木质纤维素类生物质酸水解研究进展

木质纤维素中纤维素和半纤维素经酸水解可转化为糖,糖进一步可生产燃料乙醇和其他化工产品。因此,木质纤维素酸水解制备糖是纤维素转化过程中关键步骤。本文综述了硫酸、盐酸、硝酸、磷酸、马来酸等无机、有机酸水解木质纤维素类生物质研究进展,对各种酸水解工艺的优缺点进行了分析和比较,指出了木质纤维素类生物质酸水解的研究方向。     

用基因组测绘研究能源植物

研究者们正在寻找柳枝稷以外的能源植物来生产纤维素乙醇。在过去的一年里，美国南达科他州大学（SDSU）的研究者共获得了300万美元的资助，用于研究该州出产的草原索草（prairie cordgrass），这种植物的产出效率可达到柳枝稷的两倍。     

纳米Al_2O_3对变压器绝缘纸纤维素热稳定性的影响及其机理分析

为提升电力变压器绝缘纸的热稳定性,使用纳米Al2O3对绝缘纸进行改性,通过分子模拟和试验的方法研究了纳米Al2O3对绝缘纸纤维素热稳定性的提升效果,并分析了纳米Al2O3对绝缘纸纤维素的改性机理.首先,对纳米Al2O3与纤维素的表面相互作用机理的分析表明纳米Al2O3易于掺杂到纤维素绝缘纸中,得到了Al2O3与纤维素表面相互作用结合能的公式,揭示了公式中相关参数的物理意义.然后,使用半径为5?的纳米Al2O3对纤维素进行改性,通过分子模拟技术研究了经纳米改性后的纤维素的微观参数的变化规律;同时,对改性绝缘纸和未改性绝缘纸进行了宏观热老化试验.模拟与试验结果对比分析表明,经纳米Al2O3改性的绝缘纸纤维素热稳定性有较好的提升.最后,对纳米Al2O3改性绝缘纸纤维素的机理进行了较为深入地分析,为纳米改性变压器绝缘纸性能方面的研究提供了理论支撑.     

纤维素分解混合菌群的筛选及其腐解稻草的研究Ⅰ纤维素分解混合菌群的筛选

为了得到强分解纤维素的复合微生物来配合秸秆还田,从不同生态环境的土壤中用选择性培养基进行了纤维素分解混合菌群的富集,得到了纤维素酶活性较高的混合菌群,该菌群以兼性厌气性细菌为主,能够在较短的时间内溶解滤纸。该菌群利用CMC-Na的能力比滤纸好。以稻草粉为底物时产酶的最佳尿素用量为0．1％,生长曲线表明该菌群在96h开始进入稳定生长期,筛选到了一个能够较好地腐解稻草的混合菌群。     

乙醇水蒸气重整催化剂的研究进展

燃料电池技术是未来首选的洁净、高效能源技术。本文对燃料电池制氢技术之一的乙醇水蒸气重整反应的研究进行了综述。简要介绍了乙醇水蒸气重整的反应机理；重点系统的论述了国内外对乙醇水蒸气重整制氢催化剂的研究进展。并展望了乙醇制氢燃料电池的发展前景。     

纤维素类生物质热解研究进展

从热解的机理、工艺、反应器等方面综述了国内外对纤维素类生物质热解研究的现状,讨论了生物质热解产物的组成及其理化特性,重点介绍了热解制备生物油技术。生物油既可以作为燃料油直接燃烧又可以进一步通过加氢或者裂解制备其它精细化学品,还可以从中提取有用的化学原材料。因此,纤维素类生物质热解制取生物油技术被看作是最有发展前景的生物质利用技术。     

纳米纤维素复合物新材料研究进展

本文介绍了一种新型的纳米复合材料,给出了绿色复合物的定义和分类,分析了纳米纤维素的特性和制备方法及其优缺点,综述了国外近年来纳米纤维素与不同生物高聚物复合的研究情况。与单纯的高聚物基体材料或者常规的微观和宏观的复合物相比,这类材料展示出了显著的性能改进,最大的特点是完全基于可再生的生物质制成,完全降解,并具相当的力学性能,是真正的绿色复合物。     

纤维素分解混合菌群的筛选及腐解稻草研究Ⅱ纤维素分解混合菌群对稻草的腐解

对富集筛选的纤维素分解混合菌群进行了稻草腐解试验,结果表明：施用该纤维素分解混合菌群后能够减少氨态氮素的挥发,纤维素分解混合菌群在15d内对稻草的腐解效果明显,外观分散度明显比对照要好,对照的失重率为45．80％,而处理的失重率为57．85％,比对照提高了12．05个百分点。Duncan新复极差法分析表明,失重率在1％水平差异极显著,而还原糖量、纤维素酶活以及pH值的差异均不显著,说明还原糖量、纤维素酶活以及pH值不能作为判断稻草腐解程度的指标。得到了一个稻草腐解效果较好的混合菌群,能够在外界菌群存在的条件下较好腐解稻草。     

新型微生物有望降低生物乙醇成本

美国马萨诸塞大学的微生物学家Susan B．Leschine发现了一种新型微生物，可能将会给生物乙醇的生产带来变革。     

聚乳酸及其复合材料在生物医药中的应用研究

本文综述了聚乳酸作为药物缓控释载体材料、组织工程支架材料和医用敷料的研究进展;介绍了聚乳酸．聚乙醇酸、聚乳酸,磷酸钙等复合材料在生物医药中的应用。     

Ethanol from cellulose

Summary An excess of organic waste, containing up to 60% cellulose and hemicellulose is produced worldwide. The conversion of this cellulosic material to ethanol is discussed: The two-step process consisting of a hydrolysis step to glucose and the subsequent fermentation by yeasts; and the one-step process, a fermentation of the cellulose by the anaerobic thermophileClostridium thermocellum, or by a thermophilic, anaerobic, defined mixed culture. The use of the latter seems to be very feasible., To achieve an economic process, it is suggested to combine this approach with a thermophilic fermentation of the effluent and/or stillage obtained to produce methane.Acknowledgment. Part of this work was supported by Energy and Research Development Administration contract number EY-76-509-0888-M003, and by the Deutsche Forschungsgemeinschaft.     

Chronic gestational exposure to ethanol impairs insulin-stimulated survival and mitochondrial function in cerebellar neurons

Chronic gestational exposure to ethanol has profound adverse effects on brain development. In this regard, studies using in vitro models of ethanol exposure demonstrated impaired insulin signaling mechanisms associated with increased apoptosis and reduced mitochondrial function in neuronal cells. To determine the relevance of these findings to fetal alcohol syndrome, we examined mechanisms of insulin-stimulated neuronal survival and mitochondrial function using a rat model of chronic gestational exposure to ethanol. In ethanol-exposed pups, the cerebellar hemispheres were hypoplastic and exhibited increased apoptosis. Isolated cerebellar neurons were cultured to selectively evaluate insulin responsiveness. Gestational exposure to ethanol inhibited insulin-stimulated neuronal viability, mitochondrial function, Calcein AM retention (membrane integrity), and GAPDH expression, and increased dihydrorosamine fluorescence (oxidative stress) and pro-apoptosis gene expression (p53, Fas-receptor, and Fas-ligand). In addition, neuronal cultures generated from ethanol-exposed pups had reduced levels of insulin-stimulated Akt, GSK-3β, and BAD phosphorylation, and increased levels of non-phosphorylated (activated) GSK-3β and BAD protein expression. The aggregate results suggest that insulin-stimulated central nervous system neuronal survival mechanisms are significantly impaired by chronic gestational exposure to ethanol, and that the abnormalities in insulin signaling mechanisms persist in the early postnatal period, which is critical for brain development. Received 21 January 2002; received after revision 28 February 2002; accepted 25 March 2002     

Ethanol impairs Rho GTPase signaling and differentiation of cerebellar granule neurons in a rodent model of fetal alcohol syndrome

Developmental exposure to ethanol impairs fetal brain development and causes fetal alcohol syndrome. Although the cerebellum is one of the most alcohol-sensitive brain areas, signaling mechanisms underlying the deleterious effects of ethanol on developing cerebellar granule neurons (CGNs) are largely unknown. Here we describe the effects of in vivo ethanol exposure on neurite formation in CGNs and on the activation of Rho GTPases (RhoA and Rac1), regulators of neurite formation. Exposure of 7-day-old rat pups to ethanol for 3 h moderately increased blood alcohol concentration (BAC) (∼40 mM) and inhibited neurite formation and Rac1 activation in CGNs. Longer exposure to ethanol for 5 h resulted in higher BAC (∼80 mM), induced apoptosis, inhibited Rac1, and activated RhoA. Studies demonstrated a regulatory role of Rho GTPases in differentiation of cerebellar neurons, and indicated that ethanol-associated impairment of Rho GTPase signaling might contribute to brain defects observed in fetal alcohol syndrome. Received 16 July 2006; received after revision 12 September 2006; accepted 13 October 2006     

Selected mouse lines,alcohol and behavior

Summary The technique of selective breeding has been employed to develop a number of mouse lines differing in genetic sensitivity to specific effects of ethanol. Genetic animal models for sensitivity to the hypnotic, thermoregulatory, excitatory, and dependence-producing effects of alcohol have been developed. These genetic animal models have been utilized in numerous studies to assess the bases for those genetic differences, and to determine the specific neurochemical and neurophysiological bases for ethanol's actions. Work with these lines has challenged some long-held beliefs about ethanol's mechanisms of action. For example, lines genetically sensitive to one effect of ethanol are not necessarily sensitive to others, which demonstrates that no single set of genes modulates all ethanol effects. LS mice, selected for sensitivity to ethanol anesthesia, are not similarly sensitive to all anesthetic drugs, which demonstrates that all such drugs cannot have a common mechanism of action. On the other hand, WSP mice, genetically susceptible to the development of severe ethanol withdrawal, show a similar predisposition to diazepam and phenobarbital withdrawal, which suggests that there may be a common set of genes underlying drug dependentcies. Studies with these models have also revealed important new directions for future mechanism-oriented research. Several studies implicate brain gamma-aminobutyric acid and dopamine systems as potentially important mediators of susceptibility to alcohol intoxication. The stability of the genetic animal models across laboratories and generations will continue to increase their power as analytic tools.     

Selected mouse lines, alcohol and behavior

The technique of selective breeding has been employed to develop a number of mouse lines differing in genetic sensitivity to specific effects of ethanol. Genetic animal models for sensitivity to the hypnotic, thermoregulatory, excitatory, and dependence-producing effects of alcohol have been developed. These genetic animal models have been utilized in numerous studies to assess the bases for those genetic differences, and to determine the specific neurochemical and neurophysiological bases for ethanol's actions. Work with these lines has challenged some long-held beliefs about ethanol's mechanisms of action. For example, lines genetically sensitive to one effect of ethanol are not necessarily sensitive to others, which demonstrates that no single set of genes modulates all ethanol effects. LS mice, selected for sensitivity to ethanol anesthesia, are not similarly sensitive to all anesthetic drugs, which demonstrates that all such drugs cannot have a common mechanism of action. On the other hand, WSP mice, genetically susceptible to the development of severe ethanol withdrawal, show a similar predisposition to diazepam and phenobarbital withdrawal, which suggests that there may be a common set of genes underlying drug dependencies. Studies with these models have also revealed important new directions for future mechanism-oriented research. Several studies implicate brain gamma-aminobutyric acid and dopamine systems as potentially important mediators of susceptibility to alcohol intoxication. The stability of the genetic animal models across laboratories and generations will continue to increase their power as analytic tools.     

Efficacy of ethanol as a discriminative stimulus in ethanol-preferring and ethanol-nonpreferring rats

Rats which exhibited a preference for drinking a 6% w/v solution of ethanol in a free choice situation did not differ in their sensitivity to ethanol from animals exhibiting an aversion for ethanol, as measured by leaning rates in a T-maze task in which ethanol served as a discriminative stimulus.     

Efficacy of ethanol as a discriminative stimulus in ethanol-preferring and ethanol-nonpreferring rats

Summary Rats which exhibited a preference for drinking a 6% w/v solution of ethanol in a free choice situation did not differ in their sensitivity to ethanol from animals exhibiting an aversion for ethanol, as measured by learning rates in a T-maze task in which ethanol served as a discriminative stimulus.The author is thankful to Miss Christine Currey for technical assistance.