灯盏细辛黄酮类成分对压力诱导的视网膜神经节细胞凋亡的影响

目的考察灯盏细辛中黄酮类成分(总黄酮、灯盏花素)对体外高压诱导的视网膜神经节细胞(retinal gan-glion cells,RGCs)凋亡的影响,探讨其视神经保护作用的物质基础。方法采用胰酶消化法将24只出生2~3d的SD(Sprague-Dawley)乳鼠视网膜制成细胞悬液,接种于经多聚鸟氨酸(HA)和层粘连蛋白(LN)包被的盖玻片中。培养72h后,将覆有细胞的血盖片转入加压装置中,加入黄酮类成分,继续培养48h,采用Fas蛋白免疫组化染色法及原位末端脱氧核苷酸转移酶标记(Tunel-POD)法进行检测,每天观察细胞形态,同时对部分细胞行NSE染色检查。结果细胞生长良好,NSE染色表明,85%以上的细胞为RGCs。给药组的Fas蛋白阳性表达指数和凋亡指数均明显低于模型组(P<0.05~0.01)。结论黄酮类成分均能对抗压力诱导的RGCs凋亡,为灯盏细辛视神经保护的有效组分。     

前列腺素E1对脂肪所致犬呼吸窘迫综合征的治疗作用

采用同种脂肪提取液复制犬呼吸窘迫综合征模型,观察前列腺素E_1(PGE_1)对其治疗作用。结果表明,PGE_1可改善该模型的低氧血症,降低肺毛细血管通透性,减轻肺水肿,其减轻肺损伤的机理与其抑制多形核白细胞粘附、氧自由基产生及保护Ⅱ-型肺泡上皮细胞等有关。     

Effect of dietary selenium and vitamin E on the biomechanical properties of rabbit bones

Summary It is generally agreed that combined deficiency of selenium and vitamin E leads to several abnormalities including Kashin-Beck disease which is an endemic and chronic degenerative osteoarthrosis. The abnormalities can be reversed by the administration of various forms of selenium and vitamin E.The present study was designed to investigate the effects of dietary selenium and vitamin E on bone tissue and on the biomechanical properties of bone. Young rabbits of both sexes were fed with either a selenium- and vitamin E-adequate diet (control group), or a selenium- and vitamin E-deficient diet or a selenium-excess diet. The selenium-deficient diet resulted in a significant decrease in plasma selenium level and the selenium-excess diet resulted in a significant increase in the plasma selenium level with respect to the corresponding control values (p<0.05). The diets did not affect the blood cell counts considerably but erythrocyte glutathione peroxidase activity increased (decreased) relatively when the plasma selenium level increased (decreased) (p<0.05). The light microscopic investigations of the bone tissues of the two experimental groups indicate that the findings of the present work are compatible with osteomalacia. The biomechanical properties of the bones from the three groups were determined experimentally with bending tests. Both the Se-and vitamin E-deficient diet and the Se-excess diet decreased the biomechanical strength of the bones significantly while the bones belonging to the control group always had the largest modulus of elasticity (p<0.05).     

我国丙型和戊型肝炎人群流行病学调查及流行因素的研究

为阐明丙型和戊型肝炎在我国的流行严重度和流行规律，采用描述流行病学、血清流行病学和分子流行病学相结合的研究方法，对两型肝炎的流行特征和流行因素进行了研究。结果发现；一般人群调查近９万人丙型肝炎和戊型肝炎的流行率各为２．２％和９．７％，散 生病毒性肝炎感染比率各为２．１５％和１６．４％。丙型肝炎在我国主要经血传播，与血液接触密切人群中ＨＣＶ感染率高达５０－７０％，慢性化比比例高达４０－６０％，目前供     

Prevalence and mechanism of streptokinase-induced platelet stimulation. Effect of acetylsalicylic acid.

It was recently shown that streptokinase may induce clot formation in vivo by immunoglobulin G mediated platelet stimulation. We evaluated the in vitro effect of streptokinase on platelet function in 103 subjects, of whom 52 were < or = 30 years and 51 were > or = 50 years old. Although streptokinase inhibited platelet aggregation in the majority of cases, in nine the threshold concentration of ADP required to induce irreversible aggregation decreased with streptokinase (1 million Units. l-1) by 30% or more. This observation was confirmed in five of the nine by repeated measurements indicating reproducible streptokinase-induced platelet stimulation. Among the five, two were < or = 30, and three were > or = 50 years old. In none of the five subjects did the radio allergo sorbent test detect type E immunoglobulins directed against streptokinase in the serum. In contrast, in four of the five subjects, streptokinase-induced platelet hyperaggregability was suppressed by addition of goat antibodies against human immunoglobulin G, or F(ab')2-fragments of such antibodies. Acetylsalicylic acid did not prevent streptokinase-induced platelet stimulation, but in three of five cases, led to an increase in the control threshold concentration for ADP, so that after the decrease induced by streptokinase the threshold concentration for ADP was in the same range as before acetylsalicylic acid and streptokinase administration. Thus, streptokinase led to an inhibition of platelet aggregation in the majority of subjects evaluated. In a minority of five out of 103, however, streptokinase reproducibly caused platelet stimulation, presumably mediated by immunoglobulin G.(ABSTRACT TRUNCATED AT 250 WORDS)     

维生素E对烧伤小鼠免疫功能改善及其机制

本实验研究了维生素Ｅ（ＶＥ）改善烧伤后免疫功能的作用，并对其作用机制进行了探讨。结果显示，小鼠１１％～１２％总体表面积（ＴＢＳＡ）全层皮肤烧伤后血、肝、脾中过氧化脂质（ＬＰＯ）水平升高、谷胱甘肽（ＧＳＨ）含量下降，淋巴细胞增殖反应、白介素一２（ＩＬ一２）生成、空斑形成细胞（ＩＪＦＣ）形成及迟发型超敏反应（ＤＴＨ）均处于抑制状态。投予ＶＥ后可防止烧伤动物体内ＬＰＯ水平、ＧＳＨ含量明显变化，免疫功能受抑制的程度也明显小于未投予组。以超氧化物歧化酶（ＳＯＤ）处理的作用与ＶＥ相同。体外实验显示，过氧化亚油酸可抑制淋巴细胞增殖反应以及ＩＬ一２产生、诱发淋巴细胞脂质过氧化、降低淋巴细胞内ＧＳＨ含量。淋巴细胞上述功能的抑制与ＬＰＯ水平密切相关；加入ＶＥ可抑制过氧化亚油酸对淋巴细胞的上述作用。提示ＶＥ可改善烧伤后免疫功能，其机制可能是通过抗氧化作用而发挥的。     

宫颈癌组织中HPV16 E7序列多态性分析

目的探讨广东地区宫颈癌组织中HPV16肿瘤相关性抗原E7基因序列的多态性.方法采用通用引物PCR直接测序法对宫颈癌标本中的HPV分型,从含有HPV16型的标本中采用自行设计的多重引物通过巢式PCR扩增出HPV16E7,经DNA序列测定法检测其基因变异,进而寻找其热点突变.结果50例宫颈癌组织HPV-DNA的检出率为78%,其中HPV16和HPV18型混合感染18例,单纯HPV16型感染15例.33例含有HPV16型的标本中扩增出25例HPV16E7,其中17例647位核苷酸“T”变异“C”,导致相应的蛋白质由天冬氨酸变异为丝氨酸.结论广东地区宫颈癌组织中HPV16E7DNA序列发生碱基替换的区域主要在647位至846位,热点突变点为Nt647和Nt846.     

利用T7和PR双启动子的新型表达载体的构建及其应用

构建具有λＰＲ与Ｔ７双启动动子的新型原核表达载体ｐＤＯＧ，以便使用同一载体研究不同诱导条件下，重组蛋白在大肠杆菌中表达，降解以及折叠的情况，从而选择最佳的诱导条件。方法采用ｐＢＶ２２０与ＰＥＴ－３表达载体作为原始材料，将ＰＥＴ－３上包括Ｔ７启动子与Ｔ７ｇ－１０释译起始序列的一段序列克隆到     

Alzheimer-Demenz und normales Altern Klinische,neuroradiologische, neurophysiologische und molekularbiologische Verlaufsdaten

Zusammenfassung 30 Patienten mit klinisch diagnostizierter Alzheimer-Demenz (AD) und 55 etwa gleichaltrige Kontrollprobanden wurden über einen 2-Jahres-Zeitraum prospektiv klinisch, neuroradiologisch und elektroenzephalographisch untersucht, um die longitudinalen Ver?nderungen auf diesen Untersuchungsebenen und ihre Zusammenh?nge zu studieren. In der Kontrollgruppe waren im Beobachtungszeitraum keine wesentlichen Ver?nderungen auf einer der Untersuchungsebenen zu verzeichnen. Bereits inital bestanden signifikante Unterschiede zwischen Patienten und Kontrollen hinsichtlich der kognitiven Leistung, der Ventrikelweite und der absoluten Theta- und Delta-Power. Innerhalb der Patientengruppe verschlechterten sich w?hrend des zweij?hrigen Beobachtungszeitraums die Werte der Blessed-Demenzskala um 7 ± 7 Punkte und im Mini-Mental-State Test um 8 ± 4 Punkte. Die Volumina der Seitenventrikel weiteten sich um mehr als 30 % des Ausgangswertes und die absolute Delta- oder Theta-Power stieg um mehr als 10 % des Ausgangswertes an. Hierdurch nahmen die Unterschiede zwischen Kontroll- und Patientengruppe nochmals zu. Wir konnten keine Zusammenh?nge zwischen Krankheitsbeginn, Alter, Apolipoprotein E4 Gendosis und Krankheitsverlauf belegen. Ein initial schlechter Wert der Patienten auf der Blessed-Skala war mit st?rkeren morphologischen und EEG-Ver?nderungen im Verlauf korreliert, w?hrend initial hohe Theta-Power eine st?rkere funktionelle und kognitive Verschlechterung innerhalb der Patientengruppe pr?dizierte.      

The neurochemistry of Alzheimer's disease

Our knowledge of the neurochemical pathology of AD has increased immensely the last years. Although it is now clear that mutations in the APP gene can cause some rare hereditary forms of AD, and that ApoE4 is a prominent risk factor for AD, we at present know little about the underlying cause of AD in the general population and the biochemical mechanisms by which the apolipoprotein E4 isoform affects AD pathogenesis. It is hoped that the near future will see a resolution of the current controversies in AD research, including: 1) whether APP mutations cause Alzheimer's disease by affecting Aβ deposition or the function of APP itself; 2) whether abnormal phosphorylation of tau is a central pathogenetic event, or whether it occurs as epiphenomena that reflect general neurodegeneration in a variety of disease processes; 3) Whether Aβ deposition in the brain is the central event in AD or whether it occurs as epiphenomena in a variety of brain disorders such as head trauma; and 4) whether altered tau phosphorylation occurs secondary to Aβ deposition or vice versa, and what the link is (if any) between the two processes.