脂肪族聚碳酸酯型聚氨酯互穿网络聚合物的研究

简述了脂肪族聚碳酸酯聚氨酯（ＰＣＵ）互穿网络聚合物（ＩＰＮ）的发展及最新研究动态。介绍了其制备、表征、结构与性能的关系。预示了聚碳酸酯型聚氨酯互穿网络聚合物材料的开发前景。     

聚碳酸酯二元醇的合成及应用研究进展

聚碳酸酯二元醇(PCDL)是制备聚碳酸酯型聚氨酯的重要原料,和传统的聚醚型聚氨酯和聚酯型聚氨酯相比,聚碳酸酯型聚氨酯表现出优异的耐水解性、力学性能和生物相容性。随着聚氨酯需求量的增长,聚碳酸酯二元醇的研究受到行业内的高度重视。本文先简要介绍了PCDL的合成方法,重点回顾了近十年来用于酯交换缩聚法制备PCDL的催化剂的研究进展,简述了PCDL在聚氨酯工业中的应用。未来开发非均相催化剂及高沸点的有机碱催化剂、制备不同结构的聚碳酸酯二元醇是PCDL的主要研究方向。     

聚碳酸酯二元醇及其在聚氨酯材料中的应用

本文论述了聚碳酸酯二元醇及聚碳酸酯型聚氨酯材料的发展概况，并分别简述了聚碳酸酯二元醇的合成方法、应用及聚碳酸酯型聚氨酯材料的性能与特点。     

国内外聚碳酸酯的生产及消费分析

聚碳酸酯（ＰＣ）是一种非晶型的热塑性工程塑料，学名２，２双（４羟基苯基）丙烷聚碳酸酯，即通常所称的双酚Ａ型聚碳酸酯。它与ＡＢＳ、ＰＡ、ＰＯＭ、ＰＢＴ及改性ＰＰＯ一起被称为六大通用工程塑料。ＰＣ由于具有优异的综合性能，尤以耐冲击强度高被誉为塑料之“冠”。ＰＣ树脂的可见光透过率在９０％以上，并且具有优异的电绝缘性、延伸性、尺寸稳定性及耐化学腐蚀性，还有自熄、易增强阻燃、无毒、卫生、着色等优良性能。ＰＣ广泛应用于机械、汽车、航天航空、电子、建筑、信息储存、体育、包装、光学仪器、通讯、医疗、照相器材…     

丁腈羟/聚碳酸酯基聚氨酯脲弹性体的制备和性能

用丁腈羟与聚碳酸酯二醇共混物制备聚氨酯脲弹性体,并研究了其性能.纯丁腈羟基聚氨酯脲弹性体的拉伸强度为17 MPa;随着聚碳酸酯二醇用量的增加,丁腈羟/聚碳酸酯基聚氨酯脲弹性体的拉伸强度先降低后升高,邵尔A硬度逐渐增大.纯丁腈羟基聚氨酯弹性体的热性能明显优于聚碳酸酯基聚氨酯弹性体.     

聚碳酸酯型聚氨酯／环氧树脂互穿网络聚合物交联密度及？…

用同步法合成了聚碳酸酯型聚氨酯／环氧树脂互穿网络聚合物（ＰＣＰＵ／ＥＰＩＰＮ）。红外光谱分析表明两组分间存在一定程度的化学结合。动态力学性能分析表明：由于两网络间的互穿、缠结以及接枝反应的发生,使体系中ＰＣＰＵ和ＥＰ的相容性得到改善。用溶胀法测定了ＩＰＮ体系的交联密度,结果发现形成ＩＰＮ后体系的交联密度相应比纯组分有所提高。力学性能测试表明：在ｍ（ＰＣＰＵ）／ｍ（ＥＰ）＝２５／７５处ＩＰＮ体系的力     

聚碳酸酯二元醇改性的聚氨酯微孔泡沫的研制

将聚碳酸酯二元醇(PCDL)作为配方组分,采用直接添加和将PCDL与异氰酸酯合成预聚体后再添加的不同工艺,制备了聚碳酸酯型聚氨酯微孔泡沫,并分别与普通聚氨酯微孔泡沫进行了对比.结果表明,聚碳酸酯型聚氨酯微孔泡沫的力学性能比普通聚氨酯微孔泡沫有所提高;PCDL预聚体制备的聚氨酯微孔泡沫材料耐热老化性能最佳.     

PC／TPU共混物的流变性能

用毛细管流变仪研究了聚碳酸酯（ＰＣ）及聚碳酸酯／热塑性聚氨酯弹性体（ＰＣ／ＴＰＵ）共混物的流变性能。实验结果表明：ＰＣ熔体粘度对剪切速率（γ）不敏感，而对温度（Ｔ）敏感。温度升高，ＰＣ粘度降低。加入ＴＰＵ大大改善了共混物的流动性能，使共混物的成型加工变得容易进行。当ＴＰＵ含量为４０份时，共混物的熔体粘度出现一极小值。加入不同第三组分对于降低共混物的熔体粘度效果不同，第三组分Ｅ对共混物有增粘作用     

生产聚碳酸酯树脂的"清洁"工艺

日本三菱工程塑料公司已开发出一种更符合环保要求的聚碳酸酯 (ＰＣ)树脂生产新工艺 ,并计划于明年建成生产能力为 2 0ｋｔ/ａ的装置。该公司称新工艺避免了传统工艺在双酚Ａ和光气聚合中作为溶剂使用氯代甲烷。新方法在大约 2 0 0℃和 2～ 5ｋＰａ压力下通过酯交换聚合 ,用熔融的碳酸二苯酯和双酚Ａ合成ＰＣ树脂。三菱公司称新工厂的投资大约为 42 0 0万美元。生产聚碳酸酯树脂的“清洁”工艺@郑元昌     

聚碳酸酯／聚丙烯共混物的结构与性能

在过氧化二异丙苯的引发下，用反应挤出的方法制备了聚丙烯接枝甲基丙烯酸环氧丙酯。用双螺杆挤出机制务了不同组成的聚碳酸酯／聚丙烯及ＰＣ／ＰＰ－ｇ－ＧＭＡ／ＰＰ的共混物。用电子显微镜观察了不同经组成的形态，与ＰＰ／ＰＣ共混体系相比，ＰＣ／ＰＰ／ＰＰ－ｇ－ＧＭＡ体系中的ＰＣ一ＰＰ中分散相尺寸明显降低，ＰＰ－ｇ－ＧＭＡ加入改变聚丙烯在共混物中的晶体结构及提高了聚丙烯的结晶温度，同时ＰＰ－ｇ－ＧＭＡ的加入对共     

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.