利巴韦林在体外对小鼠脾细胞NK活性的影响

采用¹²⁵I-UdR同位素释放试验,观察利巴韦林(三氮唑核苷,RTC)在体外对小鼠脾细胞自然杀伤(Nk)活性的影响。结果表明,RTC的剂量与NK活性呈负相关,在5umol·L^-1时RTC即可显著抑制NK活性。RTC与地塞米松合用对NK活性的抑制有相加作用,而RTC与γ干扰素合用则互为拮抗作用。此外,还发现RTC能明显降低刀豆蛋白A诱生的小鼠脾细胞干扰素及白细胞介素-2的产量,推测RTC对NK活性抑制的部分机理是阻碍了这些淋巴因子的生成。     

Severe anaphylactic reactions following transfusions of platelets to a patient with anti-Ch

The high-frequency Chido (Ch) antigen, found predominantly in plasma, is a determinant of the C4d fragment of the C4 molecule and is acquired by red cells during in vivo complement activation. Antibodies are made by Ch- people who lack C4S. It has often been reported that anti-Ch (and anti-Rg) do not cause hemolytic transfusion reactions. Reported here is a case of a transfusion reaction caused by anti-Ch. The antibody did not cause red cell destruction, but did cause a life-threatening anaphylactic reaction during transfusion of plasma proteins in pooled platelets. The antibody was of the IgG4 subclass and might have caused a short-term, sensitizing anaphylactic response. This case, and one previously reported in which a patient with anti-Rg experienced a severe reaction to fresh-frozen plasma and a plasma derivative, illustrates that these antibodies can cause severe, life-threatening reactions in patients who receive plasma-containing components.     

Enrichment of two glycosyl-phosphatidylinositol-anchored proteins, acetylcholinesterase and decay accelerating factor, in vesicles released from human red blood cells

Several proteins are attached to the cell membrane by a glycosyl- phosphatidylinositol (GPI) anchor. In this report, we show that during vesiculation of human RBCs in vitro, two of these proteins, acetylcholinesterase and decay accelerating factor, redistribute on the cell surface and become enriched in the released vesicles. As a result, the remnant cells are depleted of these proteins. We suggest that alterations in the architecture of the RBC membrane that precede vesiculation lead to selective polarization of GPI-anchored proteins within the domain of the membrane destined to become a vesicle. Since vesiculation occurs in many cell types, and if the loss of GPI-anchored proteins accompanies this process, it may have important biologic significance.     

Long-range mapping of the Philadelphia chromosome by pulsed-field gel electrophoresis

The Philadelphia chromosome (Ph1) of chronic myelogenous leukemia (CML) contains sequences from chromosome 9, including the ABL protooncogene, that have been translocated to the breakpoint cluster region (bcr) of chromosome 22, giving rise to a bcr-ABL fusion gene, whose product has been implicated in the genesis of CML. Although chromosome 22 translocation breakpoints in CML virtually always occur within the 5.8- kilobase (kb) bcr, chromosome 9 breakpoints have been identified within the known limits of ABL in only a few instances. For a better understanding of the variability of the breakpoints on chromosome 9, we studied the CML cell line BV173. Using pulsed-field gel electrophoresis (PFGE), large-scale maps of the t(9;22) junctions were constructed. The chromosome 9 breakpoint was shown to have occurred within an ABL intron, 160 kb upstream of the v-abl homologous sequences, but still 35 kb downstream of the 5'-most ABL exon. bcr-ABL and ABL-bcr fusion genes were demonstrated on the Ph1 and the 9q+ chromosomes, respectively; both of these genes are expressed. These results suggest that the 9;22 translocation breakpoints in CML consistently occur within the limits of the large ABL gene. RNA splicing, sometimes of very large regions, appears to compensate for the variability in breakpoint location. These studies show that PFGE is a powerful new tool for the analysis of chromosomal translocations in human malignancies.