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采用ALGOR非线性材料机械运动仿真模块模拟复合材料水雷壳体自由跌落与地面接触、碰撞、受力的全过程;分四种状态进行自由跌落过程模拟分析,研究了碰撞地面和跌落姿态对水雷壳体自由跃落碰撞过程的影响;通过碰撞过程载荷、应力、应变、位移等响应数据的分析对比,得出复合材料水雷壳体抗自由跌落冲击性能的研究结论,为复合材料水雷壳体抗冲击性能评价提供理论支撑。 相似文献
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文中主要介绍了手机后盖材料、装饰油墨、中框材料以及这些材料对粘接效果的影响。其中玻璃的成分,玻璃的加工工艺,塑胶板材的加工工艺都会影响后盖材料的内部应力及形变量;油墨的配方设计,中框材料的表面处理会影响表面性能。内部应力,形变量及表面能对粘接效果有较大影响;介绍了后盖粘接的整机要求,手机后盖粘接的主要方案及主要的胶粘剂。其中VHB胶带由于具有闭孔发泡结构,能够提供优异的抗起翘性能、贴服密封性能;具有较强的内聚力,能够保证在跌落过程中不分层,不脱落;在移除过程中不分层,干净移除。 相似文献
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采用六组不同粒级的神木粉煤为原料,质量分数1. 5%和2. 5%NaOH改性花生壳为粘结剂,通过干法冷压成型制备型煤,而后高温干馏制备改性花生壳基型焦。利用红外光谱仪表征其官能团结构,测定改性花生壳基型焦的抗压强度、跌落强度和机械强度等宏观性质。结果表明,神木煤粒度(3~1. 5) mm,质量分数2. 5%NaOH改性花生壳基型焦的性能强度更优,跌落强度98. 4%,抗压强度5 187. 15 N,抗碎强度与耐磨强度分别为82. 08%和17. 92%。NaOH浓度对型焦的性能强度影响不大。随着粉煤粒度减小,型焦宏观性能强度降低。神木煤粒度0. 425 mm,抗碎强度急剧降低至0,耐磨强度高达100%。改性花生壳基型焦红外谱线相对简单,出峰数目少,不同粒级神木煤型焦的红外谱峰峰型相似,出峰位置一致,但峰强弱略有差异。 相似文献
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LDPE/HDPE共混改进注塑制品性能的研究 总被引:1,自引:0,他引:1
将LDPE加到HDPE中,提高了制品的抗冲击性、抗跌落性和染色性,探索了注塑工艺条件;研究了用LDPE对注射级HDPE改性的流变性能;并测定了制品的力学性能。结果表明,随着LDPE用量在一定比例内的增加,冲击强度和断裂伸长率明显提高,而拉伸强度有所降低。对提桶等制品的生产和应用情况表明,用某些品种的LDPE改性1300J HDPE的某些不足的性能是可行的。 相似文献
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L. F. Gudarenko M. V. Zhernokletov S. I. Kirshanov A. E. Kovalev V. G. Kudel'kin T. S. Lebedeva A. I. Lomaikin M. A. Mochalov G. V. Simakov A. N. Shuikin I. M. Voskoboinikov 《Combustion, Explosion, and Shock Waves》2004,40(3):344-355
This paper presents results from experimental studies of the properties of Carbogal (C8F16 or perfluoro1,3dimethylcyclohexane), at high pressures and temperatures, in particular, data on single compression and recompression, temperatures, and velocity of sound. Data are given on shockwave compressibility of porous Plexiglas with an initial density 10–60 times lower than the density of the solid sample. Thermodynamically complete equations of state for Carbogal and Plexiglas are developed on the basis of a model published previously and wellknown experimental data. It is shown that calculations using the developed equations of state are in agreement with available experimental data for Carbogal up to pressures of 70 GPa and for Plexiglas over the entire examined range of pressures. 相似文献
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Pierre Meyer Ccile Notarnicola Albano C. Meli Stefan Matecki Grald Hugon Jrmy Salvador Mirna Khalil Lonard Fasson Claude Cances Jrme Cottalorda Isabelle Desguerre Jean-Marie Cuisset Pascal Sabouraud Alain Lacampagne Hugues Chevassus Franois Rivier Gilles Carnac 《International journal of molecular sciences》2021,22(23)
Duchenne muscular dystrophy (DMD) is characterized by progressive muscle wasting following repeated muscle damage and inadequate regeneration. Impaired myogenesis and differentiation play a major role in DMD as well as intracellular calcium (Ca2+) mishandling. Ca2+ release from the sarcoplasmic reticulum is mostly mediated by the type 1 ryanodine receptor (RYR1) that is required for skeletal muscle differentiation in animals. The study objective was to determine whether altered RYR1-mediated Ca2+ release contributes to myogenic differentiation impairment in DMD patients. The comparison of primary cultured myoblasts from six boys with DMD and five healthy controls highlighted delayed myoblast differentiation in DMD. Silencing RYR1 expression using specific si-RNA in a healthy control induced a similar delayed differentiation. In DMD myotubes, resting intracellular Ca2+ concentration was increased, but RYR1-mediated Ca2+ release was not changed compared with control myotubes. Incubation with the RYR-calstabin interaction stabilizer S107 decreased resting Ca2+ concentration in DMD myotubes to control values and improved calstabin1 binding to the RYR1 complex. S107 also improved myogenic differentiation in DMD. Furthermore, intracellular Ca2+ concentration was correlated with endomysial fibrosis, which is the only myopathologic parameter associated with poor motor outcome in patients with DMD. This suggested a potential relationship between RYR1 dysfunction and motor impairment. Our study highlights RYR1-mediated Ca2+ leakage in human DMD myotubes and its key role in myogenic differentiation impairment. RYR1 stabilization may be an interesting adjunctive therapeutic strategy in DMD. 相似文献
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分析了农业部、工业和信息化部第1158号公告对草甘膦生产企业的影响,介绍了草甘膦母液处理利用的技术,为草甘膦企业提供参考。 相似文献
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过氧酸和DMD的性能及其在纸浆漂白中的应用 总被引:1,自引:0,他引:1
过氧酸和二氧环丙酮是类强的亲电氧化试剂 ,在反应中可有效转移氧原子。文章综述了这类氧化剂的性能及在纸浆漂白中的作用 ,作为可替代传统氯气漂白的最有希望的无污染漂剂 ,采用过氧酸和二氧环丙酮可实现纸浆的全无氯漂白 相似文献
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桉木硫酸盐浆DMD漂白工艺条件的研究 总被引:1,自引:0,他引:1
使用新漂剂二甲基二环氧乙烷(Dimethyldioxirane,简称DMD)漂白桉木硫酸盐浆时,应严格控制反应的pH值为7.0~7.5;过氧硫酸盐和丙酮用量增加,二甲基二环氧乙烷的漂白能力随之增强;5%用量的DMD漂浆经碱抽提后脱木素能力与氧脱水素相当,但前者漂浆得率高,脱木素选择性好。 相似文献
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综述了二甲基二环氧乙烷(DMD)的制备方法、结构特点、选择性氧化的化学特性、与木质素的相关反应机理及DMD在纸浆漂白中的作用.DMD作为一种强的亲电氧化试剂,具有良好的脱木质素能力和选择性.DMD作为漂白剂单独用于纸浆漂白,可以使纸浆达到较高的白度;DMD作为多段漂段间的活化剂,可提高后续漂白的效果.不同于传统含氯漂白的污染性,DMD的低污染和高漂白效率的特点,使其在纸浆全无氯漂白方面有着良好的应用前景. 相似文献
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ABSTRACT: The dielectric/metal/dielectric (DMD) multilayer is suitable for a transparent electrode because of its high optical and high electrical properties; however, it is fabricated by an expensive and inefficient multistep vacuum process. We present a WO3/Ag/WO3 (WAW) multilayer transparent anode with solution-processed WO3 for polymer light-emitting diodes (PLEDs). This WAW multilayer not only has high transmittance and low resistance but also can be easily and rapidly fabricated. We devised a novel method to deposit a thin WO3 layer by a solution process in an air environment. A tungstic acid solution was prepared from an aqueous solution of Na2WO4 and then converted to WO3 nanoparticles (NPs) by a thermal treatment. Thin WO3 NP layers form WAW multilayer with a thermal evaporated Ag layer, and they improve the transmittance of the WAW multilayer because of its high transmittance and refractive index. Moreover, the surface of the WO3 layer is homogeneous and flat with low roughness because of the WO3 NP generation from the tungstic acid solution without aggregation. We performed optical simulation and experiments, and the optimized WAW multilayer had a high transmittance of 85% with a sheet resistance of 4 /sq. Finally, PLEDs based on the WAW multilayer anode achieved a maximum luminance of 35550 cd/m2 at 8 V, and this result implies that the solution-processed WAW multilayer is appropriate for use as a transparent anode in PLEDs. 相似文献
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Yusuke Echigoya Nhu Trieu William Duddy Hong M. Moulton HaiFang Yin Terence A. Partridge Eric P. Hoffman Joe N. Kornegay Frank A. Rohret Christopher S. Rogers Toshifumi Yokota 《International journal of molecular sciences》2021,22(23)
Duchenne muscular dystrophy (DMD) is a lethal X-linked recessive disorder caused by mutations in the DMD gene and the subsequent lack of dystrophin protein. Recently, phosphorodiamidate morpholino oligomer (PMO)-antisense oligonucleotides (ASOs) targeting exon 51 or 53 to reestablish the DMD reading frame have received regulatory approval as commercially available drugs. However, their applicability and efficacy remain limited to particular patients. Large animal models and exon skipping evaluation are essential to facilitate ASO development together with a deeper understanding of dystrophinopathies. Using recombinant adeno-associated virus-mediated gene targeting and somatic cell nuclear transfer, we generated a Yucatan miniature pig model of DMD with an exon 52 deletion mutation equivalent to one of the most common mutations seen in patients. Exon 52-deleted mRNA expression and dystrophin deficiency were confirmed in the skeletal and cardiac muscles of DMD pigs. Accordingly, dystrophin-associated proteins failed to be recruited to the sarcolemma. The DMD pigs manifested early disease onset with severe bodywide skeletal muscle degeneration and with poor growth accompanied by a physical abnormality, but with no obvious cardiac phenotype. We also demonstrated that in primary DMD pig skeletal muscle cells, the genetically engineered exon-52 deleted pig DMD gene enables the evaluation of exon 51 or 53 skipping with PMO and its advanced technology, peptide-conjugated PMO. The results show that the DMD pigs developed here can be an appropriate large animal model for evaluating in vivo exon skipping efficacy. 相似文献
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Sandrine Herbelet Boel De Paepe Jan L. De Bleecker 《International journal of molecular sciences》2020,21(23)
Glucocorticoids are drugs of choice in Duchenne muscular dystrophy (DMD), prolonging patients’ ambulation. Their mode of action at the protein level is not completely understood. In DMD, muscle tissue is replaced by fibrotic tissue produced by fibroblasts, reducing mobility. Nuclear factor of activated T-cells 5 (NFAT5) is involved in fibroblast proliferation. By treating one DMD fibroblast cell culture and one of unaffected skeletal muscle fibroblasts with methylprednisolone (MP) or hydrocortisone (HC) for 24 h or 12 d, the antiproliferative properties of glucocorticoids could be unraveled. NFAT5 localization and expression was explored by immunocytochemistry (ICC), Western blotting (WB) and RT-qPCR. NFAT5 and glucocorticoid receptor (GR) colocalization was measured by ImageJ. GR siRNA was used, evaluating GR’s influence on NFAT5 expression during MP and HC treatment. Cell proliferation was monitored by IncuCyte ZOOM. In DMD fibroblasts, treatment with MP for 24 h induced dots (ICC) positive for NFAT5 and colocalizing with GR. After 12 d of MP or HC in DMD fibroblasts, NFAT5 expression was decreased (RT-qPCR and WB) and growth arrest was observed (Incucyte ZOOM), whereas NFAT5 expression and cell growth remained unchanged in unaffected skeletal muscle fibroblasts. This study may help understand the antiproliferative properties of glucocorticoids in DMD fibroblasts. 相似文献
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Sarka Jelinkova Yvonne Sleiman Petr Fojtík Franck Aimond Amanda Finan Gerald Hugon Valerie Scheuermann Deborah Beckerov Olivier Cazorla Marie Vincenti Pascal Amedro Sylvain Richard Josef Jaros Petr Dvorak Alain Lacampagne Gilles Carnac Vladimir Rotrekl Albano C. Meli 《International journal of molecular sciences》2021,22(9)
Duchenne muscular dystrophy (DMD) is a devastating condition shortening the lifespan of young men. DMD patients suffer from age-related dilated cardiomyopathy (DCM) that leads to heart failure. Several molecular mechanisms leading to cardiomyocyte death in DMD have been described. However, the pathological progression of DMD-associated DCM remains unclear. In skeletal muscle, a dramatic decrease in stem cells, so-called satellite cells, has been shown in DMD patients. Whether similar dysfunction occurs with cardiac muscle cardiovascular progenitor cells (CVPCs) in DMD remains to be explored. We hypothesized that the number of CVPCs decreases in the dystrophin-deficient heart with age and disease state, contributing to DCM progression. We used the dystrophin-deficient mouse model (mdx) to investigate age-dependent CVPC properties. Using quantitative PCR, flow cytometry, speckle tracking echocardiography, and immunofluorescence, we revealed that young mdx mice exhibit elevated CVPCs. We observed a rapid age-related CVPC depletion, coinciding with the progressive onset of cardiac dysfunction. Moreover, mdx CVPCs displayed increased DNA damage, suggesting impaired cardiac muscle homeostasis. Overall, our results identify the early recruitment of CVPCs in dystrophic hearts and their fast depletion with ageing. This latter depletion may participate in the fibrosis development and the acceleration onset of the cardiomyopathy. 相似文献