改变生态条件除藻方法的研究

根据食物链中Ｅｌｔｏｎｉａｎ金字塔的形态和Ｋａｌｋｗｉｔｚ提出的河流污染沿程变化分带的概念，提出了改变生态条件培养高一层次生物吃掉藻类的除藻方法，并在工艺上应用浮动生物滤清器解决了这一问题，取得了较好的除藻效果。     

发酵代谢物对葡萄糖氧化酶生物合成的影响

用膜透析技术和静息细胞系统，对影响葡萄糖氧化酶（ＧＯＤ）发酵的控制因素进行了研究。静息细胞系统显示：鸟氨酸、谷氨酸、甘氨酸、丙氨酸、丝氨酸和胱氨酸等氨基酸对ＧＯＤ的合成有促进作用；葡萄糖酸和丙酮酸对ＧＯＤ的合成有阻遏作用，１．５ｍｍｏｌ／Ｌ的丙酮酸使酶活降低４６．２４％；２０ｍｍｏｌ／Ｌ的葡萄糖酸使酶活降低２１％左右，但葡萄糖酸浓度增大，有被菌体作为碳源利用的可能。利用膜透析技术可除去部分发酵过程中产生的葡萄糖酸和丙酮酸等阻遏物，减少它们对ＧＯＤ合成的分解代谢物的阻遏作用，与分批发酵相比．提高酶活４０％左右。     

人胎儿小脑皮质蒲肯野细胞发育的定量观察

本文应用体视学方法，对３５例不同月龄组的胎儿，观察其小脑皮质蒲肯野细胞在发育过程中的变化．结果发现蒲肯野细胞层在胚胎第６个月时出现，其数密度和核体密度随月龄的增长逐渐减少，细胞的体积则随月龄的增长而逐渐增大．体密度与表面积密度变化不明显．     

固定化猴头菌细胞的研究

报道了利用海藻酸钠固定化猴头菌细胞的发酵情况．就包埋剂的最佳浓度、固定化细胞的发酵条件以及固定化猴头菌细胞在深层发酵中应用的可行性进行了探讨．结果表明：最佳海藻酸钠的浓度为２％，氯化钙浓度为２％，固定化猴头菌细胞在发酵培养基内的代谢与游离细胞的代谢基本一致，发酵液中氨基酸含量最高可达８００ｍｇ／Ｌ，多糖含量最高可达１４００ｍｇ／Ｌ，固定化细胞可以连续使用３２～４８ｄ，因此固定化猴头菌细胞在工业生产中是可行的     

提高铝电解槽磁场计算精度的研究

本文讨论了计算铝电解槽磁场的各种数学模型,指出了等效数学模型存在的问题及其在计算中产生误差的原因,提出了提高磁场计算精度应采用实际数学模型,即按母线的实际形状计算各载流母线产生的磁场.     

大连水云科藻类的研究

大连地区水云科藻类有9属19种,其中前人报道过的2种,本地区新记录17种。在这17种中,有11种是我国首次记录。本文对新记录种的形态、生态与分布作简要描述。     

丁酸钠对M期同步及非同步的HeLa细胞早G_1期阻断的可逆性

本文采用早熟染色体凝集(PCC)和~3H-TdR显微自显影技术,观察丁酸钠对同步及非同步的HeLa细胞早G_1期阻断的可逆性及其可逆的进程。实验发现丁酸钠对HeLa细胞早G_1期阻断完全是可逆的,且这种可逆是在洗去丁酸钠后立即产生,丁酸钠对HeLa细胞早G_1期阻断的时间点发生在细胞进入S期前的9.5h;发现早G_1期阻断后的恢复必须再经过中、晚G_1期然后才能进入S期.     

Protein kinases mediate nitric oxide-induced apoptosis in the insect cell line IPLB-LdFB

The involvement of protein kinases (PKA, PKC and PKB) in nitric oxide (NO)-induced apoptosis with sodium nitroprusside plus N-acetyl-L-cysteine in the IPLB-LdFB cell line from the insect Lymantria dispar was investigated. The presence of protein kinase-like molecules was demonstrated by western blot analysis. The role of the kinases in programmed cell death was analysed in cytofluorimetric experiments by incubating the insect cells with H-89 (a specific inhibitor of PKA), calphostin C (an inhibitor of PKC) or wortmannin (an inhibitor of phosphatidylinositol 3-kinase). The results show that PKA is correlated with the induction and PKC and PKB with the prevention of NO-induced insect cell death. Moreover, NO-induced apoptosis involves the release of cytochrome c. Received 15 March 2002; accepted 25 March 2002     

Myelin sheaths: glycoproteins involved in their formation,maintenance and degeneration

Myelin sheaths are formed around axons by extending, biochemically modifying and spiraling plasma membranes of Schwann cells in the peripheral nervous system (PNS) and oligodendrocytes in the central nervous system (CNS). Because glycoproteins are prominent components of plasma membranes, it is not surprising that they have important roles in the formation, maintenance and degeneration of myelin sheaths. The emphasis in this review is on four integral membrane glycoproteins. Two of them, protein zero (P0) and peripheral myelin protein-22 (PMP-22), are components of compact PNS myelin. The other two are preferentially localized in membranes of sheaths that are distinct from compact myelin. One is the myelin-associated glycoprotein, which is localized at the inside of sheaths where it functions in glia-axon interactions in both the PNS and CNS. The other is the myelin-oligodendrocyte glycoprotein, which is preferentially localized on the outside of CNS myelin sheaths and appears to be an important target antigen in autoimmune demyelinating diseases such as multiple sclerosis. Received 8 April 2002; received after revision 13 May 2002; accepted 22 May 2002     

The Ror receptor tyrosine kinase family

Receptor tyrosine kinases (RTKs) participate in numerous developmental decisions. Ror RTKs are a family of orphan receptors that are related to muscle specific kinase (MuSK) and Trk neurotrophin receptors. MuSK assembles acetylcholine receptors at the neuromuscular junction [1, 2], and Trk receptors function in the developing nervous system (reviewed in [3-5]). Rors have been identified in nematodes, insects and mammals. Recent studies have begun to shed light on Ror function during development. In most species, Rors are expressed in many tissue types during development. Analyses of mutants that are defective in the single nematode Ror demonstrate a role in cell migration and in orienting cell polarity. Mice lacking one of the two Ror gene products display defects in bone and heart formation. Similarly, two different human bone development disorders, dominant brachydactyly B and recessive Robinow syndrome, result from mutations in one of the human Ror genes. Received 17 April 2001; received after revision 2 July 2001; accepted 4 July 2001