ALBERT

Beschreibung: Dieser Band enthält 72 Beiträge zu Themengebieten der Physik der festen Erde, des magnetischen und elektrischen Felds der Erde, der Physik der Atmosphäre sowie der Angewandten Geophysik, veröffentlicht durch die Deutsche Geophysikalische Gesellschaft in den Jahren 1928.

Beschreibung: 〈html〉 〈body〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0004.pdf"〉Titelseite〈/a〉〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0005.pdf"〉Gezeitenerscheinungen in der Atmosphäre〈/a〉〈br〉(Bartels, J.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0006.pdf"〉Erdmagnetische Säkularvariation und die Orientation alter Kultbauwerke〈/a〉〈br〉(Wehner, H.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0007.pdf"〉Über die Tiefenwirkung bei geoelektrischen Potentiallinienmethoden〈/a〉〈br〉(Hummel, J. N.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0008.pdf"〉Überblick über den Gang der magnetischen Vermessung der Ostsee〈/a〉〈br〉(v. Gernet, A.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0009.pdf"〉Die Wirkung der Kontinente und Ozeane auf die Differenz 〈i〉B – A〈/i〉 der Hauptträgheitsmomente der Erde im Äquator〈/a〉〈br〉(Gutenberg, B.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0011.pdf"〉Bemerkungen zu H. v. Iherings Kritik der Theorien der Kontinentverschiebungen und der Polwanderungen〈/a〉〈br〉(Wegener, A.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0012.pdf"〉Berichtigung〈/a〉〈br〉(Jung, K.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0013.pdf"〉Illustration〈/a〉〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0014.pdf"〉Über die Polhöhenschwankungen infolge der Lorentz-Kontraktion der Erde〈/a〉〈br〉(Courvoisier, L.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0015.pdf"〉Zum Uhrvergleich auf drahtlosem Wege nach der Koinzidenzhörmethode〈/a〉〈br〉(Martin, H.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0016.pdf"〉Physikalische Grundlagen einer neuen geoelektrischen Aufschlußmethode〈/a〉〈br〉(Hummel, J. N.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0017.pdf"〉Untersuchung der Potentialverteilung für einen speziellen Fall im Hinblick auf geoelektrische Potentiallinienverfahren〈/a〉〈br〉(Hummel, J. N.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0018.pdf"〉Mächtigkeitsbestimmung von Deckschichten über Spalten durch Radioaktivitätsmessungen〈/a〉〈br〉(Koenigsberger, J.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0019.pdf"〉Zur Frage der regionalen, magnetischen Anomalien Deutschlands, insbesondere derjenigen Norddeutschlands〈/a〉〈br〉(Reich, H.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0021.pdf"〉Untersuchungen über die seismische Bodenunruhe kurzer Periode〈/a〉〈br〉(Schneider, W.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0022.pdf"〉Zur Theorie elektrischer Bodenforschung〈/a〉〈br〉(Heine, W.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0023.pdf"〉Emil Wiechert †〈/a〉〈br〉(Angenheister, G.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0024.pdf"〉Die topographische Reduktion bei Drehwagenbeobachtungen〈/a〉〈br〉(Numerov, B.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0025.pdf"〉Angewandte Seismik (Zusammenfassender Bericht über Arbeiten von 1921 bis 1928)〈/a〉〈br〉(v. Schmidt, O.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0027.pdf"〉Le problème des microséismes à groupes〈/a〉〈br〉(Gherzi, E.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0028.pdf"〉Zur Empfindlichkeitsbestimmung von magnetischen Variometern und zur Eichung der magnetischen Felder von Spulen〈/a〉〈br〉(Koenigsberger, J.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0029.pdf"〉Die Schrumpfungsgeschwindigkeit des Erdradius aus astronomischen Beobachtungen〈/a〉〈br〉(Meyermann, B.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0030.pdf"〉Über eine Verbindung zwischen den mondentägigen und den sonnentägigen Variationen der magnetischen Deklination〈/a〉〈br〉(Egedal, J.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0031.pdf"〉Die Zone der anormalen Hörbarkeit im kleinen〈/a〉〈br〉(Hiller, W.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0032.pdf"〉Mitteilungen〈/a〉〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0033.pdf"〉Ein graphisches Verfahren für Drehwagenmessungen zur Berechnung der Geländewirkung und der Wirkung beliebig gestalteter Massenkörper〈/a〉〈br〉(Haalck, H.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0035.pdf"〉Beiträge zur geoelektrischen Methode〈/a〉〈br〉(Hummel, J. N.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0036.pdf"〉Zum Uhrvergleich auf drahtlosem Wege nach der Koinzidenzhörmethode〈/a〉〈br〉(Mahnkopf, H.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0037.pdf"〉Berichtigung〈/a〉〈br〉(Meyermann, B.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0038.pdf"〉Zur Frage nach der Ursache von lokalen gravimetrischen und erdmagnetischen Störungen und ihre wechselseitigen Beziehungen〈/a〉〈br〉(Haalck, H.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0040.pdf"〉Gemeinschaftliche Arbeit zwischen Seismologen und Baufachmann zur Verringerung von Erdbebenschäden〈/a〉〈br〉(Briske, R.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0042.pdf"〉Feldapparatur zur Registrierung von Zeitzeichen〈/a〉〈br〉(Köhler, R.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0043.pdf"〉Über die Schmidtsche Methode der Bestimmung der Parameter von Stabmagneten〈/a〉〈br〉(Bock, R.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0046.pdf"〉Referate der Vorträge auf der Tagung der Deutschen Geophysikalischen Gesellschaft in Hamburg vom 19. bis 21. September 1928〈/a〉〈br〉(Koenigsberger, J.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0048.pdf"〉Die Seismizität der Ozeane und Kontinente〈/a〉〈br〉(Tams, E.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0049.pdf"〉Bodenunruhe durch Brandung und durch Frost〈/a〉〈br〉(Gutenberg, B.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0050.pdf"〉Beitrag zur Schallausbreitung in der Atmospähre〈/a〉〈br〉(Kölzer, J.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0051.pdf"〉Das Magnetfeld einer elektrischen Strömung im anisotropen leitenden Halbraum〈/a〉〈br〉(Müller, M.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0052.pdf"〉Die geführten elastischen Zweimittel-Wellen〈/a〉〈br〉(Uller, K.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0053.pdf"〉Vom Jahre 1922 an im südlichen Norwegen aufgenommene Nordlichtphotogramme〈/a〉〈br〉(Störmer, C.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0055.pdf"〉Zur Frage nach der Ursache von lokalen gravimetrischen und erdmagnetischen Störungen und ihre wechselseitigen Beziehungen〈/a〉〈br〉(Haalck, H.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0057.pdf"〉Vorträge, gehalten auf der Tagung der Deutschen Geophysikalischen Gesellschaft vom 19. bis 21. September 1928〈/a〉〈br〉(Seilkopf, H.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0060.pdf"〉Statistische Mechanik der Atmosphäre〈/a〉〈br〉(Baur, F.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0061.pdf"〉Das Schwadorfer Beben vom 8. Oktober 1927〈/a〉〈br〉(Conrad, V.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0062.pdf"〉Das Periodogramm der internationalen erdmagnetischen Charakterzahlen〈/a〉〈br〉(Wenzel Pollak, L.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0064.pdf"〉Der Stand der erdmagnetischen Forschung〈/a〉〈br〉(Schmidt, A.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0065.pdf"〉Magnetische Anomalien im westlichen Mecklenburg〈/a〉〈br〉(Schuh, F.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0066.pdf"〉Bemerkungen zur numerischen und graphischen Behandlung der Krümmungsgröße〈/a〉〈br〉(Jung, K.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0067.pdf"〉Der Wasserhaushalt der Antarktis in der Eiszeit〈/a〉〈br〉(Meinardus, W.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0068.pdf"〉Übersicht über Neuerscheinungen〈/a〉〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0069.pdf"〉Vortrage, gehalten auf der Tagung der Deutschen Geophysikalischen Gesellschaft vom 19. bis 21. September 1928〈/a〉〈br〉(Tams, E.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0071.pdf"〉Über kartographische Darstellung der Seismizität〈/a〉〈br〉(Renquist, H.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0072.pdf"〉Ergebnisse von Pilotaufstiegen im Gebiete von Island〈/a〉〈br〉(Georgi, J.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0073.pdf"〉Referat über die Polarfront- und Äquatorialfronttheorien〈/a〉〈br〉(Stüve, G.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0074.pdf"〉Die Messung der Horizontal- und der Vertikalintensität mit dem Magnetron〈/a〉〈br〉(Rössiger, M.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0075.pdf"〉Untersuchungen über die lokalen Schwankungen des Erdpotentials〈/a〉〈br〉(Stoppel, R.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0076.pdf"〉Klima und Klimatafel von Hamburg〈/a〉〈br〉(Perlewitz, P.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0077.pdf"〉Neue Ergebnisse über die Struktur des Windes (Vorläufige Mitteilung)〈/a〉〈br〉(Schmidt, W.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0079.pdf"〉Lokale und regionale magnetische Anomalien in Schleswig-Holstein〈/a〉〈br〉(Reich, H.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0080.pdf"〉Die optische Station in Simferopol〈/a〉〈br〉(Tichanowsky, J.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0081.pdf"〉Das Strömungssystem der Luft über dem tropischen Atlantischen Ozean nach den Höhenwindmessungen der Meteor-Expedition〈/a〉〈br〉(Kuhlbrodt, E.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0082.pdf"〉Ergebnisse und Aufgaben der meteorologischen Strahlungsmessungen〈/a〉〈br〉(Süring, R.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0083.pdf"〉Ergebnisse von Drehwaagemessungen in Schlewig-Holstein〈/a〉〈br〉(Jung, K.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0085.pdf"〉Aufsätze〈/a〉〈br〉(Lotze, F., Brockamp, B., Haalck, H., Myrbach, O., Whipple, Cabannes, J., Dufay, J., Gherzi, E., Pochettino, A., Rostagni, A.)〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0096.pdf"〉Mitteilungen〈/a〉〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0097.pdf"〉Autorenverzeichnis〈/a〉〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0098.pdf"〉Sachverzeichnis〈/a〉〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0099.pdf"〉Literaturverzeichnis〈/a〉〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0100.pdf"〉Geophysikalische Berichte〈/a〉〈/li〉 〈li〉〈a href="https://gdz.sub.uni-goettingen.de/download/pdf/PPN101433392X_0004/LOG_0101.pdf"〉Register der Goephysikalische Berichte〈/a〉〈/li〉 〈/body〉 〈/html〉

Beschreibung: research

Beschreibung: DGG, DFG, SUB Göttingen

Beschreibung: Erfassung aller tatsächlichen oder vermuteten vektorassoziierten Krankheiten und Vektoren KATASTER-BESCHREIBUNG: viele Pathogene in Deutschland bereits vorhanden bzw. geeignete Vektoren stehen zur Verfügung, bei Einschleppung durch Reservoirwirte oder erkrankte Reisende sind autochthone Fälle zu erwarten KATASTER-DETAIL:

Beschreibung: Beispiele Ambrosia, Eichenprozessionsspinner KATASTER-BESCHREIBUNG: KATASTER-DETAIL:

Beschreibung: ausgedehnte Ambrosiaareale auch in der Lausitz und dem Berliner Raum KATASTER-BESCHREIBUNG: Neben Sensibilisierung gegen Ambrosia auch Kreuzreationen bei Sensibilisierung gegen Beifuß möglich KATASTER-DETAIL:

Beschreibung: Allgemeine Beobachtungen zum Rostbefall von Weizen im Jahr 1925 trotz langer Trockenperioden KATASTER-BESCHREIBUNG: Einfluss des Niederschlags auf die Infektion; auch kurze starke Niederschläge zwischen langen Trockenperioden sind ausreichend um einen großflächigen Befall zu bewirken. KATASTER-DETAIL: Delta Nied +, dann Infektion +;

Beschreibung: Autochthone Malaria in Deutschland, Historischer Abriss, Nachkriegsmalaria, Aktuelle malariaepidemiologische Situation KATASTER-BESCHREIBUNG: klimatische Bedingungen ermöglichen Ausreifung von Sporozoiten in heimischen Anophelesmücken, historisch erwiesen KATASTER-DETAIL:

Beschreibung: Herleitung einer Formel zur Berechnung der Plasmodium-Sporozoitenreifungszeit KATASTER-BESCHREIBUNG: Ausreifung von Pl. vivax- und Pl. falciparum-Sporozoiten im deutschen Raum möglich, Zustandekommen endemischer Malariaerregerübertragung bzw. Entstehung epidemiologisch wirksamer malariogener Potentiale dabei gebunden an das Vorhandensein von Gametozytenträgern und Überträgermücken KATASTER-DETAIL:

Beschreibung: Einfluss der Temperatur auf die Flora und ihre Verteilung in Deutschland KATASTER-BESCHREIBUNG: KATASTER-DETAIL:

Beschreibung: Zusammenhang Klima, Witterung und Ertrag von Gräsern und Klee KATASTER-BESCHREIBUNG: KATASTER-DETAIL:

Beschreibung: Einfluss von Temperatur und Niederschlag auf die Vegetation KATASTER-BESCHREIBUNG: KATASTER-DETAIL:

Beschreibung: Übersicht über die Literatur zum Einfluss des Wetters auf die Kulturpflanzen KATASTER-BESCHREIBUNG: Milder und trockener Winter wirkt positiv auf die Weizenerträge, kalter und niederschlagsreicher Winter eher negativ, Betrachung für Norddeutschland KATASTER-DETAIL:

Beschreibung: Einfluss der Witterungsfaktoren auf verschiedene Kulturen und die Betriebssysteme KATASTER-BESCHREIBUNG: KATASTER-DETAIL:

Beschreibung: Detaillierte Auflistung des Maikäferauftretens verschiedener Jahre aus dem Zeitraum 1900-1920 aus ganz Deutschland in Bezirks- teilw. sogar Gemeindeauflösung wird gegeben. Der Einfluß der Temperatur in Form von 9°C Mitteltemperatur als Grenze für die Generationenanzahl der beiden Maikäferarten Melolontha melolontha L. und Melolontha hippocastani F. wird diskutiert. Eine Karte über die Generationsdauer der beiden Maikäferarten im deutschen Reich, teilweise auf Bezirksebene, ist enthalten. KATASTER-BESCHREIBUNG: KATASTER-DETAIL:

Beschreibung: Beziehung der Witterungseinflüsse auf die Knollenerträge, Auswertungen von Kartoffelkulturstationsergebnissen KATASTER-BESCHREIBUNG: KATASTER-DETAIL:

Beschreibung: deutliche Verschiebungen der phänologischen Jahreszeiten, besonders der Frühjahrsphasen; für jede phänologische Phase negative und auch positive Trends entdeckt, z.T. auf engen Raum; Verschiebung auf Variation der Lufttemperatur zurückzuführen; Verlängerung der Vegetationsperiode, hauptsächlich durch Veränderungen im Frühjahr KATASTER-BESCHREIBUNG: KATASTER-DETAIL:

Beschreibung: einheimische und importierte  vektorassoziierte  Infektionen, Gastrointestinale  Infektionskrankheiten KATASTER-BESCHREIBUNG: KATASTER-DETAIL:

Beschreibung: Studie zu einer prognostizierten Anzahl von Tagen mit Wärme- und mit Kältestress, basierend auf Klimaszenarien für den Zeitraum 2071 bis 2100 KATASTER-BESCHREIBUNG: Prognose: größere Zahl an Todesfällen durch Hitze im Süden gegenüber dem Norden Deutschlands und zugleich größerer Rückgang der Todesfälle durch Kälte im Norden, Anstieg der Todesopferzahl durch zunehmende Hitze insgesamt größer als Rückgang der Opferzahl durch weniger Kälte KATASTER-DETAIL:

Beschreibung: Klärung der Studienlage zum potentiellen Einfluss des Klimawandels auf die Prävalenz von Haut- und Allergieerkrankungen in Deutschland KATASTER-BESCHREIBUNG: klimabedingte Veränderungen vor allem bei allergischen Erkrankungen, Hautkrebs und einzelnen erregerbedingten Dermatosen KATASTER-DETAIL:

Beschreibung: Fallbeispiel Sommer 2003 KATASTER-BESCHREIBUNG: Zunahme von Ozon in der Troposphäre bei stationären sommerlichen Hochdruckwetterlagen mit hohen Lufttemperaturen und intensiver Sonneneinstrahlung, indirekt Zunahme von Feinstaub bei Hitze (〉30°C) und Ozonbelastung (〉200 Mikrogramm pro Kubikmeter) KATASTER-DETAIL:

Beschreibung: UV-Strahlungsbeeinflussende Faktoren Azimutwinkel, Bewölkung, Aerosole, stratosphärisches Ozon, biologische Wirkung in Abhängigkeit vom Hauttyp und Sensibilisierung (Jahreszeit) KATASTER-BESCHREIBUNG: Einfluss klimatischer Veränderungen auf die Häufigkeit von Hautkrebserkrankungen sehr wahrscheinlich, bei vermutlich hoher Bedeutung des (thermisch motivierten) Expositionsverhaltens KATASTER-DETAIL:

Beschreibung: zeitliche Trends und geografische Ursprünge der Vektor-übertragenen Krankheiten in Deutschland im Hinblick auf Stärken der bestehenden Krankheitsüberwachung für Hantavirus Infektion (endemisch in Deutschland), Chikungunya-Fieber (vor kurzem Schwellenländer in Europa) und Dengue-Fieber (importiert aus tropischen Regionen) KATASTER-BESCHREIBUNG: KATASTER-DETAIL:

Beschreibung: weltweite Verbreitung der Asiatischen Tigermücke Aedes albopictus innerhalb der letzten zwei Jahrzehnte im Zusammenhang mit Chikungunya-Ausbruch im Sommer 2007 in Italien KATASTER-BESCHREIBUNG: Transportwege der Globalisierung als wesentlicher Faktor neben Klimaänderungen KATASTER-DETAIL:

Beschreibung: Gesundheitliche Bewertung ultravioletter Strahlung KATASTER-BESCHREIBUNG: KATASTER-DETAIL:

Beschreibung: Studie zu einer prognostizierten Anzahl von Tagen mit Wärme- und mit Kältestress, basierend auf Klimaszenarien für den Zeitraum 2071 bis 2100 KATASTER-BESCHREIBUNG: schätzungsweise durchschnittlicher Anstieg der Zahl der wärmeinduzierten Krankheitsfälle um einen Faktor von mehr als 3 und für hitzebedingte Krankenhausaufenthalte 6, Verlust von 0,1% bis 0.5% des BIP durch krankheitbedingten Arbeitsausfall KATASTER-DETAIL:

Beschreibung: Pollensaison, -auftreten und -arten, sowie Veränderungen der Allergenität von Pollen unter Klimawandel KATASTER-BESCHREIBUNG: zunehmende Polysensibilisierungen gegenüber Inhalationsallergien durch zunehmend invasives Traubenkraut Ambrosia artemisiifolia KATASTER-DETAIL:

Beschreibung: Lage der Hochs nördlich und südlich des 50. Breitengrades und ihre Bedeutung für die Witterung und Ernteerträge in Mitteldeutschland KATASTER-BESCHREIBUNG: KATASTER-DETAIL: Tmit+ (Janurar, Februar, März, Mai und Dezember) durch Abnahem der barometrischen Nordlagen Tmit- (August, September) durch Zunahme der barometrischen Nordlagen Nied+ (Janurar, Apri,, Mai, August, September, Dezember) durch Abnahmen der barometrischen Nordlagen (entspricht Zunahmen der Südlagen!) Nied- (Februar, März, Oktober und November) durch Abnahmen der barometrischen Nordlagen (entspricht Zunahmen der Südlagen!)

Beschreibung: Biologie und Bekämpfung von Fritfliege, Getreideblumenfliege, scheckige oder gelbe Halmfliege, Weizenfliege, Hessenfliege KATASTER-BESCHREIBUNG: Einfluss der Witterung (Temperatur, Niederschlag und Wind) auf die Schädlinge KATASTER-DETAIL: Delta T (Winter) +, Anzahl Maden der Halmfliege +; Delta Nied (September) + und Delta Wind (September) +, dann Hessenfliege -

Beschreibung: Beobachtungen zum Gelbrostbefall von Weizen, Roggen und Gerste KATASTER-BESCHREIBUNG: - KATASTER-DETAIL: -

Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, John H -- Elledge, Stephen J -- New York, N.Y. -- Science. 2002 Sep 13;297(5588):1822-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, TX 77030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12228708" target="_blank"〉PubMed〈/a〉

Beschreibung: Natural killer (NK) cells express inhibitory receptors for major histocompatibility complex (MHC) class I antigens, preventing attack against healthy cells. Mouse cytomegalovirus (MCMV) encodes an MHC-like protein (m157) that binds to an inhibitory NK cell receptor in certain MCMV-susceptible mice. In MCMV-resistant mice, this viral protein engages a related activating receptor (Ly49H) and confers host protection. These activating and inhibitory receptors are highly homologous, suggesting the possibility that one evolved from the other in response to selective pressure imposed by the pathogen.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arase, Hisashi -- Mocarski, Edward S -- Campbell, Ann E -- Hill, Ann B -- Lanier, Lewis L -- AI30363/AI/NIAID NIH HHS/ -- CA89294/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2002 May 17;296(5571):1323-6. Epub 2002 Apr 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology and the Cancer Research Institute, University of California San Francisco, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11950999" target="_blank"〉PubMed〈/a〉

Beschreibung: Higher order chromatin structure presents a barrier to the recognition and repair of DNA damage. Double-strand breaks (DSBs) induce histone H2AX phosphorylation, which is associated with the recruitment of repair factors to damaged DNA. To help clarify the physiological role of H2AX, we targeted H2AX in mice. Although H2AX is not essential for irradiation-induced cell-cycle checkpoints, H2AX-/- mice were radiation sensitive, growth retarded, and immune deficient, and mutant males were infertile. These pleiotropic phenotypes were associated with chromosomal instability, repair defects, and impaired recruitment of Nbs1, 53bp1, and Brca1, but not Rad51, to irradiation-induced foci. Thus, H2AX is critical for facilitating the assembly of specific DNA-repair complexes on damaged DNA.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4721576/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4721576/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Celeste, Arkady -- Petersen, Simone -- Romanienko, Peter J -- Fernandez-Capetillo, Oscar -- Chen, Hua Tang -- Sedelnikova, Olga A -- Reina-San-Martin, Bernardo -- Coppola, Vincenzo -- Meffre, Eric -- Difilippantonio, Michael J -- Redon, Christophe -- Pilch, Duane R -- Olaru, Alexandru -- Eckhaus, Michael -- Camerini-Otero, R Daniel -- Tessarollo, Lino -- Livak, Ferenc -- Manova, Katia -- Bonner, William M -- Nussenzweig, Michel C -- Nussenzweig, Andre -- Z99 CA999999/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2002 May 3;296(5569):922-7. Epub 2002 Apr 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, National Cancer Institute, NIH, Bethesda, MD 20892, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11934988" target="_blank"〉PubMed〈/a〉

Beschreibung: Full-length poliovirus complementary DNA (cDNA) was synthesized by assembling oligonucleotides of plus and minus strand polarity. The synthetic poliovirus cDNA was transcribed by RNA polymerase into viral RNA, which translated and replicated in a cell-free extract, resulting in the de novo synthesis of infectious poliovirus. Experiments in tissue culture using neutralizing antibodies and CD155 receptor-specific antibodies and neurovirulence tests in CD155 transgenic mice confirmed that the synthetic virus had biochemical and pathogenic characteristics of poliovirus. Our results show that it is possible to synthesize an infectious agent by in vitro chemical-biochemical means solely by following instructions from a written sequence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cello, Jeronimo -- Paul, Aniko V -- Wimmer, Eckard -- New York, N.Y. -- Science. 2002 Aug 9;297(5583):1016-8. Epub 2002 Jul 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, School of Medicine, State University of New York at Stony Brook, Stony Brook, NY 11794-5222, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12114528" target="_blank"〉PubMed〈/a〉

Beschreibung: There is a relation between stress and alcohol drinking. We show that the corticotropin-releasing hormone (CRH) system that mediates endocrine and behavioral responses to stress plays a role in the control of long-term alcohol drinking. In mice lacking a functional CRH1 receptor, stress leads to enhanced and progressively increasing alcohol intake. The effect of repeated stress on alcohol drinking behavior appeared with a delay and persisted throughout life. It was associated with an up-regulation of the N-methyl-d-aspartate receptor subunit NR2B. Alterations in the CRH1 receptor gene and adaptional changes in NR2B subunits may constitute a genetic risk factor for stress-induced alcohol drinking and alcoholism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sillaber, Inge -- Rammes, Gerhard -- Zimmermann, Stephan -- Mahal, Beatrice -- Zieglgansberger, Walter -- Wurst, Wolfgang -- Holsboer, Florian -- Spanagel, Rainer -- New York, N.Y. -- Science. 2002 May 3;296(5569):931-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max Planck Institute of Psychiatry, Kraepelinstrasse 2-10, 80804 Munich, Germany. sillaber@mpipsykl.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11988580" target="_blank"〉PubMed〈/a〉

Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gura, Trisha -- New York, N.Y. -- Science. 2003 Feb 7;299(5608):849-52.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12574616" target="_blank"〉PubMed〈/a〉

Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, Eliot -- New York, N.Y. -- Science. 2002 May 17;296(5571):1212.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12016275" target="_blank"〉PubMed〈/a〉

Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beckman, Mary -- New York, N.Y. -- Science. 2002 Feb 1;295(5556):782.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11823614" target="_blank"〉PubMed〈/a〉

Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beckman, Mary -- New York, N.Y. -- Science. 2002 Sep 6;297(5587):1626-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12215618" target="_blank"〉PubMed〈/a〉

Beschreibung: Amyotrophic lateral sclerosis (ALS) is a progressive, lethal neuromuscular disease that is associated with the degeneration of spinal and brainstem motor neurons, leading to atrophy of limb, axial, and respiratory muscles. The cause of ALS is unknown, and there is no effective therapy. Neurotrophic factors are candidates for therapeutic evaluation in ALS. Although chronic delivery of molecules to the central nervous system has proven difficult, we recently discovered that adeno-associated virus can be retrogradely transported efficiently from muscle to motor neurons of the spinal cord. We report that insulin-like growth factor 1 prolongs life and delays disease progression, even when delivered at the time of overt disease symptoms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaspar, Brian K -- Llado, Jeronia -- Sherkat, Nushin -- Rothstein, Jeffrey D -- Gage, Fred H -- AG12992/AG/NIA NIH HHS/ -- AG21876/AG/NIA NIH HHS/ -- NS33958/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2003 Aug 8;301(5634):839-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Genetics, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12907804" target="_blank"〉PubMed〈/a〉

Beschreibung: Degenerative disorders of motor neurons include a range of progressive fatal diseases such as amyotrophic lateral sclerosis (ALS), spinal-bulbar muscular atrophy (SBMA), and spinal muscular atrophy (SMA). Although the causative genetic alterations are known for some cases, the molecular basis of many SMA and SBMA-like syndromes and most ALS cases is unknown. Here we show that missense point mutations in the cytoplasmic dynein heavy chain result in progressive motor neuron degeneration in heterozygous mice, and in homozygotes this is accompanied by the formation of Lewy-like inclusion bodies, thus resembling key features of human pathology. These mutations exclusively perturb neuron-specific functions of dynein.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hafezparast, Majid -- Klocke, Rainer -- Ruhrberg, Christiana -- Marquardt, Andreas -- Ahmad-Annuar, Azlina -- Bowen, Samantha -- Lalli, Giovanna -- Witherden, Abi S -- Hummerich, Holger -- Nicholson, Sharon -- Morgan, P Jeffrey -- Oozageer, Ravi -- Priestley, John V -- Averill, Sharon -- King, Von R -- Ball, Simon -- Peters, Jo -- Toda, Takashi -- Yamamoto, Ayumu -- Hiraoka, Yasushi -- Augustin, Martin -- Korthaus, Dirk -- Wattler, Sigrid -- Wabnitz, Philipp -- Dickneite, Carmen -- Lampel, Stefan -- Boehme, Florian -- Peraus, Gisela -- Popp, Andreas -- Rudelius, Martina -- Schlegel, Juergen -- Fuchs, Helmut -- Hrabe de Angelis, Martin -- Schiavo, Giampietro -- Shima, David T -- Russ, Andreas P -- Stumm, Gabriele -- Martin, Joanne E -- Fisher, Elizabeth M C -- New York, N.Y. -- Science. 2003 May 2;300(5620):808-12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurodegenerative Disease, Institute of Neurology, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12730604" target="_blank"〉PubMed〈/a〉

Beschreibung: The protein-protein interaction between leukocyte functional antigen-1 (LFA-1) and intercellular adhesion molecule-1 (ICAM-1) is critical to lymphocyte and immune system function. Here, we report on the transfer of the contiguous, nonlinear epitope of ICAM-1, responsible for its association with LFA-1, to a small-molecule framework. These LFA-1 antagonists bound LFA-1, blocked binding of ICAM-1, and inhibited a mixed lymphocyte reaction (MLR) with potency significantly greater than that of cyclosporine A. Furthermore, in comparison to an antibody to LFA-1, they exhibited significant anti-inflammatory effects in vivo. These results demonstrate the utility of small-molecule mimics of nonlinear protein epitopes and the protein epitopes themselves as leads in the identification of novel pharmaceutical agents.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gadek, T R -- Burdick, D J -- McDowell, R S -- Stanley, M S -- Marsters, J C Jr -- Paris, K J -- Oare, D A -- Reynolds, M E -- Ladner, C -- Zioncheck, K A -- Lee, W P -- Gribling, P -- Dennis, M S -- Skelton, N J -- Tumas, D B -- Clark, K R -- Keating, S M -- Beresini, M H -- Tilley, J W -- Presta, L G -- Bodary, S C -- New York, N.Y. -- Science. 2002 Feb 8;295(5557):1086-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bioorganic Chemistry, Genentech, One DNA Way, South San Francisco, CA 94080, USA. trg@gene.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11834839" target="_blank"〉PubMed〈/a〉

Beschreibung: Activation-induced cytidine deaminase (AID) plays an essential role in class switch recombination (CSR) and somatic hypermutation (SHM) of immunoglobulin genes. We report here that deficiency in AID results in the development of hyperplasia of isolated lymphoid follicles (ILFs) associated with a 100-fold expansion of anaerobic flora in the small intestine. Reduction of bacterial flora by antibiotic treatment of AID-/- mice abolished ILF hyperplasia as well as the germinal center enlargement seen in secondary lymphoid tissues. Because an inability to switch to immunoglobulin A on its own does not lead to a similar phenotype, these results suggest that SHM of ILF B cells plays a critical role in regulating intestinal microflora.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fagarasan, Sidonia -- Muramatsu, Masamichi -- Suzuki, Keiichiro -- Nagaoka, Hitoshi -- Hiai, Hiroshi -- Honjo, Tasuku -- New York, N.Y. -- Science. 2002 Nov 15;298(5597):1424-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Chemistry, Graduate School of Medicine, Kyoto University, Yoshida, Sakyo-ku, Kyoto 606-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12434060" target="_blank"〉PubMed〈/a〉

Beschreibung: The formation and patterning of mesoderm during mammalian gastrulation require the activity of Nodal, a secreted mesoderm-inducing factor of the transforming growth factor-beta (TGF-beta) family. Here we show that the transcriptional corepressor DRAP1 has a very specific role in regulation of Nodal activity during mouse embryogenesis. We find that loss of Drap1 leads to severe gastrulation defects that are consistent with increased expression of Nodal and can be partially suppressed by Nodal heterozygosity. Biochemical studies indicate that DRAP1 interacts with and inhibits DNA binding by the winged-helix transcription factor FoxH1 (FAST), a critical component of a positive feedback loop for Nodal activity. We propose that DRAP1 limits the spread of a morphogenetic signal by down-modulating the response to the Nodal autoregulatory loop.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iratni, Rabah -- Yan, Yu-Ting -- Chen, Canhe -- Ding, Jixiang -- Zhang, Yi -- Price, Sandy M -- Reinberg, Danny -- Shen, Michael M -- New York, N.Y. -- Science. 2002 Dec 6;298(5600):1996-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Biochemistry, Division of Nucleic Acids Enzymology, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12471260" target="_blank"〉PubMed〈/a〉

Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, Martin -- Bristow, Robert -- Glazer, Peter -- Hill, Richard -- McBride, William -- McKenna, Gillies -- Muschel, Ruth -- New York, N.Y. -- Science. 2003 Dec 12;302(5652):1894; author reply 1894.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Radiation Oncology, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14671275" target="_blank"〉PubMed〈/a〉

Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Copeland, Neal G -- Jenkins, Nancy A -- O'Brien, Stephen J -- New York, N.Y. -- Science. 2002 May 31;296(5573):1617-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mouse Cancer Genetics Program, National Cancer Institute, Frederick, MD, 21702, USA. copeland@ncifcrf.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12040165" target="_blank"〉PubMed〈/a〉

Beschreibung: Animal behavior is synchronized to the 24-hour light:dark (LD) cycle by regulatory programs that produce circadian fluctuations in gene expression throughout the body. In mammals, the transcription factor CLOCK controls circadian oscillation in the suprachiasmatic nucleus of the brain; its paralog, neuronal PAS domain protein 2 (NPAS2), performs a similar function in other forebrain sites. To investigate the role of NPAS2 in behavioral manifestations of circadian rhythm, we studied locomotor activity, sleep patterns, and adaptability to both light- and restricted food-driven entrainment in NPAS2-deficient mice. Our results indicate that NPAS2 plays a substantive role in maintaining circadian behaviors in normal LD and feeding conditions and that NPAS2 is critical for adaptability to food restriction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dudley, Carol A -- Erbel-Sieler, Claudia -- Estill, Sandi Jo -- Reick, Martin -- Franken, Paul -- Pitts, SiNae -- McKnight, Steven L -- 37919/PHS HHS/ -- 4R37 MH59388/MH/NIMH NIH HHS/ -- 5T3DK07328/DK/NIDDK NIH HHS/ -- HL 64148/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2003 Jul 18;301(5631):379-83. Epub 2003 Jul 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9152, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12843397" target="_blank"〉PubMed〈/a〉

Beschreibung: Recent progress in the science of aging is driven largely by the use of model systems, ranging from yeast and nematodes to mice. These models have revealed conservation in genetic pathways that balance energy production and its damaging by-products with pathways that preserve somatic maintenance. Maintaining genome integrity has emerged as a major factor in longevity and cell viability. Here we discuss the use of mouse models with defects in genome maintenance for understanding the molecular basis of aging in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hasty, Paul -- Campisi, Judith -- Hoeijmakers, Jan -- van Steeg, Harry -- Vijg, Jan -- AG17242/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2003 Feb 28;299(5611):1355-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Medicine, University of Texas Health Science Center, San Antonio, TX 78245, USA. hastye@uthscsa.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12610296" target="_blank"〉PubMed〈/a〉

Beschreibung: Rapid turnover of the tumor suppressor protein p53 requires the MDM2 ubiquitin ligase, and both interact with p300-CREB-binding protein transcriptional coactivator proteins. p53 is stabilized by the binding of p300 to the oncoprotein E1A, suggesting that p300 regulates p53 degradation. Purified p300 exhibited intrinsic ubiquitin ligase activity that was inhibited by E1A. In vitro, p300 with MDM2 catalyzed p53 polyubiquitination, whereas MDM2 catalyzed p53 monoubiquitination. E1A expression caused a decrease in polyubiquitinated but not monoubiquitinated p53 in cells. Thus, generation of the polyubiquitinated forms of p53 that are targeted for proteasome degradation requires the intrinsic ubiquitin ligase activities of MDM2 and p300.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grossman, Steven R -- Deato, Maria E -- Brignone, Chrystelle -- Chan, Ho Man -- Kung, Andrew L -- Tagami, Hideaki -- Nakatani, Yoshihiro -- Livingston, David M -- CA15751/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2003 Apr 11;300(5617):342-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12690203" target="_blank"〉PubMed〈/a〉

Beschreibung: The active-site cysteine of peroxiredoxins is selectively oxidized to cysteine sulfinic acid during catalysis, which leads to inactivation of peroxidase activity. This oxidation was thought to be irreversible. However, by metabolic labeling of mammalian cells with 35S, we show that the sulfinic form of peroxiredoxin I, produced during the exposure of cells to H2O2, is rapidly reduced to the catalytically active thiol form. The mammalian cells' ability to reduce protein sulfinic acid might serve as a mechanism to repair oxidatively damaged proteins or represent a new type of cyclic modification by which the function of various proteins is regulated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Woo, Hyun Ae -- Chae, Ho Zoon -- Hwang, Sung Chul -- Yang, Kap-Seok -- Kang, Sang Won -- Kim, Kanghwa -- Rhee, Sue Goo -- New York, N.Y. -- Science. 2003 Apr 25;300(5619):653-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Cell Signaling Research and Division of Molecular Life Sciences, Ewha Womans University, Seoul 120-750, Korea.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12714748" target="_blank"〉PubMed〈/a〉

Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eden, Amir -- Gaudet, Francois -- Waghmare, Alpana -- Jaenisch, Rudolf -- CA87869/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2003 Apr 18;300(5618):455.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology, Nine Cambridge Center, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12702868" target="_blank"〉PubMed〈/a〉

Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heintz, Nathaniel -- New York, N.Y. -- Science. 2003 Jul 4;301(5629):59-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Rockefeller University, New York, NY 10021, USA. heintz@rockefeller.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12843383" target="_blank"〉PubMed〈/a〉

Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rajagopal, Jayaraj -- Anderson, William J -- Kume, Shoen -- Martinez, Olga I -- Melton, Douglas A -- New York, N.Y. -- Science. 2003 Jan 17;299(5605):363.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular and Cellular Biology, Howard Hughes Medical Institute, Harvard University, 7 Divinity Avenue, Cambridge, MA 02138, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12532008" target="_blank"〉PubMed〈/a〉

Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nobrega, Marcelo A -- Ovcharenko, Ivan -- Afzal, Veena -- Rubin, Edward M -- HL66728/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 17;302(5644):413.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉U.S. Department of Energy Joint Genome Institute, Walnut Creek, CA 94598, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14563999" target="_blank"〉PubMed〈/a〉

Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yewdell, Jonathan W -- New York, N.Y. -- Science. 2003 Sep 5;301(5638):1334-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892-0440, USA. jyewdell@nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12958347" target="_blank"〉PubMed〈/a〉

Beschreibung: Various chronic antidepressant treatments increase adult hippocampal neurogenesis, but the functional importance of this phenomenon remains unclear. Here, using genetic and radiological methods, we show that disrupting antidepressant-induced neurogenesis blocks behavioral responses to antidepressants. Serotonin 1A receptor null mice were insensitive to the neurogenic and behavioral effects of fluoxetine, a serotonin selective reuptake inhibitor. X-irradiation of a restricted region of mouse brain containing the hippocampus prevented the neurogenic and behavioral effects of two classes of antidepressants. These findings suggest that the behavioral effects of chronic antidepressants may be mediated by the stimulation of neurogenesis in the hippocampus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Santarelli, Luca -- Saxe, Michael -- Gross, Cornelius -- Surget, Alexandre -- Battaglia, Fortunato -- Dulawa, Stephanie -- Weisstaub, Noelia -- Lee, James -- Duman, Ronald -- Arancio, Ottavio -- Belzung, Catherine -- Hen, Rene -- New York, N.Y. -- Science. 2003 Aug 8;301(5634):805-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Neurobiology and Behavior, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12907793" target="_blank"〉PubMed〈/a〉

Beschreibung: Direct quantification of biomolecular interaction by single-molecule force spectroscopy has evolved into a powerful tool for materials and life sciences. We introduce an approach in which the unbinding forces required to break intermolecular bonds are measured in a differential format by comparison with a known reference bond (here, a short DNA duplex). In addition to a marked increase in sensitivity and force resolution, which enabled us to resolve single-base pair mismatches, this concept allows for highly specific parallel assays. This option was exploited to overcome cross-reactions of antibodies in a protein biochip application.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Albrecht, Christian -- Blank, Kerstin -- Lalic-Multhaler, Mio -- Hirler, Siegfried -- Mai, Thao -- Gilbert, Ilka -- Schiffmann, Susanne -- Bayer, Tom -- Clausen-Schaumann, Hauke -- Gaub, Hermann E -- New York, N.Y. -- Science. 2003 Jul 18;301(5631):367-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Nanotype GmbH, Lochhamer Schlag 12, 82166 Grafelfing, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12869761" target="_blank"〉PubMed〈/a〉

Beschreibung: The classical paradigm for dendritic cell function derives from the study of Langerhans cells, which predominate within skin epidermis. After an encounter with foreign agents, Langerhans cells are thought to migrate to draining lymph nodes, where they initiate T cell priming. Contrary to this, we show here that infection of murine epidermis by herpes simplex virus did not result in the priming of virus-specific cytotoxic T lymphocytes by Langerhans cells. Rather, the priming response required a distinct CD8alpha+ dendritic cell subset. Thus, the traditional view of Langerhans cells in epidermal immunity needs to be revisited to accommodate a requirement for other dendritic cells in this response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Allan, Rhys S -- Smith, Chris M -- Belz, Gabrielle T -- van Lint, Allison L -- Wakim, Linda M -- Heath, William R -- Carbone, Francis R -- New York, N.Y. -- Science. 2003 Sep 26;301(5641):1925-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, The University of Melbourne, Melbourne, Victoria 3010, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14512632" target="_blank"〉PubMed〈/a〉

Beschreibung: The CD8+ cytotoxic T cell response to pathogens is thought to be CD4+ helper T cell independent because infectious agents provide their own inflammatory signals. Mice that lack CD4+ T cells mount a primary CD8 response to Listeria monocytogenes equal to that of wild-type mice and rapidly clear the infection. However, protective memory to a challenge is gradually lost in the former animals. Memory CD8+ T cells from normal mice can respond rapidly, but memory CD8+ T cells that are generated without CD4 help are defective in their ability to respond to secondary encounters with antigen. The results highlight a previously undescribed role for CD4 help in promoting protective CD8 memory development.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2778341/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2778341/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, Joseph C -- Bevan, Michael J -- AI 19335/AI/NIAID NIH HHS/ -- R01 AI019335/AI/NIAID NIH HHS/ -- R01 AI019335-19/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2003 Apr 11;300(5617):339-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology and the Howard Hughes Medical Institute, University of Washington, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12690202" target="_blank"〉PubMed〈/a〉

Beschreibung: Mutations in MeCP2, which encodes a protein that has been proposed to function as a global transcriptional repressor, are the cause of Rett syndrome (RT T), an X-linked progressive neurological disorder. Although the selective inactivation of MeCP2 in neurons is sufficient to confer a Rett-like phenotype in mice, the specific functions of MeCP2 in postmitotic neurons are not known. We find that MeCP2 binds selectively to BDNF promoter III and functions to repress expression of the BDNF gene. Membrane depolarization triggers the calcium-dependent phosphorylation and release of MeCP2 from BDNF promoter III, thereby facilitating transcription. These studies indicate that MeCP2 plays a key role in the control of neuronal activity-dependent gene regulation and suggest that the deregulation of this process may underlie the pathology of RT T.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Wen G -- Chang, Qiang -- Lin, Yingxi -- Meissner, Alexander -- West, Anne E -- Griffith, Eric C -- Jaenisch, Rudolf -- Greenberg, Michael E -- HD 18655/HD/NICHD NIH HHS/ -- NS28829/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2003 Oct 31;302(5646):885-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14593183" target="_blank"〉PubMed〈/a〉

Beschreibung: Three distinct classes of drugs: dopaminergic agonists (such as D-amphetamine), serotonergic agonists (such as LSD), and glutamatergic antagonists (such as PCP) all induce psychotomimetic states in experimental animals that closely resemble schizophrenia symptoms in humans. Here we implicate a common signaling pathway in mediating these effects. In this pathway, dopamine- and an adenosine 3',5'-monophosphate (cAMP)-regulated phospho-protein of 32 kilodaltons (DARPP-32) is phosphorylated or dephosphorylated at three sites, in a pattern predicted to cause a synergistic inhibition of protein phosphatase-1 and concomitant regulation of its downstream effector proteins glycogen synthesis kinase-3 (GSK-3), cAMP response element-binding protein (CREB), and c-Fos. In mice with a genetic deletion of DARPP-32 or with point mutations in phosphorylation sites of DARPP-32, the effects of D-amphetamine, LSD, and PCP on two behavioral parameters-sensorimotor gating and repetitive movements-were strongly attenuated.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Svenningsson, Per -- Tzavara, Eleni T -- Carruthers, Robert -- Rachleff, Ilan -- Wattler, Sigrid -- Nehls, Michael -- McKinzie, David L -- Fienberg, Allen A -- Nomikos, George G -- Greengard, Paul -- DA10044/DA/NIDA NIH HHS/ -- MH40899/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2003 Nov 21;302(5649):1412-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular and Cellular Neuroscience, The Rockefeller University, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14631045" target="_blank"〉PubMed〈/a〉

Beschreibung: Alternative pre-messenger RNA splicing is an important mechanism for generating protein diversity and may explain in part how mammalian complexity arises from a surprisingly small complement of genes. Here, we describe "digital polony exon profiling,"a single molecule-based technology for studying complex alternative pre-messenger RNA splicing. This technology allows researchers to monitor the combinatorial diversity of exon inclusion in individual transcripts. A minisequencing strategy provides single nucleotide resolution, and the digital nature of the technology allows quantitation of individual splicing variants. Digital polony exon profiling can be used to investigate the physiological and pathological roles of alternately spliced messenger RNAs, as well as the mechanisms by which these messenger RNAs are produced.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhu, Jun -- Shendure, Jay -- Mitra, Robi D -- Church, George M -- 5U54GM62119/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2003 Aug 8;301(5634):836-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12907803" target="_blank"〉PubMed〈/a〉

Beschreibung: Disruption of the adaptor protein ELF, a beta-spectrin, leads to disruption of transforming growth factor-beta (TGF-beta) signaling by Smad proteins in mice. Elf-/- mice exhibit a phenotype similar to smad2+/-/smad3+/- mutant mice of midgestational death due to gastrointestinal, liver, neural, and heart defects. We show that TGF-beta triggers phosphorylation and association of ELF with Smad3 and Smad4, followed by nuclear translocation. ELF deficiency results in mislocalization of Smad3 and Smad4 and loss of the TGF-beta-dependent transcriptional response, which could be rescued by overexpression of the COOH-terminal region of ELF. This study reveals an unexpected molecular link between a major dynamic scaffolding protein and a key signaling pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tang, Yi -- Katuri, Varalakshmi -- Dillner, Allan -- Mishra, Bibhuti -- Deng, Chu-Xia -- Mishra, Lopa -- R01 DK56111/DK/NIDDK NIH HHS/ -- R01 DK58637/DK/NIDDK NIH HHS/ -- R03 DK53861/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2003 Jan 24;299(5606):574-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Developmental Biology, Department of Medicine, Georgetown University, Washington, DC 20007, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12543979" target="_blank"〉PubMed〈/a〉

Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hardin, P E -- Glossop, N R -- New York, N.Y. -- Science. 1999 Dec 24;286(5449):2460-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of Houston, Houston, TX 77204, USA. phardin@uh.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10636810" target="_blank"〉PubMed〈/a〉

Beschreibung: Mice lacking mCry1 and mCry2 are behaviorally arrhythmic. As shown here, cyclic expression of the clock genes mPer1 and mPer2 (mammalian Period genes 1 and 2) in the suprachiasmatic nucleus and peripheral tissues is abolished and mPer1 and mPer2 mRNA levels are constitutively high. These findings indicate that the biological clock is eliminated in the absence of both mCRY1 and mCRY2 (mammalian cryptochromes 1 and 2) and support the idea that mammalian CRY proteins act in the negative limb of the circadian feedback loop. The mCry double-mutant mice retain the ability to have mPer1 and mPer2 expression induced by a brief light stimulus known to phase-shift the biological clock in wild-type animals. Thus, mCRY1 and mCRY2 are dispensable for light-induced phase shifting of the biological clock.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Okamura, H -- Miyake, S -- Sumi, Y -- Yamaguchi, S -- Yasui, A -- Muijtjens, M -- Hoeijmakers, J H -- van der Horst, G T -- New York, N.Y. -- Science. 1999 Dec 24;286(5449):2531-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Brain Science, Kobe University School of Medicine, Kobe 650-0017, Japan. okamurah@kobe-u.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10617474" target="_blank"〉PubMed〈/a〉

Beschreibung: Angiopoietin-1 (Ang1) and vascular endothelial growth factor (VEGF) are endothelial cell-specific growth factors. Direct comparison of transgenic mice overexpressing these factors in the skin revealed that the VEGF-induced blood vessels were leaky, whereas those induced by Ang1 were nonleaky. Moreover, vessels in Ang1-overexpressing mice were resistant to leaks caused by inflammatory agents. Coexpression of Ang1 and VEGF had an additive effect on angiogenesis but resulted in leakage-resistant vessels typical of Ang1. Ang1 therefore may be useful for reducing microvascular leakage in diseases in which the leakage results from chronic inflammation or elevated VEGF and, in combination with VEGF, for promoting growth of nonleaky vessels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thurston, G -- Suri, C -- Smith, K -- McClain, J -- Sato, T N -- Yancopoulos, G D -- McDonald, D M -- HL-24136/HL/NHLBI NIH HHS/ -- HL-59157/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1999 Dec 24;286(5449):2511-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Cardiovascular Research Institute, University of California, San Francisco, CA 94143-0452, USA. gavint@itsa.ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10617467" target="_blank"〉PubMed〈/a〉

Beschreibung: Mutation at the mouse progressive ankylosis (ank) locus causes a generalized, progressive form of arthritis accompanied by mineral deposition, formation of bony outgrowths, and joint destruction. Here, we show that the ank locus encodes a multipass transmembrane protein (ANK) that is expressed in joints and other tissues and controls pyrophosphate levels in cultured cells. A highly conserved gene is present in humans and other vertebrates. These results identify ANK-mediated control of pyrophosphate levels as a possible mechanism regulating tissue calcification and susceptibility to arthritis in higher animals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ho, A M -- Johnson, M D -- Kingsley, D M -- 5T32GM07365/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Jul 14;289(5477):265-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology and Howard Hughes Medical Institute, Beckman Center B300, Stanford University School of Medicine, Stanford, CA 94305-5327, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10894769" target="_blank"〉PubMed〈/a〉

Beschreibung: The contribution of extrinsic and genetic mechanisms in determining areas of the mammalian neocortex has been a contested issue. This study analyzes the roles of the regulatory genes Emx2 and Pax6, which are expressed in opposing gradients in the neocortical ventricular zone, in specifying areas. Changes in the patterning of molecular markers and area-specific connections between the cortex and thalamus suggest that arealization of the neocortex is disproportionately altered in Emx2 and Pax6 mutant mice in opposing manners predicted from their countergradients of expression: rostral areas expand and caudal areas contract in Emx2 mutants, whereas the opposite effect is seen in Pax6 mutants. These findings suggest that Emx2 and Pax6 cooperate to regulate arealization of the neocortex and to confer area identity to cortical cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bishop, K M -- Goudreau, G -- O'Leary, D D -- NS31558/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2000 Apr 14;288(5464):344-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Neurobiology Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10764649" target="_blank"〉PubMed〈/a〉

Beschreibung: Most types of antibiotic resistance impose a biological cost on bacterial fitness. These costs can be compensated, usually without loss of resistance, by second-site mutations during the evolution of the resistant bacteria in an experimental host or in a laboratory medium. Different fitness-compensating mutations were selected depending on whether the bacteria evolved through serial passage in mice or in a laboratory medium. This difference in mutation spectra was caused by either a growth condition-specific formation or selection of the compensated mutants. These results suggest that bacterial evolution to reduce the costs of antibiotic resistance can take different trajectories within and outside a host.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bjorkman, J -- Nagaev, I -- Berg, O G -- Hughes, D -- Andersson, D I -- New York, N.Y. -- Science. 2000 Feb 25;287(5457):1479-82.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Bacteriology, Swedish Institute for Infectious Disease Control, S-171 82 Solna, Sweden.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10688795" target="_blank"〉PubMed〈/a〉

Beschreibung: An antibiotic once used to treat traveler's diarrhea might battle Alzheimer's disease as well, researchers announced here last week at the Society for Neuroscience's annual meeting. The drug dissolves Alzheimer's-like plaques in mouse brains, apparently by trapping the copper and zinc that stud these deposits. A clinical trial to test whether the drug helps people with Alzheimer's is already under way.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Helmuth, L -- New York, N.Y. -- Science. 2000 Nov 17;290(5495):1273-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11185394" target="_blank"〉PubMed〈/a〉

Beschreibung: Allergic asthma is caused by the aberrant expansion in the lung of T helper cells that produce type 2 (TH2) cytokines and is characterized by infiltration of eosinophils and bronchial hyperreactivity. This disease is often triggered by mast cells activated by immunoglobulin E (IgE)-mediated allergic challenge. Activated mast cells release various chemical mediators, including prostaglandin D2 (PGD2), whose role in allergic asthma has now been investigated by the generation of mice deficient in the PGD receptor (DP). Sensitization and aerosol challenge of the homozygous mutant (DP-/-) mice with ovalbumin (OVA) induced increases in the serum concentration of IgE similar to those in wild-type mice subjected to this model of asthma. However, the concentrations of TH2 cytokines and the extent of lymphocyte accumulation in the lung of OVA-challenged DP-/- mice were greatly reduced compared with those in wild-type animals. Moreover, DP-/- mice showed only marginal infiltration of eosinophils and failed to develop airway hyperreactivity. Thus, PGD2 functions as a mast cell-derived mediator to trigger asthmatic responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsuoka, T -- Hirata, M -- Tanaka, H -- Takahashi, Y -- Murata, T -- Kabashima, K -- Sugimoto, Y -- Kobayashi, T -- Ushikubi, F -- Aze, Y -- Eguchi, N -- Urade, Y -- Yoshida, N -- Kimura, K -- Mizoguchi, A -- Honda, Y -- Nagai, H -- Narumiya, S -- New York, N.Y. -- Science. 2000 Mar 17;287(5460):2013-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Kyoto University Faculty of Medicine, Kyoto 606-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10720327" target="_blank"〉PubMed〈/a〉

Beschreibung: Signaling proteins are thought to be tightly regulated spatially and temporally in order to generate specific and localized effects. For Rac and other small guanosine triphosphatases, binding to guanosine triphosphate leads to interaction with downstream targets and regulates subcellular localization. A method called FLAIR (fluorescence activation indicator for Rho proteins) was developed to quantify the spatio-temporal dynamics of the Rac1 nucleotide state in living cells. FLAIR revealed precise spatial control of growth factor-induced Rac activation, in membrane ruffles and in a gradient of activation at the leading edge of motile cells. FLAIR exemplifies a generally applicable approach for examining spatio-temporal control of protein activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kraynov, V S -- Chamberlain, C -- Bokoch, G M -- Schwartz, M A -- Slabaugh, S -- Hahn, K M -- AG15430/AG/NIA NIH HHS/ -- GM39434/GM/NIGMS NIH HHS/ -- R01 GM-57464/GM/NIGMS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 2000 Oct 13;290(5490):333-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, The Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11030651" target="_blank"〉PubMed〈/a〉

Beschreibung: Activation of the transcription factor nuclear factor (NF)-kappaB by proinflammatory stimuli leads to increased expression of genes involved in inflammation. Activation of NF-kappaB requires the activity of an inhibitor of kappaB (IkappaB)-kinase (IKK) complex containing two kinases (IKKalpha and IKKbeta) and the regulatory protein NEMO (NF-kappaB essential modifier). An amino-terminal alpha-helical region of NEMO associated with a carboxyl-terminal segment of IKKalpha and IKKbeta that we term the NEMO-binding domain (NBD). A cell-permeable NBD peptide blocked association of NEMO with the IKK complex and inhibited cytokine-induced NF-kappaB activation and NF-kappaB-dependent gene expression. The peptide also ameliorated inflammatory responses in two experimental mouse models of acute inflammation. The NBD provides a target for the development of drugs that would block proinflammatory activation of the IKK complex without inhibiting basal NF-kappaB activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉May, M J -- D'Acquisto, F -- Madge, L A -- Glockner, J -- Pober, J S -- Ghosh, S -- AI 33443/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2000 Sep 1;289(5484):1550-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology and Department of Molecular Biophysics and Biochemistry, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10968790" target="_blank"〉PubMed〈/a〉

Beschreibung: VDJ recombination is developmentally regulated in vivo by enhancer-dependent changes in the accessibility of chromosomal recombination signal sequences to the recombinase, but the molecular nature of these changes is unknown. Here histone H3 acetylation was measured along versions of a transgenic VDJ recombination reporter and the endogenous T cell receptor alpha/delta locus. Enhancer activity was shown to impart long-range, developmentally regulated changes in H3 acetylation, and H3 acetylation status was tightly linked to VDJ recombination. H3 hyperacetylation is proposed as a molecular mechanism coupling enhancer activity to accessibility for VDJ recombination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McMurry, M T -- Krangel, M S -- GM 41052/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2000 Jan 21;287(5452):495-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Post Office Box 3010, Duke University Medical Center, Durham NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10642553" target="_blank"〉PubMed〈/a〉

Beschreibung: Class I major histocompatibility complex (class I MHC) molecules, known to be important for immune responses to antigen, are expressed also by neurons that undergo activity-dependent, long-term structural and synaptic modifications. Here, we show that in mice genetically deficient for cell surface class I MHC or for a class I MHC receptor component, CD3zeta, refinement of connections between retina and central targets during development is incomplete. In the hippocampus of adult mutants, N-methyl-D-aspartate receptor-dependent long-term potentiation (LTP) is enhanced, and long-term depression (LTD) is absent. Specific class I MHC messenger RNAs are expressed by distinct mosaics of neurons, reflecting a potential for diverse neuronal functions. These results demonstrate an important role for these molecules in the activity-dependent remodeling and plasticity of connections in the developing and mature mammalian central nervous system (CNS).〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2175035/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2175035/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huh, G S -- Boulanger, L M -- Du, H -- Riquelme, P A -- Brotz, T M -- Shatz, C J -- 1F32EY07016/EY/NEI NIH HHS/ -- EY06912/EY/NEI NIH HHS/ -- F32 EY007016/EY/NEI NIH HHS/ -- F32 EY007016-02/EY/NEI NIH HHS/ -- F32 EY007016-03/EY/NEI NIH HHS/ -- MH48108/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2000 Dec 15;290(5499):2155-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA. gshuh@alum.mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11118151" target="_blank"〉PubMed〈/a〉

Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 2000 Apr 14;288(5464):255-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10777404" target="_blank"〉PubMed〈/a〉

Beschreibung: To determine the ability of antibodies to provide protection from Ebola viruses, monoclonal antibodies (mAbs) to the Ebola glycoprotein were generated and evaluated for efficacy. We identified several protective mAbs directed toward five unique epitopes on Ebola glycoprotein. One of the epitopes is conserved among all Ebola viruses that are known to be pathogenic for humans. Some protective mAbs were also effective therapeutically when administered to mice 2 days after exposure to lethal Ebola virus. The identification of protective mAbs has important implications for developing vaccines and therapies for Ebola virus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilson, J A -- Hevey, M -- Bakken, R -- Guest, S -- Bray, M -- Schmaljohn, A L -- Hart, M K -- New York, N.Y. -- Science. 2000 Mar 3;287(5458):1664-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Virology Division, U.S. Army Medical Research Institute of Infectious Diseases, 1425 Porter Street, Fort Detrick, Frederick, MD 21702-5011, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10698744" target="_blank"〉PubMed〈/a〉

Beschreibung: Murine T10 and T22 are highly related nonclassical major histocompatibility complex (MHC) class Ib proteins that bind to certain gammadelta T cell receptors (TCRs) in the absence of other components. The crystal structure of T22b at 3.1 angstroms reveals similarities to MHC class I molecules, but one side of the normal peptide-binding groove is severely truncated, which allows direct access to the beta-sheet floor. Potential gammadelta TCR-binding sites can be inferred from functional mapping of T10 and T22 point mutants and allelic variants. Thus, T22 represents an unusual variant of the MHC-like fold and indicates that gammadelta and alphabeta TCRs interact differently with their respective MHC ligands.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wingren, C -- Crowley, M P -- Degano, M -- Chien, Y -- Wilson, I A -- AI33431/AI/NIAID NIH HHS/ -- CA58896/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2000 Jan 14;287(5451):310-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and the Skaggs Institute for Chemical Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10634787" target="_blank"〉PubMed〈/a〉

Beschreibung: The cytokine interleukin-10 (IL-10) has shown promise in clinical trials for treatment of inflammatory bowel disease (IBD). Using two mouse models, we show that the therapeutic dose of IL-10 can be reduced by localized delivery of a bacterium genetically engineered to secrete the cytokine. Intragastric administration of IL-10-secreting Lactococcus lactis caused a 50% reduction in colitis in mice treated with dextran sulfate sodium and prevented the onset of colitis in IL-10(-/-) mice. This approach may lead to better methods for cost-effective and long-term management of IBD in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steidler, L -- Hans, W -- Schotte, L -- Neirynck, S -- Obermeier, F -- Falk, W -- Fiers, W -- Remaut, E -- New York, N.Y. -- Science. 2000 Aug 25;289(5483):1352-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Ghent University and Flanders Interuniversity Institute for Biotechnology, K. L. Ledeganckstraat 35, 9000 Gent, Belgium. lothar.steidler@dmb.rug.ac.be〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10958782" target="_blank"〉PubMed〈/a〉

Beschreibung: One of the biggest obstacles to gene therapy is the delivery of the therapeutic gene to the target tissue so that it is appropriately expressed. In his Perspective, Willard looks at the potential advantages of using a human artificial chromosome to maintain expression of a therapeutic gene and discusses some of the hurdles yet to be overcome before this gene delivery system can be tried out in the clinic.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Willard, H F -- New York, N.Y. -- Science. 2000 Nov 17;290(5495):1308-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics and Center for Human Genetics at Case Western Reserve University and the Research Institute of Universi Hospitals of Cleveland, Cleveland, OH 44106, USA. hfw@po.CWRU.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11185406" target="_blank"〉PubMed〈/a〉

Beschreibung: Caveolae are subcellular structures implicated in the import and transcytosis of macromolecules and in transmembrane signaling. To date, evidence for the existence of caveolae in hematopoietic cells has been ambiguous. Caveolae were detected in the microvilli and intracellular vesicles of cultured mouse bone marrow-derived mast cells (BMMCs). CD48, a receptor for FimH-expressing (type 1 fimbriated) Escherichia coli, was specifically localized to plasmalemmal caveolae in BMMCs. The involvement of caveolae in bacterial entry into BMMCs was indicated because caveolae-disrupting and -usurping agents specifically blocked E. coli entry, and markers of caveolae were actively recruited to sites of bacterial entry. The formation of bacteria-encapsulating caveolar chambers in BMMCs represents a distinct mechanism of microbial entry into phagocytes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shin, J S -- Gao, Z -- Abraham, S N -- AI 35678/AI/NIAID NIH HHS/ -- CA 14236/CA/NCI NIH HHS/ -- DK 50814/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2000 Aug 4;289(5480):785-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Pathology and Microbiology, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10926542" target="_blank"〉PubMed〈/a〉

Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 2000 Jan 28;287(5453):567.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10691532" target="_blank"〉PubMed〈/a〉

Beschreibung: Clinicians may soon be able to mount a multipronged attack against cholesterol, the artery-clogging lipid whose buildup in the body is a major contributor to heart attacks and other cardiovascular diseases. In work reported on page 1524, a team has pinpointed a biological master switch in mice that controls three pathways that work together to both rid the body of excess cholesterol and prevent its absorption from the intestine. The work suggests a new mechanism for reducing cholesterol, for example, with drugs that turn up the activity of the master switch, a protein known as the retinoid X receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ferber, D -- New York, N.Y. -- Science. 2000 Sep 1;289(5484):1446-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10991725" target="_blank"〉PubMed〈/a〉

Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stavnezer, J -- New York, N.Y. -- Science. 2000 May 12;288(5468):984-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, 55 Lake Avenue N., Worcester, MA 01655, USA. Janet.Stavnezer@umassmed.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10841719" target="_blank"〉PubMed〈/a〉

Beschreibung: The molecular control of self-renewal and differentiation of stem cells has remained enigmatic. Transgenic loss-of-function and overexpression models now show that the dosage of glial cell line-derived neurotrophic factor (GDNF), produced by Sertoli cells, regulates cell fate decisions of undifferentiated spermatogonial cells that include the stem cells for spermatogenesis. Gene-targeted mice with one GDNF-null allele show depletion of stem cell reserves, whereas mice overexpressing GDNF show accumulation of undifferentiated spermatogonia. They are unable to respond properly to differentiation signals and undergo apoptosis upon retinoic acid treatment. Nonmetastatic testicular tumors are regularly formed in older GDNF-overexpressing mice. Thus, GDNF contributes to paracrine regulation of spermatogonial self-renewal and differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meng, X -- Lindahl, M -- Hyvonen, M E -- Parvinen, M -- de Rooij, D G -- Hess, M W -- Raatikainen-Ahokas, A -- Sainio, K -- Rauvala, H -- Lakso, M -- Pichel, J G -- Westphal, H -- Saarma, M -- Sariola, H -- New York, N.Y. -- Science. 2000 Feb 25;287(5457):1489-93.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Programs of Developmental Biology, Molecular Neurobiology, Electron Microscopy Unit, Institute of Biotechnology, Viikki Biocenter, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10688798" target="_blank"〉PubMed〈/a〉

Beschreibung: Ectodysplasin, a member of the tumor necrosis factor family, is encoded by the anhidrotic ectodermal dysplasia (EDA) gene. Mutations in EDA give rise to a clinical syndrome characterized by loss of hair, sweat glands, and teeth. EDA-A1 and EDA-A2 are two isoforms of ectodysplasin that differ only by an insertion of two amino acids. This insertion functions to determine receptor binding specificity, such that EDA-A1 binds only the receptor EDAR, whereas EDA-A2 binds only the related, but distinct, X-linked ectodysplasin-A2 receptor (XEDAR). In situ binding and organ culture studies indicate that EDA-A1 and EDA-A2 are differentially expressed and play a role in epidermal morphogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yan, M -- Wang, L C -- Hymowitz, S G -- Schilbach, S -- Lee, J -- Goddard, A -- de Vos, A M -- Gao, W Q -- Dixit, V M -- New York, N.Y. -- Science. 2000 Oct 20;290(5491):523-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Oncology, Genentech, 1 DNA Way, South San Francisco, CA 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11039935" target="_blank"〉PubMed〈/a〉

Beschreibung: Bone morphogenetic proteins (BMPs) have multiple functions in the developing nervous system. A member of this family, BMP-9, was found to be highly expressed in the embryonic mouse septum and spinal cord, indicating a possible role in regulating the cholinergic phenotype. In cultured neurons, BMP-9 directly induced the expression of the cholinergic gene locus encoding choline acetyltransferase and the vesicular acetylcholine transporter and up-regulated acetylcholine synthesis. The effect was reversed upon withdrawal of BMP-9. Intracerebroventricular injection of BMP-9 increased acetylcholine levels in vivo. Although certain other BMPs also up-regulated the cholinergic phenotype in vitro, they were less effective than BMP-9. These data indicate that BMP-9 is a differentiating factor for cholinergic central nervous system neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lopez-Coviella, I -- Berse, B -- Krauss, R -- Thies, R S -- Blusztajn, J K -- P01 AG09525/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2000 Jul 14;289(5477):313-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry and Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA 02118, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10894782" target="_blank"〉PubMed〈/a〉

Beschreibung: Stunned myocardium is a syndrome of reversible contractile failure that frequently complicates coronary artery disease. Cardiac excitation is uncoupled from contraction at the level of the myofilaments. Selective proteolysis of the thin filament protein troponin I has been correlated with stunned myocardium. Here, transgenic mice expressing the major degradation product of troponin I (TnI1-193) in the heart were found to develop ventricular dilatation, diminished contractility, and reduced myofilament calcium responsiveness, recapitulating the phenotype of stunned myocardium. Proteolysis of troponin I also occurs in ischemic human cardiac muscle. Thus, troponin I proteolysis underlies the pathogenesis of a common acquired form of heart failure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murphy, A M -- Kogler, H -- Georgakopoulos, D -- McDonough, J L -- Kass, D A -- Van Eyk, J E -- Marban, E -- HL 44065/HL/NHLBI NIH HHS/ -- HL 63038/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2000 Jan 21;287(5452):488-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Johns Hopkins University School of Medicine, Ross Building 1144, 720 Rutland Avenue, Baltimore, MD 21205, USA. murphy@jhmi.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10642551" target="_blank"〉PubMed〈/a〉

Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Aridor, M -- Balch, W E -- New York, N.Y. -- Science. 2000 Feb 4;287(5454):816-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Biology, Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10691557" target="_blank"〉PubMed〈/a〉

Beschreibung: The mechanism underlying the intestinal fluid loss in rotavirus diarrhea, which often afflicts children in developing countries, is not known. One hypothesis is that the rotavirus evokes intestinal fluid and electrolyte secretion by activation of the nervous system in the intestinal wall, the enteric nervous system (ENS). Four different drugs that inhibit ENS functions were used to obtain experimental evidence for this hypothesis in mice in vitro and in vivo. The involvement of the ENS in rotavirus diarrhea indicates potential sites of action for drugs in the treatment of the disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lundgren, O -- Peregrin, A T -- Persson, K -- Kordasti, S -- Uhnoo, I -- Svensson, L -- New York, N.Y. -- Science. 2000 Jan 21;287(5452):491-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Goteborg University, Box 432, S-405 30 Goteborg, Sweden. ove.lundgren@fysiologi.gu.se〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10642552" target="_blank"〉PubMed〈/a〉

Beschreibung: T cell memory depends on factors that regulate expansion and death of these cells after antigenic stimulation. Mice deficient in perforin and interferon-gamma (IFN-gamma) exhibited increased expansion, altered immunodominance, and decreased death of antigen-specific CD8+ T cells after infection with an attenuated strain of Listeria monocytogenes, which was cleared from these mice. Expansion of CD8+ T cells was controlled by perforin, whereas IFN-gamma regulated immunodominance and the death phase. Thus, perforin and IFN-gamma regulate distinct elements of CD8+ T cell homeostasis independently of their role as antimicrobial effector molecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Badovinac, V P -- Tvinnereim, A R -- Harty, J T -- AI36864/AI/NIAID NIH HHS/ -- AI42767/AI/NIAID NIH HHS/ -- T32AI07511/AI/NIAID NIH HHS/ -- etc. -- New York, N.Y. -- Science. 2000 Nov 17;290(5495):1354-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Interdisciplinary Graduate Program in Immunology, University of Iowa, Iowa City, IA 52242, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11082062" target="_blank"〉PubMed〈/a〉

Beschreibung: Accelerated telomere loss has been proposed to be a factor leading to end-stage organ failure in chronic diseases of high cellular turnover such as liver cirrhosis. To test this hypothesis directly, telomerase-deficient mice, null for the essential telomerase RNA (mTR) gene, were subjected to genetic, surgical, and chemical ablation of the liver. Telomere dysfunction was associated with defects in liver regeneration and accelerated the development of liver cirrhosis in response to chronic liver injury. Adenoviral delivery of mTR into the livers of mTR(-/-) mice with short dysfunctional telomeres restored telomerase activity and telomere function, alleviated cirrhotic pathology, and improved liver function. These studies indicate that telomere dysfunction contributes to chronic diseases of continual cellular loss-replacement and encourage the evaluation of "telomerase therapy" for such diseases.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rudolph, K L -- Chang, S -- Millard, M -- Schreiber-Agus, N -- DePinho, R A -- K08 AG001019/AG/NIA NIH HHS/ -- R01HD28317/HD/NICHD NIH HHS/ -- R01HD34880/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 2000 Feb 18;287(5456):1253-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Adult Oncology, Medicine and Genetics, Dana-Farber Cancer Institute, 44 Binney Street (M413), and Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10678830" target="_blank"〉PubMed〈/a〉

Beschreibung: How do AMPA receptors that are made in the cytoplasm of excitatory neurons travel to and become localized in the distant postsynaptic membranes of dendrites? Nakagawa and Sheng, in a Perspective, suggest that the answer may lie in the stargazin protein that has now been found to interact with AMPA receptors, guiding them to the postsynaptic membrane.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nakagawa, T -- Sheng, M -- New York, N.Y. -- Science. 2000 Dec 22;290(5500):2270-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School and Massachusetts General Hospital, Boston, Massachusetts, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11188726" target="_blank"〉PubMed〈/a〉

Beschreibung: Pseudomonas aeruginosa causes severe infections, particularly of the lung, that are life threatening. Here, we show that P. aeruginosa infection induces apoptosis of lung epithelial cells by activation of the endogenous CD95/CD95 ligand system. Deficiency of CD95 or CD95 ligand on epithelial cells prevented apoptosis of lung epithelial cells in vivo as well as in vitro. The importance of CD95/CD95 ligand-mediated lung epithelial cell apoptosis was demonstrated by the rapid development of sepsis in CD95- or CD95 ligand-deficient mice, but not in normal mice, after P. aeruginosa infection.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grassme, H -- Kirschnek, S -- Riethmueller, J -- Riehle, A -- von Kurthy, G -- Lang, F -- Weller, M -- Gulbins, E -- New York, N.Y. -- Science. 2000 Oct 20;290(5491):527-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Tuebingen, Gmelinstrasse 5, 72076 Tuebingen, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11039936" target="_blank"〉PubMed〈/a〉

Beschreibung: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Balter, M -- New York, N.Y. -- Science. 2000 Sep 8;289(5485):1663-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/11001722" target="_blank"〉PubMed〈/a〉