Spécimens de caractères hébreux gravés à Venise et à Paris par Guillaume le Bé : (1546 - 1574)

publ. par H. Omont

From the Sea to Paris and back: On the interdependence of economic warfare, weather conditions and the submarine campaign 1916-1917

Starting of from Avner Offer’s comment that the First World War was not only a war of steel and gold, but also of bread and potatoes (1989: 1) and my own research on British as well as Australian preparations for economic warfare and based on sources from the entente as well as the central powers but also from the United States, Canada and Australia, may presentation will focus on the interdependence of the measures taken by entente as well as central power authorities in the second half of 1916. Already a year before both sides had become aware that this war would not only be decided on the battlefield, but that the issues of primary as well as secondary resources would be decisive. Accordingly measures that could strike the enemy in this field were discussed and put into place more and more and this at time, when weather conditions caused a reduction of harvest all over Europe, Northern America and Argentina.

Di šul-frage : redes fun di j[udiše] s[otzialisṭiše] a[rbeiṭer] p[arṭei] (P"Tz) raṭmener in lodzer šṭodṭ-raṭ, gehalṭen be-es di biudzšeṭ-debaṭen in nowember 1917

Digitalisat der Ausg. Warše [u.a.], 1920

[Der judišer ḥurban fun Poilen Galitzie un Bukowina fun ṭag-buch 674 - 677 (1914 - 1917)] : [1., 2. ṭeil]

Digitalisat der Ausg. Wilno {[u.a.], 1923

[Der judišer ḥurban fun Poilen Galitzie un Bukowina fun ṭag-buch 674 - 677 (1914 - 1917)] : [4. ṭeil]

Digitalisat der Ausg. Wilno {[u.a.], 1922

[Der judišer ḥurban fun Poilen Galitzie un Bukowina fun ṭag-buch 674 - 677 (1914 - 1917)] : [3. ṭeil]

Digitalisat der Ausg. Wilno {[u.a.], 1924

Di yidishe prese in Ṿaysrusland : (1917-1927)

tsuzamengeshṭelṭ A. Ḳirzshnits

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.