氯碱工业中杂散电流腐蚀与防护

本文概述了氯碱工业电解过程中杂散电流产生原因,腐蚀情况,在分析腐蚀机理的基础上,提出了防止杂散电流腐蚀的措施,供同行参考。     

盐水预热器杂散电流的来源与控制

隔膜电解系统中,盐水预热器 散电流的腐蚀相当严重,经过现场实际测试寻找杂散电流的来源;采用溶液等们法,消除杂散电流,以达到控制杂散电流对盐水预热器腐蚀的目的。     

浅谈电解系统中杂散电流的腐蚀与防护

介绍了电解系统中杂散电流产生的原因及造成腐蚀现象的过程，同时提出了防止杂散电流腐蚀的措施。     

金属阳极电解槽运行中杂散电流的腐蚀原因

通过对金属阳极电解槽在运行中的杂散电流的来源、存在部位、腐蚀情况的分析,提出了防止及减少杂散电流腐蚀的措施及建议。     

电焊动火过程中杂散电流对长输管道的腐蚀研究

采用杂散电流测量仪监测电焊动火过程杂散电流的变化情况,研究了电焊动火过程中管道及周围土壤中的杂散电流分布规律。结果表明,管道中的杂散电流由电焊点向管道两侧流动,杂散电流并不稳定,其变化范围很大,最大值与最小值相差几十倍;管中杂散电流随着离电焊点距离的增大逐渐减小,随着电焊机台数的增加逐渐增大,随着管道管径的增大,逐渐增大;同时在焊接过程中,土壤中的电位梯度相应增大,并随着离管道距离的增大逐渐减小。     

溶液等电位法用于盐水预热器杂散电流腐蚀的研究

采用溶液等电位原理，设计制作了能自动彻底消除杂散电流腐蚀，实现杂散电流在线监测的模拟实验装置。实验室模拟实验和氯碱厂现场试验结果均证实，用溶液等电位法消除杂散电流腐蚀是完全彻底的，监测杂散电流是准确可靠的。     

传统杂散电流测试方法在埋地钢质管道中的应用

利用传统杂散电流测试方法,对某公司的高压埋地钢制管线进行实际检测和数据分析处理。通过检测结果得出影响该高压管线疑似区域是否存在杂散电流腐蚀干扰。     

石化管道杂散电流腐蚀的防护措施研究

输油气化工管道杂散电流腐蚀的发生必须具有杂散电流源,从源头上防止杂散电流的产生显得尤为重要;在钢轨侧增大轨地过渡电阻、减小钢轨纵向电阻及设置排流收集网可以有效降低杂散电流对管道的影响;管道表面涂覆绝缘防腐层可对埋地输油管道起到绝缘屏蔽保护作用,因此电气化铁路附近埋地输油管道表面必须涂覆绝缘防腐层。同时采用阴极保护及管道排流保护的方法均可有效抑制电流腐蚀的作用。     

混凝土中掺加粉煤灰对地铁杂散电流的抑制

为减小地铁中混凝土结构的杂散电流腐蚀,本文应用交流阻抗方法对掺入不同种类高钙,低钙粉煤耧的妆浆及混凝土的交流阻抗性能进行研究。研究结果表明：在混凝土中掺加一定比例的粉煤灰可以提高其湿电阻,并降低其孔隙率,提高其密度性,故可以用作抑制城市轨道交通中的杂散电流腐蚀的措施之一。     

隔膜烧碱生产中杂散电流腐蚀产生原因及对策

介绍了隔膜烧碱生产中杂散电流腐蚀产生的原因及危害.分析了电解槽进出口系统各主要设备杂散电流产生原因,提出了针对性的解决方案.实施后,取得了良好的效果.     

污泥生物炭中氮硫行为及环境效应研究进展

污泥生物炭中氮硫元素含量高,其氮硫行为和环境效应对全球气候变化的影响不容忽视。以往的研究中,研究者往往以富碳生物炭作为主要研究对象,关注碳对全球气候变化的行为和功效,而对氮硫元素的作用关注不够。本文从原始污泥基本性质到其热解过程,再到生物炭的老化,逐步对污泥生物炭整个生命周期内氮硫的行为及其环境效应研究进行综述,并对未来应注重开展的研究方向进行展望,为生物炭中氮硫元素固定、释放及与之关联的环境效应和温室气体排放控制研究提供理论基础。分析表明,污泥中氮元素含量普遍高于硫元素,且热解过程中氮比硫更容易转移至气相产物。氮硫元素随热解温度的增加,在三相产物中的分配都是炭中持续减少,油中先增后减,气中一直增加。高温（＞800℃）条件下,气相中的氮含量高于固相,而硫元素则仍然主要存在于固相中。污泥生物炭老化及其环境效应研究表明,污泥生物炭氮硫元素与土壤的相互作用及其温室效应问题在今后的研究中应引起重视。     

Increased C-X-C Motif Chemokine Ligand 12 Levels in Cerebrospinal Fluid as a Candidate Biomarker in Sporadic Amyotrophic Lateral Sclerosis

Sporadic amyotrophic lateral sclerosis (sALS) is a fatal progressive neurodegenerative disease affecting upper and lower motor neurons. Biomarkers are useful to facilitate the diagnosis and/or prognosis of patients and to reveal possible mechanistic clues about the disease. This study aimed to identify and validate selected putative biomarkers in the cerebrospinal fluid (CSF) of sALS patients at early disease stages compared with age-matched controls and with other neurodegenerative diseases including Alzheimer disease (AD), spinal muscular atrophy type III (SMA), frontotemporal dementia behavioral variant (FTD), and multiple sclerosis (MS). SWATH acquisition on liquid chromatography-tandem mass spectrometry (LC–MS/MS) for protein quantitation, and ELISA for validation, were used in CSF samples of sALS cases at early stages of the disease. Analysis of mRNA and protein expression was carried out in the anterior horn of the lumbar spinal cord in post-mortem tissue of sALS cases (terminal stage) and controls using RTq-PCR, and Western blotting, and immunohistochemistry, respectively. SWATH acquisition on liquid chromatography-tandem mass spectrometry (LC–MS/MS) revealed 51 differentially expressed proteins in the CSF in sALS. Receiver operating characteristic (ROC) curves showed CXCL12 to be the most valuable candidate biomarker. We validated the values of CXCL12 in CSF with ELISA in two different cohorts. Besides sALS, increased CXCL12 levels were found in MS but were not altered in AD, SMA, and FTD. Therefore, increased CXCL12 levels in the CSF can be useful in the diagnoses of MS and sALS in the context of the clinical settings. CXCL12 immunoreactivity was localized in motor neurons in control and sALS, and in a few glial cells in sALS at the terminal stage; CXCR4 was in a subset of oligodendroglial-like cells and axonal ballooning of motor neurons in sALS; and CXCR7 in motor neurons in control and sALS, and reactive astrocytes in the pyramidal tracts in terminal sALS. CXCL12/CXCR4/CXCR7 axis in the spinal cord probably plays a complex role in inflammation, oligodendroglial and astrocyte signaling, and neuronal and axonal preservation in sALS.     

TrkB Receptor Signalling: Implications in Neurodegenerative,Psychiatric and Proliferative Disorders

The Trk family of receptors play a wide variety of roles in physiological and disease processes in both neuronal and non-neuronal tissues. Amongst these the TrkB receptor in particular has attracted major attention due to its critical role in signalling for brain derived neurotrophic factor (BDNF), neurotrophin-3 (NT3) and neurotrophin-4 (NT4). TrkB signalling is indispensable for the survival, development and synaptic plasticity of several subtypes of neurons in the nervous system. Substantial evidence has emerged over the last decade about the involvement of aberrant TrkB signalling and its compromise in various neuropsychiatric and degenerative conditions. Unusual changes in TrkB signalling pathway have also been observed and implicated in a range of cancers. Variations in TrkB pathway have been observed in obesity and hyperphagia related disorders as well. Both BDNF and TrkB have been shown to play critical roles in the survival of retinal ganglion cells in the retina. The ability to specifically modulate TrkB signalling can be critical in various pathological scenarios associated with this pathway. In this review, we discuss the mechanisms underlying TrkB signalling, disease implications and explore plausible ameliorative or preventive approaches.     

Early Life Events and Maturation of the Dentate Gyrus: Implications for Neurons and Glial Cells

The dentate gyrus (DG), an important part of the hippocampus, plays a significant role in learning, memory, and emotional behavior. Factors potentially influencing normal development of neurons and glial cells in the DG during its maturation can exert long-lasting effects on brain functions. Early life stress may modify maturation of the DG and induce lifelong alterations in its structure and functioning, underlying brain pathologies in adults. In this paper, maturation of neurons and glial cells (microglia and astrocytes) and the effects of early life events on maturation processes in the DG have been comprehensively reviewed. Early postnatal interventions affecting the DG eventually result in an altered number of granule neurons in the DG, ectopic location of neurons and changes in adult neurogenesis. Adverse events in early life provoke proinflammatory changes in hippocampal glia at cellular and molecular levels immediately after stress exposure. Later, the cellular changes may disappear, though alterations in gene expression pattern persist. Additional stressful events later in life contribute to manifestation of glial changes and behavioral deficits. Alterations in the maturation of neuronal and glial cells induced by early life stress are interdependent and influence the development of neural nets, thus predisposing the brain to the development of cognitive and psychiatric disorders.     

Sp7 Transgenic Mice with a Markedly Impaired Lacunocanalicular Network Induced Sost and Reduced Bone Mass by Unloading

The relationship of lacunocanalicular network structure and mechanoresponse has not been well studied. The lacunocanalicular structures differed in the compression and tension sides, in the regions, and in genders in wild-type femoral cortical bone. The overexpression of Sp7 in osteoblasts resulted in thin and porous cortical bone with increased osteoclasts and apoptotic osteocytes, and the number of canaliculi was half of that in the wild-type mice, leading to a markedly impaired lacunocanalicular network. To investigate the response to unloading, we performed tail suspension. Unloading reduced trabecular and cortical bone in the Sp7 transgenic mice due to reduced bone formation. Sost-positive osteocytes increased by unloading on the compression side, but not on the tension side of cortical bone in the wild-type femurs. However, these differential responses were lost in the Sp7 transgenic femurs. Serum Sost increased in the Sp7 transgenic mice, but not in the wild-type mice. Unloading reduced the Col1a1 and Bglap/Bglap2 expression in the Sp7 transgenic mice but not the wild-type mice. Thus, Sp7 transgenic mice with the impaired lacunocanalicular network induced Sost expression by unloading but lost the differential regulation in the compression and tension sides, and the mice failed to restore bone formation during unloading, implicating the relationship of lacunocanalicular network structure and the regulation of bone formation in mechanoresponse.     

Physiological effects of alarm chemosignal emitted during the forced swim test

Two experiments were conducted. In the first, male rats were immersed for 25 min in fresh water or water previously swum in by another rat. Control rats were not immersed in water. Rats tested in water previously swum in by another rat were significantly less immobile than rats tested in fresh water. Water immersion resulted in significant increases in serum corticosterone, glucose, and phosphorus levels, a decrease in potassium levels, and a higher phosphorus/potassium ratio, compared to nonimmersed controls regardless of water condition. When the two water-immersed groups were compared, rats tested in previously swum water had significantly higher glucose and significantly lower potassium levels and a higher phosphorus/potassium ratio than rats tested in fresh water. Immobility times were significantly correlated with the phosphorus/potassium ratio. In the second experiment, blood gases were measured prior to testing and at 25 min after immersion in rats tested in fresh and previously swum water. Rats in soiled water hypoventilated to a significantly greater extent than rats in fresh water but did not differ significantly in blood oxygenation. These two studies demonstrate that alarm chemosignals can produce physiological effects in conspecifics.     

咪鲜胺在粤浙两地水稻和土壤中残留动态

为了评价咪鲜胺在水稻上使用后的残留动态及环境安全性，在广东、浙江两地同时进行了咪鲜胺在水稻上的残留动态试验。结果表明：在广东地区，咪鲜胺在植株中的半衰期为2．59d，在土壤中的半衰期为2．46d，在稻田水的半衰期为0．46d；在浙江地区，咪鲜胺在植株中的半衰期为3．08d，在土壤中的半衰期为1．89d，在稻田水的半衰期为1．52d。收获的水稻糙米中咪鲜胺最终残留量均低于0．5mg／kg。     

Hepatic and Adipose Tissue Depot-Specific Changes in Lipid Metabolism in Late-Onset Obese (LOB) Rats

Transgenic Late-onset OBesity (LOB) rats slowly develop a male-specific, autosomal dominant, obesity phenotype with a specific increase in peri-renal white adipose tissue (WAT) depot and preserved insulin sensitivity (Bains et al. in Endocrinology 145:2666–2679, 2004). To better understand the remarkable phenotype of these rats, the lipid metabolism was investigated in male LOB and non-transgenic (NT) littermates. Total plasma cholesterol (C) levels were normal but total plasma triacylglycerol (TAG) (2.8-fold) and hepatic TAG content (25%) was elevated in LOB males. Plasma VLDL-C and VLDL-TAG levels were higher while plasma apoB levels were 60% lower in LOB males. Increased hepatic TAG secretion explained the increased VLDL levels in LOB males. The hepatic gene expression of FAS, SCD-1, mitochondrial (mt)GPAT, and DGAT2 was up-regulated in both old obese and young non-obese LOB rats. Lipoprotein lipase (LPL) activity in heart and epididymal white adipose tissue (WAT) was unchanged, while LPL activity was increased in peri-renal WAT (30%) and decreased in soleus muscle (40%). Moreover, FAS, SCD-1 and DGAT2 gene expression was increased in peri-renal, but not in epididymal WAT. Basal lipolysis was reduced or unchanged and β-adrenergic stimulated lipolysis was reduced in WAT from both old obese and young non-obese LOB rats. To summarize, the obese phenotype of LOB male rats is associated with increased hepatic TAG production and secretion, a shift in LPL activity from skeletal muscle to WAT, reduced lipolytic response in WAT depots and a specific increase in expression of genes responsible for fatty acid and TAG synthesis in the peri-renal depot. F. Frick and R. Hume contributed equally to this work.     

Role of Glucocorticoid Signaling and HDAC4 Activation in Diaphragm and Gastrocnemius Proteolytic Activity in Septic Rats

Sepsis increases glucocorticoid and decreases IGF-1, leading to skeletal muscle wasting and cachexia. Muscle atrophy mainly takes place in locomotor muscles rather than in respiratory ones. Our study aimed to elucidate the mechanism responsible for this difference in muscle proteolysis, focusing on local inflammation and IGF-1 as well as on their glucocorticoid response and HDAC4-myogenin activation. Sepsis was induced in adult male rats by lipopolysaccharide (LPS) injection (10 mg/kg), and 24 h afterwards, rats were euthanized. LPS increased TNFα and IL-10 expression in both muscles studied, the diaphragm and gastrocnemius, whereas IL-6 and SOCS3 mRNA increased only in diaphragm. In comparison with gastrocnemius, diaphragm showed a lower increase in proteolytic marker expression (atrogin-1 and LC3b) and in LC3b protein lipidation after LPS administration. LPS increased the expression of glucocorticoid induced factors, KLF15 and REDD1, and decreased that of IGF-1 in gastrocnemius but not in the diaphragm. In addition, an increase in HDAC4 and myogenin expression was induced by LPS in gastrocnemius, but not in the diaphragm. In conclusion, the lower activation of both glucocorticoid signaling and HDAC4-myogenin pathways by sepsis can be one of the causes of lower sepsis-induced proteolysis in the diaphragm compared to gastrocnemius.