Dealing with damage: Plasma membrane repair mechanisms.

Eukaryotic cells have developed repair mechanisms, which allow them to reseal their membrane in order to prevent the efflux of cytoplasmic constituents and the uncontrolled influx of calcium. After injury, the Ca(2+)-concentration gradient fulfils a dual function: it provides guidance cues for the repair machinery and directly activates the molecules, which have a repair function. Depending on the nature of injury, the morphology of the cell and the severity of injury, the membrane resealing can be effected by lysosomal exocytosis, microvesicle shedding or a combination of both. Likewise, exocytosis is often followed by the endocytic uptake of lesions. Additionally, since plasmalemmal resealing must be attempted, even after extensive injury in order to prevent cell lysis, the restoration of membrane integrity can be achieved by ceramide-driven invagination of the lipid bilayer, during which the cell is prepared for apoptotic disposal. Plasmalemmal injury can be contained by a surfeit of plasma membrane, which serves as a trap for toxic substances: either passively by an abundance of cellular protrusions, or actively by membrane blebbing.

Ca2+-dependent repair of pneumolysin pores: A new paradigm for host cellular defense against bacterial pore-forming toxins

Pneumolysin (PLY), a key virulence factor of Streptococcus pneumoniae, permeabilizes eukaryotic cells by forming large trans-membrane pores. PLY imposes a puzzling multitude of diverse, often mutually excluding actions on eukaryotic cells. Whereas cytotoxicity of PLY can be directly attributed to the pore-mediated effects, mechanisms that are responsible for the PLY-induced activation of host cells are poorly understood. We show that PLY pores can be repaired and thereby PLY-induced cell death can be prevented. Pore-induced Ca2+ entry from the extracellular milieu is of paramount importance for the initiation of plasmalemmal repair. Nevertheless, active Ca2+ sequestration that prevents excessive Ca2+ elevation during the execution phase of plasmalemmal repair is of no less importance. The efficacy of plasmalemmal repair does not only define the fate of targeted cells but also intensity, duration and repetitiveness of PLY-induced Ca2+ signals in cells that were able to survive after PLY attack. Intracellular Ca2+ dynamics evoked by the combined action of pore formation and their elimination mimic the pattern of receptor-mediated Ca2+ signaling, which is responsible for the activation of host immune responses. Therefore, we postulate that plasmalemmal repair of PLY pores might provoke cellular responses that are similar to those currently ascribed to the receptor-mediated PLY effects. Our data provide new insights into the understanding of the complexity of cellular non-immune defense responses to a major pneumococcal toxin that plays a critical role in the establishment and the progression of life-threatening diseases. Therapies boosting plasmalemmal repair of host cells and their metabolic fitness might prove beneficial for the treatment of pneumococcal infections.

Engineered liposomes sequester bacterial exotoxins and protect from severe invasive infections in mice

Gram-positive bacterial pathogens that secrete cytotoxic pore-forming toxins, such as Staphylococcus aureus and Streptococcus pneumoniae, cause a substantial burden of disease. Inspired by the principles that govern natural toxin-host interactions, we have engineered artificial liposomes that are tailored to effectively compete with host cells for toxin binding. Liposome-bound toxins are unable to lyse mammalian cells in vitro. We use these artificial liposomes as decoy targets to sequester bacterial toxins that are produced during active infection in vivo. Administration of artificial liposomes within 10 h after infection rescues mice from septicemia caused by S. aureus and S. pneumoniae, whereas untreated mice die within 24-33 h. Furthermore, liposomes protect mice against invasive pneumococcal pneumonia. Composed exclusively of naturally occurring lipids, tailored liposomes are not bactericidal and could be used therapeutically either alone or in conjunction with antibiotics to combat bacterial infections and to minimize toxin-induced tissue damage that occurs during bacterial clearance

Edut Adonai: Katechismus der mosaischen Religionslehre

von E. Kley

Lied - Es ritten fünf Reiter zum Thore hinaus : Ade! Ade! Ade! ; etc. etc.

Bibliograph. Nachweis: Wolf, Sylvia: Politische Karikaturen in Deutschland 1848/49. Mittenwald 1982. – I.49 Nr. 16

Das Vergeltungsprincip im biblischen und talmudischen Strafrecht

Halle, Univ., Diss., 1892

Geschichte der alttestamentlichen Religion

von Eduard König

"Was hat die jüdische Gemeinde Königsbergs König Friedrich I. im besondern zu verdanken?" : Vortrag, gehalten am 15. Januar 1901 im Verein für jüd. Geschichte u. Litteratur zu Königsberg i. Pr.

von Ed. Birnbaum

Salomon Sulzer, Professor und Obercantor : biographische Skizze

von Eduard Kulke

Ahasver "der ewige Jude" nach seiner ursprünglichen Idee und seiner literarischen Verwertung

betrachtet von Eduard König

Geschichtliche Darstellung der Israelitischen Freischule zu Hamburg bei Gelegenheit der Feier ihres fünfundzwanzigjährigen Bestehens (am 31 October 1841)

mitgetheilt von Eduard Kley

Gesänge zum gottesdienstlichen Gebrauch an den Sabbath u. Festtagen der israelitischen Gemeinde zu Liegnitz : mit besonderer Berücksichtigung der bisher gebräuchlichen Gesänge

gesichtet, ausgew. und durch 90 eigene Kompositionen verm. und hrsg. von Eduard Hamburger

Psalm 24 (Vers 7-10) Śeʼu sheʻarim : für Chor und Solostimmen mit Orgel- und Harfenbegleitung ad libitum

componirt von Ed. Birnbaum

Das verjudete Frankreich : Versuch einer Tagesgeschichte

von Eduard Drumont