由铁鳞制备纳米氧化铁可见光光催化剂

以铁鳞为原料,采用水热法成功制备不同形貌的纳米Fe2 O3光催化剂。探讨了不同浓度的盐酸、液固比及反应时间对铁鳞浸出规律的影响。系统研究了铁鳞浸出液的纯度对于水热法制备纳米Fe2 O3的微观形貌和光催化性能的影响。结果表明：8 g铁鳞与150 mL浓度为3 mol·L-1的盐酸溶液在100℃回流反应2 h,铁鳞的浸出率达到约93%且浸出液纯度较高。浸出液中的杂质离子改变了纳米Fe2 O3的微观形貌和晶体的择优生长方向。另外,以铁鳞为原料制备出的纳米Fe2 O3可见光光催化性能较好,光降解罗丹明B溶液60 min后,其降解率可达87%左右。     

Design of optimum solid oxide membrane electrolysis cells for metals production

Oxide to metal conversion is one of the most energy-intensive steps in the value chain for metals production. Solid oxide membrane (SOM) electrolysis process provides a general route for directly reducing various metal oxides to their respective metals, alloys, or intermetallics. Because of its lower energy use and ability to use inert anode resulting in zero carbon emission, SOM electrolysis process emerges as a promising technology that can replace the state-of-the-art metals production processes. In this paper, a careful study of the SOM electrolysis process using equivalent DC circuit modeling is performed and correlated to the experimental results. A discussion on relative importance of each resistive element in the circuit and on possible ways of lowering the rate-limiting resistive elements provides a generic guideline for designing optimum SOM electrolysis cells.     

氧化钨纳米棒的制备及其形貌控制

报道了一种利用溶胶-凝胶法和水热法相结合制备纳米氧化钨的新方法.首先在丙醇-四丁基溴化铵-环己烷体系中,由钨酸钠和盐酸反应出发制备凝胶状的钨酸,然后将其置于高压反应釜中200℃下处理12 h即可制得氧化钨纳米棒.使用X-射线衍射分析仪(XRD)和扫描电子显微镜(SEM)对产物的结构与形貌进行表征.     

过硫酸盐溶液吸收烟气中NO的动力学研究

在鼓泡吸收反应器中,以过硫酸盐溶液为氧化剂吸收脱除烟气中NO,以双膜理论为基础,研究了吸收过程中的传质动力学。对NO的氧化吸收过程进行了分析,建立了气液传质模型,测定了动力学参数：比相界面(a)和气相传质系数(K_G)。结果显示：温度为75 _oC,过硫酸盐溶液浓度在0.05-0.2M范围内,NO浓度≤1 000 ppm,NO的反应级数为0.5,过硫酸钠的反应级数为1,并确定了过硫酸盐溶液吸收NO总的传质速率方程。     

掺杂预合成添加剂对氧化锌压敏电阻性能影响

为了提高氧化锌(ZnO)压敏电阻的电学性能,采用常规烧结并在ZnO压敏电阻中掺杂预先合成的BiSbO₄和Zn₂SiO₄,研究不同掺杂比例对ZnO压敏电阻的微观结构、电学性能、通流能力的影响.结果表明:ZnO压敏电阻在掺杂BiSbO₄和Zn₂SiO₄后,能够有效抑制ZnO晶粒变大,晶体结构变得致密均匀,致密性有所提高,有效提高压敏特性和通流能力.BiSbO₄和Zn₂SiO₄掺杂比例为3∶1的样品综合性能比较优异,样品的致密度为5.58 g·cm^-3,压敏电位梯度达到425 V·mm^-1,非线性系数为70,漏电流为1.2×10^-7 A·cm^-2,能量耐受能力达到334.21 J·cm^-3,残压比为2.5.     

Endothelium-derived nitric oxide and vascular physiology and pathology

In 1980, Furchgott and Zawadzki demonstrated that the relaxation of vascular smooth muscle cells in response to acetylcholine is dependent on the anatomical integrity of the endothelium. Endothelium-derived relaxing factor was identified 7 years later as the free radical gas nitric oxide (NO). In endothelium, the amino acid L-arginine is converted to L-citrulline and NO by one of the three NO synthases, the endothelial isoform (eNOS). Shear stress and cell proliferation appear to be, quantitatively, the two major regulatory factors of eNOS gene expression. However, eNOS seems to be mainly regulated by modulation of its activity. Stimulation of specific receptors to various agonists (e.g., bradykinin, serotonin, adenosine, ADP/ATP, histamine, thrombin) increases eNOS enzymatic activity at least in part through an increase in intracellular free Ca²⁺. However, the mechanical stimulus shear stress appears again to be the major stimulus of eNOS activity, although the precise mechanisms activating the enzyme remain to be elucidated. Phosphorylation and subcellular translocation (from plasmalemmal caveolae to the cytoskeleton or cytosol) are probably involved in these regulations. Although eNOS plays a major vasodilatory role in the control of vasomotion, it has not so far been demonstrated that a defect in endothelial NO production could be responsible for high blood pressure in humans. In contrast, a defect in endothelium-dependent vasodilation is known to be promoted by several risk factors (e.g., smoking, diabetes, hypercholesterolemia) and is also the consequence of atheroma (fatty streak infiltration of the neointima). Several mechanisms probably contribute to this decrease in NO bioavailability. Finally, a defect in NO generation contributes to the pathophysiology of pulmonary hypertension. Elucidation of the mechanisms of eNOS enzyme activity and NO bioavailability will contribute to our understanding the physiology of vasomotion and the pathophysiology of endothelial dysfunction, and could provide insights for new therapies, particularly in hypertension and atherosclerosis.     

Inhaled and exhaled nitric oxide

Inhaled nitric oxide (NO) is used to treat various cardiopulmonary disorders associated with pulmonary hypertension. The rationale is based on the fact that NO, given by inhalation, only dilates those pulmonary vessels that perfuse well-ventilated lung units. As a result, pulmonary gas exchange is improved while pulmonary vascular resistance is reduced and pulmonary blood flow is increased. Inhaled NO has been succesfully applied to treat persistent pulmonary hypertension of the newborn, reducing the need for extracorporeal life support. Although pulmonary hypertension and altered vasoreactivity contribute to profound hypoxaemia in adult and paediatric acute respiratory distress syndrome (ARDS), the benefit of inhaled NO still remains to be established in patients with ARDS. ARDS is a complex response of the lung to direct or indirect insults, leading to pulmonary vasoconstriction and various inflammatory responses. Recent randomized trials suggest that inhaled NO only causes a transient improvement in oxygenation. Whether this effect is important in the long-term management of ARDS remains to be established. NO, measured in the exhaled breath, is an elegant and non-invasive means to monitor inflammation of the upper and lower respiratory tract. In the normal upper airways, the bulk of exhaled NO originates from the paranasal sinuses. Exhaled NO is increased in nasal allergy and decreased in cystic fibrosis, nasal polyposis and chronic sinusitis. That NO production is increased in asthmatic airways is also well established. However, several questions still need to be addressed, in particular evaluation of the sensitivity and specificity of the measurement techniques, and assessment of the bronchodilator action of endogenous NO.     

氧化异烟酸铜 (Ⅱ )配合物的晶体结构分析(英文)

在二水氧化异烟酸铜配合物中，铜原子分别与异烟酸中的两个氧原子和两个水分子中的氧原子按反式结构形成四配位体，配位几何构形是平面正方形结构， Cu－ O键长位于 1. 942(3)和 1. 945(2)之间.     

Nitric oxide biosynthesis, nitric oxide synthase inhibitors and arginase competition for L-arginine utilization

Nitric oxide (NO) is a recently discovered mediator produced by mammalian cells. It plays a key role in neurotransmission, control of blood pressure, and cellular defense mechanisms. Nitric oxide synthases (NOSs) catalyze the oxidation of L-arginine to NO and L-citrulline. NOSs are unique enzymes in that they possess on the same polypeptidic chain a reductase domain and an oxygenase domain closely related to cytochrome P450s. NO and superoxide formation as well as NOS stability are finely regulated by Ca²⁺/calmodulin interactions, by the cofactor tetrahydrobiopterin, and by substrate availability. Strong interactions between the L-arginine-metabolizing enzymes are clearly demonstrated by competition between NOSs and arginases for L-arginine utilization, and by potent inhibition of arginase activity by N^ω-hydroxy-L-arginine, an intermediate in the L-arginine to NO pathway.