Il matrimonio di C. A. Vecchj

[von] Ermanno Loevinson

A Jewish Calendar for sixtyfour years, detailing the new moons, festivals, and fasts : ... to which are added tabl. for continuing the calendar to A. M. 6000-2240 C. Ae. and a chronological table ...

by E. H. Lindo

Na 1 Nachlass Max Horkheimer, 4 - Korrespondenzen u.a. mit Richard Bach (p. I 2, 131-358)

24 Briefe zwischen Richard Bach und Max Horkheimer, 1938-1940; 2 Briefe zwischen Alfred Chalk und Max Horkheimer, 17.10.1939, 14.11.1939; 3 Briefe von Morduch Lexandrowitsch und der American Consulate General, 1939; 4 Briefe von der American Consulate General und Max Horkheimer, 1938-1939; 1 Brief von Max Horkheimer an das Amtstgericht Berlin, 15.03.1939; 1 Brief von Max Horkheimer an Stiedry, 05.12.1938; 1 Brief von Max Horkheimer an den Collector of Custom, 26.10.1938; 2 Briefe zwischen Josef Maier und Carson Alexandrowitsch, 28.06.1938, 29.06.1938; 1 Brief von Margarete Baruch an Alice Maier, 11.04.1938; 1 Brief von Emanuel List an Carson Alexandrowitsch, 23.02.1938; 1 Abschrift des Briefes von der Metropolitan Opera Association New York an Morduch Lexandrowitsch, 22.02.1938; 1 Brief von Jacques Barzun an Max Horkheimer, 09.07.1947; 4 Briefe zwischen K. Baschwitz und Max Horkheimer, 1938-1946; 2 Briefe zwischen E. Bauer und Max Horkheimer, 08.04.1935, 27.05.1935; 4 Briefe zwischen Fritz Bauer und Max Horkheimer, 1937-1938; 2 Briefe zwischen Lina Bauer und Max Horkheimer, 20.07.1942, 16,08,1942; 4 Briefe zwsichen Rudolf Bauer und Max Horkheimer, 1937; 15 Briefe zwischen Gertrud Bauer und Max Horkheimer, 1938-1941; 1 Brief von Max Horkheimer an den Collector of Customs, 15.03.1940; 2 Briefe zwischen I. Hannah Davidson vom Jewish Community Center San Francisco und Max Horkheimer, 19.09.1938, 29.09.1938; 2 Briefe zwsichen I. Bauer und Max Horkheimer, 25.09.1938, 29.09.1938; 1 Brief von Max Horkheimer an Klopfer, 27.09.1938; 3 Briefe zwischen Y.M.H.A. - Y.W.H.A The Jewish Center of Saint Louis und Max Horkheimer, 19.09.1938, 1938; 1 Brief von Max Horkheimer an Julius Rosenberg, 17.09.1938; 1 Brief von Max Horkheimer an das Jwish Center Salt Lake City, Utah, 07.09.1938; 1 Brief von Max Horkheimer an das Jewish Community Center San Fransisco, 07.09.1938; 3 Briefe zwischen dem New York Section of the National Council of Jewish Women und Max Horkheimer, 07.04.1938, 1938; 2 Briefe zwischen Baum und Max Horkheimer, 12.03.1946, 25.05.1946; 1 Brief von Max Horkheimer an Charles A. Beard , 12.12.1934; 1 Brief von Charles A. Beard an C. A. Beard; 5 Briefe von Friedrich Pollock an Charles A. Beard, 1940-1941; 5 Briefe zwischen Lilo Beck und Max Horkheimer, 1940-1941; 7 Briefe zwischen Maximilian Beck und Max Horkheimer, 1939-1940; 1 Brief von Paul Tillich an Max Horkheimer , 01.10.1940; 1 Brief von dem Emergency Committee in Aid of Displaced Foreign Scholars New York an Max Horkheimer, 19.04.1940; 5 Briefe zwischen Konrad Bekker und Max Horkheimer, 1936-1939; 2 Briefe von Max Horkheimer an Ludwig Bendix, 1921, 1937; 1 Brief von Peter Bendmann an Max Horkheimer; 1 Brief von Max Horkheimer an Ruth Benedict, 30.07.1937; 1 Brief von Eric Russel Bentley an Max Horkheimer, 30.01.1945; 1 Brief von George Berg an Max Horkheimer, 12.07.1945; 2 Briefe zwischen Egon Bergel und Max Horkheimer, 18.08.1938, 22.08.1938; 1 Brief von Marie Jahoda an Max Horkheimer, 14.07.1928; 1 Brief von Theodor W. Adorno an Kurt Bergel, 09.09.1939; 15 Briefe zwischen Klaus Berger und Max Horkheimer, 1936-1943; 1 Brief von Frederick Pollock an Philip M. Hayden von der Columbia University New York, 05.03.1942; 1 Brief von Hans Venedey an Max Horkheimer, 05.03.1938; 1 Brief von Max Horkheimer an Ida Berger-Chevant, 18.02.1939;

Na 1 Nachlass Max Horkheimer, 581 - Korrespondenzen mit Friedrich (Frederick) Pollock und Henryk Grossmann (p. VI 34, 199-464)

1 Brief von Edith Kriss an Margot von Mendelssohn, 13.10.1943; 1 Brief von Margot von Mendelssohn an Max Horkheimer, 23.01.1944; 1 Brief von Max Horkheimer an Henryk Grossman, 10.04.1944; 1 Brief von Nevitt Sanford an Max Horkheimer, 21.01.1944; 2 Briefe zwischen Richard C. Rothschild und Frederick Pollock, 1944; 1 Brief von Frederick Pollock an das Registrar for Voting in New York Country, [1944]; 1 Brief von Theodor W. Adorno an Frederick Pollock, 07.06.1944;

Hydrographic measurements from C.S.S. Hudson Cruise 82-002, Canadian Technical Report of Hydrography and Ocean Sciences No. 118, 112 pp (digital version)

This archive consists of the hydrographic data collected on Cruise 82-002 of C.S.S. Hudson, April 11 to May 2, 1982. 78 stations were occupied on a line running near 48°N from the mouth of the English Channel to the Grand Banks of Newfoundland. Pressure, temperature and salinity were measured by a Guildline digital CTP system. Salinity, dissolved oxygen, silicate, nitrate and phosphate were measured from water samples collected on the CTP upcasts. CTP and discrete bottle data and associated derived parameters are tabulated at standard levels. This is the digital version of the printed report (of 1989, see further details), published in 2006 with the information system Pangaea.

La construcción de comunidades políticas en el Río de La Plata : Tucumán, Catamarca y Santiago del Estero entre 1810-1838

Fil: Iramain, Pablo Sebastián. Universidad Nacional de La Plata. Facultad de Humanidades y Ciencias de la Educación; Argentina.

La construcción de comunidades políticas en el Río de La Plata : Tucumán, Catamarca y Santiago del Estero entre 1810-1838

Fil: Iramain, Pablo Sebastián. Universidad Nacional de La Plata. Facultad de Humanidades y Ciencias de la Educación; Argentina.

La construcción de comunidades políticas en el Río de La Plata : Tucumán, Catamarca y Santiago del Estero entre 1810-1838

Fil: Iramain, Pablo Sebastián. Universidad Nacional de La Plata. Facultad de Humanidades y Ciencias de la Educación; Argentina.

Targeted overexpression of protein kinase C β2 isoform in myocardium causes cardiomyopathy

Increased cardiovascular mortality occurs in diabetic patients with or without coronary artery disease and is attributed to the presence of diabetic cardiomyopathy. One potential mechanism is hyperglycemia that has been reported to activate protein kinase C (PKC), preferentially the β isoform, which has been associated with the development of micro- and macrovascular pathologies in diabetes mellitus. To establish that the activation of the PKCβ isoform can cause cardiac dysfunctions, we have established lines of transgenic mice with the specific overexpression of PKCβ2 isoform in the myocardium. These mice overexpressed the PKCβ2 isoform transgene by 2- to 10-fold as measured by mRNA, and proteins exhibited left ventricular hypertrophy, cardiac myocyte necrosis, multifocal fibrosis, and decreased left ventricular performance without vascular lesions. The severity of the phenotypes exhibited gene dose-dependence. Up-regulation of mRNAs for fetal type myosin heavy chain, atrial natriuretic factor, c-fos, transforming growth factor, and collagens was also observed. Moreover, treatment with a PKCβ-specific inhibitor resulted in functional and histological improvement. These findings have firmly established that the activation of the PKCβ2 isoform can cause specific cardiac cellular and functional changes leading to cardiomyopathy of diabetic or nondiabetic etiology.

Inactivation of the α C protein antigen gene, bca, by a novel shuttle/suicide vector results in attenuation of virulence and immunity in group B Streptococcus

The α C protein of group B Streptococcus (GBS) is a major surface-associated antigen. Although its role in the biology and virulence of GBS has not been defined, it is opsonic and capable of eliciting protective immunity. The α C protein is widely distributed among clinical isolates and is a potential protein carrier and antigen in conjugate vaccines to prevent GBS infections. The structural gene for the α C protein, bca, has been cloned and sequenced. The protein encoded by bca is related to a class of surface-associated proteins of Gram-positive cocci involved in virulence and immunity. To investigate the potential roles of the α C protein, bca null mutants were generated in which the bca gene was replaced with a kanamycin resistance cassette via homologous recombination using a novel shuttle/suicide vector. Studies of lethality in neonatal mice showed that the virulence of the bca null mutants was attenuated 5- to 7-fold when compared with the isogenic wild-type strain A909. Significant differences in mortality occurred in the first 24 h, suggesting that the role of the α antigen is important in the initial stages of the infection. In contrast to A909, bca mutants were no longer killed by polymorphonuclear leukocytes in the presence of α-specific antibodies in an in vitro opsonophagocytic assay. In contrast to previous studies, α antigen expression does not appear to play a role in resistance to opsonophagocytosis in the absence of α-specific antibodies. In addition, antibodies to the α C protein did not passively protect neonatal mice from lethal challenge with bca mutants, suggesting that these epitopes are uniquely present within the α antigen as expressed from the bca gene. Therefore, the α C protein is important in the pathogenesis of GBS infection and is a target for protective immunity in the development of GBS vaccines.

Cytochrome c′ folding triggered by electron transfer: Fast and slow formation of four-helix bundles

Reduced (FeII) Rhodopseudomonas palustris cytochrome c′ (Cyt c′) is more stable toward unfolding ([GuHCl]1/2 = 2.9(1) M) than the oxidized (FeIII) protein ([GuHCl]1/2 = 1.9(1) M). The difference in folding free energies (ΔΔGf° = 70 meV) is less than half of the difference in reduction potentials of the folded protein (100 mV vs. NHE) and a free heme in aqueous solution (≈−150 mV). The spectroscopic features of unfolded FeII–Cyt c′ indicate a low-spin heme that is axially coordinated to methionine sulfur (Met-15 or Met-25). Time-resolved absorption measurements after CO photodissociation from unfolded FeII(CO)–Cyt c′ confirm that methionine can bind to the ferroheme on the microsecond time scale [kobs = 5(2) × 104 s−1]. Protein folding was initiated by photoreduction (two-photon laser excitation of NADH) of unfolded FeIII–Cyt c′ ([GuHCl] = 2.02–2.54 M). Folding kinetics monitored by heme absorption span a wide time range and are highly heterogeneous; there are fast-folding (≈103 s−1), intermediate-folding (102–101 s−1), and slow-folding (10−1 s−1) populations, with the last two likely containing methionine-ligated (Met-15 or Met-25) ferrohemes. Kinetics after photoreduction of unfolded FeIII–Cyt c′ in the presence of CO are attributable to CO binding [1.4(6) × 103 s−1] and FeII(CO)–Cyt c′ folding [2.8(9) s−1] processes; stopped-flow triggered folding of FeIII–Cyt c′ (which does not contain a protein-derived sixth ligand) is adequately described by a single kinetics phase with an estimated folding time constant of ≈4 ms [ΔGf° = −33(3) kJ mol−1] at zero denaturant.