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The recent discovery of superconductivity in infinite-layer nickelates generates tremendous research endeavors, but the ground state of their parent compounds is still under debate. Here, we report experimental evidences for the dominant role of Kondo scattering in the underdoped Nd1-xSrxNiO2 thin films. A resistivity minimum associated with logarithmic temperature dependence in both longitudinal and Hall resistivities are observed in the underdoped Nd1-xSrxNiO2 samples before the superconducting transition. At lower temperatures down to 0.04 K, the resistivities become saturated, following the prediction of the Kondo model. A linear scaling behavior $\sigma _{{\boldsymbol{xy}}}^{{{\boldsymbol AHE}}}{\rm{\ }}\sim{\rm{\ }}{\sigma }_{{\boldsymbol{xx}}}$ between anomalous Hall conductivity $\sigma _{{\boldsymbol{xy}}}^{{\boldsymbol{AHE}}}$ and conductivity ${\sigma }_{{\boldsymbol{xx}}}{\rm{\ }}$is revealed, verifying the dominant Kondo scattering at low temperature. The effect of weak (anti-)localization is found to be secondary. Our experiments can help clarifying the basic physics in the underdoped Nd1-xSrxNiO2 infinite-layer thin films.

Gravity dams are important infrastructures, and their failure can affect public security. In this work, physical modeling was conducted to determine the dynamic responses and types of damag...

To evaluate the effect of interleukin-19 (IL-19) treatment on epidural fibrosis and its mechanism of action with transforming growth factor β (TGF-β).Initially, IL-19 (10, 20, 50 and 100 ng/L) was used to pretreat rat fibroblasts. TGF-β (10 μg/L) was then applied to activate fibroblasts. The protein expression levels of TGF-β receptor, extracellular-signal-regulated kinase (Erk) and p-38 were measured by Western blotting. In addition, we performed laminectomy at T10 vertebral plate in rats, followed by injection of IL-19 in caudal vein one week after injury. Furthermore, IL-19, TGF-β and fibrosis indexes were measured by quantitative Real-time polymerase chain reaction (qRT-PCR) and Western blotting at 7 and 28 days after injury, respectively.Concentration-dependent IL-19 significantly down-regulated TGF-β receptor expression and inhibited phosphorylated Erk (p-Erk) and phosphorylated p38 (p-p38). In vivo, IL-19 reduced the expressions of TGF-β and connective tissue growth factor (CTGF) at 7 days. Furthermore, IL-19 significantly suppressed extracellular matrix productions formation, including α smooth muscle actin (α-SMA) and collagen-1 (COL-1), and fibronectin at 28 days.IL-19 inhibited TGF-β expression via Erk and p38 pathway. Moreover, it decreased CTGF expression to suppress α-SMA, COL-1 and fibronectin in scar tissues, thereby preventing spinal cord from compression of scar tissues.

To investigate the regulatory role of microRNA-490-3p in the recovery process of spinal cord injury (SCI) and its underlying mechanism.Expression levels of microRNA-490-3p and MK2 in peripheral blood of SCI patients and healthy controls were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Glial cells C8-D1A and C8-B4 were induced by H2O2 for constructing in vitro SCI model, followed by detection of microRNA-490-3p and MK2 levels. After glial cells were transfected with microRNA-490-3p mimic or inhibitor, respectively, cell apoptosis and levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were detected. Bioinformatics was used to predict the binding site between microRNA-490-3p and MK2, which was further verified by dual-luciferase reporter gene assay. After construction of MK2 overexpression plasmid, rescue experiments were carried out to confirm the regulatory effect of microRNA-490-3p on MK2 in mediating SCI recovery.MicroRNA-490-3p expression was remarkably lower, whereas MK2 expression was higher in peripheral blood of SCI patients than those of healthy controls. Downregulated microRNA-490-3p and upregulated MK2 were observed in glial cells after H2O2 induction in C8-D1A and C8-B4 cells. Overexpression of microRNA-490-3p remarkably decreased levels of TNF-α and IL-6, as well as alleviated apoptosis in glial cells. Both protein and mRNA levels of MK2 were negatively regulated by microRNA-490-3p. Dual-luciferase reporter gene assay confirmed that MK2 was the target gene of microRNA-490-3p. Finally, rescue experiments verified that the regulatory effects of microRNA-490-3p on alleviating inflammation and apoptosis after SCI were reversed by MK2 overexpression.MicroRNA-490-3p is lowly expressed in glial cells after SCI. Overexpression of microRNA-490-3p alleviates inflammation and apoptosis via targeting MK2, thereafter promoting SCI recovery.

Circular RNAs (circRNAs) have recently shown capabilities as gene regulators in mammals. In this study, we aimed to evaluate the effects and mechanism of circ_0009910 in gastric cancer (GC).Circ_0009910 expression was quantified by Real-time PCR in human GC cell lines and tissues. Association between circ_0009910 levels and clinicopathological factors and patient's prognosis was analyzed. The roles of circ_0009910 in regulating GC cell proliferation, colony formation, migration, and invasion were evaluated in vitro. Western blot analysis was conducted to detect the expressions of molecular markers of epithelial-mesenchymal transition (EMT).Circ_0009910 expression level was elevated in GC tissues and cell lines and associated with clinical stage (p = 0.032), distant metastasis (p = 0.028) and differentiation (p = 0.007). Kaplan-Meier survival analysis indicated that circ_0009910 expression in positive group has a worse overall survival compared to the negative group (p = 0.0013). Multivariate analysis showed that circ_0009910 was an independent risk factor for GC (HR = 2.346, 95% CI: 1.673-3.775, p = 0.006). Knockdown of circ_0009910 expression can suppress BGC823 and AGS cells proliferation, migration and invasion in vitro experiments. The results of Western blot indicated that knockdown of circ_0009910 increased expression of E-cadherin and decreased expression of the mesenchymal markers, snail and N-cadherin.Altogether, we demonstrate that circ_0009910 acts as a prognostic biomarker and promote cell proliferation, migration, invasion and EMT in GC, indicating that circ_0009910 may be a novel potential biomarker and therapeutic target of GC.

MLN4924 is a second-generation small molecule inhibitor with anti-cancer activity that inhibits neddylation activation enzyme (NAE), subsequently blocking the neddylation-dependent activation of Cullin-RING E3 ligases (CRLs). Mof4 family associated protein 1 (MRFAP1) is a highly conserved, short half-life protein and one of the most up-regulated proteins in response to MLN4924 treatment. MRFAP1 has been identified as a novel cell cycle-related protein and a regulatory component monitoring and preventing genomic instability. However, whether MRFAP1 plays a role in MLN4924-mediated cancer cell death remains elusive.The expression of MRFAP1 in gastric cancer clinic samples was detected by Real-time PCR and Western blot. CRISPR (clustered regularly interspaced short palindromic repeats)/Cas9 system was used to knockout MRFAP1 gene in both AGS and SGC-7901 cells. The proliferation of GC cells was measured by CCK8 assay. The cell cycle distribution of GC cells was determined by fluorescence-activated cell sorting (FACS) assay. Co-immunoprecipitation assay was used to determine the interaction between MRFAP1 and P27.MRFAP1 was downregulated in clinic gastric cancer samples at post-translational level. Overexpression of MRFAP1 decreased gastric cancer cells proliferation. CRISPR-mediated knockout of MRFAP1 increased the cytotoxicity of MLN4924 by augmenting MLN4924-induced G2/M arrest and apoptosis against gastric cancer cells. At the molecular level, we found that MLN4924 induced the interaction between P27 and MRFAP1, the latter associated with P27, which was further stabilized in response to MLN4924 treatment.We showed a protective role of MRFAP1 in gastric cancer cells with MLN4924 treatment and suggested the potential possibility to combine MLN4924 with MRFAP1 inhibition to treat gastric cancer.

C29H20O7, monoclinic, P121/c1 (no. 14), a = 9.583(4) Å, b = 25.30(1) Å, c = 19.975(9) Å, β = 96.732(8)°, V = 4809.0 Å3, Z = 8, Rgt(F) = 0.071, wRref(F2) = 0.189,T = 298 K.

C23H24O11, monoclinic, P1211 (no. 4), a = 6.081(3) Å, b = 7.838(3) Å, c = 22.60(1) Å, β = 92.127(7)°, V = 1076.4 Å3, Z = 2, Rgt(F) = 0.072, wRref(F2) = 0.226, T = 298 K.

A new mathematical model is presented for plane strain bending and springback analysis in sheet metal forming. This model combines effects associated with bending and stretching, considers stress and strain distributions and different thickness variations in the thickness direction, and takes force equilibrium into account. An elastic-plastic material model and Hill’s nonquadratic yield function are incorporated in the model. The model is used to obtain force, bending moment, and springback curvature. A typical two-dimensional draw bending part is divided into five regions along the strip, and the forces and moments acting on each region and the deformation history of each region are examined. Three different methods are applied to the two-dimensional draw bending problems: the first using the new model, the second using the new model but also including a kinematic directional hardening material model to consider the bending and unbending deformation in the wall, and the third using membrane theory plus bending strain. Results from these methods, including those from the recent benchmark program, are compared.

Although many genetic alterations are known to be associated with human transitional cell carcinoma (TCC) of the urinary bladder, relatively little is known about the roles of these molecular defects, singular or in combination, in bladder tumorigenesis. We have developed a transgenic mouse model of bladder tumorigenesis using a 3.6-kb promoter of uroplakin II gene to drive the urotheliums-specific expression of oncogenes. In this study, we demonstrate that transgenic mice bearing a low copy number of SV40T transgene developed bladder carcinoma in situ (CIS), whereas those bearing high copies developed CIS as well as invasive and metastatic TCCs. These results indicate that the SV40T inactivation of p53 and retinoblastoma gene products, defects frequently found in human bladder CIS and invasive TCCs, can cause the aggressive form of TCC. Our results also provide experimental proof that CIS is a precursor of invasive TCCs, thus supporting the concept of two distinct pathways of bladder tumorigenesis (papillary versus CIS/invasive TCC). This transgenic system can be used for the systematic dissection of the roles of individual or combinations of specific molecular events in bladder tumorigenesis.

Reactive oxygen species solution produced by strong ionization discharging plasma was used to kill Escherichia coli by spraying. Several effect factors such as pH value, solution temperature, spraying time and exposure time were observed in this study, and their effects on killing rate of Escherichia coli were discussed and analysed. Results show that the treating efficiency of ROS solution for Escherichia coli is higher in alkaline solution than that in acid solution. The killing rate of Escherichia coli increases while the spraying time and exposure time are longer and the temperature is lower. The effects of different factors on killing rate of Escherichia coli are as follows: spraying time > pH value > exposure time > solution temperature.

This paper presents a dynamic simulating model of the dielectric barrier discharge (DBD), structured as an equivalent electric circuit of the streamer and glow discharge generated alternately in DBD. The main parameters of DBD have been established by means of analysing the structural characteristics of a single discharge cell. An electrical comprehensive Simulink /MATLAB model was developed in order to reveal the interaction of the adjacent two discharge cell. A series of simulations was carried out in order to estimate the key structural parameters that affect the alternate streamer and glow discharge mode. The comparison results of experimental and simulate indicate that there exists a close similarity of the current waveforms graphic. Therefore, we can grasp a deep understanding mechanism of the dielectric barrier discharge and optimize the plasma reactor.