Field work in the Outback:Planning and processing a geological diploma mapping in Central Australia

Der Finke Gorge National Park liegt im Zentrum des Australischen Kontinents. Aufgrund der großen Dimensionen des Landes sind weite Teile nur unzureichend und kleinmaßstäblich geologisch kartiert. Im Rahmen dieser Arbeit sollte der Versuch unternommen werden, den National Park unter Zuhilfenahme von Fernerkundungsdaten, wie Landsat TM-, ASTER-Daten, hochauflösenden stereographischen Luftbildern, digitalen Geländemodellen (DGM) und Vegetationskarten großmaßstäblich zu kartieren (1:10000). Die vorliegende Arbeit knüpft an die Untersuchungen von BUDE & PRINZ (2003) an und soll diese durch Geländebefunde ergänzen. Darüber hinaus soll der Bericht Erfahrungen hinsichtlich der Planung und Durchführung einer derartigen geologischen Geländearbeit vermitteln.The Finke Gorge National Park is situated in the centre of the Australian continent. Due to the great dimension of the outback, most of its parts are mapped geologically at a small scale. In this work we try to produce a detailed 1:10000 geological map of the National Park by applying field methods supported by remote sensing data like Landsat TM-, ASTER-Data, high resolution stereographic aerial views, digital terrain modells (DTM) and detailed geobotanic vegetation maps. This study continues the efforts of BUDE & PRINZ (2003), as it includes ground proof for representative areas. Furthermore this report gives an idea of the essential preparations in the forefield of such a geological field campaign

On-chip light detection using monolithically integrated quantum dot micropillars

This work was supported by the German Research Foundation (DFG) under Grants RE2974/9-1 and SCHN1376/1-1. The research leading to these results has received funding from the European Research Council under the European Union's Seventh Framework ERC Grant Agreement No. 615613.We demonstrate the on-chip detection of light using photosensitive detectors based on quantum dot (QD) micropillar cavities. These microscale detectors are applied exemplarily to probe the emission of a monolithically integrated, electrically pumped whispering gallery mode microlaser. Light is detected via the photocurrent induced in the electrically contacted micropillar detectors under reverse-bias. In order to demonstrate the high potential and applicability of the microdetector presented, we determine the threshold current of an integrated microlaser to be (54 ± 4) μA, in very good agreement with the value of (53 ± 4) μA inferred from optical data. Within this work we realize the monolithic integration of a laser and a detector in a single device operating in the regime of cavity-quantum electrodynamics. Our results thus advance the research on microscale sensor technology towards the few-photon quantum limit and pave the way for on-chip opto-electronic feedback experiments.PostprintPeer reviewe

Rmi1 stimulates decatenation of double Holliday junctions during dissolution by Sgs1-Top3

double Holliday junction (dHJ) is a central intermediate of homologous recombination that can be processed to yield crossover or non-crossover recombination products. To preserve genomic integrity, cells possess mechanisms to avoid crossing over. We show that Saccharomyces cerevisiae Sgs1 and Top3 proteins are sufficient to migrate and disentangle a dHJ to produce exclusively non-crossover recombination products, in a reaction termed "dissolution." We show that Rmi1 stimulates dHJ dissolution at low Sgs1-Top3 protein concentrations, although it has no effect on the initial rate of Holliday junction (HJ) migration. Rmi1 serves to stimulate DNA decatenation, removing the last linkages between the repaired and template DNA molecules. Dissolution of a dHJ is a highly efficient and concerted alternative to nucleolytic resolution that prevents crossing over of chromosomes during recombinational DNA repair in mitotic cells and thereby contributes to genomic integrity

The Biology and control of the septoria diseases of winter wheat in western Oregon

The septoria diseases of winter wheat are a limiting factor to wheat production in the Willamette Valley. This publication will describe the symptoms and development of the septoria diseases, including the influence of environmental conditions, the reactions of different cultivars to Septoria, the impact of Septoria on yield, and control methods.Published May 1996. Facts and recommendations in this publication may no longer be valid. Please look for up-to-date information in the OSU Extension Catalog: http://extension.oregonstate.edu/catalo

Oveson : a soft white winter wheat

Published September 1987. Facts and recommendations in this publication may no longer be valid. Please look for up-to-date information in the OSU Extension Catalog: http://extension.oregonstate.edu/catalo

ruvA Mutants that resolve Holliday junctions but do not reverse replication forks

RuvAB and RuvABC complexes catalyze branch migration and resolution of Holliday junctions (HJs) respectively. In addition to their action in the last steps of homologous recombination, they process HJs made by replication fork reversal, a reaction which occurs at inactivated replication forks by the annealing of blocked leading and lagging strand ends. RuvAB was recently proposed to bind replication forks and directly catalyze their conversion into HJs. We report here the isolation and characterization of two separation-of-function ruvA mutants that resolve HJs, based on their capacity to promote conjugational recombination and recombinational repair of UV and mitomycin C lesions, but have lost the capacity to reverse forks. In vivo and in vitro evidence indicate that the ruvA mutations affect DNA binding and the stimulation of RuvB helicase activity. This work shows that RuvA's actions at forks and at HJs can be genetically separated, and that RuvA mutants compromised for fork reversal remain fully capable of homologous recombination

Longitudinal Cytokine Profiling Identifies GRO-α and EGF as Potential Biomarkers of Disease Progression in Essential Thrombocythemia.

Myeloproliferative neoplasms (MPNs) are characterized by deregulation of mature blood cell production and increased risk of myelofibrosis (MF) and leukemic transformation. Numerous driver mutations have been identified but substantial disease heterogeneity remains unexplained, implying the involvement of additional as yet unidentified factors. The inflammatory microenvironment has recently attracted attention as a crucial factor in MPN biology, in particular whether inflammatory cytokines and chemokines contribute to disease establishment or progression. Here we present a large-scale study of serum cytokine profiles in more than 400 MPN patients and identify an essential thrombocythemia (ET)-specific inflammatory cytokine signature consisting of Eotaxin, GRO-α, and EGF. Levels of 2 of these markers (GRO-α and EGF) in ET patients were associated with disease transformation in initial sample collection (GRO-α) or longitudinal sampling (EGF). In ET patients with extensive genomic profiling data (n = 183) cytokine levels added significant prognostic value for predicting transformation from ET to MF. Furthermore, CD56+CD14+ pro-inflammatory monocytes were identified as a novel source of increased GRO-α levels. These data implicate the immune cell microenvironment as a significant player in ET disease evolution and illustrate the utility of cytokines as potential biomarkers for reaching beyond genomic classification for disease stratification and monitoring.The serum cytokine studies were supported by a research grant from the Rosetrees Trust. NFØ was supported by grants from the Danish Lundbeck Foundation and Danish Cancer Society, J.G. was supported by fellowships from Bloodwise and the Kay Kendall Leukaemia Fund; and M.S.S. is the recipient of a Biotechnology and Biological Sciences Research Council Industrial Collaborative Awards in Science and Engineering PhD Studentship. Work in the R.C.S. laboratory was supported by grants from the Stiftung Blutspendezentrum SRK beider Basel, the Swiss National Science Foundation (31003A-147016/1 and 31003A_166613), and the Swiss Cancer League (KLS-2950-02-2012 and KFS-3655-02-2015). A.K. was supported by the Else Kröner-Fresenius Foundation. Work in the A.R.G. laboratory is supported by the Wellcome Trust, Bloodwise, Cancer Research UK, the Kay Kendall Leukaemia Fund, and the Leukemia and Lymphoma Society of America. Work in the D.G.K. laboratory is supported by a Bloodwise Bennett Fellowship (15008), a European Hematology Association Non-Clinical Advanced Research Fellowship, and an ERC Starting Grant (ERC-2016-STG–715371). D.G.K. and A.R.G. are supported by a core support grant from the Wellcome Trust and Medical Research Council to the Wellcome MRC Cambridge Stem Cell Institute, the National Institute for Health Research Cambridge Biomedical Research Centre, and the CRUK Cambridge Cancer Centre