损毁和刺激垂体对大鼠痛阈的影响

采用局限性损毁和刺激垂体的方法,以行为测痛为指标,观察大鼠垂体在痛觉调节中的作用以及地塞米松（Ｄｅｘ）对其影响。实验结果显示,损毁垂体中间叶（ＩＬ）及邻近的前叶（ＡＬ）,大鼠痛阈明显低于手术前的痛阈（Ｐ＜０．０１）。电刺激垂体的上述同样部位,大鼠痛阈明显高于手术基础值及自身假刺激值（Ｐ＜０．００１）。经Ｄｅｘ处理的动物,电刺激垂体不再引起痛阈升高。结果表明,大鼠垂体ＩＬ及靠近ＡＬ与痛调节有关,这种     

由大肠杆菌中提取重组猪生长激素的研究

 本文通过研究提出了一种由大肠杆菌细胞中提取重组猪生长激素的方法。提取回收率为52.4％,纯度为94.1％,具有生物学活性。     

双拷贝人α型心钠素基因的组建及大肠杆菌分泌型克隆与表达

将单拷贝人α心钠素基因3′端用Ban Ⅱ酶解除去包括终止密码在内的36个碱基对,代之以人工合成的含Glu-Lys-Phe-Glu连接片段与另一单拷贝人α心钠素基因的5′端串连成编码60肽的双拷贝心钠素基因,克隆于大肠杆菌分泌型表达载体pIN-Ⅲ-OmpA_2质粒中,表达生成60肽的双拷贝人α型心钠素衍生物,在信号肽的作用下分泌至胞膜间质并自动切割为60肽的外源基因产物。分子量约8K的表达产物用分子筛或超滤膜分离后再经HPLC纯化,表达产物具有明显的心钠素放免活性和舒张血管活性。     

Exogenous C1q reconstitutes a secondary deficiency of C5-deficient AKR mouse macrophages for FcR-dependent cellular cytotoxicity and phagocytosis

Studies originally designed to assess the putative role of endogenous C5 in macrophage activation for antibody-dependent cellular cytotoxicity (ADCC) yielded unanticipated results. Resident and inflammatory peritoneal macrophages from C5-deficient AKR mice were found to have significantly lower capacity for FcR-dependent ADCC activation and phagocytosis of IgG-opsonized SRBC targets than did C5-competent C3HeB/FeJ (C3H) mice. Reconstitution of the ADCC response of AKR macrophages was accomplished initially with C5-sufficient C3H mouse serum, which suggested that endogenous C5 may be required for ADCC activation. However, further investigation largely eliminated C5 involvement in that a heat-labile component of C5-deficient AKR serum was shown to be active in the reconstitution of ADCC activation of AKR macrophages. Macrophages from AKR mice were found to have significantly lower levels of C1q mRNA synthesis, endogenous C1q levels, and C1q secretion than did C3H mouse macrophages as determined by Northern blot, Western blot, and presynthetic radiolabeling analysis, respectively. The addition of purified exogenous C1q to IgG-opsonized SRBC targets fully reconstituted ADCC activation for AKR inflammatory peritoneal macrophages to levels of normally FcR-responsive C3H macrophages. Similarly, exogenous C1q augmented FcR-dependent phagocytosis of AKR macrophages but had no effect on macrophages from responsive C3H mice. Our results indicate that AKR mice have a deficiency for FcR-dependent cellular cytotoxicity and phagocytosis that is related to their low potential for C1q synthesis and secretion rather than to their established genetic deficiency for C5 synthesis. We tentatively conclude that endogenous C1q is required as an accessory molecule for macrophage FcR-dependent effector functions and that C5 is not a prerequisite for ADCC activation.     

Functional analysis of the 3′-terminal sequence of the maize controlling element (Ac) by internal replacement and deletion mutagenesis

Using deletion analysis of the Ac transposable element, we have shown that replacement of internal sequences from base pairs 181–3559 does not abolish transposition. We have done sequential deletion analysis of the 3'-end of the Ac element and found that deletion of the major transposase binding sites (AAACGG) abolishes transposition. But, surprisingly, we found a 3'-terminal deletion of the transposase binding sites which also contained a 71-bp internal sequence between base pairs 3559 and 3630 retained transposition ability. This 71-bp internal sequence did not have a transposase (ORFa) binding motif. These data suggest that two different domains may be involved in the minimal sequence necessary for transposition. Finally, we have identified functional prokaryotic promoter sequences and ARS sequences within the 5' and 3'-termini of Ac, but cannot ascribe any function to these sequences.     

真正柑桔果树群植物的分支学研究

本文用相容性分析方法(Compatability snalysis)分析了真正柑桔果树群(芸香科Rutaceae-柑桔亚科Aurantioideae-柑桔族(Citreae)-柑桔亚族(Citrinae)植物内各属间的分支学关系。给出了建立在7个相容性性状组成的最大族所决定的分支图。性状极性的确定使用了外群法。结果表明,柑桔属(Citrus L.)和多蕊桔属(Clymenia Swing)构成一个单系类群,他们的姐妹群是金柑属(Fortunella Swing.)。被认为起源于中国的3个属,柑桔属(Citrus)、金柑属(Fortunella)和积属(Poncirus Raf.)并未构成一个单系类群。本文还利用分支关系分析和讨论了真正柑桔果树群的种系发生关系。     

转移及非转移肿瘤移植后615小鼠血液流变学变化的研究

血道高转移瘤株FC、淋巴合并血道高转移瘤株U14、淋巴道高转移瘤株H22、非转移瘤株P615分别接种于336只纯系近交615小鼠.不同时间取血并处死动物,进行组织学及血液流变学检查.将转移瘤发展过程分为潜伏期、侵袭期、转移早、中、晚期,非转移瘤发展过程分为潜优期、增殖期、囊腔形成期及中心坏死期.本实验结果显示,不同转移能力及途径肿瘤发展的不同时期血液流变学变化规律不同,因而表明肿瘤侵袭、转移与血液流变学变化之间存在互为因果的紧密关系.其临床诊断及治疗意义被讨论.