Monoclonal antibodies to mouse complement receptor type 1 (CR1). Their use in a distribution study showing that mouse erythrocytes and platelets are CR1-negative

mAb to murine C receptor type 1 (CR1) were produced and three of them were characterized. One antibody, designated as 8C12, immunoprecipitated a protein of 190,000 Mr from a detergent extract of surface-labeled spleen cells and stained spleen B but not T lymphocytes in fluorescent flow cytometry. It inhibited both CR1-mediated rosette formation and the cofactor activity of CR1 for factor I-mediated cleavage of C3b, suggesting that it recognizes the ligand-binding site of CR1. The two other antibodies, designated as 7G6 and 7E9, recognized different epitopes from that recognized by 8C12, and they cross-reacted with a protein of 150,000 Mr that is present in a spleen extract. The distribution of CR1 in murine hemopoietic cells was studied by binding experiments with radiolabeled 8C12 and fluorescent flow cytometry. When CR1 was not detected by 8C12 alone, the two other antibodies were used in combination with 8C12 to confirm the negative results. Almost all B lymphocytes from the spleen, lymph nodes, and peripheral blood were CR1 positive. Most of the Thy-1-positive lymphocytes from these tissues were CR1 negative. Thymus lymphocytes were also CR1 negative. Peritoneal macrophages and chemotactic factor stimulated but not unstimulated peripheral blood granulocytes were CR1 positive. In contrast to human E, mouse E were CR1 negative. This pattern of distribution was consistent with previous results obtained by rosette assays. Although mouse platelets cause immune adherence hemagglutination with C3b-bearing SRBC, they are CR1 negative. Three other lines of evidence also indicated that platelets are CR1 negative. First, no band of CR1 was demonstrated by immunoprecipitation with 8C12 of an extract of surface-labeled platelets. Second, 8C12, which inhibited rosette formation by lymphocytes, alone or in combination with 7G6 and 7E9, did not inhibit immune adherence between platelets and C3b-bearing SRBC. Third, polyclonal rabbit IgG prepared from anti-mouse CR1 antiserum did not inhibit immune adherence by platelets. These results strongly suggest that the C3b-binding factor(s) on mouse platelets is different from CR1 and that processing of C3b-bearing immune complexes in mouse blood may be mediated by a new and as yet unidentified C3b-binding factor(s).     

从“湖北光敏感核不育水稻”的未受精子房和花药培养出单倍体植株

采用10种诱导培养基,培养湖北光敏感核不育水稻农垦58品种的未受精子房和花药。共培养未受精子房2790个,获得胚囊愈伤组织17块,最高诱导频率达3.33%,其中2块分化出绿苗。培养花药16740个,获得花药愈伤组织15块,最高诱导频率为0.92%,其中3块分化出苗,2丛白苗,1株绿苗。胚囊植株和花粉植株经根尖染色体检查为单倍体,2n=x=12。实验证明,液体培养、2,4-D0.2-0.5 mg/1、低温预处理对诱导胚囊愈伤组织及花粉愈伤组织的形成具良好效果。     

大鼠应激性胃粘膜损害与eAMPCa~2及能量代谢变化的关系

本文采用放射免疫测定法、原子吸收光谱分析法和生化酶分析法,测定了大鼠在经受束缚加浸水急性应激四小时内,胃组织cAMP Ca~(2+)及在ATP、ADP、AMP和能量代谢的短期动态变化,同时观察了胃粘膜的损害程度。结果发现胃粘膜损害面积密度随着应激时间延长而逐渐增加;胃组织cAMP和Ca~(2+)则进行性降低;两者呈密切负相关;胃组织能量代谢却略有增强。若预先给以CaCl_2,再予应激,则有减轻应激性胃粘膜损害的作用。     

TPA对原代白血病细胞的诱导分化作用

本文报告了TPA对32例不同类型白血病细胞的体外分化诱导结果。TPA(1.6×10~-7M)可诱导急性非淋巴细胞(ANLL)白血病细胞迅速出现单核巨噬细胞分化标志:细胞贴壁、胞浆丝状伪足形成,具有类似巨噬细胞的形态改变及相应的细胞化学反应特征。急性淋巴细胞白血病(ALL)和桨细胞白血病(PCL)细胞不发生上述变化,表现为细胞聚集成闭现象。慢性淋巴细胞白血病(CLL)出现桨细胞样形态转化。初发与复发病例的诱导反应相类似。TPA体外诱导分化实验,有助于了解病人白血病细胞的分化潜能,对于鉴别粒单系和淋巴系两类白血病,尤其对于用常规方法分型困难的低分化白血病有一定的临床诊断意义。     

柴达木盆地荒漠土壤蓝藻群落的初步研究

本文分析了柴达木盆地东部和中部具有代表性地区的丘陵、戈壁和沙丘的蓝藻种类组成、生物量及主要的土壤化学成分;采用了模糊聚类、系统聚类及多元线性回归等方法分析藻类的群落及其与环境因子的关系。共鉴定出21种蓝藻,其中6种为国内首次报道。研究表明:土壤含磷量、总盐量及与粘性和湿度有关的土壤结构是决定柴达木盆地蓝藻群落组成的重要因素。     

Plant-microbial interaction under gnotobiotic conditions: A scanning electron microscope study

Inoculation of canola seeds withPseudomonas putida GR12-2 stimulates root elongation under gnotobiotic conditions. Transformation ofP. putida GR12-2 with the broad-host-range plasmid pGSS15 abolishes the enhancement of root elongation. With scanning electron microscopy it was found that both transformed and nontransformedP. putida GR12-2 are capable of binding to canola seed coats. In addition, it was observed that 4 days after the initial inoculation the roots of bothP. putida GR12-2- and GR12-2/pGSS15-treated seedlings were free of adhering bacteria despite the fact that it was subsequently shown that both bacterial strains are capable of binding to roots. Thus, adhesion to roots is not necessary for the initial phase of enhanced root elongation that is induced byP. putida GR12-2 under gnotobiotic conditions.