人参皂甙Rg1对老年大鼠免疫功能的调节作用

已知老年机体免疫功能的降低与淋巴细胞增殖能力的减弱和白细胞介素-2(IL-2)产生减少有密切关系。以老年大鼠免疫功能为主要研究对象,首次发现人参皂甙Rg1无论体内给药还是体外实验均能选择性增强老年大鼠脾淋巴细胞增殖能力和IL-2的产生与释放,采用Northern和Western印迹分析法证明,Rg₁可明显促进IL-2基因和蛋白的表达,表现在IL-2mRNA和IL-2蛋白含量的显著增加。值得注意的是,在同样的条件下,Rg₁对青年大鼠免疫功能的影响并不显著,由此可以认为Rg1一种“免疫调节剂”,而并非单纯的“免疫增强剂”。     

Markers of oxidative stress and antioxidant activity in plasma and erythrocytes in neonatal respiratory distress syndrome

Markers of oxidative stress and antioxidant activity in plasma and erythrocytes were studied for 14 d after birth in infants with neonatal respiratory distress syndrome ( n = 9) and controls ( n = 36). In plasma, the total radical trapping antioxidant capacity and the chain-breaking antioxidants vitamin C, sulfhydryl groups and bilirubin were similar. The differences in uric acid levels were not consistent, but vitamin E levels and vitamin E/total-lipid ratio were lower in the neonatal respiratory distress group ( p < 0.01). In erythrocytes, the antioxidant enzymes glutathione peroxidase, glutathione reductase and superoxide dismutase did not differ postnatally. Indicators of oxidative damage in plasma (sulfhydryl/protein ratio and thiobarbituric acid reactive substances) showed the same postnatal course in both groups and were not influenced by oxygen therapy. In erythrocytes the reduced/oxidized glutathione ratio showed no consistent differences. In conclusion, this study, using erythrocytes and plasma, does not provide convincing evidence of oxidative damage and diminished antioxidant defenses in preterm infants with neonatal respiratory distress syndrome.     

催产素对妊娠末期大鼠蜕膜细胞内游离钙的刺激作用

妊娠末期催产素刺激子宫蜕膜细胞产生与分娩有关的前列腺素,但其作用方式仍未知。本实验分离妊娠19d大鼠蜕膜细胞,测定了催产素作用后蜕膜细胞内游离钙的变化,结果加入0.001～1μmol·L^-1催产素后,蜕膜细胞内[Ca²⁺]i出现瞬息增加,其峰值与催产素浓度呈剂量依赖关系,且此作用有自身钝化现象。说明催产素可能激活妊娠末期大鼠蜕膜细胞内的肌醇磷酯蛋白激酶C系统。给妊娠末期大鼠ip硫酸去氢表雄酮钠盐后分离的蜕膜细胞,催产素作用引起[Ca²⁺]i瞬息增加峰值较对照升高。     

Cloning, functional activities and in vivo tissue distribution of rat NKR-P1+ TCR alpha beta + cells

We have successfully cloned nine NKR-P1+ TCR alpha beta + cells from PVG rat spleens, utilizing murine macrophage inflammatory protein-1 alpha (MIP-1 alpha) and IL-2. These clones are either double negative (DN, CD4-CD8-), which included clones 3.31, 3.71, 4.19, 4.59 and 4.65, or single positive (SP, CD4+CD8-), which included clones 1.64, 3.8, 3.76 and 3.78. No CD8+ clone was recovered. All nine clones are restricted in terms of their expression of the V beta antigens, since they express V beta 8.2 but not V beta 8.5, V beta 10 or V beta 16. These clones are agranular and they fall to generate NK or LAK activity upon incubation with IL-2, IL-12 or their combination. On the basis of their production of intracellular cytokines they can be divided into three categories: (I) SP clones (1.64, 3.8, 3.76 and 3.78) do not produce IL-2 or IL-4, but produce IFN-gamma and IL-12, and they vary in their production of IL-1, RANTES or tumor necrosis factor (TNF)-alpha; (II) DN clones 4.59 and 4.65 produce IL-1 alpha and IFN-gamma only, and fall to produce other cytokines; and (III) DN clones 3.31, 3.71 and 4.19 produce IL-1 alpha, IL-1 beta, IL-2, IL-12, IFN-gamma, RANTES and TNF-alpha. From all the clones examined only DN clones 3.31 and to a lesser degree 4.19 produce IL-4. In vivo tissue localization of clones 3.8, 3.31 and 4.59 shows that these cells distribute into the liver and bone marrow 24 h post i.v. administration. Their accumulation in the liver and bone marrow along with their ability to secrete various cytokines suggest that these cells may influence the generation, differentiation or apoptosis of immune or hematopoietic cells.      

Neurological sequelae in patients recovered from fulminant hepatic failure.

Two teenage patients with fulminant hepatic failure progressing to grade 4 encephalopathy with clinical signs of cerebral oedema are described, in whom permanent neurological injury (involving the brain stem in one and the cerebral cortex in the other) was the sequel to an otherwise full recovery. The present day management of cerebral oedema may, as in these two cases, ensure the survival of patients with fulminant hepatic failure who would previously have been likely to die from the effects of raised intracranial pressure. As a result it is now possible more recovered cases will be seen with residual neurological deficits, a previously very rarely recorded event.     

In vivo response of murine gamma delta T cells to a heat shock protein-derived peptide.

Recent results suggested that a large subset of heat shock protein HSP-60 reactive peripheral lymphoid gamma delta T cells preexists in normal adult mice, all members of which respond to a single segment of this common HSP. However, the experimental evidence supporting this idea involved in vitro peptide responses of gamma delta T-cell hybridomas generated from unprimed spleen cells. Here, we report an attempt to elicit a gamma delta T-cell response in vivo by stimulation of adult C57BL/10 mice with HSP-60 or an HSP-60-derived peptide fragment comprising amino acids 180-196 of mycobacterial HSP-60. Whereas no gamma delta T-cell response was detectable in mice injected with the intact protein, stimulation with the peptide altered the reactive gamma delta T-cell population in vivo. These changes were detected among hybridomas generated with cells restimulated in vitro and included a large increase in hybridizable gamma delta T cells, a nearly maximal increase in the relative frequency of HSP-60-reactive cells, and structural changes in expressed T-cell receptors of HSP-60-reactive cells. Interestingly, we failed to elicit a detectable alpha beta T-cell response to the particular peptide stimulatory for gamma delta T cells, although at least three other HSP-60 epitopes were recognized. Our data show that normal gamma delta T cells can respond in vivo to small peptide antigens. The gamma delta T-cell response to the HSP-60-derived peptide studied here is apparently independent of antigen-specific alpha beta T-cell reactivity.     

Epstein–Barr virus in the pathogenesis of oral cancers

Epstein–Barr virus (EBV) is a ubiquitous gamma‐herpesvirus that establishes a lifelong persistent infection in the oral cavity and is intermittently shed in the saliva. EBV exhibits a biphasic life cycle, supported by its dual tropism for B lymphocytes and epithelial cells, which allows the virus to be transmitted within oral lymphoid tissues. While infection is often benign, EBV is associated with a number of lymphomas and carcinomas that arise in the oral cavity and at other anatomical sites. Incomplete association of EBV in cancer has questioned if EBV is merely a passenger or a driver of the tumorigenic process. However, the ability of EBV to immortalize B cells and its prevalence in a subset of cancers has implicated EBV as a carcinogenic cofactor in cellular contexts where the viral life cycle is altered. In many cases, EBV likely acts as an agent of tumor progression rather than tumor initiation, conferring malignant phenotypes observed in EBV‐positive cancers. Given that the oral cavity serves as the main site of EBV residence and transmission, here we review the prevalence of EBV in oral malignancies and the mechanisms by which EBV acts as an agent of tumor progression.