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Precipitates are the primary source of strength for the Al-Mg-Si alloy. Aluminum alloy in the peak-aged state mainly contains ß" and ß' precipitates. Most of the literature has only considered the strengthening effect of ß". Here, we develop a single-crystal intensity model including both precipitate enhancement effects for the first time. This model was subsequently implemented into a crystal plastic finite-element method to model the uniaxial tensile process of a polycrystalline aggregate model of Al-Mg-Si alloy. The simulation results for uniaxial stretching are in good agreement with the experimental results, confirming that the constitutive parameters used for the single-crystal strength model with two precipitates are based on realistic physical implications. Furthermore, by comparing the uniaxial tensile simulation results of a peak-aged alloy considering the actual precipitated phase composition of the alloy with those assuming that the precipitated phase is only the ß" phase, the predicted tensile strength of the former is around 5.65% lower than that of the latter, suggesting that the two kinds of precipitation should be separately considered when simulating the mechanical response of Al-Mg-Si alloy. It is highly expected that the present simulation strategy is not limited to Al-Mg-Si alloys, and it can be equally applied to the other age-enhanced alloys.

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The effect of surface integrity on the hot fatigue performance of Ti2AlNb alloy was investigated. A turning process was used to prepare the standard specimens for hot fatigue tests. The surface integrity characterization and axial fatigue tests were performed. The results show that the influence of surface roughness on the hot fatigue performance of the Ti2AlNb alloy is a secondary factor. The compressive residual stress and enhanced microhardness in the surface layer has a significant effect on the hot fatigue life and they are dominant in the hot fatigue behavior of the Ti2AlNb alloy. Through the investigation on the characteristics of the fatigue fractures, the fatigue propagation process was significantly suppressed because of the strong residual compressive stress and microhardness distribution on the surface layer of the Ti2AlNb specimen.

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OBJECTIVE: To explore the molecular basis for two brothers affected with globozoospermia. METHODS: Whole exome sequencing was carried out for both patients. Candidate variant was verified by Sanger sequencing and quantitative real-time PCR (qRT-PCR). RESULTS: Whole exome sequencing, Sanger sequencing and qRT-PCR verification revealed a heterozygous c.384dup (p.Glu129*) variant in the DPY19L2 gene in the two brothers and their mother. A large heterozygous deletion, spanning approximately 164.5 kb and encompassing the entire DPY19L2 gene, was detected on chromosome 12 of the two patients and their father. CONCLUSION: The c.384dup (p.Glu129*) variant and deletion of the DPY19L2 gene probably underlie the pathogenesis of globozoospermia in the two patients, which was in keeping with the autosomal recessive inheritance of disease in this pedigree.

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The transplantation of Schwann cells (SCs) could successfully promote axonal regeneration. This is likely to attribute to the adhesion molecules expression and growth factors secretion of SCs. But which factor(s) play a key role has not been precisely studied. In this study, an outgrowth assay using dorsal root ganglia (DRG) neuron-SC co-culture system in vitro was performed. Co-culture of SCs or application of SC-conditioned medium (CM) substantially and significantly increased DRG neurite outgrowth. Further, nerve growth factor and NGF receptor (TrkA) mRNA were highly expressed in Schwann cells and DRG neuron, respectively. The high concentration of NGF protein was detected in SC-CM. When K-252a, a specific inhibitor of NGF receptor was added, DRG neurite outgrowth was significantly decreased in a concentration-dependent manner. These data strongly suggest that SCs play important roles in neurite outgrowth of DRG neurons by secreted NGF.

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Oligodendrocyte precursor cells (OPCs) are bipotential progenitor cells that can differentiate into myelin-forming oligodendrocytes or functionally undetermined type II astrocytes. Transplantation of OPCs is an attractive therapy for demyelinating diseases. However, due to their bipotential differentiation potential, the majority of OPCs differentiate into astrocytes at transplanted sites. It is therefore important to understand the molecular mechanisms that regulate the transition from OPCs to oligodendrocytes or astrocytes. In this study, we isolated OPCs from the spinal cords of rat embryos (16 days old) and induced them to differentiate into oligodendrocytes or type II astrocytes in the absence or presence of 10% fetal bovine serum, respectively. RNAs were extracted from each cell population and hybridized to GeneChip with 28,700 rat genes. Using the criterion of fold change > 4 in the expression level, we identified 83 genes that were up-regulated and 89 genes that were down-regulated in oligodendrocytes, and 92 genes that were up-regulated and 86 that were down-regulated in type II astrocytes compared with OPCs. The up-regulated genes, such as activating transcription factor 3 and myelin basic protein in oligodendrocytes or claudin 11 in type II astrocytes, might contribute to OPC differentiation and represent constitutive components of oligodendrocytes or type II astrocytes. The down-regulated genes in both oligodendrocytes and type II astrocytes, such as transcription factor 19, might be involved in maintaining self-renewal and/or represent the property of OPCs. These results provide new insights into the elucidation of the molecular mechanisms, by which OPCs differentiate to oligodendrocytes or type II astrocytes.

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The PKC signaling pathway has been implicated in diverse cellular functions. Here, we sought to investigate the role of PKC-alpha÷beta in C6 glioma cell migration. We found that both PKC-alpha and PKC-beta were expressed by C6 glioma cells, but only PKC-alpha was markedly activated in serum-treated C6 cells. Go6976, a PKC-alpha÷beta specific inhibitor, was found to cause a dose-dependent reduction of PKC-alpha activation and cell migration induced by serum in C6 cells. These results collectively indicated that the PKC-alpha signaling pathway is necessary for glioma cell migration. Our findings may provide an insight into a better understanding to the malignant progression of gliomas.

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In the title compound, [Cu(C(13)H(9)NO(3))(C(5)H(5)N)], the Cu(II) atom is coordinated in a distorted square-pyramidal geometry, with two N and two O atoms in the basal positions and one O atom in the apical position. The apical Cu-O bond [2.3520 (16) Å] is much longer than the basal Cu-O and Cu-N bonds [1.9139 (14)-2.0136 (17) Å]. The carboxyl-ate group bridges Cu(II) atoms, forming a zigzag chain along the a axis.