寄生云杉树蜂的枝跗瘿蜂一新种(膜翅目:瘿蜂总科:枝跗瘿蜂科)

枝跗瘿蜂科(Ibahidae)是个小科,所有种类均寄生蛀干害虫树蜂科(Siricidae)的幼虫。我国大陆的本科种类由杨忠岐1991年首次作了报道。现记述采自祁连山林区的另1新种。该种寄生于为害青海云杉(Picea crassifolia Kom.)的黄肩长尾树蜂(Xeris spec-trum spectrum)等树蜂的幼虫。新种的模式标本保存于西北林学院天敌昆虫研究室。至此,我国大陆共有本科种类3种,加上台湾的1个种,我国共有4种:     

环螽属二新种及一新记录种：（直翅目：螽斯总科,露螽科）

环螽属Letana Walker,1869(=Pyrrhicia Stal,1873)迄今已知22种,分布中国、越南、泰国、缅甸、尼泊尔、印度和斯里兰卡等国。作者在整理这个属的标本时发现2新种和1新纪录种,分别采自中国(西藏)和尼泊尔,现记述于后。模式标本均保存在中国科学院上海昆虫研究所。     

人参根系发育形态学的研究

人参(Panax qinseng C. A. Meyer)属于直根系植物,有次生构造。一年生苗只具有主根和侧根。二年以上的人参常在根状茎上长出不定根,即人参根系包括主根和不定根及其各级分枝。主根初生木质部为三原型,侧根和不定根及其分枝多为二原型,偶见三原型。根系随参龄的增加而增大。每年末级分枝自基部于休眠前萎缩、脱落,并在萎缩部分的上一级支根内部产生越冬根原基,越冬根原基是翌年形成全部吸收根的基础。一年生人参由中柱鞘产生一圈初生树脂道,由形成层产生一圈(或二圈)次生树脂道,以后次生树脂道的圈数随参龄的增加而每年增加一圈,自第五年开始渐缓。根内淀粉粒含量随发育时期的变化而相应变化,其积累高峰出现在果后期。研究人参根系发育形态学不仅对全面正确认识人参根系具有理论意义,而且对改进人参栽培管理和评价人参质量具有指导意义。     

银额果蝇的B染色体研究:1.昆明群体的Bs数目和频率

本研究发现银额果蝇昆明群体有丝分裂中期核型中存在B染色体,出现频率为69.1%。目前,在已研究过的来自各个地区的银额果蝇中,昆明群体的B染色体频率最高。B染色体数目为1-6条。该群体内单雌系间的B染色体数目不同,个体间和细胞间的B染色体数目也不同。在核型中,B染色体最小,形态稳定,点状,C-带和G-带呈阳性。     

神经节苷脂对6-OHDA损毁交感神经末梢的对抗作用

单次6-OHDA (15mg/kg.i.p.)注射后24h,可使雌性成年小鼠颌下腺内儿茶酚胺荧光神经末梢几乎完全消失;同时用 HPLC 测得腺体内去甲肾上腺素(NA)和多巴胺(DA)的含量下降至正常值的3—4%以下。随着受损交感神经末梢再生过程,NA 和 DA 水平有缓慢的恢复。在损毁2周时 NA 和 DA 含量分别达到正常水平的50%和28%,且在4周时完全恢复。在注射6-OHDA 的同时,和在损伤后12h 内给动物注射4次神经节苷脂(每次50mg/kg.i.p.)并在其后的一周內每天注射一次,可使颌下腺内 NA 含量维持在正常水平;在损毁后4h 及损毁前4d 开始施用神经节苷脂,也可不同程度地对抗交感神经末梢损伤,但作用强度不如前者。实验结果提示:(1)神经节苷脂通过减弱6-OHDA 及其代谢产物的损伤效应能够保护交感神经末梢膜,它可能还有促损伤末梢再生性长芽的作用;(2)损伤后神经节苷脂处理得越早,其效果越好。     

促性腺激素诱导猕猴排卵周期中卵巢纤溶酶原激活因子与抑制因子的变化

在用 PMSG 和 hUG 诱导猕猴排卵过程中,我们研究了 pA 和它的抑制因子 PAI-1与排卵的关系。实验结果表明,由促性腺激素所诱导出的卵巢 tPA 活性的增加与排卵密切相关,在排卵前达到高峰,而排卵后明显下降;uPA 只在排卵后的颗粒细胞大量出现;PAI-1分泌高峰比 tPA 峰值早出现12—24小时;排卵来临时,tPA 的明显上升导致 PAl-1的空然下降。上述实验结果说明,卵巢中 tPA 和 PAI-1活性的这种平衡性的变化可能在排卵机制和维持卵巢的正常生理功能中起重要作用,而 uPA 或许与黄体形成的调节有某些关系。     

大鼠中枢神经系统衰老的形态学研究Ⅳ.大脑皮质锥体细胞树突棘的数量变化

用6、12与31个月的雄性Wistar大鼠的大脑Krieg 2、3区皮质,对其V层大锥体细胞的五段50μm长度内的树突棘做形态学定量研究。在Golgi法的切片中共计数了三个年龄组的151个细胞的725段树突的棘密度。结果表明,老年大鼠比成年和青年大鼠的棘密度普遍下降。其中以基树突与侧树突棘度下降最显著(减少24％左右),顶树突只中段有明显减少。老年大鼠锥体细胞还常出现胞体、树突及其分支的明显形态改变。     

Reduced cyclosporin accumulation in multidrug-resistant cells

Cyclosporin accumulation was reduced by 50% or more in multidrug- resistant CHRC5 CHO cells with high levels of P-glycoprotein expression compared to drug sensitive AuxB1 CHO cells. This difference could be overcome by verapamil which is known to interact with P-glycoprotein and reverse multidrug resistance. The difference in cyclosporin accumulation between sensitive and resistant cells decreased with increasing cyclosporin concentrations suggesting that cyclosporine itself regulated its own accumulation through interaction with P-glycoprotein. Indeed, cyclosporin also reversed differences in vinblastine accumulation between resistant and sensitive cell lines. Since P-glycoprotein is highly expressed in the kidney which is also a target for cyclosporin toxicity, the effects of verapamil on cyclosporin accumulation were studied in two renal cell lines, rat mesangial cells and LLCPK1, cells. Verapamil increased cyclosporin accumulation by approximately 70%. These results suggest that cellular cyclosporine accumulation is regulated at least in part by its interaction with P-glycoprotein.     

Antibodies to peptide determinants in transforming growth factor beta and their applications

Polyclonal antibodies have been raised to a series of synthetic peptides which correspond to essentially all regions of the transforming growth factor beta 1 (TGF-beta 1) molecule. All antisera were evaluated for their abilities to react with TGF-beta 1 and TGF-beta 2 in either the native or reduced form in enzyme-linked immunosorbent assays, Western blots, and immunoprecipitation assays. While all antisera demonstrated some ability to recognize TGF-beta 1 in these systems, there was limited cross-reactivity with TGF-beta 2, suggesting that substantial sequence or conformational differences exist between the two growth factors. On Western blots 5-10 ng of purified human platelet TGF-beta 1 could be detected when probed with affinity-purified peptide antisera generated against peptides corresponding to residues 48-77, 50-75, and 78-109 of the 112 amino acid TGF-beta 1 monomer. Antisera raised against peptides 50-75 and 78-109 were most effective in immunoprecipitating reduced and native 125I-TGF-beta 1, respectively. The antisera also were tested for their effectiveness in blocking the binding of 125I-TGF-beta 1 to its receptor. Anti-peptide 78-109 and anti-peptide 50-75 blocked 80% and 40% of the binding, respectively, while antibodies against amino-terminal peptides were without effect. These data suggest that the carboxyl-terminal region of TGF-beta 1 may play a significant role in the binding of the native ligand to its receptor.     

Altered plasma membrane ultrastructure in multidrug-resistant cells

Multidrug resistance is mediated by P-glycoprotein, an integral plasma membrane component which is thought to function as a drug export pump. This model can explain drug resistance, but fails to account for the broader pleiotropy of the multidrug resistance phenotype. We report here a freeze-fracture study revealing increases in the densities of protoplasmic face intramembrane particles in multidrug-resistant Chinese hamster ovary (CHO) and human leukemic cells. The intramembrane particle density in a CHO cell revertant which had lost the characteristics of the multidrug resistance phenotype was indistinguishable from that of the drug-sensitive parental cell line. This demonstration of a global multidrug resistance-linked change in plasma membrane architecture may have significant implications for understanding the variety of concurrent membrane-related changes which are not easily explained by the current model for multidrug resistance.