Phagocyte-derived catecholamines enhance acute inflammatory injury

It is becoming increasingly clear that the autonomic nervous system and the immune system demonstrate cross-talk during inflammation by means of sympathetic and parasympathetic pathways. We investigated whether phagocytes are capable of de novo production of catecholamines, suggesting an autocrine/paracrine self-regulatory mechanism by catecholamines during inflammation, as has been described for lymphocytes. Here we show that exposure of phagocytes to lipopolysaccharide led to a release of catecholamines and an induction of catecholamine-generating and degrading enzymes, indicating the presence of the complete intracellular machinery for the generation, release and inactivation of catecholamines. To assess the importance of these findings in vivo, we chose two models of acute lung injury. Blockade of alpha2-adrenoreceptors or catecholamine-generating enzymes greatly suppressed lung inflammation, whereas the opposite was the case either for an alpha2-adrenoreceptor agonist or for inhibition of catecholamine-degrading enzymes. We were able to exclude T cells or sympathetic nerve endings as sources of the injury-modulating catecholamines. Our studies identify phagocytes as a new source of catecholamines, which enhance the inflammatory response.     

在基本的认知物理学习系统中相互作用的多媒体的应用(下)

现代社会要求理工科学生在大学教育中逐渐掌握各种科学研究的手段及个人技能,以满足21世纪的需要．我们描述了一个帮助学生发展这种技能及在实际科学研究中的认知过程,系统技术在这个学习系统的许多方面起到非常重要的作用,我们描述了在各种国际测量表中描述的教育目标,描述了部分满足这个目标的学习系统,描述了技术在这个系统中的作用以及这个学习系统的有效性评估．