矿渣微晶玻璃的制备及展望

本文介绍了制备矿渣微晶玻璃的方法-熔融法和烧结法，总结了两种方法各自的优缺点，综述了基础玻璃的组成和晶核剂对制备矿渣微晶玻璃的主晶相及性能的影响；从矿渣微晶玻璃现状出发，展望了矿渣微晶玻璃的未来发展。     

矿渣微晶玻璃的制备及展望

介绍了制备矿渣微晶玻璃的方法-熔融法和烧结法，总结了两种方法各自的优点及存在的问题，着重综述了基础玻璃的组成和晶核剂对制备矿渣微晶玻璃的主晶相及性能的影响；从矿渣微晶玻璃现状出发，展望了矿渣微晶玻璃的未来发展趋势。     

矿渣微晶玻璃熔窑设备的设计体会

针对湘潭、招远矿渣微晶玻璃中试线及国内现有生产线存在的普遍问题,结合多年来的研究设计及生产经验,讨论了影响矿渣微晶玻璃正常生产的因素,根据实验结果概述了矿渣微晶玻璃熔窑及成形等关键设备的结构设计,提出了有利于提高熔化热效率和熔化率、改进矿渣微晶玻璃的熔化质量的设备的优化组合。     

整体析晶法矿渣微晶玻璃的研制

以宝钢高炉矿渣为原料整体析晶法制备矿渣微晶玻璃,通过DTA确定微晶玻璃的热处理制度,通过XRD确定玻璃的主晶相,利用SEM观察微晶玻璃的显微形貌,并对微晶玻璃的抗折强度进行测试。     

矿渣微晶玻璃熔设备的设计体会

针对湘潭、招远矿渣微晶玻璃中试线及国内现有生产线存在的普遍问题,结合多年来的研究设计及生产经验,讨论了影响矿渣微晶玻璃正常生产的因素,根据实验结果概述了矿渣微晶玻璃熔窑及成形等关键设备的结构设计,提出了有利用提高熔化热效率和熔化率、改进矿渣微晶玻璃的熔化质量的设备的优化组合。     

富铁矿渣微晶玻璃的研究与开发

对富铁矿渣微晶玻璃的开发与研究现状进行了评述,重点介绍了富铁矿渣的特点、富铁矿渣微晶玻璃的工艺和性能研究现状以及其研究开发前景。     

利用工业废渣制备微晶玻璃进展

工业废渣大量排放造成了严重的环境污染,利用工业废渣制备矿渣微晶玻璃受到国内外的广泛关注.本文总结了目前已研究过用来制备微晶玻璃的工业废渣,并对其制备工艺、矿渣微晶玻璃成核和晶体长大等关键技术进行了阐述.认为工业废渣转制微晶玻璃是一项很有前景的材料开发和环保技术.     

矿渣微晶玻璃专家系统类比设计模型

类比学习是利用过去的经验来求解新问题的一种思维过程,是专家系统中实现知识自动获取的重要方法。根据矿渣微晶玻璃设计的基本特征,详细介绍了矿渣微晶玻璃类比设计的基本原理、类比因素以及类比准则。选择属性类比作为专家系统类比设计的主要方式,以矿渣的成分作为类比因素,以经过修正的综合类似度作为类比准则,结合矿渣微晶玻璃实例库和人工神经网络模型建立了专家系统类比设计模块。实验结果证明,该类比设计模块具有很好的设计效果,是矿渣微晶玻璃设计的有效方法之一。     

矿渣微晶玻璃产品的研究与开发

对矿渣微晶玻璃的开发与研究情况进行了评述 ,重点介绍了矿渣微晶玻璃生产线的研究与发展成果 ,对工艺与关键设备开发过程做了详细介绍     

钢渣微晶玻璃的制造和应用

一、前言利用工业废渣制造矿渣微晶玻璃,近二十年来得到了迅速的发展。矿渣微晶玻璃具有较高的机械强度、耐磨、良好的电学性能和化学稳定性,已成为一种良好的结构材料。当前的矿渣微晶玻璃主要采用高炉炉渣来制造,这是因为高炉炉渣的化学组成比较稳定,并适应CaO-AL_2O_3-SiO_2系微晶玻璃的要求。平炉、电炉和转炉炼钢所得钢渣因其变     

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。     

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.     

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.     

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.     

Molecular mechanisms of aging and immune system regulation in Drosophila

Aging is a complex process that involves the accumulation of deleterious changes resulting in overall decline in several vital functions, leading to the progressive deterioration in physiological condition of the organism and eventually causing disease and death. The immune system is the most important host-defense mechanism in humans and is also highly conserved in insects. Extensive research in vertebrates has concluded that aging of the immune function results in increased susceptibility to infectious disease and chronic inflammation. Over the years, interest has grown in studying the molecular interaction between aging and the immune response to pathogenic infections. The fruit fly Drosophila melanogaster is an excellent model system for dissecting the genetic and genomic basis of important biological processes, such as aging and the innate immune system, and deciphering parallel mechanisms in vertebrate animals. Here, we review the recent advances in the identification of key players modulating the relationship between molecular aging networks and immune signal transduction pathways in the fly. Understanding the details of the molecular events involved in aging and immune system regulation will potentially lead to the development of strategies for decreasing the impact of age-related diseases, thus improving human health and life span.