Targeted disruption of the mouse transforming growth factor-beta 1 gene results in multifocal inflammatory disease.

Transforming growth factor-beta 1 (TGF-beta 1) is a multifunctional growth factor that has profound regulatory effects on many developmental and physiological processes. Disruption of the TGF-beta 1 gene by homologous recombination in murine embryonic stem cells enables mice to be generated that carry the disrupted allele. Animals homozygous for the mutated TGF-beta 1 allele show no gross developmental abnormalities, but about 20 days after birth they succumb to a wasting syndrome accompanied by a multifocal, mixed inflammatory cell response and tissue necrosis, leading to organ failure and death. TGF-beta 1-deficient mice may be valuable models for human immune and inflammatory disorders, including autoimmune diseases, transplant rejection and graft versus host reactions.     

Mechanism for the learning deficits in a mouse model of neurofibromatosis type 1.

Neurofibromatosis type I (NF1) is one of the most common single-gene disorders that causes learning deficits in humans. Mice carrying a heterozygous null mutation of the Nfl gene (Nfl(+/-) show important features of the learning deficits associated with NF1 (ref. 2). Although neurofibromin has several known properties and functions, including Ras GTPase-activating protein activity, adenylyl cyclase modulation and microtubule binding, it is unclear which of these are essential for learning in mice and humans. Here we show that the learning deficits of Nf1(+/-) mice can be rescued by genetic and pharmacological manipulations that decrease Ras function. We also show that the Nf1(+/-) mice have increased GABA (gamma-amino butyric acid)-mediated inhibition and specific deficits in long-term potentiation, both of which can be reversed by decreasing Ras function. Our results indicate that the learning deficits associated with NF1 may be caused by excessive Ras activity, which leads to impairments in long-term potentiation caused by increased GABA-mediated inhibition. Our findings have implications for the development of treatments for learning deficits associated with NF1.     

格值诱导空间的若干特征定理

讨论了格值诱导空间及相关的弱诱导空间和满层空间的代数特征和拓扑特征。     

一类新型双杂环衍生物的合成及其杀菌活性

三唑并嘧啶类杂环衍生物由于其分子结构中同时包含了三唑及嘧啶这两类重要的活性结构单元 ,因而往往表现出广泛的生物活性[1～ 4] ,既可以用于医药 ,也可以用于农药 .因此 ,近年来关于三唑并嘧啶类衍生物的合成及其生物活性的研究受到了人们的广泛关注 -二甲基 - 1 ,2 ,4-三唑     

山东威海卫饮用天然矿泉水生成背景与水质评价的研究

本文论述了山东威海卫饮用天然矿泉水的生成条件，对其界限指标、限量指标、污染物指标、微生物指标等进行了综合评价，确定其为重碳酸型的含锶、偏硅酸优质矿泉水．     

一个计算金属半径的近似公式

本文提出一个计算金属原子半径新的近似公式，并计算了５８种金属的原子半径，其结果与实验测定值非常接近。     

氮－烃类二元低温混合工质的工作机理分析

用ＰＲ方程计算氮－烃类二元混合物的自由焓，提出判别氨－烃类二元混合物互溶性的方法，并计算了该类混合工质的汽液平衡、液液平衡和汽液液平衡特性，为寻求新的混合工质对提供了一种有效的理论预测方法。     

炼钢─连铸─热轧直接热装一体化计划

从计划角度重点分析了钢铁生产中炼钢、连铸、热轧三者之间联接的较高模式－直接热装轧制计划系统的实现方式，并给出了较为具体的方案。     

临界等温线的推算──几个立方型状态方程的比较

对ＰＴ方程等几个立方型状态方程描述氩的临界等温线的能力作比较研究。在临界压力以下区域．ＰＴ方程、ＨＳ－ＳＲＫ方程和ＳＲＫ方程推算精度较好，ＡＡＤ＜０．４％。在临界压力以上区域，所讨论的五个方程都不能提供具有合理精度的描述。     

超氧物歧化酶对糖尿病模型大鼠血液和晶状体中自由基及其清除剂的影响

本工作发现糖尿病大鼠晶状体和血液中的ＬＰＯ、ＭＤＡ水平高于正常大鼠，而Ｔ－ＳＯＤ、Ｃｕ·Ｚｎ－ＳＯＤ水平降低（Ｐ＜Ｏ．０１）．观察用不同剂量ＳＯＤ及不同时间的治疗方案，结果大剂量比小剂量，长时间比短时间更能改善自由基和清除剂的状况，提示糖尿病患者晶状体中自由基代谢异常，这可能和糖尿病性白内障有关；表明ＳＯＤ可能是防治糖尿病性白内障的良药．