Alexander disease: putative mechanisms of an astrocytic encephalopathy

Alexander disease (AXD) is the first primary astrocytic disorder. This encephalopathy is caused by dominant mutations in the glial fibrillary acidic protein (GFAP) gene, encoding the main intermediate filament of astrocyte. Pathologically, this neurodegenerative disease is characterised by dystrophic astrocytes containing intermediate filament aggregates associated with myelin abnormalities.More than 20 GFAP mutations have been reported. Many of them cluster in highly conserved regions between several intermediate filaments. Contrary to other intermediate filament-related diseases, AXD seems to be the consequence of a toxic gain of function induced by aggregates. This is supported by the phenotype of mice overexpressing human GFAP. Nevertheless, GFAP null mice display myelin abnormalities and blood-brain barrier dysfunction that are present in AXD.Given the pivotal role of astrocytes in brain physiology, there are many possibilities for astrocytes to dysfunction and to impair the functions of other cells. Physiopathological hypotheses are discussed in the frame of AXD.Received 11 April 2003; received after revision 22 July 2003; accepted 31 July 2003Both authors contributed equally to this work.     

我国古代"情志相胜,以情胜情"的心理疗法及其对现代心理治疗的影响

我国中医学源远流长,其"情志相胜,以情胜情"的心理治疗理念、相应的具体治疗方法及案例,对于分析现代人的心理疾病、并针对性地进行临床治疗具有重要的作用.     

Axonal transport of neurofilaments in normal and disease states

Neurofilaments are among the most abundant organelles in neurones. They are synthesised in cell bodies and then transported into and through axons by a process termed 'slow axonal transport' at a rate that is distinct from that driven by conventional fast motors. Several recent studies have now demonstrated that this slow rate of transport is actually the consequence of conventional fast rates of movement that are interrupted by extended pausing. At any one time, most neurofilaments are thus stationary. Accumulations of neurofilaments are a pathological feature of several human neurodegenerative diseases suggesting that neurofilament transport is disrupted in disease states. Here, we review recent advances in our understanding of neurofilament transport in both normal and disease states. Increasing evidence suggests that phosphorylation of neurofilaments is a mechanism for regulating their transport properties, possibly by promoting their detachment from the motor(s). In some neurodegenerative diseases, signal transduction mechanisms involving neurofilament kinases and phosphatases may be perturbed leading to disruption of transport. Received 11 July 2001; received after revision 30 August 2001; accepted 31 August 2001     

Arginase expression in peritoneal macrophages and increase in circulating polyamine levels in mice infected with Schistosoma mansoni

We investigated the nitric oxide (NO) synthase and arginase pathways in resident peritoneal macrophages of mice infected with the tropical parasite Schistosoma mansoni. The two enzymes may have opposite effects, insofar as NO may be involved in the killing of the parasite whereas arginase may stimulate parasite growth via polyamine synthesis. We determined the effects of the infection on the expression and activity of the two enzymes in macrophages, before and after cytokine activation. Cells from infected mice expressed the hepatic type I arginase, whereas in control cells, the enzyme was expressed only after cytokine activation, as were NO synthase II and type II arginase in both groups of cells. Moreover, we found that in infected mice, arginase expression in macrophages was associated with a ten fold increase in the concentration of circulating ornithine-derived polyamines. This may be of pathological importance, since parasitic helminths are though to be dependent on their hosts for the uptake and interconversion of polyamines. Received 13 March 2001; received after revision 4 May 2001; accepted 7 June 2001     

Programmed cell clearance

Apoptosis, a physiological process of self-annihilation, is essential during development and for the maintenance of tissue homeostasis. Considerable efforts have been made in recent years to elucidate the molecular mechanisms that govern this mode of cellular demise; however, the subsequent recognition and removal of apoptotic corpses by neighboring phagocytes has received less attention. Nevertheless, macrophage engulfment of apoptotic cells is known to be important in the remodeling of tissues, and contributes to the resolution of inflammation through the removal of effete cells prior to the release of noxious cellular constituents. Moreover, apoptotic cells are a potential source of self-antigens, and clearance of cell corpses is thought to preclude the induction of autoimmune responses. The view is thus emerging that tissue homeostasis is dependent not only on the balance between mitosis and apoptosis, but also on the rate of apoptosis versus that of cell clearance. This review aims to discuss the mechanisms and consequences of macrophage recognition and disposal of apoptotic cells, a process which will be referred to as programmed cell clearance.Received 16 April 2003; received after revision 22 May 2003; accepted 26 May 2003     

纳米硅对三峡库区柑橘青霉菌的药效试验

对三峡库区柑橘果实贮藏期间携带微生物进行了分离,青霉菌(Penicillium)为主要的致病菌;不同药剂处理接种青霉菌的柑橘果实,实验表明多菌灵抑菌效果最好,防效达到65.4%,其次是纳米硅达到53.4%;对青霉菌的抑菌■试验表明,多菌灵抑制效果最好,抑制率为90%,纳米硅为88%.说明纳米硅对柑橘青霉病有一定的防治效果,并因其无公害有施用价值.     

周口店北京人遗址环境地质条件及地质病害机理分析

自周口店北京人遗址区被发现后的几十年以来,由于自然和人为因素的影响,在各发掘点内出现了诸多不同类型的地质病害,严重威胁着遗址区的安全与保护.基于此,通过现场及室内试验对遗址区环境工程地质条件进行了分析并在此基础上通过岩石薄片镜下鉴定、岩石化学分析及崩解试验等对影响遗址区病害的因素及机理做了分析.结果发现,周口店遗址区7个发掘点共有20处类型不一、规模不等、变形程度不同的潜在地质病害点.其破坏的原因可以归结为地质、环境及人类活动3个因素,其中着重讨论了环境因素的影响.环境因素分析结果表明,不同地点处由于其胶结物成份不同所以环境因素对其的影响方式也不同.图12,表3,参8.     

宋代的牲畜疫病及政府的应对——以宋代政府诏令为中心的讨论

历代政府对耕牛和马都给予了保护性的政策。两宋时期,耕牛和马作为农业生产的主要动力与运输工具,由于国营牧监的南移和饲养方式的变化,导致了疫病的频繁发生和流行,从而引起了宋代政府的高度重视。以宋代政府诏令为中心,探讨宋代牲畜疫病的流行情况及特点,牲畜疫病的病因及对农业生产、交通运输和军事战争所产生的重大影响,分析和疏理宋代通过政府诏令对不同时期发生的牲畜疫病所采取的应对措施。同时,还探讨北宋和南宋政府在牲畜疫病应对上的不同,以及这种不同与两宋时期的政治军事和社会经济之间的关系。     

铁路接头病害预防与整治探讨

结合工作中实际养护经验,分析了铁路接头产生病害的原因,在对接头病害原因进行分析的基础上,提出了防止铁路病害的措施与方法.     

Protective effect of sodium butyrate on the cell culture model of Huntington disease

This study aimed to develop a cell culture model of Huntington disease and observe the effect of sodium butyrate on this cell culture model. Exon 1 of both a wild type and a mutant IT15 gene from the genomic DNA of a healthy adult and a patient with Huntington disease was amplified and cloned into the eukaryotic expression vector pEGFP-C1. Human neuroblastoma SH-SY5Y cells were transiently transfected with these recombinant plasmids in the absence and presence of sodium butyrate (0.1, 0.2, 0.5, 1.0 mmol/L). The MTT assay was used to measure cell viability. The results indicated that the N-terminal fragment of mutant huntingtin formed perinuclear and intranuclear aggregates and caused a decrease of SH-SY5Y cell viability. Sodium butyrate inhibited the decrease of SH-SY5Y cell viability caused by the N-terminal fragment of mutant huntingtin. This suggests that sodium butyrate has a protective effect on this cell culture model of Huntington disease.