矽肺发病的当代概念和设想

矽肺是一种因吸入各种形式的结晶型二氧化硅(SiO_2)所引起的慢性炎症性和纤维性的肺部疾病。本文主要讨论有细胞免疫或体液免疫反应参与的炎症和纤维化活动的交替作用,从而导致矽肺的发生这样一个假想的发病机理。粉尘的沉积与清除及矽肺的病理学特点吸入的粉尘在呼吸道不同部位的沉积取决于颗粒的大小、形状、质量、空气动力学特性和其他物理性质。一般0.5～5μm的粉尘可到达呼吸道下部,并沉积在小气道或肺泡,而<0.5μm的粉尘可悬浮于呼出气流中或沉积于肺泡内。沉积于气道纤毛上皮的粘膜荚     

Stimulation of Indole Alkaloid Content in Vanadium-Treated Catharanthus roseus Suspension Cultures

Addition of vanadyl sulphate to cell suspensions of CATHARANTHUS ROSEUS was found to increase ajmalicine, catharanthine, and tryptamine levels. Up to 500 microg/g dry weight catharanthine and 131.0 microg/g dry weight ajmalicine were detected in vanadyl sulphate-treated cells. This represents an approximate increase of 50% over control levels. This stimulation was found to be dependent upon the concentration of vanadyl sulphate administered and upon the cell age. High tryptamine levels were not correlated with increased tryptophan decarboxylase activity. Vanadium content of the cells was found to reach a maximum within 1 min following vanadyl sulphate treatment as measured by Instrumental Neutron Activation Analysis.     

Neurobiological structure of the revised limit cycle reciprocal interaction model of REM cycle control

SUMMARY  New data bearing on the neurobiological basis of REM sleep and on mechanisms of EEG synchronization/desynchronization are presented. The revision of the limit cycle reciprocal interaction model (LCRIM) of REM cycle control incorporates new information on monoamine inhibition of mesopontine cholinergic neurons and of cholinergic mechanisms promoting REM sleep. New data also show cortical slow-wave activity is controlled by thalamocortical neurons' membrane potential level, which, in turn, is strongly controlled during sleep by brainstem cholinergic input arising from REM-on neurons. This new knowledge leads to a neurobiologi-cally justified integration of the LCRIM and of the two-process model of sleep control.