Tolerance i merkantilismens tidsalder - de religiøse fristeder i hertugdømmerne Slesvig og Holsten

Tolerance in the Age of MercantilismIn 1684, Jews were allowed to settle in the core regions of Denmark. But already in the beginning of the 17th century, cities in the Duchies of Schleswig and Holstein, where the Danish king, through complex dynastic and historical circumstances, held the title of duke, were opened up for Jewish settlers – they were even invited to move there.The settlement of Altona is well known and well researched, but the smaller settlements are equally interesting. Glückstadt on the Elbe was founded in 1616, and by 1620, Sephardi Jewish merchants, mainly from Hamburg and Amsterdam, were invited to settle and were given the same rights as their Christian counterparts. Despite some ups and down due to the Thirty Years War, Glückstadt flourished throughout the 1600s, but by the end of the century, the financial situation changed due to new patterns of commerce, and by 1733, the Sephardi community no longer existed. A small Ashkenazi settlement was also allowed, but with fewer privileges, and due to emancipation, it was gradually dissolved and had ceased to exist by the end of the 19th century.In Friedrichstadt, founded in 1621, the preferred minority was originally the Protestant Remonstrants. Catholics, Quakers and others followed, and in 1675, the first Ashkenazi Jews are recorded to have settled in the town, and there is evidence that the different minorities (Christian and Jewish) cooperated in several areas. A new synagogue was built in 1847, but when emancipation reached the Duchies in the mid-1850s, the community dissolved due to emigration and emancipation. Rendsburg, part of the royal Danish realm already in the late 16th century and of strategic importance, was through the 17th century heavily fortified through the construction of the new fortress-cum-district Neuwerk. The new fortress was open to non-Protestant, but not Catholic, residents, who were given equal rights as their Lutheran counterparts – as long as their affluence was sufficient to ensure the ownership of a house and their religious practices were held out of the public eye. By the year 1700, the Ashkenazi community had their own burial ground in a nearby village, but services had to be held in private homes until the beginning of the 19th century. However, with the gradual emancipation in the 19th century (Denmark proper, 1814; the Duchies, 1854), and the Prussian victory in 1864, which made both Schleswig and Holstein part of the Germany-to be, Rendsburg-Neuwerk followed the destiny of the other communities

Reduced Expression of Fibroblast Growth Factor Receptor 2IIIb in Hepatocellular Carcinoma Induces a More Aggressive Growth

Fibroblast growth factor receptor 2 isoform b (FGFR2-IIIb) is highly expressed in hepatocytes and plays an important role in liver homeostasis and regeneration. Here, we analyzed the expression and function of FGFR2-IIIb in hepatocellular carcinoma (HCC). FGFR2-IIIb expression in HCC tissues and cell lines was lower than in primary human hepatocytes and nontumorous tissue. FGFR2-IIIb-negative HCCs showed a significantly higher Ki-67 labeling index, and loss of FGFR2-IIIb expression correlated significantly with vascular invasion and more advanced tumor stages. A decrease in FGFR-2IIIb expression in HCC cell lines was not related to promoter hypermethylation. However, PCR analysis indicated that chromosomal deletion at 10q accounted for the loss of FGFR2 expression in a subset of HCC cells. FGFR2-IIIb re-expression in stable transfected HCC cell lines induced a higher basal apoptosis rate and a significantly reduced proliferation and migratory potential in vitro. In nude mice, FGFR2-IIIb re-expressing HCC cells grew significantly slower, and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay revealed higher apoptosis rates. The antitumorigenic effects of FGFR2-IIIb expression in HCC cells were not affected by keratinocyte growth factor or an inhibitor of FGFR-phosphorylation, indicating that they are independent of tyrosine kinase activation. In conclusion, our data indicate that FGFR2-IIIb inhibits tumorigenicity of HCC cells. Identification of the molecular mechanisms promoting regeneration in normal tissue while suppressing malignancy may lead to novel therapeutic targets of this highly aggressive tumor

A high-resolution anatomical atlas of the transcriptome in the mouse embryo.

Ascertaining when and where genes are expressed is of crucial importance to understanding or predicting the physiological role of genes and proteins and how they interact to form the complex networks that underlie organ development and function. It is, therefore, crucial to determine on a genome-wide level, the spatio-temporal gene expression profiles at cellular resolution. This information is provided by colorimetric RNA in situ hybridization that can elucidate expression of genes in their native context and does so at cellular resolution. We generated what is to our knowledge the first genome-wide transcriptome atlas by RNA in situ hybridization of an entire mammalian organism, the developing mouse at embryonic day 14.5. This digital transcriptome atlas, the Eurexpress atlas (http://www.eurexpress.org), consists of a searchable database of annotated images that can be interactively viewed. We generated anatomy-based expression profiles for over 18,000 coding genes and over 400 microRNAs. We identified 1,002 tissue-specific genes that are a source of novel tissue-specific markers for 37 different anatomical structures. The quality and the resolution of the data revealed novel molecular domains for several developing structures, such as the telencephalon, a novel organization for the hypothalamus, and insight on the Wnt network involved in renal epithelial differentiation during kidney development. The digital transcriptome atlas is a powerful resource to determine co-expression of genes, to identify cell populations and lineages, and to identify functional associations between genes relevant to development and disease