151 research outputs found
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
Police Chemistry
Johann von Justi, the foremost literary cameralist of his generation, served as chief police commissioner in Göttingen between 1755 and 1757. While in Göttingen, Justi offered lectures at the university on the “economic, police and cameral sciences.” He also arrested vagrants, wrote on chemistry, disciplined unruly students, conducted chemical experiments, supervised the pricing of Göttingen\u27s staple goods, engaged in a public controversy with a prominent Berlin chemist, edited and published a bi-weekly periodical (Göttingische Policey-Amts Nachrichien), and worked with the university\u27s curator to refashion the academic structure of the sciences. Taken together, these various activities reflected his broad vision for social and academic change, a vision with important implications for the form and content of the sciences. Drawing on archival material in Göttingen, on articles from the Policey-Amts Nachrichten, and on Justi\u27s other cameralist and chemical writings, I use his everyday experiences as a local police official to explore the meaning of his chemical work. I argue that Justi\u27s chemistry was suffused with the cameralist dreams and ambitions of a small-town police commissioner. It is what I call police chemistry
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
ChemInform Abstract: Synthesis and Antibacterial Activity of (1′R,5R,6R)-2-tert-Butyl-6-(1′- hydroxyethyl)penem-3-carboxylic Acid.
The first component of complement. I. Purification and properties of native C1.
Abstract
The first component of complement has been purified by using affinity chromatography on Sepharose-bound IgG. Unlike earlier procedures that yield the activated form of C1, in this method C1 is maintained in the native form by the protease inhibitor p-nitrophenyl, p'-guanidinobenzoate (NPGB). The procedure requires only two steps and yields pure C1 as judged both by SDS-PAGE analysis and by effective molecule calculations. The yields have varied from 30 to 50% in over 50 preparations. The functional properties of the purified native C1 correspond to those of C1 in serum. The dose-response activity profile is nonlinear, but becomes linear when C1 IS ALLOWED TO SELF-ACTIVATE. From SDS-PAGE analysis of the self-activated C1, all the C1r and C1s subcomponents are converted to the activated split products, indicating that all C1 molecules are biologically active. The recovery of C1 activity is dependent on the use of a heterologous source for the IgG on the affinity absorbant. The conditions of binding and elution from the Sepharose-IgG column are critical, indicating that immunoglobulin-bound C1 is rapidly inactivated under physiologic conditions by serum inactivators. The activation of the purified C1 in fluid phase has been explored both in the presence and absence of C1-inhibitor.</jats:p
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Multiple Forms of Properdin
Abstract
Properdin exists in at least three functionally different forms. The form which is isolated by the most rapid (two-step) procedure from fresh serum we designate native properdin (nP). Purified nP is characterized by its inability to bind to solid phase C3b, to stabilize the labile C3/C5 convertase, to form a soluble C3 convertase in serum, and by its capacity to reconstitute P-depleted serum with respect to C3 consumption by zymosan or inulin. The second form of P, designated pre-P, is characterized by its ability to bind reversibly to solid phase C3b, to stabilize the labile C3/C5 convertase formed with multiple C3b molecules, and to reconstitute P-depleted serum in a manner analogous to nP. The third form is active P, referred to as P̄. It is characterized by its ability to bind irreversibly to solid phase C3b, to stablize the labile C3/C5 convertase as well as the single C3b C3 convertase and to assemble the soluble C3 convertase when added to serum independent of zymosan or inulin.</jats:p
X-ray Topography Study of Surface Damage in Single-Crystal Sapphire
ABSTRACTX-ray diffraction topography was used to investigate the relationship between subsurface damage, near-surface microstructure, and fracture strength in a series of sapphire modulus of rupture (MOR) bars which had been fabricated to proof test fabrication processes. The strength of the bars was determined by failure in four point bending. The tensile surface of the bars was also examined using optical microscopy and non-contacting surface profilometry. Both show that the bars have good surface finish, with a typical RMS roughness of 0.7 nm. No correlation was found between RMS surface finish and fracture strength. Although the bars appeared to be indistinguishable, topographs taken prior to fracture testing revealed that they are of two distinct types. Type 1 has an oriented microstructure consisting of a pattern of linear features running the length of the bars. Type 2 was typical of well-polished sapphire, containing individual dislocations and occasional damage from handling. We attribute the Type 1 microstructure to fabrication damage that was not removed by subsequent processing and/or polishing. Fracture strength data showed that the Type I (damaged) bars had strengths less than 70 % of the bars without damage. Topography is sensitive to near-surface damage that can be correlated to fracture strength. Neither low magnification optical microscopy nor conventional surface finish statistics could be correlated to strength.</jats:p
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