大鼠单克隆抗体夹心ELISA法检测肝病病人血清中p21^ras蛋白

本文应用抗癌基因ｒａｓ表达产物Ｐ２１ｒａｓ蛋白的大鼠单克隆抗体建立的双抗体夹心ＥＬＩＳＡ法，检测了肝癌及癌病变前病人血清中ｐ２１ｒａｓ蛋白的浓度。所获阳性检出率分别为：慢性乙型肝炎为１３．０％（１２／９２），肝硬化为２７．８％（１０／３６）和肝癌为５０．０％（８／１６）。另外，对试验方法的敏感性、特异性及稳定性，以及检测Ｐ２１ｒａｓ蛋白与ＡＦＰ的关系进行了评价。结果表明，Ｐ２１ｒａｓ蛋白的过高表达发生在肝细胞癌变之前。提示在慢性乙型肝炎及肝硬化病人血清中检出Ｐ２１ｒａｓ蛋白，是预测肝细胞癌变的危险信号。     

棘球蚴内容物导致肺损害的研究

目的 :观察棘球蚴囊内容物攻击兔所至肺功能和形态的损害。建立囊型包虫肺栓塞的动物模型。方法 :取囊型包虫内容物 ,分离出囊砂 ,与囊液配成 5 %的悬浊液。 2 1只家兔 ,分 3组 :Ⅰ :生理盐水组 ,Ⅱ :澄清囊液组 ,Ⅲ :囊砂悬浊液组。每只家兔都置入股动脉导管及股静脉导管。依照上述分组按 2mL/kg体重分别自静脉导管注射生理盐水、澄清囊液或含囊砂的悬浊液。于注射后 ( 5、30、6 0min)动态监测MAP、血气指标及血清血管活性物质(ET - 1、TXB2 、6 -keto -PGF1α)水平的变化。指标测定后 ,行肺部ECT检查。最后取出动物肺脏行光镜病检。结果 :Ⅲ组和Ⅱ组在注射后均出现MAP、血气指标的明显降低 (P <0 .0 5 )和血清TXB2 、6 -keto -PGF1α的升高 (P <0 .0 5 ) ,尤以Ⅲ组最明显 (P <0 .0 5 )。各组动物血清ET - 1水平在注射前后无明显变化 (P >0 .0 1)。ECT显示Ⅲ组动物肺部放射性缺损 ,Ⅱ组动物肺部放射性减弱。Ⅲ组肺脏病检见头节广泛栓塞于肺小动脉、微小动脉中 ,肺脏呈“急性呼吸窘迫综合症样”改变。Ⅱ组肺组织出现淤血、水肿及炎细胞浸润。结论 :Ⅲ组动物基本能够模拟出囊型包虫病肺栓塞的临床表现。囊液中有形成分在肺损害中起着重要的作用。TXB2 、6 -keto -PGF1α参与了肺损伤病理过程。     

Genetic control of serum IgE levels: a study of low molecular weight protein tyrosine phosphatase

Protein tyrosine phosphatases (PTPases) have recently been recognized as important modulators of various signal transduction pathways in immune cells. Genetic polymorphisms have been described in genes codifying for members of this family of enzymes, and the genetics of PTPases is predicted to play an important role in the etiology of immune diseases and of their clinical variability. The low molecular weight protein tyrosine phosphatase (ACP1 or LMPTP) is one of the few PTPases with a known genetic polymorphism, and has been proposed to be associated with atopic dermatitis in a small sample from an Italian population. In this paper we describe the association of the ACP1 polymorphism with total IgE levels in two independent samples from English and Italian populations. In both the samples the mean value of serum IgE is lower among subjects carrying the BC genotype than in other ACP1 genotypes. The BC genotype is associated with the highest total ACP1 enzymatic activity. Our data suggest that one or both of the ACP1 isoforms exert an inhibitory role on some signal transduction pathway relevant for IgE hyperproduction.     

2型糖尿病患者血清von Willebrand因子变化与微血管并发症的关系

目的 :探讨 2型糖尿病患者的微血管内皮细胞功能损伤与微血管并发症之间的关系。方法 :从 3 3 4名 2型糖尿病患者中选择合并微血管并发症但未合并大血管并发症者 3 2人作为微血管并发症组 ,并选择年龄与之匹配的无大血管及微血管并发症 55人作为无并发症组 ,观察二组患者血清vonWillebrand因子 (vWF)水平 ,并与年龄相接近的正常对照组 ( 4 0例 )比较。结果 :血清vWF水平正常对照组 0 .92U± 0 .44U/ml;无并发症组 1.15U± 0 .42U /ml ;微血管并发症组 1.3 7U± 0 .44U/ml;三组之间均有显著性差异 (P <0 .0 5～ 0 .0 1)。多因素Logistic回归分析表明vWF、空腹血糖分别与糖尿病人是否合并微血管病变显著相关 (ExpB分别为 3 .0 2 3 ,1.3 3 7,P <0 .0 5～ 0 .0 1) ,以vWF为应变量的多元逐步回归分析表明年龄、糖尿病病程、甘油三酯分别与vWF呈显著独立正相关 (B =0 .53 ,0 .3 5,0 .2 9,P <0 .0 5～ 0 .0 1)。结论 :在糖尿病患者中存在不同程度的微血管内皮细胞的损伤 ,此变化随着微血管并发症的进展呈进行性加重。以vWF升高所反映的微血管内皮细胞损伤是一项值得临床推广的研究方法     

Independent integration of genes controlling the invasive properties and streptomycin resistance of enteropathogenic strain Escherichia coli 0124

CrossingEscherichia Coli K12 Hfr AB313 with an enteropathogenic strain ofE. coli of the serological group 0124 yielded recombinants which had lost their invasiveness. The loss of invasiveness of these recombinants was not due to the acquisition of genes controlling resistance to streptomycin.I. P. Pavlov First Leningrad Medical Institute. (Presented by Academician of the Academy of Medical Sciences of the USSR N. N. Zhukov-Verezhnikov.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 82, No. 9, pp. 1144–1145, September, 1976.     

Effect of hypothermia on renal sodium reabsorption

Summary The relationship between sodium reabsorption and oxygen consumption was studied in an isolated rabbit kidney preparation perfused with blood at 37, 28 and 19° C. When the temperature was lowered from 37° C to 28° C and to 19°C the rate of oxygen consumption and of the maximal P.A.H. excretion (Tm P.A.H.) decreased more than that of sodium reabsorption.TheQ ₁₀ for sodium reabsorption is about 1.8, while that for maximal P.A.H. excretion is 2.5. Some hypothesis on the possible mechanisms of the lowQ ₁₀ of the Na⁺ reabsorption are forwarded.Preliminary reports have been published [Boll. Soc. Ital. Biol. Sper.43, 1019–1023 (1966) and44, 1784–1787 (1967);45, 860–862 (1969) and45, 863–865 (1969)].     

健脾补肾药对脾虚大鼠细胞因子水平的影响

目的 :观察健脾补肾方药对实验性脾虚证大鼠细胞因子的影响 ,探讨脾虚证与细胞因子的关系及脏腑相关的意义。方法 :选用SD雄性大鼠 ,随机分为 :正常对照组 ,脾虚模型组 ,健脾补肾方高、低剂量组 ,通过大黄复制脾虚证动物模型 ,并用健脾补肾方药进行防治。采用放射免疫分析观察各组动物血清肿瘤坏死因子(TNF)、白细胞介素 - 6 (IL - 6 )、白细胞介素 - 2 (IL - 2 )水平的变化。结果 :脾虚模型组大鼠血清TNF、IL - 6、IL - 2含量均比正常对照组显著降低 (p <0 0 1) ,而健脾补肾方药能明显升高TNF、IL - 6、IL - 2含量 ,使体重增加 ,脾脏和胸腺组织的重量增加。结论 :脾虚证的发生与细胞因子网络调节系统的失衡有关 ,而健脾补肾中药对实验性脾虚证有较好的防治作用 ,脾肾相关理论对实践有指导意义。     

Haplotype analysis of the BRCA2 9254delATCAT recurrent mutation in breast/ovarian cancer families from Spain

A frame-shift 9254del5 mutation was independently identified in 12 families, eleven of them with Spanish ancestors, in a BRCA2 screening performed in 841 breast and/or ovarian cancer families and in 339 women with breast cancer diagnosed before the age of 40 at different centers in France and Spain. We sought to analyze in detail the haplotype and founder effects of the 9254del5 and to estimate the time of origin of the mutation. Eight polymorphic microsatellite markers and two BRCA2 polymorphisms were used for the haplotype analyses. The markers were located flanking the BRCA2 gene spanning a region of 6.1 cM. Our results suggest that these families shared a common ancestry with BRCA2 9254del5, which is a founder mutation originating in the Northeast Spanish, with an estimated age of 92 (95% CI 56-141) generations.     

Endomorphin-2 modulates productions of TNF-alpha,IL-1beta,IL-10, and IL-12, and alters functions related to innate immune of macrophages

We evaluate immunological effects of opioid peptide endomorphin-2 on the production of cytokines related to inflammation and Th1/Th2 balance, and functions related to innate immune of rat peritoneal macrophages. Endomorphin-2 inhibited TNF-, IL-10, and IL-12 productions, but potentiated IL-1 production by macrophages. Moreover, endomorphin-2 potentiated macrophage adhesion to fibronectin, and the expression of adhesion molecule Mac-1 on macrophages. In contrast, endomorphin-2 suppressed phagocytosis of opsonized E. coli by macrophages, without affecting phagocytosis of non-opsonized E. coli. In addition, endomorphin-2 inhibited macrophage chemotaxis, and the production of superoxide anion by macrophages. These results suggest that endomorphin-2 may alter macrophage functions such as cytokine productions and functions related to innate immune.