999 resultados para Plotino, 205-270


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1 Brief von Max Horkheimer an Abel, 16.03.1936; 3 Briefe zwischen Hubert Abrahamsohn und Max Horkheimer, 1935-1936, 21.12.1936; 2 Briefe zwischen Emanuel Adler und Max Horkheimer, 12.04.1946, 26.04.1946; 2 Briefe zwischen Max Adler und Max Horkheimer, 16.03.1935, 29.03.1935; 1 Brief von Eva Ahamson an Max Horkheimer, 01.11.1944; 2 Briefe der Aircraft Warning Service Brentwood an Max Horkheimer, Mai 1942; 6 Briefe zwischen Librairie Félix Alcan und Max Horkheimer, 1935, 18.12.1935; 11 Briefe zwischen Franz Alexander und Max Horkheimer, 1938-1940; 2 Briefe zwischen der American Historical Review New York und Max Horkheimer, 01.04.1941, 07.04.1941; 1 Brief von Paul Reiwald an Max Horkheimer, 18.10.1940; 2 Briefe zwischen Helen Manice Alexander und Max Horkheimer, 1936; 2 Briefe zwischen Bernardine Allen und Max Horkheimer, 17.06.1938, 24.06.1938; 1 Brief der Alumni Federation of Columbia University an Max Horkheimer, 21.07.1942; 1 Brief der American Friends Service Comittee an Max Horkheimer, 10.12.1940; 3 Briefe zwischen der American Academy of Political and Social Science Philadelphia und Max Horkheimer, 1939,1940, 16.01.1939; 1 Brief der American Automobile Association Washington an Max Horkheimer, 22.03.1938; 1 Brief der American Association for the Advancement of Science Washington an Max Horkheimer, 16.08.1937; 2 Briefe von Max Horkheimer an den American Consulate General Berlin, 1939; 1 Brief von Max Horkheimer an den American Consulate General Havana, 03.03.1941; 4 Briefe von Max Horkheimer an den American Consul London, 1939-1941; 2 Briefe von Max Horkheimer an den American Consulate General Stuttgart, 1939-1941; 1 Brief von Max Horkheimer an den American Consul Zürich, 1939; 1 Brief von Friedrich Pollock an den American Council of Learned Society, Washington, 27.06.1941; 2 Briefe von Max Horkheimer an die American Friends of German Freedom New York, 1941; 4 Briefe der American Historical Association Washington an Max Horkheimer, 1937-1938; 1 Brief von Max Horkheimer an den American Red Cross Westwood Office, 21.06.1943; 18 Briefe zwschen der American Society for the Prevention of Cruelty to Animals New York und Max Horkheimer, 1936-1941; 1 Brief von Max Horkheimer an die American Women's Volunteer Service Pacific Palisades, 27.07.1942; 23 Briefe zwischen Eugene Anderson und Max Horkheimer, 1937-1941; 2 Briefe zwischen Norah Andreae und Max Horkheimer, 27.10.1944, 09.09.1946; 1 Brief von Rosa Nebel-Schenk, 04.03.1946; 1 Brief von der National Catholic Welfare Conference, 14.08.1944; 12 Briefe zwischen Werner Andreae und Max Horkheimer, 1945-1954; 1 Brief von Julius Marx an Werner Andreae, 10.05.1946, 11.05.1950; 2 Briefe von Josef Messinger an Werner Andreae, 23.10.1946, ohne Datum; 3 Briefe zwischen dem Advokatenbüro Hodler und Max Horkheimer, 1946, 09.05.1946;

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58 Briefe zwischen dem Professor Ludwig von Friedeburg (Kultusminister) und Max Horkheimer, 1953-1973; Gutachten über die Habilitationsschrift von Friedeburg 1959 (Blatt 53-66); Antrittsvorlesung von Friedeburg: "Universität und Öffentlichkeit" 1967 (Blatt 159-173); Sonderdrucke und Fragebogen;

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Frankfurter Latern

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Frankfurter Latern, Devrient, Paris, Mathilde Heine, Anlage (nicht enthalten): Gedicht aus Heinrich Heines Nachlaß, "Brendelche Schnud", Dr. Heine, Dresden, Nizza

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Vorbesitzer: Michelangelo Gualandi

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p63, a p53 family member, is a transcription factor that has complex roles in cancer. This study focuses on the role of the ∆Np63α isoform in bladder cancer (BC). Epithelial – mesenchymal transition (EMT) is a physiological process that plays an important part in metastasis and drug resistance. At the molecular level, EMT is characterized by the loss of the epithelial marker E-cadherin, and the acquisition of the transcriptional repressors of E-cadherin (ZEB1, ZEB2, TWIST, SNAI1 and SNAI2). Recent publications highlight the role of microRNAs belonging to the miR-200 family and miR-205 in preventing EMT through suppression of ZEB1 and ZEB2. p53, the homologue of p63, is implicated in regulating EMT by modulating the expression of miR-200c; however, the mechanisms underlying miR-205 control remain unclear. Here we show that ∆Np63α regulates the transcription of miR-205 and controls EMT in human BC cells. We observed a strong correlation between the expression of ∆Np63α, miR-205 and E-cadherin in a panel of BC cell lines (n=28) and also in bladder primary tumors from a cohort of patients (n=98). A remarkably inverse correlation is observed between ∆Np63α and ZEB1/2 in cell lines. Stable knockdown (KD) ∆Np63α in UC6, an “epithelial” BC cell line, decreased the expression of miR-205 and induced ZEB1/2 expression, the effects that were reversed by expression of exogenous miR-205. Moreover, overexpressing ∆Np63α in UC3, a “messenchymal” BC cell line, brought about opposite results, an increase in miR-205 expression and a reduction in ZEB1/2 expression. Modulation of ∆Np63α expression resulted in a parallel change in the expression of miR-205 and miR-205 “host” gene (miR-205HG). Nuclear run-on and chromatin immunoprecipitation experiments demonstrated that ∆Np63α regulates the transcription of miR-205 through controlling the recruitment of RNA Polymerase II to the promoter of miR-205HG. Interestingly, high miR-205 expression correlated with poor clinical outcome in BC patients, consistent with our recent publication highlighting the enrichment of ∆Np63 in a lethal subset of muscle invasive BC. In summary, our data present the important roles of ∆Np63α in preventing EMT mediated by miR-205. Our study also identifies miR-205 as a potential molecular marker to predict clinical outcome in BC patients.

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http://lib.dr.iastate.edu/carver_narratives/1030/thumbnail.jpg

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Primary Objectives - Describe and quantify the present strength and variability of the circulation and oceanic processes of the Nordic Seas regions using primarily observations of the long term spread of a tracer purposefully released into the Greenland Sea Gyre in 1996. - Improve our understanding of ocean processes critical to the thermaholine circulation in the Nordic Seas regions so as to be able to predict how this region may respond to climate change. - Assess the role of mixing and ageing of water masses on the carbon transport and the role of the thermohaline circulation in carbon storage using water transports and mixing coefficients derived from the tracer distribution. Specific Objectives Perform annual hydrographic, chemical and SF6 tracer surveys into the Nordic regions in order to: - Measure lateral and diapycnal mixing rates in the Greenland Sea Gyre and in the surrounding regions. - Document the depth and rates of convective mixing in the Greenland Sea using the SF6 and the water masses characteristics. - Measure the transit time and transport of water from the Greenland Sea to surrounding seas and outflows. Document processes of water mass transformation and entrainment occurring to water emanating from the central Greenland Sea. - Measure diapycnal mixing rates in the bottom and margins of the Greenland Sea basin using the SF6 signal observed there. Quantify the potential role of bottom boundary-layer mixing in the ventilation of the Greenland Sea Deep Water in absence of deep convection. Monitor the variability of the entrainment of water from the Greenland Sea using time series auto-sampler moorings at strategic positions i.e., sill of the Denmark Strait, Labrador Sea, Jan Mayen fracture zone and Fram Strait. Relate the observed variability of the tracer signal in the outflows to convection events in the Greenland Sea and local wind stress events. Obtain a better description of deepwater overflow and entrainment processes in the Denmark Strait and Faeroe Bank Channel overflows and use these to improve modelling of deepwater overflows. Monitor the tracer invasion into the North Atlantic using opportunistic SF6 measurements from other cruises: we anticipate that a number of oceanographic cruises will take place in the north-east Atlantic and the Labrador Sea. It should be possible to get samples from some cruises for SF6 measurements. Use process models to describe the spread of the tracer to achieve better parameterisation for three-dimensional models. One reason that these are so resistant to prediction is that our best ocean models are as yet some distance from being good enough, to predict climate and climate change.