Complement system activation contributes to the ependymal damage induced by microbial neuraminidase

Background In the rat brain, a single intracerebroventricular injection of neuraminidase from Clostridium perfringens induces ependymal detachment and death. This injury occurs before the infiltration of inflammatory blood cells; some reports implicate the complement system as a cause of these injuries. Here, we set out to test the role of complement. Methods The assembly of the complement membrane attack complex on the ependymal epithelium of rats injected with neuraminidase was analyzed by immunohistochemistry. Complement activation, triggered by neuraminidase, and the participation of different activation pathways were analyzed by Western blot. In vitro studies used primary cultures of ependymal cells and explants of the septal ventricular wall. In these models, ependymal cells were exposed to neuraminidase in the presence or absence of complement, and their viability was assessed by observing beating of cilia or by trypan blue staining. The role of complement in ependymal damage induced by neuraminidase was analyzed in vivo in two rat models of complement blockade: systemic inhibition of C5 by using a function blocking antibody and testing in C6-deficient rats. Results The complement membrane attack complex immunolocalized on the ependymal surface in rats injected intracerebroventricularly with neuraminidase. C3 activation fragments were found in serum and cerebrospinal fluid of rats treated with neuraminidase, suggesting that neuraminidase itself activates complement. In ventricular wall explants and isolated ependymal cells, treatment with neuraminidase alone induced ependymal cell death; however, the addition of complement caused increased cell death and disorganization of the ependymal epithelium. In rats treated with anti-C5 and in C6-deficient rats, intracerebroventricular injection of neuraminidase provoked reduced ependymal alterations compared to non-treated or control rats. Immunohistochemistry confirmed the absence of membrane attack complex on the ependymal surfaces of neuraminidase-exposed rats treated with anti-C5 or deficient in C6. Conclusions These results demonstrate that the complement system contributes to ependymal damage and death caused by neuraminidase. However, neuraminidase alone can induce moderate ependymal damage without the aid of complement

Ionospheric gas dynamics of satellites and diagnostic probes

The gas dynamics of interactions of a tenuous ionosphere with moving satellites and probes that have bearings on the diagnostics of the ionosphere are discussed. Emphasis is on the cases where the body is moving at mesothermal speeds, namely intermediate between the thermal speeds of ions and electrons of the ambient ionosphere. Methods of collision-free plasma kinetics with self-consistent field are used. The development of the topics for discussion starts with stationary Langmuir probe which entails the basic mechanism of body-plasma interaction that becomes further intricated as the body moves at a higher and higher speed. Applications of the theory of plasma interaction to meteors which move in the ionosphere are also presented.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/43801/1/11214_2004_Article_BF00212707.pd

An improved version of barodesy for clay

Barodesy is a constitutive model based on proportional paths and the asymptotic behaviour of soil. It was originally developed for sand in 2009 by Kolymbas, and a version for clay was introduced in 2012. A shortcoming of former barodetic models was that tensile stresses can occur for certain dilative deformations. In this article, an improved version of barodesy for clay and a simplified calibration procedure are proposed. Basic features are shown, and simulations of element tests are compared with experimental data of several clay types.(VLID)452075