Über die Köpfe hinweg? Überlegungen, Einwände und Thesen aus der Perspektive Studierender

[Abstract fehlt

Frankfurt am Main/Mainz, Deutschland. Spuren archäologischer Wissensgenerierung. Propylaeum-VITAE, ein von der DFG gefördertes Verbundprojekt zur archäologischen Wissenschaftsgeschichte

In 2017 the biographical information system Propylaeum-VITAE launched, which is hosted by the Specialist Information Service of Classics »Propylaeum« at the university library Heidelberg. The online database is a tool not only for researching biographical information of former scholars of classical studies, pre- and protohistory but also to analyse their personal networks, the generation of knowledge as well as the genesis and development of concepts and methods in classical studies. Based on this, in August 2020 the German Research Foundation approved a project, applied by the RGK, RGZM and Heidelberg University Library, called »Spuren Archäologischer Wissensgenerierung (Traces of archaeological knowledge)«. The project aims to expand Propylaeum-VITAE systematicaly and to index archival and bibliographical sources stored in the Archives and Libraries of the RGZM, RGK and further cooperation partners via the biographical information system

Functional and Structural Profiling of the Human Thrombopoietin Gene Promoter*S⃞

Human thrombopoietin (TPO) is involved in cardiovascular disease as it regulates megakaryocyte development and enhances platelet adhesion/aggregation. The THPO promoter structure is still controversial. By reverse transcription-PCR, we confirm that THPO transcription is cell line-dependently initiated at two alternative promoters, which we newly designated P1a and P1. We subsequently electrophoretically scanned and resequenced these portions in 95 and 57 patients with cardiovascular disease, respectively, and identified seven variants (–1450/del58bp, C-920T [rs2855306], A-622G, C-413T [rs885838], C+5A, G+115A, and C+135T). After subcloning of 1032 bp of THPO P1 in pGL3-basic vector, five molecular haplotypes (MolHaps1–5) were observed: [A–622-C–413-C+5-G+115; wild type (wt)], [A–622-T–413-C+5-G+115], [G–622-T–413-C+5-G+115], [A–622-C–413-A+5-G+115], [A–622-C–413-C+5-A+115], and analyzed in reporter gene assays in HEK293T and HepG2 cells. MolHaps 2, 4, and 5 were significantly more active than wt (all p values ≤0.01) in HEK293T cells, MolHap3 exerted a substantial loss of promoter activity (p < 0.0001 in HEK293T and p < 0.01 in HepG2, compared with wt). Electrophoretic mobility shift assays revealed that A-622G and C-413T individually differed from MolHaps in their DNA-protein interaction patterns. Supershift and chromatin immunoprecipitation assays identified CCAAT/enhancer-binding protein δ as the binding protein exclusively for the –622A allelic portion