过程强化的若干新进展

本文从现代过程工业发展的需求出发，介绍了过程强化的历史和现状，分析了近年来过程强化的特点。本文还结合实例对化工过程强化的作用和存在的问题等进行了讨论。     

姬松茸高产栽培模式研究

为充分利用当地丰富的秸秆和牛粪资源，及早在北方地区开发生产姬松茸这一珍稀品种。从姬松茸的选育、栽培模式比较试验结果可看出，合理控制温湿度，改进覆土方式，加强病虫害预防是保证高产的有效措施。     

热连轧精轧机组温度模型的改进

从实际生产数据入手,研究了温度模型设定精度的现状及设定精度与各影响因素之间的关系,同时还消化了原来的温度模型程序并将其移植到微机上.经大量的离线统计回归分析,提出了一个行之有效的温度模型改进方案.该改进方案的思路同样适合其他热轧生产线.     

辨析企业人才的"留"与"流"

论述了辨证认识与处理好人才的“留”与“流”的关系，指出了只有做好人才管理工作，慎重地考虑人才的留用，才能使企业长期、持续、健康、稳定地发展。     

微波辐射合成7-羟基-4-甲基香豆素

以浓硫酸为催化剂，采用微波辐射技术，由间苯二酚与乙酰乙酸乙酯缩合制备7－羟基－4－4甲基香豆素。结果表明，微波辐射合成7－羟基－4－4甲基香豆素的最以应条件为：间苯二酚5.5g，乙酰乙酸乙酯6.8ml，浓硫酸1.5ml，微波功率240W，微波辐射时间6min，产率84．1％，不采用微波辐射，反应时间大于10h，产率78％，红外光谱分析表明，7－羟基－4－4甲基香豆素的特征峰与7－羟基－4－甲基香豆素的各官能团的吸收峰吻合，测定7－羟基－4－甲基香豆素的熔点为189－192℃。     

用GC/MS、GC分析中药前胡中白花前胡丙素、丁素和紫花前胡苷元

为快速鉴别中药白花前胡（Peucedanum praeruptorum Dunn.）和紫花前胡（Peucedanum decursinum Maxim.），用气相色谱/质谱（GC/MS），气相色谱法（GC）分别定性，定量分析白花前胡丙素（Pd-1a），丁素（Pd-Ⅱ）和紫花前胡苷元（Nodakenetin），在白花前胡中检出白花前胡丙素（M/Z 386）和丁素（M/Z 426)，但未检出紫花前胡苷元，在紫花前胡中检出紫花前胡苷元（M/Z 246），但未检出白花前胡丙素和丁素，线性关系：YPd-1a=1.111XPd-1a 0.021(n=6 r=0.9995)，线性范围：0.175～1.919μg，YPd-Ⅱ=1.189XPd-Ⅱ-0.013(n=6 r=0.9996),线性范围：0.086～0.950μg。YNodakenetin=0.901XNodkenetin-0.024（n=6 r=0.9999），线性范围：0.089～1.062μg，回收率：白花前胡丙素97.29%，白花前胡丁素98.81%，紫花前胡苷元96.34%，分析结果表明，不同产地药材样品中各自特征成分含量不同，分析中未能找到白花前胡和紫花前胡苷元共有的相同的有效成分或指标性成分。表明可用GC/MS区分白花前胡和紫花前胡苷元，但未能用统一的化学对照品进行质量控制。     

强直电流伸展弧CVD硬质合金金刚石涂层工具

采用自行研制的强电流直流扩展电弧设备对酸浸和渗硼预处理的YG6刀片进行了金刚石薄膜涂层沉积，并对放于不同位置的沉积刀片表面涂层的激光Raman谱和SEM形貌进行了分析、研究。结果表明：渗硼预处理工艺优于酸浸预处理工艺；在渗硼处理的GY6刀片上，沉积的金刚石薄膜涂层具有大面积、均匀性好和质量高的特点。     

Timed bromocriptine administration reduces body fat stores in obese subjects and hyperglycemia in type II diabetics.

Obese postmenopausal female volunteers were given timed daily oral dosages of bromocriptine, and tested for reduction of body fat stores. This dopamine agonist has been shown to reset circadian rhythms that are altered in obese animals and to reduce body fat levels in several animal models. The participants were instructed not to alter their existing exercise and eating behavior during treatment. Skinfold measurements were taken on 33 subjects as indices of body fat. The measurements (e.g., suprailiac) were reduced after six weeks by about 25%, which represents a reduction of 11.7% of the total body fat. These dramatic decreases in body fat, which are equivalent to that produced by severe caloric restriction, were accompanied by more modest reductions of body weight (2.5%), indicating a possible conservation of protein that is usually lost as a consequence of such caloric restriction. The effects of bromocriptine treatment on body fat and hyperglycemia were also examined in non-insulin dependent diabetics being treated with oral hypoglycemics (7 subjects) or insulin (7 subjects). Total body fat was reduced by 10.7% and 5.1% in diabetics on oral hypoglycemics and insulin, respectively, without any significant reductions in body weight. Hyperglycemia was reduced in most of the 15 diabetic subjects treated leading to euglycemia and even cessation of hypoglycemic drugs in 3 of the 7 subjects during 4-8 weeks of bromocriptine treatment. These findings support the hypothesis that obesity and type II diabetes may be treated effectively with bromocriptine when administered at the proper times and dosages.     

Preferential excretion of glycated albumin in C57BL-Ks-J mice: effects of diabetes.

Urinary excretion of glycated albumin was quantitated in genetically hyperglycemic mice (C57BL-Ks-J, db/db mice), a model for non-insulin-dependent diabetes mellitus, and compared with their non-diabetic littermates. The data indicated a preferential excretion of glycated albumin in non-diabetic mice. This phenomenon of 'editing' of glycated albumin is decreased significantly in diabetic mice. Quantitative measurements of overall excretion of glycated albumin suggested that the loss of editing in diabetic mice is due to the dilution of glycated albumin by the unmodified albumin which is excreted in large amounts in diabetic mice. Therefore, the loss of editing observed in this model resembled the one we characterized in insulin-dependent diabetic humans and a streptozotocin-diabetic rat model.