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11.
Sepsis is a clinical syndrome that is usually induced by bacterial infections. It is generally assumed that the syndrome results from an excessive triggering of endogenous inflammatory mediators by the invading microorganisms. These mediators include substances released by activated monocytes, macrophages, endothelial cells and neutrophils such as cytokines, reactive oxygen species and proteases, as well as activation products of coagulation, fibrinolysis, contact and complement systems. Recent studies have suggested that cytokines and complement activation products may have overlapping biological activities. In addition, multiple interactions in vitro as well as in vivo between cytokines and complement have been described. Here we will review some of these recent studies and will discuss their relevance for the pathogenesis of sepsis and septic shock.  相似文献   
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Measurements of simultaneous force and intracellular Ca2+ concentration ([Ca2+]i) in rat uterine smooth muscle have been made to elucidate the mechanisms involved when force produced spontaneously, by high-K+ depolarization or carbachol is altered by a change of intracellular pH (pHi). Rises in force and [Ca2+]i were closely correlated for all forms of contraction, with the Ca2+ transient peaking before force. In spontaneously active preparations, alkalinization significantly increased, and acidification decreased, force and [Ca2+]i. Inhibition of the sarcoplasmic reticulum ATPase (cyclopiazonic acid) did not affect these changes, whereas removal of external Ca2+ abolished both responses, suggesting that the effect of pHi is on Ca2+ entry. Alkalinization caused a prolongation of the action potential complex, associated with a potentiation of contractile activity. Acidification produced hyperpolarization and abolition of action potentials and spontaneous activity, but did not prevent brief applications of carbachol or high-K+ from producing depolarization and increasing force, suggesting no impairment of the mechanism of generation of the action potential. For depolarized preparations, acidification increased tonic force and [Ca2+]i; the increase in the calcium signal persisted in zero-external calcium. In the presence of carbachol, acidification transiently increased force and [Ca2+]i, followed by a reduction in both. It is concluded that changes in pHi act at more than one step in excitation-contraction coupling and that changes in [Ca2+]i can account for most of the changes in uterine force. Received: 1 April 1996 /Accepted: 8 May 1996  相似文献   
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The triphenyl and tributyl phosphine initiated polymerization of maleic anhydride was investigated. The structure of the macro zwitterions, formed under the given reaction conditions, depended on the initiator employed. If the polymerization was initiated by triphenyl phosphine, the macromolecules contained succinic anhydride units and cyclopentanone derivatives, formed from further rearrangement. If, however, tributyl phosphine was employed as initiator, the polymers were mostly made up of conjugated ketoolefinic units. IR, NMR and mass spectrometric measurements were carried out to determine the structure of the polymers. Existence of the macro zwitterions was proved by high voltage electrophoresis. The semi-conductor properties of the polymers containing conjugated ketoolefinic units are discussed. Spectroscopic investigation of the kinetics of the triphenyl phosphine initiated polymerization of maleic anhydride showed that the initiation reaction of the ylide, formed with the monomer, proceeded about 90 times slower than the propagation reaction due to addition of the monomer to the growing chain-end.  相似文献   
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Laudationes     
Ohne ZusammenfassungHerr Professor Dr.James E. Rothman wurde 1950 in Haverhill/Mass. geboren, studierte am Yale-College und am Department of Biological Chemistry, Harvard Medical School sowie am Department of Biology, Massachusetts Inst. of Technology von 1967–1978. Daraufhin wurde er Assistant Professor, 3 Jahre später Associate Professor und nach weiteren 3 Jahren Professor am Department of Biochemistry, Stanford University. Seit 1988 ist er Squibb Professor of Molecular Biology am Department of Biology an der Princeton University.Herr Prof. Dr.K.W.A. Wirtz wurde 1942 in Utrecht geboren, erhielt seine Ausbildung in Biochemie und Physiologie an den Universitäten von Utrecht und Cornell Univ. Ithaka und promovierte mit einer Arbeit unter Prof. L.L.M. van Deenen (Heinrich-Wieland-Preis 1971). Unterbrochen durch längere Aufenthalte im Ausland, wurde er 1973 Assistant Professor und 1980 Professor für Biochemie an seiner heutigen Wirkungsstätte.  相似文献   
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