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In the present work, a new surface mechanical strengthening (SMS) technique named stress ultrasonic rolling (SUR), which is ultrasonic rolling (UR) assisted with a uniaxial tensile elastic stress field, was reported and successfully conducted on 5 % wt TiB2/7050Al composite. Based on the experimental analysis and numerical simulation, the effects of SUR on surface integrity and fatigue performance of the composite were comprehensively investigated. Compared with ordinary UR, SUR further enhanced the fatigue strength at 106 cycles of the composite by 5 % and prolonged the fatigue life of the composite under the stress level of 532.8 MPa by 1.8 to 3.3 times, which are attributed to the comprehensive effect of excellent surface finish, larger and deeper compressive residual stress (RSc) layer, dispersed TiB2particles distribution in the surface, and superficial nanocrystalline structures. Besides, the assistance of uniaxial tensile elastic stress field did not increase the amount of surface plastic deformation, which indicates the RSc generated by SUR should have similar mechanical and thermal stability to that produced by ordinary UR treatment.

How enhancers activate their distal target promoters remains incompletely understood. Here we dissect how CTCF-mediated loops facilitate and restrict such regulatory interactions. Using an allelic series of mouse mutants, we show that CTCF is neither required for the interaction of the Sox2gene with distal enhancers, nor for its expression. Insertion of various combinations of CTCF motifs, between Sox2and its distal enhancers, generated boundaries with varying degrees of insulation that directly correlated with reduced transcriptional output. However, in both epiblast and neural tissues, enhancer contacts and transcriptional induction could not be fully abolished, and insertions failed to disrupt implantation and neurogenesis. In contrast, Sox2expression was undetectable in the anterior foregut of mutants carrying the strongest boundaries, and these animals fully phenocopied loss of SOX2 in this tissue. We propose that enhancer clusters with a high density of regulatory activity can better overcome physical barriers to maintain faithful gene expression and phenotypic robustness.

C15H13BrO2, monoclinic, P21/c(no. 14), a= 5.6574(9) Å, b= 9.7821(16) Å, c= 24.251(4) Å, β= 93.265(4)°, V= 1339.9(4) Å3, Z= 4, Rgt(F) = 0.0428, wRref(F2) = 0.0930, T= 273 K.

In-situ ceramics particle reinforced aluminum matrix composites are favored in the aerospace industry due to excellent properties. However, the hard ceramic particles as the reinforcement phase bring challenges to machining. To study the effect of in-situ TiB2particles on machinability and surface integrity of TiB2/2024 composite and TiB2/7075 composite, milling experiments were performed, and compared with conventional 2024 and 7075 aluminum alloys. In-situ TiB2particles clustered at the grain boundaries and dispersed inside the matrix alloy grains hinder the dislocation movement of the matrix alloy. Therefore, the milling force and temperature of the composites are higher than those of the aluminum alloys due to the increase of the strength and the decrease of the plasticity. In the milling of composites, abrasive wear is the main wear form of carbide tools, due to the scratching of hard nano-TiB2particles. The composites containing in-situ TiB2particles have machining defects such as smearing, micro-scratches, micro-pits and tail on the machined surface. However, in-situ TiB2particles impede the plastic deformation of the composites, which greatly reduces cutting edge marks on the machined surface. Therefore, under the same milling parameters, the surface roughness of TiB2/2024 composite and TiB2/7075 composite is much less than that of 2024 and 7075 aluminum alloy respectively. Under the milling conditions of this experiment, the machined subsurface has no metamorphic layer, and the microhardness of the machined surface is almost the same as that of the material. Besides, compared with 2024 and 7075 aluminum alloy, machined surfaces of TiB2/2024 composite and TiB2/7075 composite both show tensile residual stress or low magnitude of compressive residual stress.

C26H26CuN2O5, triclinic, P= 1̄ (no. 2), a= 8.8090(5) Å, b= 11.4984(6) Å, c= 12.3941(7) Å, α= 90.11°, β= 106.017(2)°, γ= 100.180(2)°, V= 1185.95(11) Å3, Z= 2, Rgt(F)= 0.0315, wRref(F2)= 0.0869, T = 293 K.

C24H24N2O3, monoclinic, P21/n(no. 14), a= 13.674(3) Å, b= 7.3900(14) Å, c= 20.862(4) Å, β= 106.728(7)°, V= 2018.9(7) Å3, Z= 4, Rgt(F) = 0.0633, wRref(F2) = 0.1804, T = 293 K.

C22H15N3O2, triclinic, P1‾$P‾{1}$(no. 2), a= 5.7613(4) Å, b= 12.3545(7) Å, c= 13.3427(8) Å, α= 110.002(2)°, β= 98.837(2)°, γ= 94.263(2)°, V= 873.55(9) Å3, Z= 2, Rgt(F) = 0.0471, wRref(F2) = 0.1376, T= 293 K.

C15H11N3O2, triclinic, P1̄ (no. 2), a= 8.4680(5) Å, b= 9.7578(5) Å, c= 10.2101(6) Å, α= 104.578(5)°, β= 111.882(6)°, γ= 106.589(5)°, V= 686.77(8) Å3, Z= 2, Rgt(F) = 0.0394, wRref(F2) = 0.1261, T= 250(2) K.

C9H9BrO3, monoclinic, P21n(no. 14), a= 10.8914(4) Å, b= 4.6335(2) Å, c= 18.4554(8) Å, β= 97.278(2)°, V= 923.85(7) Å3, Z= 4, T= 225 K, Rgt(F) = 0.0385, wRref(F2) = 0.0902.

C10H6ClN3OS, monoclinic, C2/c(no. 15), a= 18.3141(4) Å, b= 7.31845(15) Å, c= 17.7885(4) Å, β= 110.495(3)°, V= 2233.30(9) Å3, Z= 8, T= 150(2), Rgt(F) = 0.0331, wRref(F2) = 0.0904.

C34H54N10O6S6, monoclinic, P21(no. 4), a= 11.8434(5) Å, b= 11.2298(6) Å, c= 17.0706(8) Å, β= 94.661(2)°, V= 2262.86(19) Å3, Z= 4, Rgt(F) = 0.0287, wRref(F2) = 0.0809, T= 150(2) K.

Supplemental Digital Content is available in the text.Interleukin-24 (IL-24) is an ideal tumor-suppressor gene, but the mechanisms underlying its antitumor specificity remain to be elucidated. The best way to investigate these problems is to begin from the initiation of corresponding signaling cascades activated by IL-24 with screening and identifying those proteins that interacted with IL-24. With the aim of identifying these initial interactions, a yeast two-hybrid screening was performed by transforming AH109 cells containing PGBKT7-IL-24 with a liver cDNA plasmid library. These cells were then plated on synthetic nutrient medium (SD/-Trp/-Leu/-His) for the first screening and on quadruple dropout medium containing X-α-gal for the second screening. Positive colonies were further verified by repeating the MATE experiments, co-immunoprecipitation (Co-IP) analysis, and fluorescence resonance energy transfer (FRET) assays in vitro. Following the yeast two-hybrid screening, 15 genes were selected for sequencing, with two genes, HLA-Cand NDUFA13, further verified using Co-IP assays and FRET assays. Both HLA-C and NDUFA13 were found to interact with IL-24. We found that HLA-C and NDUFA13 could interact with IL-24 and it may be involved in the signal induced by IL-24. Overall, this study contributes further insight into the cancer-specific apoptosis-inducing abilities of IL-24 to potentially enhance its therapeutic potential, and it also provides outlets for other biological functions of IL-24.

C27H24N4O2monoclinic, P21/c(no. 14), a= 5.8073(2) Å, b= 31.2564(9) Å, c= 24.8105(8) Å, β= 90.13°, V= 4503.5(2) Å3, Z= 8, Rgt(F) = 0.0644, wRref(F2) = 0.1854, T= 150(2) K.

C13H14Cl1N3, orthorhombic, Pma2 (no. 28), a= 6.7623(2) Å, b= 21.1431(6) Å, c= 8.8708(2) Å, Z= 4, V= 1268.31(6) Å3, Rgt(F) = 0.0362, wRref(F2) = 0.0969, T= 200(2) K.

C38H58N10O6S4, monoclinic, P21(no. 4), a= 11.9542(5) Å, b= 11.4057(5) Å, c= 17.2763(8) Å, β= 96.380(1)° V= 2340.97(18) Å3, Z= 4, Rgt(F) = 0.0325, wRref(F2) = 0.0836, T= 200 K.

C22H18N2O4S3, monoclinic, P21/c(no. 14), a= 9.632(2) Å, b= 10.000(3) Å, c= 22.760(6) Å, β= 93.196(18)°, V= 2188.9(10) Å3, Z= 4, Rgt(F) = 0.0354, wRref(F2) = 0.0933, T= 293(2) K.

C12H8ClN3O, monoclinic, C2/c(no. 15), a= 19.2743(18) Å, b= 7.3515(7) Å, c= 17.8170(16) Å, β= 112.593(2)°, V= 2330.8(4) Å3, Z= 8, Rgt(F) = 0.0333, wRref(F2) = 0.0906, T= 153(2) K.

C30H23NO2, orthorhombic, Pbca(no. 61), a= 10.7674(16) Å, b= 19.542(3) Å, c= 20.970(3) Å, V= 4412.5(11) Å3, Z= 8, Rgt(F) = 0.0350, wRref(F2) = 0.0963, T= 153 K.