Grammatica Hebraica : punctis massoreticis libera

Francisci Mascleffi ; ed. Luca Franc. Lalande

Der Einsiedler auf der Johannis-Klippe : Küsten-Roman ; aus dem Schwedischen

von Emilie (Flygare-) Carlén

Die Einkommensteuer-Frage

Boberach: Der Berichterstatter begründet für die Erste Kammer die Ablehnung des Regierungsentwurfs zur Mahl-, Schlacht- und Klassensteuer und die Beibehaltung dieser Steuern

First isolation of a rhabdovirus from perch Perca fluviatilis in Switzerland

Perca fluviatilis is a fish species of increasing interest to the Swiss fish farming industry. In recent years, recirculation systems have been specifically set up to increase production. In one of these farms, abnormal spiral swimming associated with elevated mortalities occurred in repeated batches of imported perch shortly after stocking on several occasions. No bacterial or parasitic etiology was detected, but a virus grown in bluegill fry (BF-2) cells was identified as perch rhabdovirus. Subsequent investigations of other samples suggested a viral tropism for the central nervous system (CNS). Phylogenetic analysis of the partial N and entire G gene sequences positioned this isolate in genogroup C of the species Perch rhabdovirus, with high nucleotide and amino acid (aa) sequence identities with the DK5533 strain isolated in Denmark in 1989. Comparative studies using other closely related isolates allowed the distinction of 2 serological Patterns among perch rhabdoviruses and the identification of a proline substitution by a serine in Position 147 of the glycoprotein potentially involved in antigenic differentiation. Even if perch imported onto the farm tested negative by virus isolation prior to transport, they may have been the origin of this outbreak since CNS tissue was not included in the samples that were analyzed. Another possibility might be a sub-clinical infection with a viral load in resident fish too low to be detected. This study reports the first isolation of a perch rhabdovirus in Switzerland, and emphasizes the necessity of optimizing diagnostic tools that facilitate better control of the risks associated with fish translocation.

Meta-analysis identifies seven susceptibility loci involved in the atopic march.

Eczema often precedes the development of asthma in a disease course called the 'atopic march'. To unravel the genes underlying this characteristic pattern of allergic disease, we conduct a multi-stage genome-wide association study on infantile eczema followed by childhood asthma in 12 populations including 2,428 cases and 17,034 controls. Here we report two novel loci specific for the combined eczema plus asthma phenotype, which are associated with allergic disease for the first time; rs9357733 located in EFHC1 on chromosome 6p12.3 (OR 1.27; P=2.1 × 10(-8)) and rs993226 between TMTC2 and SLC6A15 on chromosome 12q21.3 (OR 1.58; P=5.3 × 10(-9)). Additional susceptibility loci identified at genome-wide significance are FLG (1q21.3), IL4/KIF3A (5q31.1), AP5B1/OVOL1 (11q13.1), C11orf30/LRRC32 (11q13.5) and IKZF3 (17q21). We show that predominantly eczema loci increase the risk for the atopic march. Our findings suggest that eczema may play an important role in the development of asthma after eczema.

Mutation Update of the CLCN5 Gene Responsible for Dent Disease 1

Dent disease is a rare X-linked tubulopathy characterized by low molecular weight proteinuria, hypercalciuria, nephrocalcinosis and/or nephrolithiasis, progressive renal failure, and variable manifestations of other proximal tubule dysfunctions. It often progresses over a few decades to chronic renal insufficiency, and therefore molecular characterization is important to allow appropriate genetic counseling. Two genetic subtypes have been described to date: Dent disease 1 is caused by mutations of the CLCN5 gene, coding for the chloride/proton exchanger ClC-5; and Dent disease 2 by mutations of the OCRL gene, coding for the inositol polyphosphate 5-phosphatase OCRL-1. Herein, we review previously reported mutations (n = 192) and their associated phenotype in 377 male patients with Dent disease 1 and describe phenotype and novel (n = 42) and recurrent mutations (n = 24) in a large cohort of 117 Dent disease 1 patients belonging to 90 families. The novel missense and in-frame mutations described were mapped onto a three-dimensional homology model of the ClC-5 protein. This analysis suggests that these mutations affect the dimerization process, helix stability, or transport. The phenotype of our cohort patients supports and extends the phenotype that has been reported in smaller studies.

Itinera mundi

Vorlage d. Digitalisats aus d. Besitz d. Theol. Hochschule St. Georgen

Na 1 Nachlass Max Horkheimer, 514 - Korrespondenzen mit Theodor W. Adorno (p. VI 4, 1 - 214)

150 Briefe zwischen Theodor W. Adorno, Gretel Adorno und Max Horkheimer; 1 Brief von Edith B. Berlebach an Theodor W. Adorno, 19.11.1961; 1 Brief von Theodor W. Adorno an Edith B. Berlebach, 16.11.1961; 2 Briefe zwischen dem Institut für staatsbürgerliche Bildung in Rheinland-Pflalz (Mainz) und Theodor W. Adorno, 11.09.1961; 1 Brief der American Council of Learned Societies (New York) an Max Horkheimer, 29.08.1961; 1 Brief von dem Kuratorium Unteilbares Deutschland (Bonn) an Theodor W. Adorno, 06.06.1961; 1 Brief des Hessichen Ministers für Erziehung und Volksbildung an Theodor W. Adorno, 05.06.1961; 1 Brief von Theodor W. Adorno an Walter Schlesinger, 06.12.1962; 1 Brief von Walter Schlesinger an Max Horkheimer, 02.08.1963; 1 Brief von Theodor W. Adorno an W. R. Beyer, 05.05.1962; 1 Brief von Theodor W. Adorno an Pierre de Bie, 16.03.1962; 1 Brief von Edgar Morin an Theodor W. Adorno, 07.02.1962;