Formation of Polymethyl(methylene)aluminum

Sinn H, Hinck H, Bandermann F, Grützmacher H-F. Formation of Polymethyl(methylene)aluminum. Angewandte Chemie, International Edition in English. 1968;7(3):217

Polymere Werkstoffe mit neuen Eigenschaften durch stereospezifische Polymerisation funktionalisierter Monomerer mit homogenen Uebergangsmetallkatalysatoren Schlussbericht

The goal was to develop catalyst systems on metallocene basis which are suitable to polymerize methyl methacrylate highly sterospecifically to syndiotactic polymers for increasing the glass temperature. From ab initio calculations with zirconocene systems, energetically different reaction procedures resulted with which this goal could possibly be attained. From these procedures we selected the one with neutral species as active centres. Subsequently, a series of suitable, differently substituted and bridged zirconocenes was synthesized and activated for the polymerization of methyl methacrylate with tritylborate. It materialized that, independent of the substitution at the zircon atom, only a slightly significant increase in the syndiotacticity of methyl methacrylate can be attained with neutral active species. However, with these results, the test area within which further investigations should be performed is considerably restricted. In further tests, cationic species should be employed as active centres, since these were to open the path next favourable to the one aimed at with a view to energy consumption. Promising results could be obtained when polymerizing acrylonitrile with the same catalyst systems. The work is still in full progress.(orig.)Es war das Ziel, auf Metallocenbasis Katalysatorsysteme zu entwickeln, mit denen Methylmethacrylat hochstereospezifisch zur Erhoehung der Glastemperatur zu syndiotaktischen Polymeren polymerisiert werden kann. Aus ab initio Rechnungen an Zirkonocensystemen ergaben sich energetisch unterschiedliche Reaktionswege, auf denen das Ziel erreicht werden koennte. Aus ihnen wurde der mit neutralen Spezies als aktiven Zentren ausgewaehlt. Danach wurde eine Reihe geeigneter unterschiedlich substitutierter und verbrueckter Zirkonocene synthetisiert und zur Polymerisation von Methylmethacrylat mit Tribylborat aktiviert. Es zeigte sich, dass mit neutralen aktiven Spezies unabhaengig von der Substitution am Zirkonatom nur eine geringe signifikante Erhoehung der Syndiotaktizitaet von Methylmethacrylat erzielt werden kann. Die Ergebnisse schraenken aber das Versuchsfeld, in dem weitere Untersuchungen stattfinden sollten, erheblich ein. In weiteren Arbeiten sollten kationische Spezies als aktive Zentren eingesetzt werden, da sie einen naechst energetisch guenstigen Weg oeffnen sollten. Erfolgversprechende Ergebnisse ergaben sich bei der Polymerisation von Acrylnitril mit den gleichen Katalysatorsystemen. Die Arbeiten sind noch in vollem Gang. (orig.)SIGLEAvailable from TIB Hannover: DtF QN1(104,14) / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekBundesministerium fuer Bildung und Forschung, Berlin (Germany)DEGerman

CXCL5-secreting pulmonary epithelial cells drive destructive neutrophilic inflammation in tuberculosis

Successful host defense against numerous pulmonary infections depends on bacterial clearance by polymorphonuclear leukocytes (PMNs); however, excessive PMN accumulation can result in life-threatening lung injury. Local expression of CXC chemokines is critical for PMN recruitment. The impact of chemokine-dependent PMN recruitment during pulmonary Mycobacterium tuberculosis infection is not fully understood. Here, we analyzed expression of genes encoding CXC chemokines in M. tuberculosis–infected murine lung tissue and found that M. tuberculosis infection promotes upregulation of Cxcr2 and its ligand Cxcl5. To determine the contribution of CXCL5 in pulmonary PMN recruitment, we generated Cxcl5(–/–) mice and analyzed their immune response against M. tuberculosis. Both Cxcr2(–/–) mice and Cxcl5(–/–) mice, which are deficient for only one of numerous CXCR2 ligands, exhibited enhanced survival compared with that of WT mice following high-dose M. tuberculosis infection. The resistance of Cxcl5(–/–) mice to M. tuberculosis infection was not due to heightened M. tuberculosis clearance but was the result of impaired PMN recruitment, which reduced pulmonary inflammation. Lung epithelial cells were the main source of CXCL5 upon M. tuberculosis infection, and secretion of CXCL5 was reduced by blocking TLR2 signaling. Together, our data indicate that TLR2-induced epithelial-derived CXCL5 is critical for PMN-driven destructive inflammation in pulmonary tuberculosis