Stürmer des Ghetto : Essays

von Z. F. Finkelstein

[Rezension]

Louis Finkelstein

Zu den Takkanot des Rabbenu Gerschom

Louis Finkelstein

Simon Samiel Frug

Z. F. Finkelstein

Na 1 Nachlass Max Horkheimer, 14 - Korrespondenzen u.a. mit Hugo Fischer und Karl August Wittfogel (p. I 7, 224-429)

1 Brief von Max Horkheimer an Rosel Favez, 03.12.1935; 5 Briefe zwischen Sidney B. Fay von der Bureau of International Search Cambridge, Massachusetts und Max Horkheimer, 1939-1941; 1 Brief von Max Horkheimer an James Feibleman, 02.03.1942; 5 Briefe von Hans Feibelmann an Max Horkheimer, 1936-1937; 2 Briefe zwischen Babette Feigenbaum und Max Horkheimer, 29.04.1941, 05.05.1941; 1 Brief von Arthur Feiler an Max Horkheimer, 15.10.1939; 1 Brief von Max Horkheimer an Adolf Feitler, 03.01.1935; 3 Briefe zwischen Frederick V. Filed von dem American Council Institute of Pacific Relations und Max Horkheimer, 1937, 05.04.1937; 9 Briefe zwischen Thea Field, Lowell Field und Max Horkheimer, 1935-1941; 1 Brief von Max Horkheimer an Finkelstein, 18.09.1941; 7 Briefe zwischen Harry Finkelstein und Max Horkheimer, 1936-1940; 1 Brief von Louis Finkelstein an Robert MacIver, 29.05.1940; 2 Briefe zwischen Louis Finkelstein und Max Horkheimer, 06.06.1940, 04.06.1940; 15 Briefe zwischen Hugo Fischer und Max Horkheimer, 1937-1938; 1 Brief von Hugo Fischer an P. Tillich; 1 Brief von Hugo Fischer an Karl A. Wittfogel, 17.06.1940; 2 Briefe von Max Horkheimer an Ernest Manheim, April 1942; 1 Brief von Alexander Farquharson an Max Horkheimer, 20.01.1940; 3 Briefe zwischen dem Institute of International Education, New York Edgar J. Fisher und Max Horkheimer, Oktober 1938, 18.10.1938; 10 Briefe zwischen Paul Fischer und Max Horkheimer, 1938-1940; 2 Briefe zwischen der Hessian Hills School New York und Max Horkheimer, 21.02.1938, 28.02.1938; 2 Briefe zwischen Dorothy Canfield Fisher und Max Horkheimer, 24.01.1939, 19.01.1939; 1 Brief von Ossip K. Flechtheim an Max Horkheimer, 04.01.1941; 2 Briefe zwischen der University of Minnesota, Minneapolis und Max Horkheimer, 02.08.1945, 15.09.1945; 3 Briefe zwischen Leo Löwenthal und Max Horkheimer, 1943-1945, 17.08.1945; 2 Briefe zwischen der University of Denver, Colorado und Max Horkheimer, 11.05.1943, 28.05.1943; 1 Brief von dem Institute Universitaire De Hautes Etudes Internationales Genf an Max Horkheimer, 25.01.1939; 1 Brief von Hans Kelsen an Max Horkheimer, 30.01.1939; Lebenslauf und 2 Empfehlungsschreiben von Max Fleischmann für Prof. Edwin Borchard; 1 Brief von der Columbia University in the City of New York an Franz Neumann, 17.04.1940; 3 Briefe zwischen Philipp Flesch und Max Horkheimer, 26.03.1940, 1939-1940; 17 Briefe zwischen Babette Fletcher, Theo Fletcher und Max Horkheimer, 1941-1950; 1 Brief von Max Horkheimer an Abraham Flexner, 07.06.1939; 1 Brief von Robert Fließ an Max Horkheimer, 24.10.1938; 1 Brief von der Foreign Policy Association New York an Max Horkheimer, 03.11.1934; 1 Brief von Max Horkheimer an Rudolf Forster, 10.01.1940; 2 Briefe von der Fortune Time & Life Building New York und Max Horkheimer, 1938-1940; 4 Briefe zwischen Siegmund H. Foulkes (Fuchs) und Max Horkheimer, 1936-1937, 31.12.1936; 5 Briefe zwischen Elsie M. Foulstone und Max Horkheimer, 1941; 1 Brief von Mary Fox an Max Horkheimer, 09.12.1938; 5 Briefe zwischen Ernst Fraenkel und Max Horkheimer, 1936-1938; 1 Heiratsanzeige Liesl Frank; 7 Briefe zwischen Philipp Frank und Max Horkheimer, 1937-1939; 6 Briefe zwischen Lothar G. Frank und Max Horkheimer, 1941; 7 Briefe zwischen Felix Frankfurter und Max Horkheimer, 1937-1941; 2 Briefe zwischen Joseph Freeman und Max Horkheimer, 22.11.1944; 1 Brief von der Free Synagogue New York an Max Horkheimer, 14.11.1938; 2 Briefe zwsichen Benjamin Freilichmann und Max Horkheimer, 07.01.1939, 23.01.1939; 2 Briefe zwischen dem Frenkel Travel Service New York und Max Horkheimer, 21.02.1936, 23.02.1936; 2 Briefe zwischen Hugo Freund und Max Horkheimer, 14.11.1938, 18.11.1938; 2 Briefe zwischen Julius A. Jr. Freynick und Max Horkheimer, 11.09.1939, 18.09.1939;

A RELIGIÃO NO CONFLITO ENTRE ISRAEL E PALESTINA NO CONTEXTO DA CRIAÇÃO DO ESTADO JUDAICO: ASPECTOS HISTÓRICOS (1896-1948)

O presente trabalho analisa o papel da religião no conflito entre Israel e Palestina, principalmente no contexto da implantação do Estado de Israel, em 1948. A análise toma como delimitação histórica do conflito o período de 1896 a 1948, quando ocorre a migração das primeiras levas de judeus para os territórios palestinos. A pergunta inicial é sobre como judeus e muçulmanos se relacionavam nos primeiros anos de imigração até a criação do Estado de Israel. O problema principal a ser esclarecido é como a construção cultural ocidental em relação aos palestinos interferiu no conflito, principalmente no que tange à tomada da terra e à construção de um novo país dentro de um já existente, socialmente, religiosamente e culturalmente. Finalmente a pesquisa pergunta pela repercussão do conflito entre israelenses e palestinos no campo religioso protestante, principalmente entre grupos conservadores e fundamentalistas deste ramo do cristianismo. A pesquisa é totalmente bibliográfica e toma como referência as teorias pós-coloniais para debater a história do território, no que se refere aos aspectos religiosos do conflito.

A “REVOLTA” DE JEÚ E A ESTELA DE DÃ: Um Estudo Em 2 Reis 10,28-36

A pesquisa tem por objetivo trabalhar o evento da Revolta de Jeú, em conjunto com a Estela de Dã, tendo como ponto de partida para tal, a exegese da perícope de 2 Reis 10-28,36. A história Deuteronomista apresenta o ato da Revolta de Jeú como sendo um feito demasiadamente importante, na restauração do culto a Javé em Israel, a partir de um contexto onde o culto a outras divindades, em Israel Norte, estava em pleno curso. No entanto, a partir da análise conjunta da Estela de Dã, que tem como provável autor o rei Hazael de Damasco, somos desafiados a ler esta história pelas entrelinhas não contempladas pelo texto, que apontam para uma participação ativa de Hazael, nos desfechos referentes a Revolta de Jeú, como sendo o responsável direto que proporcionou a subida de Jeú ao trono em Israel, clarificando desta forma este importante período na história Bíblica. Para tal análise, observar-se-á três distintos tópicos, ligados diretamente ao tema proposto: (1) A Revolta de Jeú e a Redação Deuteronomista, a partir do estudo exegético da perícope de 2 Reis 10,28-36, onde estão descritas informações pontuais sobre período em que Jeú reinou em Israel; (2) Jeú e a Estela de Dã, a partir da apresentação e análise do conteúdo da Estela de Dã, tratando diretamente dos desdobramentos da guerra em Ramote de Gileade, de onde se dá o ponto de partida à Revolta de Jeú; e por fim (3) O Império da Síria, onde a partir da continuidade da análise do conteúdo da Estela de Dã, demonstraremos a significância deste reino, além de apontamentos diretamente ligados ao reinado de Hazael, personagem mui relevante no evento da Revolta de Jeú.

Translocation of inserted foreign epitopes by a channelforming protein

Certain bacterial protein toxins are able to insert themselves into, and at least partially across, lipid bilayer membranes in the absence of any auxiliary proteins, by using unknown mechanisms to overcome the high energy barrier presented by the hydrophobic bilayer core. We have previously shown that one such toxin, colicin Ia, translocates a large, hydrophilic part of itself completely across a lipid bilayer in conjunction with the formation of an ion-conducting channel. To address the question of whether the colicin can translocate any arbitrary amino acid sequence, we have altered the translocated segment by inserting, singly, two different foreign epitopes. Colicins containing either epitope retain significant bactericidal activity and form channels of normal conductance in planar bilayers. Furthermore, antibodies added on the side of the bilayer opposite that to which the colicin was added interact specifically with the corresponding epitopes, producing an inhibition of channel closing. Thus, the inserted epitopes are translocated along with the rest of the segment, suggesting that a surprisingly small part of colicin Ia, located elsewhere in the molecule, acts as a nonspecific protein translocator.

Loss of the gene encoding mannose 6-phosphate/insulin-like growth factor II receptor is an early event in liver carcinogenesis

This report shows that loss of heterozygosity at the mannose 6-phosphate/insulin-like growth factor II receptor (M6P/IGF2R) locus occurred in 5/8 (63%) dysplastic liver lesions and 11/18 (61%) hepatocellular carcinomas (HCCs) associated with the high risk factors of hepatitis virus infection and liver cirrhosis. Mutations in the remaining allele were detected in 6/11 (55%) HCCs, including deletions in a polydeoxyguanosine region known to be a target of microsatellite instability. M6P/IGF2R allele loss was also found in cirrhotic tissue of clonal origin adjacent to these dysplastic lesions and HCCs, demonstrating that M6P/IGF2R inactivation occurs early in liver carcinogenesis. In conclusion, HCCs frequently develop from clonal expansions of phenotypically normal, M6P/IGF2R-mutated hepatocytes, providing further support for the idea that M6P/IGF2R functions as a liver tumor-suppressor gene.

Reconstitution of human replication factor C from its five subunits in baculovirus-infected insect cells

Human replication factor C (RFC, also called activator 1) is a five-subunit protein complex (p140, p40, p38, p37, and p36) required for proliferating cell nuclear antigen (PCNA)-dependent processive DNA synthesis catalyzed by DNA polymerase δ or ɛ. Here we report the reconstitution of the RFC complex from its five subunits simultaneously overexpressed in baculovirus-infected insect cells. The purified baculovirus-produced RFC appears to contain equimolar levels of each subunit and was shown to be functionally identical to its native counterpart in (i) supporting DNA polymerase δ-catalyzed PCNA-dependent DNA chain elongation; (ii) catalyzing DNA-dependent ATP hydrolysis that was stimulated by PCNA and human single-stranded DNA binding protein; (iii) binding preferentially to DNA primer ends; and (iv) catalytically loading PCNA onto singly nicked circular DNA and catalytically removing PCNA from these DNA molecules.

Statistical significance of protein structure prediction by threading

In this study, we estimate the statistical significance of structure prediction by threading. We introduce a single parameter ɛ that serves as a universal measure determining the probability that the best alignment is indeed a native-like analog. Parameter ɛ takes into account both length and composition of the query sequence and the number of decoys in threading simulation. It can be computed directly from the query sequence and potential of interactions, eliminating the need for sequence reshuffling and realignment. Although our theoretical analysis is general, here we compare its predictions with the results of gapless threading. Finally we estimate the number of decoys from which the native structure can be found by existing potentials of interactions. We discuss how this analysis can be extended to determine the optimal gap penalties for any sequence-structure alignment (threading) method, thus optimizing it to maximum possible performance.

Prevalence of germ-line mutations in p16, p19ARF, and CDK4 in familial melanoma: analysis of a clinic-based population.

Five to ten percent of individuals with melanoma have another affected family member, suggesting familial predisposition. Germ-line mutations in the cyclin-dependent kinase (CDK) inhibitor p16 have been reported in a subset of melanoma pedigrees, but their prevalence is unknown in more common cases of familial melanoma that do not involve large families with multiple affected members. We screened for germ-line mutations in p16 and in two other candidate melanoma genes, p19ARF and CDK4, in 33 consecutive patients treated for melanoma; these patients had at least one affected first or second degree relative (28 independent families). Five independent, definitive p16 mutations were detected (18%, 95% confidence interval: 6%, 37%), including one nonsense, one disease-associated missense, and three small deletions. No mutations were detected in CDK4. Disease-associated mutations in p19ARF, whose transcript is derived in part from an alternative codon reading frame of p16, were only detected in patients who also had mutations inactivating p16. We conclude that germ-line p16 mutations are present in a significant fraction of individuals who have melanoma and a positive family history.

In vitro reconstitution of human replication factor C from its five subunits.

Replication factor C (RFC, also called Activator I) is part of the processive eukaryotic DNA polymerase holoenzymes. The processive elongation of DNA chains requires that DNA polymerases are tethered to template DNA at primer ends. In eukaryotes the ring-shaped homotrimeric protein, proliferating cell nuclear antigen (PCNA), ensures tight template-polymerase interaction by encircling the DNA strand. Proliferating cell nuclear antigen is loaded onto DNA through the action of RFC in an ATP-dependent reaction. Human RFC is a protein complex consisting of five distinct subunits that migrate through SDS/polyacrylamide gels as protein bands of 140, 40, 38, 37, and 36 kDa. All five genes encoding the RFC subunits have been cloned and sequenced. A functionally identical RFC complex has been isolated from Saccharomyces cerevisiae and the deduced amino acid sequences among the corresponding human and yeast subunits are homologous. Here we report the expression of the five cloned human genes using an in vitro coupled transcription/translation system and show that the gene products form a complex resembling native RFC that is active in supporting an RFC-dependent replication reaction. Studies on the interactions between the five subunits suggest a cooperative mechanism in the assembly of the RFC complex. A three-subunit core complex, consisting of p36, p37, and p40, was identified and evidence is presented that p38 is essential for the interaction between this core complex and the large p140 subunit.

Systems feasibility study: states' assistance in defect recall campaigns. Final report, Volume I.

National Highway Traffic Safety Administration, Washington, D.C.

Systems feasibility study: states' assistance in defect recall campaigns. Final report, Volume II.

National Highway Traffic Safety Administration, Washington, D.C.