两种活性炭平炉的有效能(火用)分析

本文对活性炭平炉进行了有效能分析,发现普通平炉能耗主要是烟气带走了大量有效能,占总输入有效能51.3％,而SL—SY型平炉只占9.0％,后者因此所节省的炭,以得率20.0％（干基）计,相当于比前者多生产51.5％的活性炭。     

活性炭吸附汽油蒸气动力学性能测定

在蒸发油气吸附回收处理技术中，将活性炭作为首选吸附剂，重点考察研究其吸附汽油蒸气动力学性能。试验结果表明，活性炭的饱和吸附率随吸附操作温度增大而降低，新鲜活性炭在20℃时的饱和吸附率高达34％，30℃时为30％，活性炭吸附存在劣化度，再生难彻底，影响其使用寿命，活性炭吸附油气速度较快，不同活性炭的吸附饱和时间略有差别，一般在40min内已经达到或基本接近饱和，活性炭吸附塔压降很小，总平均为0．142Pa/cm。     

厌氧流化床处理含酚废水的发酵效能

采用厌氧活性炭流化床反应器处理中等浓度含酚有机废水，经过３８４天连续运行，在稳定状态下，投入的有机基质（酚和乙酸钠）被彻底降解，有９２％以上转化为甲烷，仅有４％左右同化为生物体，有机物去除率达到９４％以上，结果表明，这是一种发酵效能高，处理效果好的有机废水处理方法。     

中孔活性炭吸附等温式

在 BET吸附理论和杨氏气体吸附理论的基础上 ,应用内插法拟合 ,找到了与实验曲线相吻合的中孔活性炭吸附等温式 ,并对其机理进行探讨     

苯酚在干污泥上的吸附性能研究

采取实验方法，以城市污水处理厂剩余污泥为原料制取干污泥作为吸附剂，研究了其在不同温度下对苯酚的吸附行为。结果表明，干污泥对苯酚的吸附在30℃温度下吸附速率最快，吸附过程遵循二级吸附动力学模型，并且Lagergren一级速率方程也可以较好地描述干污泥对苯酚的吸附；25℃时，干污泥对苯酚的吸附行为用Langmuir模型描述时相关性最好，其方程式为G=909．091×0．0031Ce／（1＋0．0031Ce），其最大吸附量为909．091mg·g^-1，k=0．0031。     

白皮松不定芽增殖和生长研究

研究了基本培养基、激素、活性炭和GA3在白皮松不定芽增殖和生长培养过程中的作用。结果表明,采用MS培养基白皮松不定芽的增殖系数均超过5。培养基中加入0.05mg/L分裂素时不定芽的增殖系数最高达到6.7。培养基中添加活性炭对不定芽增殖的影响不大,但对不定芽的生长,特别是不定芽的伸长具有明显效果,在3g/L活性炭的培养基中,高度大于2cm的嫩梢达到42.3%,大于4cm的嫩梢达到28.4%。在基本培养基中添加GA3有助于白皮松不定芽的伸长,但GA3质量浓度过高又会抑制其伸长。     

苯酚废水处理的试验研究

通过试验对比了活性炭吸附法、电解法、活性炭填充电极电解法处理苯酚废水的效果,探讨了其反应机理。在对影响处理苯酚废水去除率的各种要素如反应时间、电流密度、原水浓度、pH值等进行条件试验后,得出了去除苯酚静态试验的最佳条件。对活性炭填充电极电解法处理苯酚废水而言,电流密度、原水浓度、pH值的影响不大,最佳反应时间为60 m in,最佳NaC l投加量为0.2%。     

降低"雪青"梨的外植体褐化研究

以"雪青"梨为材料,以第6代茎尖愈伤组织为外植体,采用L9(34)正交设计,研究不同因素对降低外植体褐化的作用.3因素设为基本培养基(A)、培养基中巯基乙醇(B)和活性炭(C)浓度;每因素设3个水平,A分别为1/4MS,MS和1/2 MS无机盐浓度,B分别为0.5,0.1和0g/L,C分别为2.5,5和0g/L.外植体接种在不同的MS基本培养基中(均含2,4-D 2 mg/L,6-BA 0.1 mg/L,琼脂8g/L,蔗糖30g/L,pH=5.8),于25±1℃,2 000k光照培养,30d后统计褐化率.试验结果表明降低外植体褐化的最优水平组合为A1B1C2,B,C对试验结果的影响达显著水平(P＜0.05),不同水平间差异显著(P＜0.05).以1/4 MS为基本培养基,并于1/4MS+MC 0.5g/L+AC 5g/L培养基中光照培养,褐化率可降至5%.     

Cyclosporine A inhibits intima proliferation of rat abdominal aortas injured by balloon

AIM: To observe the effect of cyclosporine A on intima hyperplasia of rat abdominal aortas injured by balloon.METHODS: Thirty-six healthy adult male SD rats were randomly divided into 3 groups: sham group (n=12), balloon-injured group (n=12) and cyclosporine A treatment group (n=12).From the 3rd day before injury to the 30th day after injury, the rats in cyclosporine A treatment group were treated with cyclosporine A at a dose of 12.5 mg/kg everyday, while the rats in sham group and balloon-injured group were fed with the same volume of water.On the 30th day after injury, the specimens were obtained from the rats.HE staining and immunohistochemistry were used to measure the expression level of calcineurin (CaN) in arterial wall.Pathological changes of the arterial wall were observed under light microscope.The expression of CaN and nuclear factor 3 of activated T-cells(NFATc3) in the abdominal aortas was detected by the technique of real-time PCR.RESULTS: Intimal hyperplasia was observed in balloon-injured rats.The neointima was not uniform in thickness on the 30th day.The thickness of the intimal layers and the ratio of the intimal to the medial layers in cyclosporine A group were obviously lower than those in balloon group(P<0.05).Immunohistochemistry revealed that calcineurin expression increased after balloon injury, but the expression of calcineurin in cyclosporine A group was obviously decreased as compared with balloon group (P<0.05).The results of real-time PCR showed that the mRNA expression of calcineurin and NFATc3 in cyclosporine A group was significantly lower than that in balloon-injured group (P<0.05).CONCLUSION: Cyclosporine A attenuates restenosis by suppressing the CaN-NFATc signaling pathway.     

Proliferative effect of PDGF and anti-proliferative activity of AMPK on vascular smooth muscle cells

AIM: To investigate the proliferative effect of platelet-derived growth factor (PDGF) and anti-proliferative activity of AMP-activated protein kinase (AMPK) on vascular smooth muscle cells (VSMCs). METHODS: The proliferation of VSMCs cultured with PDGF and activation of AMPK were observed. VSMCs were divided in 4 groups: control group; PDGF group; 5-aminoimidazole-4 -carboxamide-1-β-D-riboside (AICAR) group and AICAR+PDGF group. The time course of AMPK activation was determined. The protein level of mTOR was also measured. RESULTS: Compared with control group, the proliferative rate in PDGF group was significantly increased. The growth of VSMCs was inhibited in a time-dependent manner and the activity of p-mTOR was significantly decreased in AICAR group. Compared with control group, the expression of p-AMPK in PDGF group was significantly decreased, and that in AICAR group and AICAR+PDGF group was significantly increased. The expression of p-AMPK in AICAR+PDGF group was higher than that in PDGF group. The activity of p-mTOR in PDGF group was significantly higher than that in control group, while that of AICAR group and AICAR+PDGF group was significantly decreased. The expression of p-mTOR in AICAR+PDGF group was lower than that in PDGF group. CONCLUSION: Stimulation of VSMCs with PDGF promotes the cell proliferation, which can be inhibited by AICAR. The proliferation of VSMCs activated by AMPK is probably correlated with the down-regulation of mTOR expression.