脾虚三证模型大鼠脂质过氧化损伤的比较

目的：探讨实验性脾虚大鼠脂质过氧化损伤的差异性,方法：采用饮食加劳倦等 合因素分别复制脾虚不同主型动物模型,观察各模型组和治疗组的脂质过氧化物（LPO）的含量和谷胱甘肽过氧化物酶（GSH－Px) ,超氧化物歧化酶（SOD）,心肌黄酶（DTD）活性变化。结果,各脾虚模型大鼠LPO呈不同程度升高,各种抗氧化酶活性不同程度下降,且且间差异显著,各治疗组药物具有降低LPO,升高抗氧化酶活性的作用,结论：脂质过氧化损伤是脾虚三证的共同症理生理基础。     

脾虚三证模型大鼠脂质过氧化损伤的比较

目的 :探讨实验性脾虚大鼠脂质过氧化损伤的差异性。方法 :采用饮食加劳倦等复合因素分别复制脾虚不同证型动物模型。观察各模型组和治疗组的脂质过氧化物 (L PO)的含量和谷胱甘肽过氧化物酶 (GSH- Px)、超氧化物岐化酶 (SOD)、心肌黄酶 (DTD)的活性变化。结果 :各脾虚模型大鼠 L PO呈不同程度升高 ,各种抗氧化酶活性不同程度下降 ,且组间差异显著。各治疗组药物具有降低 L PO、升高抗氧化酶活性的作用。结论 :脂质过氧化损伤是脾虚三证的共同病理生理基础。     

治萎防变胶囊对慢性萎缩性胃炎模型大鼠SOD、GSH-Px活性及MDA、LPO含量的影响

目的探讨治萎防变胶囊对慢性萎缩性胃炎(CAG)模型大鼠胃组织超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性及丙二醛(MDA)、脂质过氧化物(LPO)含量的影响。方法采用综合法成功复制CAG动物模型。施药治疗后分别对各组大鼠胃组织超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性及丙二醛(MDA)、脂质过氧化物(LPO)含量进行检测。结果与空白组比较,模型组大鼠胃组织SOD、GSH-Px活性显著下降(P0.01,P0.05),MDA、LPO含量显著升高(P0.01,P0.01);与模型组比较,治萎防变胶囊可显著提高SOD、GSH-Px活性(P0.05,P0.05),显著降低MDA、LPO含量(P0.05,P0.05),且以治萎防变胶囊大剂量组作用显著。结论治萎防变胶囊具有提高机体抗氧化酶活力,减轻自由基损伤和抑制脂质过氧化物反应的作用。     

碱性成纤维细胞生长因子对大鼠急性心肌损伤保护作用的实验观察

目的研究碱性成纤维细胞生长因子(BasicFibroblastGrowthFactor,bFGF)预处理对异丙肾上腺素(Isoprenaline,Iso)致大鼠急性心肌损伤的保护机制。方法将Wistar雄性大白鼠随机分成3组:对照组、Iso损伤组、bFGF预处理组,用光镜观察心肌组织的病理变化,生化方法检测心肌酶,硫代巴比妥酸荧光方法测定心肌组织脂质过氧化物MDA的水平,DTNB直接显色法测定心肌组织谷胱甘肽过氧化物酶活性,无机磷法测定心肌线粒体H 鄄ATP酶水解活性。结果Iso损伤组心肌坏死较重,心肌酶和心肌组织脂质过氧化物MDA的水平明显增高,心肌组织谷胱甘肽过氧化物酶活性及心肌线粒体H 鄄ATP酶水解活性减低;bFGF预处理组心肌坏死明显减轻,心肌酶及心肌组织脂质过氧化物MDA的水平下降,心肌组织谷胱甘肽过氧化物酶活性及心肌线粒体H 鄄ATP酶水解活性增加(P<0.05)。结论bFGF可通过抑制脂质过氧化,提高抗氧化酶活性和改善心肌能量代谢而减轻大鼠心肌损伤。     

辅酶Q_(10)对移植心脏再灌注损伤保护的实验研究

本文以大鼠腹腔心脏移植为模型,实验组在心脏移植前注入辅酶Q_(10)(CoQ_(10)),术后测定供心组织:1.实验组超氧化物岐化酶(SOD),谷胱甘肽过氧化物酶(GSH-Px)均高于对照组(P<0.01,P<0.05),过氧化脂质(LPO)明显低于对照组(P<0.01),2.超微结构显示实验组的改变较对照组明显减轻.提示:心脏移植前应用CoQ_(10)可明显降低供心氧自由基产生,同时增强机体内源抗氧化酶活性,保护心肌结构,减轻移植心肌组织的损伤.     

苍脂颗粒剂对鼠胃粘膜细胞保护作用的研究

为了探讨苍脂颗粒剂治疗脾胃病的胃粘膜保护作用，采用利血平模拟的大鼠脾虚证及亚急性阿斯匹林胃粘膜损伤模型，测定其对非蛋白质流基物质（NPSH）、谷胱甘肽过氧化物酶（GSH－px）、过氧化氢酶（CAT）、超氧化物歧化酶（SOD）及血浆过氧化脂质（LPO）等具有胃粘膜细胞保护作用物质的含量或活性的影响。结果显示，苍脂颗粒剂可以明显改善脾虚伴慢性胃粘膜病变大鼠及亚急性阿期匹林胃粘膜损伤大鼠的粘膜损伤程度，显著提高胃粘膜NPSH（F＜0．01）、GSH-px（P＜0．01）等细胞保护物质的水平．提示苍脂颗粒剂具有一定的胃粘膜细胞保护作用。     

大黄泻下与劳倦过度单、复因素造模脾虚小鼠过氧化与抗氧化改变的比较研究

目的：探讨单因素与复合因素造模法对脾虚动物模型生物膜结构和功能改变的规律及其机制。方法：70只小白鼠随机分为4组,即大黄泻下造模（A）组20只,劳倦过度造模（C）组20只,大黄泻上加劳倦过度造模（AC）组20只,空白对照（O）组10只。观察各组小白鼠丙二醛（MDA）、共轭双烯（CD）、过氧化氢酶（Cat)、超氧化物歧化酶（SOD）及过氧化物酶（GSH－Px）的变化,结果：3种方法塑造的脾虚小鼠模型均出现了体重下降,MDA、CD升高,Cat,SO,GSH-Px下降,且脂质过氧化损伤程度和抗氧化氧化酶活性下降程度以AC组为最重。结论：脾虚造模方法以大黄泻下加劳倦过度法为优,复因素脾虚造模法要优于单因素脾虚造模法。     

车前子多糖对大鼠肝线粒体自由基防御功能的影响

目的探讨车前子多糖(PSP)对大鼠肝线粒体自由基防御功能的影响。方法差速离心法提取雄性SD大鼠肝线粒体,采用硫酸亚铁-维生素C(Fe2+-Vit C)激发剂,建立大鼠肝线粒体脂质过氧化(LPO)模型,比色法测定丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)和抗氧化物酶(T-AOC)活性,观察PSP对各生化指标的影响。结果 PSP浓度在25、50和100 mg/L范围时,MDA含量分别为3.94±0.15,3.65±0.18和2.88±0.20,均显著低于模型组6.47±0.48(P<0.01),表明PSP对肝线粒体脂质过氧化有抑制作用,而对抗氧化物酶类活性均有激活作用,与模型组比较,均明显升高(P<0.01)。结论 PSP对大鼠肝线粒体自由基的防御功能可产生一定的影响,对治未病起到一定的防治作用。     

内皮素-1致大鼠急性肺损伤中脂质过氧化物含量的变化

目的 :旨在研究ET 1对大鼠肺和全身脂质过氧化损伤作用 ,以明确ET 1致大鼠ALI的作用机制。方法 :2 8只健康雄性Wistar大鼠 ,随机分为两组 :内皮素组经股静脉持续滴注ET 1,对照组用生理盐水代替。检测两组动物实验前后呼吸频率、血气分析、支气管肺泡灌洗液 (BALF)中蛋白含量、白细胞及分类计数、肺系数、肺组织学检查以及肺实质、BALF、全血中脂质过氧化物 (LPO)、超氧化物歧化酶 (SOD)、谷胱甘肽 (GSH)的含量。结果 :ET 1诱导出大鼠ALI ,内皮素组较对照组肺实质、BALF中LPO含量升高 ,SOD含量下降 (P <0 .0 1) ,全血LPO含量升高 ,SOD含量下降 (P<0 .0 5 ) ,BALF中GSH含量下降 (P <0 .0 1)。结论 :ET 1能够引起大鼠肺部脂质过氧化损伤效应。ET 1可能是机体内源性的致肺损伤因子之一。     

苍脂颗粒剂对鼠胃粘膜细胞保护作用的研究

为了探讨苍脂颗粒剂治疗脾胃病的胃粘膜保护作用，采用利血平模拟的大鼠脾虚证及亚急性阿斯匹林胃粘膜损伤模型，测定其对非蛋白质巯基物质，谷胱甘肽过氧化物酶，过氧化氢酶，超氧化物歧化酶及血浆过氧化脂质等具有胃粘膜细胞保护作用物质的含量或活性的影响。结果显示，苍脂颗粒剂可以明显改善脾虚伴慢性胃粘膜病变大鼠及亚急性阿斯匹林胃粘膜损伤大鼠的粘膜损伤程度，显著提高胃粘膜ＮＰＳＨ，ＧＳＨ－ｐｘ等细胞保护物质的水平，     

Kappa-Chain Deficiency

A decreased concentration of immunoglobulin molecules of one light chaintype () was found in a young girl withrecurrent respiratory infections anddiarrhea. She had, in addition, decreased A and E globulin, partialalbinism, and intestinal lactase deficiency. No eosinophils were detectedin blood, bone marrow, or nasalsmears. Radiolabeled - and -typemolecules survived equally well, suggesting that the synthesis of moleculesbearing -chains was decreased. Thepatient improved considerably with theregular administration of -globulin. Itis possible that biological as well aschemical differences exist between immunoglobulins of the two light-chaintypes and that an optimal immuneresponse is dependent on a normalcomplement of - and -chains.

Submitted on April 25, 1972 Revised on July 10, 1972 Accepted on July 21, 1972     

Plasma and Erythrocyte Folate in Iron Deficiency and Folate Deficiency

Erythrocyte and plasma folate levels were studied before treatment in 20patients with iron deficiency anemia and in 23 patients with megaloblasticanemia due to folate deficiency. Fourteen of the cases of iron deficiency anemiawere also studied after treatment with oral iron alone. Fifty-seven normalpersons were used as controls.

The mean erythrocyte folate (ng./ml. packed cells) was significantly increased in iron deficiency anemia and significantly depressed in folate deficiency anemia. After treatment with oral iron alone, the mean erythrocytefolate level fell to normal in the iron deficiency anemia group. The mean corpuscular folate (ng. x 108^-8) was also significantly raised in iron deficiency:in eight of 10 cases this fell after treatment, but the overall fall was not significant. The plasma folate rose in iron deficiency anemia after oral irontreatment.

Submitted on August 8, 1969 Accepted on November 17, 1969     

Erythrocyte Glutathione-Peroxidase Deficiency

S ummary Glutathione peroxidase deficiency is the most recently described erythrocyte enzyme abnormality. This enzyme occupies a critical position in the pathways leading to the decomposition of peroxides in the erythrocyte. On the basis of our studies of patients with GSH-P deficiency, it appears that a spectrum of disease quite similar to that found in G-6-PD deficiency is present; this includes compensated haemolytic disease, drug-induced haemolysis and neonatal jaundice.     

慢性心力衰竭气虚证、气阴两虚证、气阳虚证的临床特点分析

目的研究气虚类慢性心力衰竭不同证型的临床特点。方法纳入118例气虚类(含气阴两虚及气阳虚)慢性心力衰竭(CHF)患者,采集其相关临床症状、体征、检验检查,比较分析气虚证、气阴两虚证、气阳虚证的不同临床特点。结果扩张性心肌病患者辨证多为气阳虚;气虚证、气阴两虚证、气阳虚证心力衰竭严重程度不同,气阳虚证患者心力衰竭程度最严重。结论心力衰竭气虚证、气阴两虚证、气阳虚证在原发疾病和心力衰竭病情程度上有不同特点:扩张性心肌病患者辨证多为气阳虚,气阳虚证患者心力衰竭程度最严重。     

The Mode of Inheritance of PTA Deficiency: Evidence for the Existence of Major PTA Deficiency and Minor PTA Deficiency

Plasma thromboplastin antecedent (PTA) activity was measured with aquantitative assay in the available members of the families of eight propositiwith severe PTA deficiency. PTA deficiency was found to exist in two forms:major PTA deficiency, characterized by PTA levels of up to 20 per cent of ourstandard reference plasma and by the potential for serious surgical bleeding,and minor PTA deficiency, characterized by PTA levels between 30 and 65per cent of our standard reference plasma and by the absence of significantsurgical bleeding. Minor PTA deficiency was found in parents and childrenof subjects with major PTA deficiency.

It would appear that the gene for PTA deficiency is an incompletely recessive or "intermediate" gene which produces major PTA deficiency in the homozygote and minor PTA deficiency in the heterozygote.

Submitted on March 27, 1961 Accepted on May 16, 1961     

Iron Deficiency and Dyserythropoiesis

S ummary . In 10 patients with Fe deficiency significant dyserythropoiesis was found. The degree of dyserythropoiesis provided a reliable indication of the severity of the iron deficiency as measured by the serum iron and total iron binding capacity; a positive correlation ( P < 0.002.) being found between the % incidence of dyserythropoiesis in the bone marrow and both the serum iron and % iron saturation. The frequent occurrence of basophilic stippling in the erythroblasts of these patients suggested that the presence or absence of stippling does not help differentiate between iron deficiency and other causes of hypochromic anaemia.