12 research outputs found

    FEM Research on Welding Thermal Deformation of Copper Alloy Sheet and Optimization of Welding Sequence

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    To reduce the residual stress and deformation of the copper alloy sheet after welding, and improve the welding quality of the copper alloy sheet, the finite element method (FEM) research on welding thermal deformation and welding sequence optimization was carried out. First, a finite element model of copper alloy sheet welding was established based on ANSYS, the mechanical property parameters of the model at high temperature were determined, and the thermal–structural coupling calculation was performed on the model. Then, the change trend and magnitude of the residual stress and deformation of the model after welding were analyzed. Finally, different welding sequence schemes were designed, and numerical simulation calculations were carried out. The results of the welding sequence solution show that the change trend of the residual stress after welding of the base metal under different welding sequences is basically the same; repeated heating of the base metal at the same position causes large residual stress; the weldment vertical plate is subjected to opposing forces in the x-axis and y-axis directions at the same time. Among four welding schemes, the welding scheme that alternately welds symmetrically from the start and end positions of the weld seam to the middle position of the plate causes the least welding deformation. Compared with the other three schemes, its deformation reduces by 26.6%, 18.3%, and 19.4%, respectively

    White and Grey Matter Changes in the Language Network during Healthy Aging

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    <div><p>Neural structures change with age but there is no consensus on the exact processes involved. This study tested the hypothesis that white and grey matter in the language network changes during aging according to a “last in, first out” process. The fractional anisotropy (FA) of white matter and cortical thickness of grey matter were measured in 36 participants whose ages ranged from 55 to 79 years. Within the language network, the dorsal pathway connecting the mid-to-posterior superior temporal cortex (STC) and the inferior frontal cortex (IFC) was affected more by aging in both FA and thickness than the other dorsal pathway connecting the STC with the premotor cortex and the ventral pathway connecting the mid-to-anterior STC with the ventral IFC. These results were independently validated in a second group of 20 participants whose ages ranged from 50 to 73 years. The pathway that is most affected during aging matures later than the other two pathways (which are present at birth). The results are interpreted as showing that the neural structures which mature later are affected more than those that mature earlier, supporting the “last in, first out” theory.</p></div

    Consistency among WM/GM and between WM and GM matter changes in Group 1.

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    <p>The correlation matrix among all ROIs, including both GM and WM matter, are given.</p

    Linear regression fit results.

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    <p>(A) shows fitting result when using grand-averaged cortical thickness as the dependent variable in Group 1. (B) shows fitting result when using age as the dependent variable in Group 1. (C) Re-examination of Group 1's ROI in Group 2's data. Age is the dependent variable. Note that the red line is the linear fit result, whereas the green lines are the confidence internal (95%). For all three panels, the x-axis corresponds to the actual age or cortical thickness, whereas the y-axis corresponds to the age or cortical thickness produced by the regression model.</p

    Neural structural changes with age in Group 1.

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    <p>(A) shows FA changes. Note that the skeletonized results are “thickened” to help visualization. Left SLF-IFC/Prg, left superior longitudinal fasciculus underlying the inferior frontal cortex and precentral gyrus; Left SLF-TP, left superior longitudinal fasciculus underlying the temporal-parietal association cortex; Left and right IFOF-IFC, left and right inferior fronto-occipital fasciculus underlying the inferior frontal cortex; Right FM-MeFC, right forceps minor underlying the medial frontal cortex; Left bCC, left body of corpus callosum. (B) shows cortical thickness changes. The colored blobs (blue for cortical thickness, red for FA) indicate brain areas that correlated negatively with age. Left IFC, left inferior frontal cortex; Left Prg, left precentral gyrus. No positive correlations were found.</p

    Deficiency of BAP1 inhibits neuroblastoma tumorigenesis through destabilization of MYCN

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    Abstract The transcription factor MYCN is frequently amplified and overexpressed in a variety of cancers including high-risk neuroblastoma (NB) and promotes tumor cell proliferation, survival, and migration. Therefore, MYCN is being pursued as an attractive therapeutic target for selective inhibition of its upstream regulators because MYCN is considered a “undruggable” target. Thus, it is important to explore the upstream regulators for the transcription and post-translational modification of MYCN. Here, we report that BRCA1-associated protein-1 (BAP1) promotes deubiquitination and subsequent stabilization of MYCN by directly binding to MYCN protein. Furthermore, BAP1 knockdown inhibits NB tumor cells growth and migration in vitro and in vivo, which can be rescued partially by ectopic expression of MYCN. Importantly, depletion of BAP1 confers cellular resistance to bromodomain and extraterminal (BET) protein inhibitor JQ1 and Aurora A kinase inhibitor Alisertib. Furthermore, IHC results of NB tissue array confirmed the positive correlation between BAP1 and MYCN protein. Altogether, our work not only uncovers an oncogenic function of BAP1 by stabilizing MYCN, but also reveals a critical mechanism for the post-translational regulation of MYCN in NB. Our findings further indicate that BAP1 could be a potential therapeutic target for MYCN-amplified neuroblastoma

    Correlation analysis of MR elastography and Ki-67 expression in intrahepatic cholangiocarcinoma

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    Abstract Background Intrahepatic cholangiocarcinoma (iCCA) is an aggressive primary liver cancer with dismal outcome, high Ki-67 expression is associated with active progression and poor prognosis of iCCA, the application of MRE in the prediction of iCCA Ki-67 expression has not yet been investigated until now. We aimed to evaluate the value of magnetic resonance elastography (MRE) in assessing Ki-67 expression for iCCA. Results In the whole cohort, 97 patients (57 high Ki-67 and 40 low Ki-67; 58 males, 39 females; mean age, 58.89 years, ranges 36–70 years) were included. At the multivariate analysis, tumor stiffness (odds ratio (OR) = 1.669 [95% CI: 1.307–2.131], p < 0.001) and tumor apparent diffusion coefficient (ADC) (OR = 0.030 [95% CI: 0.002, 0.476], p = 0.013) were independent significant variables associated with Ki-67. Areas under the curve of tumor stiffness for the identification of high Ki-67 were 0.796 (95% CI 0.702, 0.871). Tumor stiffness was moderately correlated with Ki-67 level (r = 0.593, p < 0.001). When both predictive variables of tumor stiffness and ADC were integrated, the best performance was achieved with area under the curve values of 0.864 (95% CI 0.780–0.926). Conclusion MRE-based tumor stiffness correlated with Ki-67 in iCCA and could be investigated as a potential prognostic biomarker. The combined model incorporating both tumor stiffness and ADC increased the predictive performance. Critical relevance statement MRE-based tumor stiffness might be a surrogate imaging biomarker to predict Ki-67 expression in intrahepatic cholangiocarcinoma patients, reflecting tumor cellular proliferation. The combined model incorporating both tumor stiffness and apparent diffusion coefficient increased the predictive performance. Key points • MRE-based tumor stiffness shows a significant correlation with Ki-67. • The combined model incorporating tumor stiffness and apparent diffusion coefficient demonstrated an optimized predictive performance for Ki-67 expression. • MRE-based tumor stiffness could be investigated as a potential prognostic biomarker for intrahepatic cholangiocarcinoma. Graphical Abstrac
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