Dr. Adolf Jellinek : Gedenkblatt zur Feier seines vor 25 Jahren am 6. Oct. 1857 ... erfolgten Amtsantrittes als Prediger der israelitischen Gemeinde in Wien

von Joel Müller. Hrsg. von Ch. D. Lippe

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.

Sēfer ʿAṣîrat ham-maggēfā : doś zainin (segules u-refues) den (oilem) for tzu šṭelin wi man zol (nizehar) zain (be-es ha-ḥadaš)... ḥatîmat gedôlê rôfe'îm miq-q"q Berlin

Digitalisat der Ausg. Frankfurṭ-de-Odr, 1770/71

Leila Ada : Leben und Ende einer israelitischen Jungfrau

[Osborn W. Trenery Heighway]

Bekanntmachung : Aufruf zur Ablieferung von Brotscheinen für Mazzen ... vom 16. März 1916

der Vorstand der Israelitischen Gemeinde [Frankfurt a. M.]

B cells in ADA deficiency

Deficiency of the enzyme adenosine deaminase (ADA) results in severe lymphopenia in humans. Mice with an inactivating mutation in the ADA gene also exhibit profound lymphopenia, as well as pulmonary insufficiency and ribcage abnormalities. In fact, the mouse model has a phenotype that is remarkably similar to that of the human disease, making the mice valuable tools for unraveling the mechanism of lymphocyte destruction in absence of this housekeeping gene. T cell deficiency in ADA deficiency has been extensively studied by others, revealing a block in early thymocyte development. In contrast, our studies revealed that early B cell development in the bone marrow is normal. ADA-deficient mice, however, exhibit profound defects in germinal center formation, preventing antigen-dependent B cell maturation in the spleen. ADA-deficient spleen B cells display significant defects in proliferation and activation signaling, and produce more IgM than their normal counterparts, suggesting that extrafollicular plasmablasts are overrepresented. B cells from ADA-deficient mouse spleens undergo apoptosis more readily than those from normal mouse spleens. Levels of ADA's substrates, adenosine and 2′-deoxyadenosine, are elevated in both bone marrow and spleen in ADA-deficient mice. S ′-adenosyihomoeysteine hydrolase (SAH hydrolase) activity is significantly inhibited in both locales, as well. dATP levels, though, are only elevated in spleen, where B cell development is impaired, and not in bone marrow, where B cell ontogeny is normal. This finding points to dATP as the causative agent of lymphocyte death in ADA deficiency. ADA deficiency results in inhibition of the enzyme ribonucleotide reductase, thereby depleting nucleoside pools needed for DNA repair. Another mouse model that lacks a functional gene encoding a protein involved in DNA repair and/or cell cycle checkpoint regulation, p53-binding protein 1, exhibits blocks in T and B cell development that are similar to those seen in ADA-deficient mice. Unraveling the mechanisms of lymphocyte destruction in ADA deficiency may further understanding of lymphocyte biology, facilitate better chemotherapeutic treatment for lymphoproliferative diseases, and improve gene and enzyme therapy regimens attempted for ADA deficiency. ^