Molecular pathogenesis of apolipoprotein E-mediated amyloidosis in late-onset Alzheimer’s disease

Apolipoprotein E (apoE) ɛ4 allele is a genetic risk factor for late-onset familial and sporadic Alzheimer’s disease (AD). In the central nervous system, apoE is secreted mainly by astrocytes as a constituent of high-density lipoproteins. A recent study using apoE knockout mice provided strong evidence that apoE promotes cerebral deposition of amyloid β protein (Aβ). However, no clear explanation of the pathogenesis of apoE-induced AD has been provided. Here we discuss two possible mechanisms by which apoE might enhance Aβ deposition. One is the intracellular pathway in which apoE is internalized by neurons and induces lysosomal accumulation of Aβ and amyloidogenic APP (amyloid precursor protein) fragments, leading to neuronal death. The other is the extracellular pathway in which apoE-containing lipoproteins are trapped by Aβ1–42 deposits mobilizing soluble Aβ peptides and consequently enlarge amyloid plaques. These two mechanisms may operate at different stages of AD pathogenesis and suggest a chaperone-like function for the apoE molecule. Received 4 February 1999; received after revision 9 April 1999; accepted 23 April 1999     

Arachidonic acid release by ionomycin and phorbol ester is similar in C127 epithelial cells expressing wild-type or mutated (ΔF508) cystic fibrosis transmembrane conductance regulator

The Ca²⁺ ionophore ionomycin induced cytosolic [Ca²⁺]_i elevation as well as strong activation of Cl⁻ efflux in mouse mammary epithelial cell lines expressing wild-type or mutated (deletion of phenylalaline 508) cystic fibrosis transmembrane conductance regulator (CFTR) or vector. Ionomycin-induced Cl⁻ efflux was abolished by the intracellular Ca²⁺ chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid, whereas both activators and inhibitors of phospholipase A₂ had no effect, indicating the involvement of Ca²⁺-dependent Cl^- channels. Stimulation of arachidonic acid release by ionomycin and phorbol ester was not significantly different between wild-type or mutated cell lines, whereas vector-transfected cells exhibited a significant higher release, which was shown to be due to larger amount of immunoreactive cytosolic phospholipase A₂. These results indicate that phospholipase A₂ activity of C127 cells was not influenced by the presence of wild-type or mutated CFTR. Received 27 April 1999; received after revision 11 June 1999; accepted 23 July 1999     

制取四溴双酚A的新方法

提出了在H2O2存在下,以双酚A、溴化钠及盐酸为原料制备四溴双酚A的新方法,讨论了加料温度、H2O2用量、投料顺序及时间等工艺条件对制取四溴双酚A产率的影响. 在选定的实验条件下制取四溴双酚A的产率可达96.5%.     

Pipelined Flash A/D转换电路参量的裕度函数

推出了A/D转换量化界面的电路连续参量V_(mj)、K、ΔV_(jt)和V_(jt min)4者的上、下裕度函数,建立极限裕度的数学模型,提出在满足整体极限裕度的前提下,追求整体电路最低成本之下的稳定的难题。     

评岛尾永康的《中国化学史》

文章对于日本学者撰写的第一部《中国化学史》进行了分析评论，认为该书具有的主要特点是：（１）时代性，概括了直到１９９２年以前的最新研究成果；（２）严谨性，运用文献丰富，以求得出严密结论；（３）辩驳性，注意从不同见解的争论中进行阐述，自然得出结论；（４）社会性，注意把化学发展置于整个社会中考察，揭示深层动因；（５）比较性，注意把中国化学发展置于世界范围考察，体现中国的特点和作用；（６）形象性，运用相当丰富的图片进行叙述，具体、生动；（７）日本视野性，以日本学者特有的角度阐述中国化学发展，具有独到之处。文章还指出了该书一些需要改进和提高之处。     

论有机体代謝过程中能量供应的偶联反映和对ATP的再认识

本文着重阐述了有机体能量代谢过程中ATP—CP系统、有氧氧化和无氧酵解三大供能系统的偶联反应。并对ATP恢复的影响因素作了分析,同时介绍了作者对ATP的再认识和理解。     

Immunogenicity of recombinant fowl-pox virus co-expressing structural protein precursor P1-2A and proteinase 3C of FMDV

Two recombinant plasmids, pUTA2P1 and pUTAL3CP1, were constructed by inserting structural protein precursor P1-2A and proteinase 3C of foot-and-mouth disease virus (FMDV) into fowl-pox virus (FPV) recombinant vectors pUTA-2 and pUTA-16-LacZ respectively, and two recombinant FPVs (vUTA2P1 and vUTAL3CP1) screened by the RT-PCR, IFA assay and Western blotting assay were obtained successfully. Mice injected respectively with rFPVs were induced high level specific anti-FMDV antibodies, increasing of T subtypes, and higher cytotoxicities of splenocytes than those of control groups. These results indicated that a new method was used to construct a potential candidate vaccine of FMDV.     

关于《兄终弟继质疑》的质疑

同世界许多民族一样,历史上壮族姓氏家族观念根深蒂固,壮族社会中长期流行“兄终弟继”或称为“夫兄弟婚”的传统婚俗。侬全福与侬夏卿是侬氏家族中的远房兄弟,侬全福被交趾王杀害后,其妻阿侬投奔于侬夏卿处,并与侬夏卿结为夫妻,其后,共同支持侬智高反抗交趾和北宋王朝。这应是不争的历史事实。     

Enzymes and receptors in the leukotriene cascade

Leukotrienes are a family of paracrine hormones derived from the oxidative metabolism of arachidonic acid. These lipid mediators are recognized as important signal molecules in a variety of inflammatory and allergic conditions affecting the skin, joints, gastrointestinal and respiratory systems, in particular asthma. Such conditions are typified by local pain, tissue edema, hyperemia and functional losses. In the tissues, immunocompetent cells accumulate at the site of injury which contribute to tissue damage and perpetuation of the disease process. Leukotrienes can elicit most, if not all, of these signs and symptoms. Thus, leukotriene B₄ is one of the most powerful chemotactic agents known to date and participates in the recruitment of leukocytes. The cysteinyl leukotrienes, on the other hand, contract smooth muscles, particularly in the peripheral airways and microcirculation. Recently, drugs which block the formation and action of leukotrienes have been introduced as novel antiasthmatic medications. This chapter reviews the biochemistry, molecular biology and cell biology of the key enzymes and cognate receptors in the leukotriene cascade.     

Effects of calcineurin on LTP of rats <Emphasis Type="Italic">in vivo</Emphasis>

Calcineurin (CN) is thought to play a role in the synaptic plastivity and long-term potentiation (LTP) in the hippocampus. Based on two LTP models in vivo, a specific inhibitor cyclosporin A (CsA) of CN was observed, which affected LTP in the hippocampal dentate gyrus of the rats. The results indicated that CsA blocked LTP induced by high frequency stimulation (HFS) partly, but it had no effect on the decrease of the onset and peak latency of population spikes (PS) except that it reduced the increase of the amplitude after HFS. On the other hand, CsA blocked LTP induced by ginsenosides (GSS) completely. It suppressed the GSS-enhanced amplitude of PS reversibly and blocked the decrease of the peak latency of PS induced by the GSS. These results suggest that the postsynaptic CN plays a role in the induction of LTP in the hippocampus of the rats.