青年学生A型行为类型的比较研究

采用行为类型问卷 ,对安徽省合肥、安庆、六安三市的部分大、中学校高中三年级、大学一年级、大学四年级学生及研究生 763人进行测试 ,结果显示青年学生群体的 A型行为特征( TH+ CH总分 )与普通人群无明显差异。但 CH分即争强好胜 ,敌意倾向明显高于普通人群。就高三学生调查结果看 ,在此阶段约 1 1 %的人 A+型行为就已形成。而大学的学习生活 ,既没有使大学生中 A型人的人数比例增加 ,也未见 A型行为总的特征明显增强。提示青年学生 A型行为早在中学阶段已形成 ,因此对其预防和干预应在早期进行     

Deficiency of fibrinolytic enzyme activities in the serum of patients with Alzheimer-type dementia

Previously we reported that there is a kallikrein deficiency in the cerebral tissue of patients with Alzheimer-type dementia. The present study was performed to investigate protease changes in the serum of these patients. The results showed that the kallikrein activity was normal, but that the activities of plasmin and urokinase were significantly low. The present findings indicate a derangement in the clotting and fibrinolytic systems in Alzheimer patients.     

转基因植物研究进展

介绍了转基因植物的发展历史,已获得转基因植物的物种,转基因技术及转基因植物在生产上的应用.     

Early circulating erythroid progenitors (BFU-E) in sickle cell anemia

Sickle cell anemia (SS) patients can be divided into two sub-populations according to peripheral HbF levels. Patients with low (<9%) HbF levels (LFSS) are characterized by an increased number of circulating BFU-E in active DNA synthesis, and release of burst promoting activity (BPA) by unstimulated low density (LD) adherent cells. In contrast, circulating BFU-E from SS patients with high (>9%) HbF levels (HFSS) are normal in number, largely in resting phase, and their LD cells do not release BPA-like activity.More recently further heterogeneity has been found among these two groups. In LFSS patients GM-CSF is constitutively produced by unstimulated monocytes. In contrast, HFSS patients' adherent cell depletion increases cycling of BFU-E in culture. CM from HFSS patients inhibits BFU-E expression in culture. Hence, LD adherent cells from HFSS patients may release an inhibitory factor(s). The nature of this factor has to be determined.In addition, there are distinct subpopulations of BFU-E responsiveness to growth factor (GM-CSF, IL-3): a) LFSS patients have a homogeneous BFU-E population, equally responsive to GM-CSF and IL-3; b) HFSS patients, in addition to this subpopulation, have a subset of BFU-E dependent exclusively on IL-3 which is 20 to 40% of the total number of circulating BFU-E. This is similar to BFU-E from normal individuals. Hence, LFSS BFU-E represent an actively proliferating population, equally responsive to GM-CSF and IL-3, controlled by at least constitutively produced GM-CSF and possibly other factors.These observations suggest a significant modification in BFU-E behavior in the subset of SS patients with low HbF levels and high hemopoietic stress. The heterogenous regulation of BFU-E in SS disease seems to be an epiphenomenon of HbF levels, and not vice-versa.     

湖北省高校1971～1990年间教职工全死因回顾性整群抽样调查

通过对湖北省高校近20年教职工死因调查,报道了该省高校1971～1990年20年间共死亡教职工680人,总死亡率为329.462/10万的情况。前三位死因顺位依次为恶性肿瘤、脑血管病、心血管病。恶性肿瘤的前三位死因顺位是肝癌、肺癌、胃癌。死亡年龄分布40岁以上占死亡总数的90.15％。同时对不同职别、性别群体的死因进行了分析,对有关因素略作讨论,并提出高校应积极开展健康教育、建立与完善健康咨询、推行综合健康医学模式等教职工的最佳保健方案。     

几个大白菜品种农艺和品质性状及抗病和抗冻能力的比较研究

对5个大白菜品种在4个试验点进行田间试验,重点比较了品种81—5和青杂3号的农艺、品质性状和抗病、抗冻能力。品种81—5苗期生长势、成株紧实度、单株重及亩产量几项性状均明显优越;品质性状总体上看也比较好,表现是含水量和纤维素含量低、蛋白质总量和维生素C及糖分含量高,但游离氨基酸和人体必需的8种蛋白质氨基酸含量较低;对软腐病等主要病害的抗性、耐贮性和抗冻能力均较强,原生质体对冻害损伤的抵抗力较品种青杂3号高40％以上。     

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     

Myosins from plants

Molecular cloning and sequence analysis of myosin genes from Arabidopsis thaliana and electron microscopic observation of a myosin from characean alga have revealed that overall structure of plant unconventional myosins is similar to that of the class V myosins. These plant unconventional myosins have two heads, a coiled-coil tail of varied length and a globular tail piece at the end. The tail piece is probably a site for membrane interaction. Characean myosin is of special interest because it can translocate actin filaments at a velocity several times faster than muscle myosin, which must have evolved to support the quick movement of animals in the struggle for their lives.     

Caffeine as a psychomotor stimulant: mechanism of action

The popularity of caffeine as a psychoactive drug is due to its stimulant properties, which depend on its ability to reduce adenosine transmission in the brain. Adenosine A₁ and A_2A receptors are expressed in the basal ganglia, a group of structures involved in various aspects of motor control. Caffeine acts as an antagonist to both types of receptors. Increasing evidence indicates that the psychomotor stimulant effect of caffeine is generated by affecting a particular group of projection neurons located in the striatum, the main receiving area of the basal ganglia. These cells express high levels of adenosine A_2A receptors, which are involved in various intracellular processes, including the expression of immediate early genes and regulation of the dopamine- and cyclic AMP-regulated 32-kDa phosphoprotein DARPP-32. The present review focuses on the effects of caffeine on striatal signal transduction and on their involvement in caffeine-mediated motor stimulation.Received 8 July 2003; received after revision 7 September 2003; accepted 6 October 2003     

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.