粉尘爆炸与厂房泄压关系的探讨

本文从粉尘爆炸泄压的角度进行分析,指出哈尔滨亚麻纺织厂原厂房设计存在三个问题:(1)没有足够的泄压面积;(2)单个厂房过于狭长;(3)中央换气室和通风管道(地沟)相联,在管道(地沟)中产生粉尘爆炸。这种厂房设计只要一处产生局部粉尘爆炸,极易造成全厂连续爆炸的后果。     

从两个爆炸事故实例看工业厂房泄压面积的重要性

本文结合爆炸实例讨论了工业厂房防爆的育关规定,指出了泄压设施的合理设计和泄压材料的正确选择是极其重要的。     

爆炸泄压的简易设计法

<正> 防止化工建筑物或其它建筑物内部爆炸引起其自身毁坏的最简单、也是最好的方法是在墙上或屋顶设置泄压板,这种泄压板很容易被冲破。关于泄压板面积要多大的问题,本文介绍一种简单易用的方程,这个方     

粉尘爆炸泄压面积计算

随着粉料处理工业的日益发展,人们逐渐认识到许多粉尘是具有爆炸危险的。为保护设备及人员安全,需要在处理粉料的设备上安装泄爆装置(如防爆门或爆破片)。在选择泄爆装置时,经常碰到泄压面积大小的计算问题,因此重点介绍粉尘泄爆原理及泄压面积的计算。     

原油泄压罐紧急泄压设施的设计选择

以某原油输送中泄压罐泄压设施为例,采用API国际标准,简述原油紧急泄放装置瞬间泄放的计算方法以及设计中原油泄压罐的泄压流量最大面积与储罐顶面积的比值选定。     

基于泄压阀失效的泄压系统分析与优化

为了探究先导式泄压阀失效后管道存在的风险,以实际成品油管道的泄压系统为例,基于SPS瞬态模拟方法,对泄压阀失效工况进行动态仿真模拟,重点分析泄压阀失效后油品最大泄放流速和累计泄放量,提出泄压系统优化举措,设置逻辑保护程序.结果表明:泄压阀失效时泄压管线最大流速达19.7 m/s,18 min累计泄放量达370 m3,易...     

探究油库工艺管线泄压方式

油库工艺管线在实际使用中,可能会出现憋压等问题,导致管线设备受到损坏,影响油库运行效率。而采取泄压技术能够解决这一问题,确保管线设备运行的完整性以及安全性。基于此,首先,确定油库工艺管线泄压的作用,其次,分析当前采取的泄压方式,最后,研究油库工艺管线泄压方式优化措施,为今后我国油库工艺管线的稳定安全运行提供条件。     

A301型低温低压氨合成催化剂工业应用实例及几个问题的探讨

介绍了Ｆｅ１－ｘＯ基Ａ３０１型低温低压氨合成催化剂工业应用实例,并讨论了工业应用中的几个问题,指出Ａ３０１型催化剂的工业应用具有的节能效果和效益,可达到高产量、高效益、长寿命的目的,因此是一种值得大力推广扩新型催化剂。文章认为在中、小型化肥厂的应用中,合成新鲜气中的痕量硫的慢性累积性中毒以及合成回路设备和管道的内漏是影响催化剂使用效果和使用寿命的主要原因。分析了Ａ３０１型催化剂在大型合成氨厂的有利     

二丙基硅烷双酚A环氧树脂的表征及固化性能研究

采用红外光谱（FT—IR）和核磁共振（^29Si NMR）对3,3’-二（3-三甲氧基硅丙基）双酚A环氧树脂（SEP）进行了结构表征,并对其性能和固化进行了研究。该树脂为含烷氧硅基的环氧树脂,室温下可流动,室温下黏度比E51大,在60℃以上黏度相近。采用表干时间、DSC和FT-IR等对SEP的湿固化研究结果表明,该环氧树脂通过硅氧烷水解缩合而固化,表干时间随固化温度升高而减小。该环氧树脂可以像E-51一样用胺类固化剂进行固化,低温下凝胶时间稍长,90％以上比较接近。     

PP1, PP2A and PP2B Interplay in the Regulation of Sperm Motility: Lessons from Protein Phosphatase Inhibitors

Male fertility relies on the ability of spermatozoa to fertilize the egg in the female reproductive tract (FRT). Spermatozoa acquire activated motility during epididymal maturation; however, to be capable of fertilization, they must achieve hyperactivated motility in the FRT. Extensive research found that three protein phosphatases (PPs) are crucial to sperm motility regulation, the sperm-specific protein phosphatase type 1 (PP1) isoform gamma 2 (PP1γ2), protein phosphatase type 2A (PP2A) and protein phosphatase type 2B (PP2B). Studies have reported that PP activity decreases during epididymal maturation, whereas protein kinase activity increases, which appears to be a requirement for motility acquisition. An interplay between these PPs has been extensively investigated; however, many specific interactions and some inconsistencies remain to be elucidated. The study of PPs significantly advanced following the identification of naturally occurring toxins, including calyculin A, okadaic acid, cyclosporin, endothall and deltamethrin, which are powerful and specific PP inhibitors. This review aims to overview the protein phosphorylation-dependent biochemical pathways underlying sperm motility acquisition and hyperactivation, followed by a discussion of the PP inhibitors that allowed advances in the current knowledge of these pathways. Since male infertility cases still attain alarming numbers, additional research on the topic is required, particularly using other PP inhibitors.     

Disorder of Sex Development Due to 17-Beta-Hydroxysteroid Dehydrogenase Type 3 Deficiency: A Case Report and Review of 70 Different HSD17B3 Mutations Reported in 239 Patients

The 17-beta-hydroxysteroid dehydrogenase type 3 (17-β-HSD3) enzyme converts androstenedione to testosterone and is encoded by the HSD17B3 gene. Homozygous or compound heterozygous HSD17B3 mutations block the synthesis of testosterone in the fetal testis, resulting in a Disorder of Sex Development (DSD). We describe a child raised as a female in whom the discovery of testes in the inguinal canals led to a genetic study by whole exome sequencing (WES) and to the identification of a compound heterozygous mutation of the HSD17B3 gene (c.608C>T, p.Ala203Val, and c.645A>T, p.Glu215Asp). Furthermore, we review all HSD17B3 mutations published so far in cases of 17-β-HSD3 deficiency. A total of 70 different HSD17B3 mutations have so far been reported in 239 patients from 187 families. A total of 118 families had homozygous mutations, 63 had compound heterozygous mutations and six had undetermined genotypes. Mutations occurred in all 11 exons and were missense (55%), splice-site (29%), small deletions and insertions (7%), nonsense (5%), and multiple exon deletions and duplications (2%). Several mutations were recurrent and missense mutations at codon 80 and the splice-site mutation c.277+4A>T each represented 17% of all mutated alleles. These findings may be useful to those involved in the clinical management and genetic diagnosis of this disorder.