Johann Meilof : zur Geschichte des römischen Rechts in Livland im 15. Jahrhunderte

http://www.ester.ee/record=b4114660~S1*es

Livländische Forschungen

http://www.ester.ee/record=b4008463*es

Geschichte Kaiser Friedrichs des Zweiten und seiner Reiche. Bd. 2, 1235-1250. Abth. 1, Vom Mainzer Reichstage bis zur zweiten Excommunication des Kaisers

http://tartu.ester.ee/record=b1573613~S1*es

Reisefrüchte aus Italien und anderes zur deutsch-italischen Geschichte

von Ed. WinkelmannAus: [Forschungen zur deutschen Geschichte ; 18.1878]In Fraktur(VLID)9511

Philipp von Schwaben und Otto IV. von Braunschweig

von Eduard WinkelmannMikrofiche-Ausg. im Verl. Universitäts- und Stadtbibliothek, Köln, erschienenIn FrakturErschienen: Bd. 1 -

Mutant Adenosine Deaminase 2 in a Polyarteritis Nodosa Vasculopathy

BackgroundPolyarteritis nodosa is a systemic necrotizing vasculitis with a pathogenesis that is poorly understood. We identified six families with multiple cases of systemic and cutaneous polyarteritis nodosa, consistent with autosomal recessive inheritance. In most cases, onset of the disease occurred during childhood

Rudolf Ladenburg and the first quantum interpretation of optical dispersion

In 1921, the experimental physicist Rudolf Ladenburg put forward the first quantum interpretation of optical dispersion. Theoretical physicists had tried to explain dispersion from the point of view of quantum theory ever since 1913, when Niels Bohr proposed his quantum model of atom. Yet, their theories proved unsuccessful. It was Ladenburg who gave a breakthrough step toward our quantum understanding of dispersion. In order to understand Ladenburg’s step, I analyze Ladenburg’s experimental work on dispersion prior to 1913, the reasons why the first theories of dispersion after 1913 were not satisfactory, and Ladenburg’s 1921 proposal. I argue that Ladenburg’s early experimental work on dispersion is indispensable to understand his 1921 paper. The specific kind of experiments he performed before 1913, the related interpretative problems, and the way he tried to solve them, led him reapproach the dispersion problem in 1921 in a way that was completely different from the way theoretical physicists had done it before

A Mutation in VPS35, Encoding a Subunit of the Retromer Complex, Causes Late-Onset Parkinson Disease

To identify rare causal variants in late-onset Parkinson disease (PD), we investigated an Austrian family with 16 affected individuals by exome sequencing. We found a missense mutation, c.1858G>A (p.Asp620Asn), in the VPS35 gene in all seven affected family members who are alive. By screening additional PD cases, we saw the same variant cosegregating with the disease in an autosomal-dominant mode with high but incomplete penetrance in two further families with five and ten affected members, respectively. The mean age of onset in the affected individuals was 53 years. Genotyping showed that the shared haplotype extends across 65 kilobases around VPS35. Screening the entire VPS35 coding sequence in an additional 860 cases and 1014 controls revealed six further nonsynonymous missense variants. Three were only present in cases, two were only present in controls, and one was present in cases and controls. The familial mutation p.Asp620Asn and a further variant, c.1570C>T (p.Arg524Trp), detected in a sporadic PD case were predicted to be damaging by sequence-based and molecular-dynamics analyses. VPS35 is a component of the retromer complex and mediates retrograde transport between endosomes and the trans-Golgi network, and it has recently been found to be involved in Alzheimer disease