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Dll1 Haploinsufficiency in Adult Mice Leads to a Complex Phenotype Affecting Metabolic and Immunological Processes
Isabel Rubio-Aliaga, Gerhard K. H. Przemeck, Helmut Fuchs, Valérie Gailus-Durner, Thure Adler, Wolfgang Hans, Marion Horsch, Birgit Rathkolb, Jan Rozman, Anja Schrewe, Sibylle Wagner, Sabine M. Hoelter, Lore Becker, Thomas Klopstock, Wolfgang Wurst, Eckhard Wolf, Martin Klingenspor, Boris T. Ivandic, Dirk H. Busch, Johannes Beckers, Martin Hrabé de Angelis
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0006054
Abstract: Background The Notch signaling pathway is an evolutionary conserved signal transduction pathway involved in embryonic patterning and regulation of cell fates during development and self-renewal. Recent studies have demonstrated that this pathway is integral to a complex system of interactions, involving as well other signal transduction pathways, and implicated in distinct human diseases. Delta-like 1 (Dll1) is one of the known ligands of the Notch receptors. The role of the Notch ligands is less well understood. Loss-of-function of Dll1 leads to embryonic lethality, but reduction of Delta-like 1 protein levels has not been studied in adult stage. Methodology/Principal Findings Here we present the haploinsufficient phenotype of Dll1 and a missense mutant Dll1 allele (Dll1C413Y). Haploinsufficiency leads to a complex phenotype with several biological processes altered. These alterations reveal the importance of Dll1 mainly in metabolism, energy balance and in immunology. The animals are smaller, lighter, with altered fat to lean ratio and have increased blood pressure and a slight bradycardia. The animals have reduced cholesterol and triglyceride levels in blood. At the immunological level a subtle phenotype is observed due to the effect and fine-tuning of the signaling network at the different levels of differentiation, proliferation and function of lymphocytes. Moreover, the importance of the proteolytic regulation of the Notch signaling network emphasized. Conclusions/Significance In conclusion, slight alterations in one player of Notch signaling alter the entire organism, emphasizing the fine-tuning character of this pathway in a high number of processes.
Pleiotropic effects in Eya3 knockout mice
Torben S?ker, Claudia Dalke, Oliver Puk, Thomas Floss, Lore Becker, Ines Bolle, Jack Favor, Wolfgang Hans, Sabine M H?lter, Marion Horsch, Magdalena Kallnik, Eva Kling, Corinna Moerth, Anja Schrewe, Christian Stigloher, Stefanie Topp, Valerie Gailus-Durner, Beatrix Naton, Johannes Beckers, Helmut Fuchs, Boris Ivandic, Thomas Klopstock, Holger Schulz, Eckhard Wolf, Wolfgang Wurst, Laure Bally-Cuif, Martin de Angelis, Jochen Graw
BMC Developmental Biology , 2008, DOI: 10.1186/1471-213x-8-118
Abstract: Expression analysis of Eya3 by in-situ hybridizations and β-Gal-staining of Eya3 mutant mice revealed abundant expression of the gene throughout development, e.g. in brain, eyes, heart, somites and limbs suggesting pleiotropic effects of the mutated gene. A similar complex expression pattern was observed also in zebrafish embryos.The phenotype of young adult Eya3 mouse mutants was systematically analyzed within the German Mouse Clinic. There was no obvious defect in the eyes, ears and kidneys of Eya3 mutant mice. Homozygous mutants displayed decreased bone mineral content and shorter body length. In the lung, the tidal volume at rest was decreased, and electrocardiography showed increased JT- and PQ intervals as well as decreased QRS amplitude. Behavioral analysis of the mutants demonstrated a mild increase in exploratory behavior, but decreased locomotor activity and reduced muscle strength. Analysis of differential gene expression revealed 110 regulated genes in heart and brain. Using real-time PCR, we confirmed Nup155 being down regulated in both organs.The loss of Eya3 in the mouse has no apparent effect on eye development. The wide-spread expression of Eya3 in mouse and zebrafish embryos is in contrast to the restricted expression pattern in Xenopus embryos. The loss of Eya3 in mice leads to a broad spectrum of minor physiological changes. Among them, the mutant mice move less than the wild-type mice and, together with the effects on respiratory, muscle and heart function, the mutation might lead to more severe effects when the mice become older. Therefore, future investigations of Eya3 function should focus on aging mice.Eya3 is one of four mammalian orthologous genes (Eya1-4) of eyes absent (eya) in Drosophila melanogaster [1,2]. Previous investigations demonstrated that a homozygous knockout of eya function in D. melanogaster results in severe embryonic defects and absence of compound eyes due to eye progenitor cell death [3,4]. Like eyes absent in Drosophil
Standardized, Systemic Phenotypic Analysis of UmodC93F and UmodA227T Mutant Mice
Elisabeth Kemter, Petra Prückl, Birgit Rathkolb, Kateryna Micklich, Thure Adler, Lore Becker, Johannes Beckers, Dirk H. Busch, Alexander A. G?tz, Wolfgang Hans, Marion Horsch, Boris Ivandic, Martin Klingenspor, Thomas Klopstock, Jan Rozman, Anja Schrewe, Holger Schulz, Helmut Fuchs, Valérie Gailus-Durner, Martin Hrabé de Angelis, Eckhard Wolf, Bernhard Aigner
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0078337
Abstract: Uromodulin-associated kidney disease (UAKD) summarizes different clinical features of an autosomal dominant heritable disease syndrome in humans with a proven uromodulin (UMOD) mutation involved. It is often characterized by hyperuricemia, gout, alteration of urine concentrating ability, as well as a variable rate of disease progression inconstantly leading to renal failure and histological alterations of the kidneys. We recently established the two Umod mutant mouse lines UmodC93F and UmodA227T on the C3H inbred genetic background both showing kidney defects analogous to those found in human UAKD patients. In addition, disease symptoms were revealed that were not yet described in other published mouse models of UAKD. To examine if further organ systems and/or metabolic pathways are affected by Umod mutations as primary or secondary effects, we describe a standardized, systemic phenotypic analysis of the two mutant mouse lines UmodA227T and UmodC93F in the German Mouse Clinic. Different genotypes as well as different ages were tested. Beside the already published changes in body weight, body composition and bone metabolism, the influence of the Umod mutation on energy metabolism was confirmed. Hematological analysis revealed a moderate microcytic and erythropenic anemia in older Umod mutant mice. Data of the other analyses in 7-10 month-old mutant mice showed single small additional effects.
Accumulation of Gel Particles in the Sea-Surface Microlayer during an Experimental Study with the Diatom Thalassiosira weissflogii  [PDF]
Luisa Galgani, Anja Engel
International Journal of Geosciences (IJG) , 2013, DOI: 10.4236/ijg.2013.41013
Abstract:

Since the early 80’s, the sea-surface microlayer (SML) has been hypothesized as being a gelatinous film. Recent studies have confirmed this characteristic, which confers properties that mediate mass and energy fluxes between ocean and atmosphere, including the emission of primary organic aerosols from marine systems. We investigated SML thickness and composition in five replicate indoor experiments between September and December 2010. During each experiment, the SML and underlying seawater were sampled from four seawater tanks: one served as control, and three were inoculated with Thalassiosira weissflogii grown in chemostats at 180, 380 and 780 ppm pCO2. We examined organic material enrichment factors in each tank, paying particular attention to gel particles accumulation such as polysaccharidic Transparent Exopolymer Particles (TEP) and the proteinaceous Coomassie Stainable Particles (CSP). While previous studies have observed carbohydrates and TEP enrichment in the microlayer, little is yet known about proteinaceous gel particles in the SML. Our experiments show that CSP dominate the gelatinous composition of the SML. We believe that the enrichment in CSP points to the importance of bacterial activity in the microlayer. Bacteria may play a pivotal role in mediating processes at the air-sea interface thanks to their exudates and protein content that can be released through cell disruption.

Post-Stroke Inhibition of Induced NADPH Oxidase Type 4 Prevents Oxidative Stress and Neurodegeneration
Christoph Kleinschnitz,Henrike Grund,Kirstin Wingler,Melanie E. Armitage,Emma Jones,Manish Mittal,David Barit,Tobias Schwarz,Christian Geis,Peter Kraft,Konstanze Barthel,Michael K. Schuhmann,Alexander M. Herrmann,Sven G. Meuth,Guido Stoll,Sabine Meurer,Anja Schrewe,Lore Becker,Valérie Gailus-Durner,Helmut Fuchs,Thomas Klopstock,Martin Hrabé de Angelis,Karin Jandeleit-Dahm,Ajay M. Shah,Norbert Weissmann,Harald H. H. W. Schmidt
PLOS Biology , 2012, DOI: 10.1371/journal.pbio.1000479
Abstract: Ischemic stroke is the second leading cause of death worldwide. Only one moderately effective therapy exists, albeit with contraindications that exclude 90% of the patients. This medical need contrasts with a high failure rate of more than 1,000 pre-clinical drug candidates for stroke therapies. Thus, there is a need for translatable mechanisms of neuroprotection and more rigid thresholds of relevance in pre-clinical stroke models. One such candidate mechanism is oxidative stress. However, antioxidant approaches have failed in clinical trials, and the significant sources of oxidative stress in stroke are unknown. We here identify NADPH oxidase type 4 (NOX4) as a major source of oxidative stress and an effective therapeutic target in acute stroke. Upon ischemia, NOX4 was induced in human and mouse brain. Mice deficient in NOX4 (Nox4?/?) of either sex, but not those deficient for NOX1 or NOX2, were largely protected from oxidative stress, blood-brain-barrier leakage, and neuronal apoptosis, after both transient and permanent cerebral ischemia. This effect was independent of age, as elderly mice were equally protected. Restoration of oxidative stress reversed the stroke-protective phenotype in Nox4?/? mice. Application of the only validated low-molecular-weight pharmacological NADPH oxidase inhibitor, VAS2870, several hours after ischemia was as protective as deleting NOX4. The extent of neuroprotection was exceptional, resulting in significantly improved long-term neurological functions and reduced mortality. NOX4 therefore represents a major source of oxidative stress and novel class of drug target for stroke therapy.
Post-Stroke Inhibition of Induced NADPH Oxidase Type 4 Prevents Oxidative Stress and Neurodegeneration
Christoph Kleinschnitz ,Henrike Grund,Kirstin Wingler,Melanie E. Armitage,Emma Jones,Manish Mittal,David Barit,Tobias Schwarz,Christian Geis,Peter Kraft,Konstanze Barthel,Michael K. Schuhmann,Alexander M. Herrmann,Sven G. Meuth,Guido Stoll,Sabine Meurer,Anja Schrewe,Lore Becker,Valérie Gailus-Durner,Helmut Fuchs,Thomas Klopstock,Martin Hrabé de Angelis,Karin Jandeleit-Dahm,Ajay M. Shah,Norbert Weissmann,Harald H. H. W. Schmidt
PLOS Biology , 2010, DOI: 10.1371/journal.pbio.1000479
Abstract: Ischemic stroke is the second leading cause of death worldwide. Only one moderately effective therapy exists, albeit with contraindications that exclude 90% of the patients. This medical need contrasts with a high failure rate of more than 1,000 pre-clinical drug candidates for stroke therapies. Thus, there is a need for translatable mechanisms of neuroprotection and more rigid thresholds of relevance in pre-clinical stroke models. One such candidate mechanism is oxidative stress. However, antioxidant approaches have failed in clinical trials, and the significant sources of oxidative stress in stroke are unknown. We here identify NADPH oxidase type 4 (NOX4) as a major source of oxidative stress and an effective therapeutic target in acute stroke. Upon ischemia, NOX4 was induced in human and mouse brain. Mice deficient in NOX4 (Nox4?/?) of either sex, but not those deficient for NOX1 or NOX2, were largely protected from oxidative stress, blood-brain-barrier leakage, and neuronal apoptosis, after both transient and permanent cerebral ischemia. This effect was independent of age, as elderly mice were equally protected. Restoration of oxidative stress reversed the stroke-protective phenotype in Nox4?/? mice. Application of the only validated low-molecular-weight pharmacological NADPH oxidase inhibitor, VAS2870, several hours after ischemia was as protective as deleting NOX4. The extent of neuroprotection was exceptional, resulting in significantly improved long-term neurological functions and reduced mortality. NOX4 therefore represents a major source of oxidative stress and novel class of drug target for stroke therapy.
Semiblind Channel Estimation for IFDMA in Case of Channels with Large Delay Spreads
Anja Sohl,Anja Klein
EURASIP Journal on Advances in Signal Processing , 2011, DOI: 10.1155/2011/857859
Abstract:
Tears on the screen: Bodily emotionalism in Reality-Tv
Hirdman,Anja;
Observatorio (OBS*) , 2011,
Abstract: our contemporary culture is in many aspects obsessed with emotions and authenticity. the media figures as a key locus in this development. however, the function and display of emotions vary depending on media type and genre. the article studies the construction of bodily emotionalism in reality-tv where corporeal signs such as tears confirm the display of emotional authenticity. it argues that authenticity appears to be synonymous with foremost the exposure of so called primary emotions, which are considered expressions for more direct and less controlled impulses. the specific value placed on tears in our culture is discussed in relation to televisions emotional script, the authentic claims of the genre and as a cultural longing after transparency where the ′truth′ resides within the body.
Brief Report on the Extended Linear Sigma Model
Habersetzer, Anja
High Energy Physics - Phenomenology , 2013,
Abstract: We present a chiral effective model which exhibits all the known symmetry features of the QCD Lagrangian. The extended Linear Sigma Model (eLSM) includes (pseudo-)scalar and (axial-) vector mesons, glueballs, and baryons. It has proven to be a useful tool to understand the nature of the low-energy resonances. It can be used to describe the masses and decay widths of the known low-energy mesons and to disentangle the complicated picture of resonances in the low-energy range. We can answer some of the open questions in the low-energy region, e.g. the resonance (f_0(1500)) is a predominantly glueball state and the resonance (f_0(1370)) is most likely the chiral partner of the pion. We could also find that the resonance (N(1650)) is favoured as the chiral partner of the nucleon (N(939)). In addition the temperature dependence of the chiral condensate and the glueball condensate can be used to study the phase diagram at nonzero temperatures and densities. At nonzero density we achieve nuclear matter saturation.
GMA-Jahrestagung in Greifswald vom 02.-05. Oktober 2008 []
Ratzmann, Anja
GMS Zeitschrift für Medizinische Ausbildung , 2008,
Abstract:
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