Waves of genomic hitchhikers shed light on the evolution of gamebirds (Aves: Galliformes) : research article

Background The phylogenetic tree of Galliformes (gamebirds, including megapodes, currassows, guinea fowl, New and Old World quails, chicken, pheasants, grouse, and turkeys) has been considerably remodeled over the last decades as new data and analytical methods became available. Analyzing presence/absence patterns of retroposed elements avoids the problems of homoplastic characters inherent in other methodologies. In gamebirds, chicken repeats 1 (CR1) are the most prevalent retroposed elements, but little is known about the activity of their various subtypes over time. Ascertaining the fixation patterns of CR1 elements would help unravel the phylogeny of gamebirds and other poorly resolved avian clades. Results We analyzed 1,978 nested CR1 elements and developed a multidimensional approach taking advantage of their transposition in transposition character (TinT) to characterize the fixation patterns of all 22 known chicken CR1 subtypes. The presence/absence patterns of those elements that were active at different periods of gamebird evolution provided evidence for a clade (Cracidae + (Numididae + (Odontophoridae + Phasianidae))) not including Megapodiidae; and for Rollulus as the sister taxon of the other analyzed Phasianidae. Genomic trace sequences of the turkey genome further demonstrated that the endangered African Congo Peafowl (Afropavo congensis) is the sister taxon of the Asian Peafowl (Pavo), rejecting other predominantly morphology-based groupings, and that phasianids are monophyletic, including the sister taxa Tetraoninae and Meleagridinae. Conclusions The TinT information concerning relative fixation times of CR1 subtypes enabled us to efficiently investigate gamebird phylogeny and to reconstruct an unambiguous tree topology. This method should provide a useful tool for investigations in other taxonomic groups as well

10 Minuten Reformation

Am 31. Oktober 2017 jährte sich der sog. Thesenanschlag Martin Luthers zum 500. Mal. Luther hatte als Theologieprofessor gravierende Fehlentwicklungen seiner Kirche und Gesellschaft angeprangert und konkrete Thesen präsentiert, wie diese Missstände beseitigt werden könnten. Dabei sah Luther seine Kirche, seine Gesellschaft, sogar die ganze Welt in höchster existentieller Gefahr. Die ökumenische Hochschulgemeinde von KHG und ESG in Hildesheim nahm das geschichtsträchtige Datum zum Anlass, um mit Lehrenden unterschiedlicher wissenschaftlicher Fachbereiche an der Universität Hildesheim darüber zu diskutieren, welche gesellschaftlichen „Reformationen“ heute erforderlich sind, je aus der Perspektive des jeweiligen Fachbereiches. Die Statements sollten an unterschiedlichen Orten der Universität gehalten werden, jeweils mittwochs zur programmatischen Uhrzeit um fünf vor zwölf. Ziel des hochschulöffentlichen Diskurs-Projektes war es, essentielle Dringlichkeitsgebote („Thesen“) aus einzelnen Wissenschaftsdisziplinen zu sammeln und in den Dialog zu bringen. Heraus gekommen sind zehn 10-Minuten-Statements von charmanter Eigenwilligkeit und enormer hochschulpolitischer und gesellschaftlicher Brisanz. Es sind Zeitdiagnosen und Veränderungsappelle aus der Sozialwissenschaft, der Kulturpolitik und der Psychologie, der Theater- und der Erziehungswissenschaft, der Theologie, der Philosophie und der englischen Sprachwissenschaft, der Informationswissenschaft und aus der Welt der verfassten Studierendenschaft. Die Statements liegen in diesem Buch nun schriftlich vor und provozieren Widerspruch oder Zustimmung, auf jeden Fall aber die Lust, darüber ins Gespräch zu kommen, unter Lehrenden und Studierenden

Oral insulin immunotherapy in children at risk for type 1 diabetes in a randomised controlled trial

AIMS/HYPOTHESIS Oral administration of antigen can induce immunological tolerance. Insulin is a key autoantigen in childhood type 1 diabetes. Here, oral insulin was given as antigen-specific immunotherapy before the onset of autoimmunity in children from age 6~months to assess its safety and immune response actions on immunity and the gut microbiome. METHODS A phase I/II randomised controlled trial was performed in a single clinical study centre in Germany. Participants were 44 islet autoantibody-negative children aged 6~months to 2.99~years who had a first-degree relative with type 1 diabetes and a susceptible HLA DR4-DQ8-containing genotype. Children were randomised 1:1 to daily oral insulin (7.5~mg with dose escalation to 67.5~mg) or placebo for 12~months using a web-based computer system. The primary outcome was immune efficacy pre-specified as induction of antibody or T cell responses to insulin and measured in a central treatment-blinded laboratory. RESULTS Randomisation was performed in 44 children. One child in the placebo group was withdrawn after the first study visit and data from 22 insulin-treated and 21 placebo-treated children were analysed. Oral insulin was well tolerated with no changes in metabolic variables. Immune responses to insulin were observed in children who received both insulin (54.5%) and placebo (66.7%), and the trial did not demonstrate an effect on its primary outcome (p = 0.54). In exploratory analyses, there was preliminary evidence that the immune response and gut microbiome were modified by the INS genotype Among children with the type 1 diabetes-susceptible INS genotype (n = 22), antibody responses to insulin were more frequent in insulin-treated (72.7%) as compared with placebo-treated children (18.2%; p = 0.03). T cell responses to insulin were modified by treatment-independent inflammatory episodes. CONCLUSIONS/INTERPRETATION The study demonstrated that oral insulin immunotherapy in young genetically at-risk children was safe, but was not associated with an immune response as predefined in the trial primary outcome. Exploratory analyses suggested that antibody responses to oral insulin may occur in children with a susceptible INS genotype, and that inflammatory episodes may promote the activation of insulin-responsive T cells. TRIAL REGISTRATION Clinicaltrials.gov NCT02547519 FUNDING: The main funding source was the German Center for Diabetes Research (DZD e.V.)