中国古典园林三维造型研究

论述了采用层次结构化及参数化三维造型方法，建立一个以造型函数库为核心，从而构造各类、各级园林景观构件表面模型的方法和过程。对于某些非建筑类的园林配景构件，采用了Ｆｒａｃｔａｌ方法进行造型。     

新型实用布线算法──L─M算法

本文提出新型布线算法，集李氏迷宫法与线搜索法的长处为一体，以饱和带法进行动态排序，以线搜索法确定借孔位置，然后用李氏法进行单层布线，获得最佳路径，从而达到线型好，布通率高的效果。     

Suitable fixation condition for rat liver using microwave irradiation and its application to the immunohistochemistry of glutamate dehydrogenase

In 50 patients auditory threshold and brain stem evoked potential studies were carried out before and after myelography. Due to the analysis of amplitudes and latencies of auditory brain stem measurements, significant functional disorders of the hearing organ and the auditory pathway could be demonstrated. In most of the patients these functional disorders were found to be subclinical, whereas 12 patients showed alterations extending from a subjectively slight hearing loss to an audiometrically objectified acute hearing loss depending on its intensity in each case. The reasons of these functional disorders could not be clarified. An open cochlear aqueduct through which perilymph enters the subarachnoidal space leading to a secondary endolymphatic hydrops can be considered as the cause in cases where manifest symptoms develop. The changes in brain stem audiometry can be additionally explained by changes in osmolality of the inner ear fluids which may lead to the development of an endolymphatic hydrops.     

超细Fe3O4粒子表面包覆酞菁钴性质研究

本文研究了合成载氧体的金属有机化学液相淀积法制造工艺，所得产物经ＴＥＭ、ＸＰＳ、Ｍｏｓｓ－ｂａｕｅｒ谱和Ｂ－Ｈ仪等手段，研究了它的结构和磁性能。实验表明，酞青钴以薄层形式包覆在Ｆｅ＿３Ｏ＿４的表面，封闭了Ｆｅ＿３Ｏ＿４的表面孔洞，稳定了Ｆｅ＿３Ｏ＿４的物相，增强了磁性能。     

Fastmet工艺评述

介绍了Ｆａｓｔｍｅｔ工艺及发展状况，并对工艺特点和指标进行了分析。使用冷固结含碳球团和转底炉使该工艺可直接采用粉矿和提高生产效率，但因硫含量高、铁品位低而产品质量较差。不过投资和生产成本与传统工艺比较却占有较大优势。     

~（131）Ⅰ—MIBG比活度对鼠心肌交感神经囊泡内外摄取的影响

研究了两种比活度的１３１Ⅰ－ＭＩＢＧ在正常及利血平抑制后在鼠体内的分布，结果表明：注射后４ｈ，正常鼠心肌对３．２２ＴＢｑ／ｇ的ＭＩＢＧ摄取为９．０８％ＩＤ／ｇ，明显高于对１８．５ＧＢｑ／ｇ的摄取（４．８７％ＩＤ／ｇ）。计算表明，比活度主要影响了鼠心肌交感神经囊泡内摄取，而与囊泡外摄取无关．当ＭＩＢＧ用于心肌显像时，高比活度的ＭＩＢＧ有利于诊断。     

Expression of polyglutamine-expanded Huntingtin activates the SEK1-JNK pathway and induces apoptosis in a hippocampal neuronal cell line

Huntington's disease is one of a growing number of hereditary neurodegenerative disorders caused by expansion of a polyglutamine stretch at the NH2 terminus of huntingtin. To explore whether polyglutamine-expanded huntingtin induces neuronal toxicity, I examined the expression of the full-length of huntingtin with 16, 48, or 89 polyglutamine repeats in a rat hippocampal neuronal cell (HN33). Expression of mutated huntingtin with 48 or 89 polyglutamine repeats stimulated c-Jun amino-terminal kinases (JNKs) activity and induced apoptotic cell death in HN33 cells while expression of normal huntingtin with 16 polyglutamine repeats had no toxic effect. The JNK activation precedes apoptotic cell death and co-expression of a dominant negative mutant form of stress-signaling kinase (SEK1) nearly completely blocked activation of JNKs and neuronal apoptosis mediated by mutated huntingtin. Taken together, my studies demonstrate that expression of polyglutamine-expanded huntingtin induces neuronal apoptosis via activation of the SEK1-JNK pathway.     

Trends and variations in neonatal length of in-hospital stay in Canada

The objectives of this study were to evaluate the possible mechanisms involved in prolongation of bleeding time in pre-eclamptic patients receiving a magnesium sulfate infusion to prevent convulsions. Eighteen pre-eclamptic patients near term or at term (4 cases 33 to 35 weeks; the remainder > 36 weeks) were studied. Fifteen of them received magnesium sulfate infusion; 3 did not and served as controls. Bleeding time (modified Ivy method with Surgicutt), platelet count, platelet aggregation pattern, as well as serum arachidonic acid metabolites [thromboxane B2 (TxB2) and 6-Keto-prostaglandin F1 alpha (6-Keto-PGF1 alpha)] werde done on admission to the labor floor (before magnesium infusion) and repeated at discontinuation of the infusion, 12-24 hours postpartum; the controls received the second test 24 hours postpartum. Thirteen of 15 patients receiving magnesium sulfate had an increase in bleeding time from an average of 6 minutes 31 seconds to 11 minutes 56 seconds, an 82% rise (p < 0.004). In 2 there was a decrease. Among the 3 controls the averages were 6 minutes 38 seconds and 6 minutes 3 seconds. The total magnesium given ranged from 52.5 to 145 grams. Platelet counts averaged 251,000/mm3 (range 145,000-519,000). Platelet aggregation pattern done in 11 patients and was normal and unchanged after magnesium in 10 of the patients with increased bleeding time and one control. TxB2 and 6-Keto-PGF1 alpha levels did not change significantly either after magnesium administration (688 and 135 pgm/ml, to 654 and 117) or in controls (695 and 230 pgm/ml, to 445 and 225). Likewise, the ratio of these 2 substances did not change in either group (6.3 to 6.6, and 4.2 to 2.2). There was no correlation between duration of infusion or total magnesium given and directions of small changes observed. This study confirms a prior preliminary observation that magnesium sulfate infusion, as currently used to prevent eclamptic convulsions, induces a significant prolongation of bleeding time. This effect is mediated neither by changes in platelets count or aggregation pattern, nor by changing the level or ratios of serum arachidonic acid metabolites (TxB2 and 6-Keto-PGF1 alpha). Further studies are needed to clarify the mechanism of this clinically important observation of increased bleeding following magnesium sulfate infusion.     

Chemistry of the pyrrolo[1,2-alpha]benzimidazole antitumor agents: influence of the 7-substituent on the ability to alkylate DNA and inhibit topoisomerase II

This study addresses the influence the 7-substituent on the cytotoxicity of pyrrolo[1,2-alpha]-benzimidazole quinones possessing a 6-aziridinyl group (PBIs) and a 6-acetamido group (APBIs). Reduction of a PBI to the aziridinyl hydroquinone results in both nucleophile trapping (alkylation) and 1,5-sigmatropic shift reactions. The latter process is essentially an internal redox reaction wherein the hydroquinone causes reductive opening of the aziridinyl ring. The 7-substituent controls the fate of the aziridinyl ring by means of steric and electronic effects. An electron-rich 7-substituent favors the 1,5-sigmatropic shift reaction. If the 7-substituent distorts the 6-aziridinyl group from the conformation required for the 1,5-sigmatropic shift, then nucleophile trapping occurs. The 7-methyl substituent results in significant nucleophilic trapping, and the 7-unsubstituted and 7-methoxy substituents favor the 1,5-sigmatropic reaction. Thus, the 7-methyl PBIs show the most cytotoxicity of the analogues studied. The APBIs are cytotoxic only as quinones, and reduction to the hydroquinone results in loss of activity. Consistent with this observation, the change from 7-methyl to the more electron-rich 7-methoxy results in a substantial loss of APBI cytotoxicity as well as decreased topoisomerase II inhibition. The mechanism of inhibition is thought to involve the interacalation of only electron deficient APBIs into DNA.     

Suppressive effect of corticosteroids on the gene expression of interleukin-5 and eosinophil activation in asthmatics

Although cortico steroids are effective anti-inflammatory agents in ameliorating asthma symptoms and bronchial hperreactivity, their mechanism of action is unknown. Interleukin (IL)-5 is known to play a key role in regulating eosinophil proliferation and activation. Therefore, we examined the changes of IL-5 mRNA expressions in PBMC semi-quantitatively with RT-PCR as well as serum ECP levels and MCH-PC20 values in asthmatics before and after being treated with corticosteroids. The results revealed that there were significant decrease in the level of IL-5 mRNA and serum ECP concentration after therapy (P < 0.05) and there was remarkable improvement in the values of MCH-PC20 and FEV1% (P < 0.05). It was also found that the changes of serum ECP levels or MCH-PC20 values were accompanied by a reduction in IL-5 mRNA expression (r = 0.5426 or 0.4857, P < 0.05). These results suggested that the therapeutic effects of corticosteroids in asthma may result from modulation of IL-5 gene expression with consequent inhibition of eosinophil activation.