Mechanism of Kenaf Retting Using Aerobes

The experimental results showed that the duration of microbial retting processing of kenaf fibers by using aerobic microbe was four times shorter than that by using anaerobic microbe. The residual gum percentage, breaking strength, breaking elongation and linear density of aerobic retted kenaf bundle fibers did not show significantly difference with that of anaerobic retted kenaf bundle fibers by ANOVA-Tukey's studentized test at a = 5% except for the softness. The bioenergetic principle and the calculation of the amount of ATP produced during the decomposition processing of kenaf gums were used to explain why the retting duration in the case of using aerobic microbes was much shorter than that of using anaerobic microbes.     

[FeFe] hydrogenases and their evolution: a genomic perspective

Most hydrogenases (H2ases), the enzymes that produce or oxidize dihydrogen, possess dimetallic active sites and belong to either one of two phylogenetically distinct classes, the [NiFe] and the [FeFe] H2ases. These families of H2ases share a number of similarities regarding active site structure and reaction mechanism, as a result of convergent evolution. They are otherwise alien to each other, in particular with respect to protein sequence and structure, maturation mechanisms, and distribution among the realms of life. One of the interesting features of [FeFe] H2ases is their occurrence in anaerobic bacteria, anaerobic protists, and mitochondriate eukaryotes. They thus have the potential to report on important evolutionary events, including transitions from the prokaryote to the eukaryote lifestyle. Genome sequences yield a variety of [FeFe] H2ase sequences that have been implemented to shed light on the evolution of these proteins and their host organisms.     

Progress in molecular parasitology

Summary Substantial progress has been made in the last ten years in understanding the structural and functional organization of parasitic protozoa and helminths and the complex physiological relationships that exist between these organisms and their hosts. By employing the new powerful techniques of biochemistry, molecular biology and immunology the genomic organization in parasites, the molecular basis of parasite's variation in surface antigens and the biosynthesis, processing, transport and membrane anchoring of these and other surface proteins were extensively investigated. Significant advances have also been made in our knowledge of the specific and often peculiar strategies of intermediary metabolism, cell compartmentation, the role of oxygen for parasites and the mechanisms of antiparasitic drug action. Further major fields of interest are currently the complex processes which enables parasites to evade the host's immune defense system and other mechanisms which have resulted in the specific adaptations which enabled parasites to survive within their host environments. Various approaches in molecular and biochemical parasitology and in immunoparasitology have been proven to be of high potential for serodiagnosis, immunoprophylaxis and drug design.This paper is based on a review presented at a workshop on Molecular Parasitology, organized by the Swiss Society of Tropical Medecine and Parasitology at the University of Neuchâtel, March 1985.     

生物能力学原理在红麻好氧性微生物脱胶中的应用

用实验证实了红麻纤维在微生物好氧条件下的脱胶速度比在厌氧条件下快四倍,且前者残胶率也低于后者.根据生物能力学原理并通过ATP数量计算从理论上论证了上述的实验结果.     

生物能量学理论及其虾蟹类的研究进展

生物能量学是研究能量在生物体内转换的科学．本文重点介绍动物个体水平上的能量转换的基本理论和方法．能量收支方程为：C=G＋R＋U＋F，其中，R=SDA＋Rs＋Ra；虾蟹类能量收支方程为：C=G＋R＋U＋F＋E研究上式各组分与环境因子和内源因子的关系，及各组分间的定量关系是生物能量学的主要内容．本文还介绍了虾蟹类生物能量学研究一些新进展，如各种生态因子对虾蟹类能量收支的影响、SDA与营养因子关系的研究和虾蟹类响应环境突变的能量学机制的研究等．最后．对生物能量学在种群营养动力学研究方面的应用、种群水平的生物能量学研究和生物能量学在水产养殖以及在育种方面的应用等方面作了展望．     

Morphine but not fentanyl and methadone affects mitochondrial membrane potential by inducing nitric oxide release in glioma cells

We have observed that treatment of human glioma cells with morphine in the nanomolar range of concentration affects the mitochondrial membrane potential. The effect is specific to morphine and is mediated by naloxone-sensitive receptors, and is thus better observed on glioma cells treated with desipramine; moreover, the mitochondrial impairment is not inducible by fentanyl or methadone treatment and is prevented by the nitric oxide (NO) synthase inhibitor L-NAME. We conclude that in cultured glioma cells, the morphine-induced NO release decreases the mitochondrial membrane potential, as one might expect based on the rapid inhibition of the respiratory chain by NO. The identification of new intra-cellular pathways involved in the mechanism of action of morphine opens additional hypotheses, providing a novel rationale relevant to the therapy and toxicology of opioids.Received 19 August 2004; received after revision 16 September 2004; accepted 7 October 2004