乙二醇蒸发器大开孔结构应力分析与强度校核

基于分析设计法,利用有限元软件ABAQUS对乙二醇蒸发器大开孔结构和补强圈结构进行应力分析,并进行强度校核,讨论了内压对应力强度的影响规律。结果发现,应力集中位于接管与筒体连接部位,强度校核符合要求,满足强度要求的极限载荷为0.77MPa。     

不同形式补强圈对吊装强度影响

针对大型萃取精馏塔,利用有限元方法分析了3种形式的补强圈对其吊装强度的影响,为大型塔设备吊装提供合理方案。     

Formation of Furan Fatty Alkyl Esters from their Bis‐Epoxide Fatty Esters

Reactions of epoxidized alkyl soyate with four different alcohols: ethanol, isopropyl alcohol, 2‐ethylhexanol, benzyl alcohol, in the presence of Brønsted acid catalyst, were investigated. Products, not reported in prior studies of similar reactions, were found. These were furan fatty acid alkyl esters (FFE, mixture of alkyl 8‐(5‐hexyl‐2‐furyl) octanoate and alkyl 9‐(5‐pentyl‐2‐furyl)nonanoate) which were unambiguously identified by means of GC–MS and two‐dimensional NMR. Evidence suggests that the FFE are formed by an acid‐catalyzed rearrangement of the epoxidized linoleates. The FFE were formed in presence of all four alcohols tested and in the presence of either sulfuric acid or Amberlyst 15 catalyst. Yields of up to 13 %, as quantified by GC and NMR spectroscopies, were observed.     

曲匹地尔合成工艺的研究

以氨基碳酸胍和甲酸为原料加入环合剂POCl3和缩合剂DCC-HOBT,使反应时间缩短了,生成的中间体5-甲基-7羟基-1,2,4-三氮唑[1,5-a]嘧啶收率高,重结晶用新型复合溶剂在产率、质量与文献[1-2]相比有较大提高与改善,收率由61%[1-2]提高到75%。     

水环压缩机组在乙炔生产中的应用

介绍了水环压缩机组的主要设备、工作原理及在乙炔生产中的应用．总结了水环压缩机组的开停车操作、异常故障处理和日常维护。     

Q345/40Cr钢双金属环件的热处理工艺及组织性能

对热辗扩Q345钢/40Cr钢双金属环件进行860～950℃淬火和520～610℃回火处理,并对热处理后的组织和性能进行了观察、分析和测试。双金属环件在890℃淬火后,进行不同温度回火,测试其力学性能。结果表明,淬火后晶粒细化,随着淬火温度的升高,晶粒变大。40Cr钢硬度先下降后升高,Q345钢硬度稍微下降,结合层靠近40Cr钢一侧硬度先下降后升高,靠近Q345钢一侧硬度下降。在860℃淬火时,40Cr钢一侧合金元素未完全溶解,在890℃淬火效果最佳。随着回火温度的升高,双金属环件的抗拉强度和硬度下降;40Cr钢的伸长率提高,Q345钢和结合层的伸长率先升高后降低;双金属环件的冲击性能提高。结合层断口在Q345钢一侧。双金属环件在890℃淬火、550℃回火后综合性能最好,可以满足实际使用要求。     

压力平衡气动比例阀设计与试验研究

比例阀与电磁阀的不同之处在于能够实现流量的连续调节,因此其设计方法也不同。介绍自行研制的气动比例阀结构,概述其工作原理,详细介绍了动阀芯结构尺寸、线圈组件设计方法,通过增加密封膜片使阀芯受力平衡,使阀芯在运动过程中只受电磁力和弹簧力作用,更容易实现动态平衡并降低电磁铁功耗。为了提高输出电磁力的水平特性,对隔磁环进行了参数化仿真研究,最终确定最优隔磁环参数θ2=60°,Δh=0.2 mm,θ1=90°, h=1 mm。根据动态平衡确定了弹簧力范围,通过Inventor软件确定了复位弹簧参数,最后对气动比例阀的流量特性进行了试验。试验结果表明：该气动阀的输出流量能够随控制电压实现连续变化,满足比例阀的基本性能。     

航空轴承内圈滚道磨削残余应力的工艺优化及试验研究

对国内外8Cr4Mo4V钢制航空轴承套圈滚道磨削残余应力进行了对比试验,根据航空轴承内套圈滚道磨削工艺特点,基于ABAQUS建立轴承内套圈滚道磨削残余应力的有限元分析模型并进行了数值计算,对内套圈滚道的残余应力进行了检测、分析及验证,进而优化了轴承内套圈滚道磨削工艺。结果表明：通过增加喷丸工序、适当提高进给速度和终磨采用220目白刚玉砂轮替代石墨砂轮可有效提高轴承内圈滚道残余压应力。     

Ring‐Opening/Expansion Rearrangement of Cycloprop[2,3]inden‐1‐ols Catalyzed by p‐Toluenesulfonic Acid

A divergent approach to generate either 1‐hydroxymethylindenes (which could then be converted to benzofulvenes through a dehydration reaction) or naphthalenes by the rearrangement of cycloprop[2,3]inden‐1‐ols is reported. The effect of the cyclopropyl ring substitution pattern on ring‐opening/expansion rearrangements of the substrates was systemically studied.

     

Rare Variants in Genes Encoding MuRF1 and MuRF2 Are Modifiers of Hypertrophic Cardiomyopathy

Modifier genes contribute to the diverse clinical manifestations of hypertrophic cardiomyopathy (HCM), but are still largely unknown. Muscle ring finger (MuRF) proteins are a class of muscle-specific ubiquitin E3-ligases that appear to modulate cardiac mass and function by regulating the ubiquitin-proteasome system. In this study we screened all the three members of the MuRF family, MuRF1, MuRF2 and MuRF3, in 594 unrelated HCM patients and 307 healthy controls by targeted resequencing. Identified rare variants were confirmed by capillary Sanger sequencing. The prevalence of rare variants in both MuRF1 and MuRF2 in HCM patients was higher than that in control subjects (MuRF1 13/594 (2.2%) vs. 1/307 (0.3%), p = 0.04; MuRF2 22/594 (3.7%) vs. 2/307 (0.7%); p = 0.007). Patients with rare variants in MuRF1 or MuRF2 were younger (p = 0.04) and had greater maximum left ventricular wall thickness (p = 0.006) than those without such variants. Mutations in genes encoding sarcomere proteins were present in 19 (55.9%) of the 34 HCM patients with rare variants in MuRF1 and MuRF2. These data strongly supported that rare variants in MuRF1 and MuRF2 are associated with higher penetrance and more severe clinical manifestations of HCM. The findings suggest that dysregulation of the ubiquitin-proteasome system contributes to the pathogenesis of HCM.