development of novel therapeutics against HCV infection. [Copyright &y& Elsevier]