Large Housing Estates of Berlin, Germany

Large estates of towers and slabs can be found all over the German capital, and the differences between those which before 1990 were situated on different sides of the Berlin Wall are often hard to tell for the layperson. They stand witness to the dream of modern living and acceptable housing conditions for the whole population, which in the decades after the Second World War inspired the socialist regime in the East in the same way as the welfare state in the West. In terms of political background and social significance, however, the Plattenbauten (slab buildings) in the East were rather distinct from the Wohnblöcke (dwelling blocks) in the West. Not only were those in the East far more frequent – in 1990 about one third of East Berliners call a large housing estate their home, compared to about only five percent of West Berliners – they also constituted an environment that was closely aligned to the East German regime’s socio-political goals. This chapter will summarize the history of large housing estates in both East and West Berlin, pointing out commonalities and differences that determine significance and perception of these buildings to date

Sporadic congenital nonautoimmune hyperthyroidism caused by P639S mutation in thyrotropin receptor gene

Germline mutations of thyrotropin receptor (TSHR) gene determining a constitutive activation of the receptor were identified as a molecular cause of familial or sporadic congenital nonautoimmune hyperthyroidism (OMIM: 609152) (Nat Genet 7:396-401, 1994; N Engl J Med 332:150-154, 1995; Acta Endocrinol (Copenh) 100:512-518, 1982). We report the case of an Italian child subjected to the first clinical investigation at 24 months for an increased growth velocity; biochemical investigation showed high FT4 and FT3 serum values and undetectable thyrotropin in the absence of anti-thyroid antibodies; the thyroid gland was normal at ultrasound examination. Treatment with methimazole was started at the age of 30 months when her growth velocity was high and the bone age was advanced. DNA was extracted from her parents', brother's, and the patient's blood. Exons 9 and 10 of the TSHR gene were amplified by polymerase chain reaction and subjected to direct sequencing. In proband, a heterozygous substitution of cytosine to thymine determining a proline to serine change at position 639 (P639S) of the TSHR was detected while the parents and brothers of the propositus, all euthyroid, showed only the wild-type sequence of the TSHR gene. This mutation was previously described as somatic in patients affected by hyperfunctioning thyroid nodules and as germline in a single Chinese family affected by thyrotoxicosis and mitral valve prolapse. This constitutively activating mutation is able to activate both the cyclic AMP and the inositol phosphate metabolic pathways when expressed in a heterologous system. In conclusion, we describe the first case of sporadic congenital nonautoimmune hyperthyroidism caused by de novo germinal P639S mutation of TSHR