271 research outputs found

    Befragung zum Status-Quo der Tierhaltung bei 287 süddeutschen Bio-Betrieben (Demeter- und Bioland)[Inquiry to the status quo of livestock husbandry in organic farms in southern germany]

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    Fazit: Die gegenüber früheren Untersuchungen gestiegenen Bestandsgrößen weisen darauf hin, daß sich im ökologischen Landbau ein ähnlicher Strukturwandel wie in der konventionellen Landwirtschaft vollzieht (Wachstum und Spezialisierung). Die Auswertung zeigt ferner, daß die Betriebe zunehmend bemüht sind, bereits jetzt den zukünftigen Haltungsvorschriften der EU-Verordnung zu entsprechen. Fast alle Betriebe führen Weidegang durch und trotz der relativ geringen Bestandsgröße haben die meisten Betriebe bereits Laufställe; Auslaufmöglichkeiten fallen demgegenüber allerdings noch ab

    Entwicklung, Erprobung, Umsetzung und Evaluation von Strategien in den Bereichen Tiergesundheit, Haltung, Fütterung, Management in der ökologischen Ferkelerzeugung

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    Die ökologische Ferkelerzeugung weist hinsichtlich Tiergesundheit, Leistungsfähigkeit und Wirtschaftlichkeit große Defizite auf. Die Ursachen sind komplex und betreffen u.a. Fütterung, Haltung und Hygiene. Für diese Bereiche sollten durch Exakt- und Praxisversuche Lösungsansätze entwickelt werden. Teilprojekte umfassten folgende Themen: Der Einfluss unterschiedlicher Raufutter in der Fütterung tragender Sauen, die Wirkung einer Inulinzugabe sowie vom Extrudieren von Ackerbohnen in Sauen- und Ferkelfutter, die Bewertung alternativer Desinfektionsverfahren, ein Vergleich von Einzelhaltung versus kombinierte Einzel- und Gruppenhaltung säugender Sauen sowie die Optimierung des Ferkelliegebereichs in der Ferkelaufzucht. Zentrale Ergebnisse: - Die verschiedenen Raufuttervarianten (Kleegrassilage, Heu, Maissilage, Topinamburknollen) hatten keine negativen Effekte auf Körperkonstitution und Reproduktionsleistungen der Sauen. - Die Saugferkel der mit Inulin versorgten Sauen entwickelten sich gegenüber der Kontrollgruppe während der Säugezeit leistungsmäßig besser, während der Ferkelaufzucht gab es keine Leistungssteigerungen. Der Einsatz von getoasteten Ackerbohnen führte zu signifikant besseren Ferkelzunahmen gegenüber dem Einsatz von extrudierten Ackerbohnen. - Keines der getesteten alternativen Desinfektionsverfahren (Heißwasserdampf, elektroaktiviertes Wasser, Abflammen) ist eine Alternative zur chemischen Desinfektion bezüglich Keimreduktion, Arbeitsaufwand und Kosten. - Gruppensäugen führt bei Sauen zu erhöhter Aktivität sowie zu spezifischen Verhaltensanpassungen. Leistungseinbußen konnten weder für Sauen noch für Ferkel dokumentiert werden. „Gruppensäugen“ führt zu einem höheren Arbeitszeitbedarf und steigenden Baukosten. - Der Liegebereich für Aufzuchtferkel ist in vielen Betrieben nicht optimal und durch z. T. einfache Maßnahmen (Abdichten des Liegenestes, Wärmedämmung des Bodens, Bodenheizung, Anbringen einer weiteren Wärmequelle) für die Tiere zu verbessern

    An investigation of horizontal transfer of feed introduced DNA to the aerobic microbiota of the gastrointestinal tract of rats

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    Background: Horizontal gene transfer through natural transformation of members of the microbiota of the lower gastrointestinal tract (GIT) of mammals has not yet been described. Insufficient DNA sequence similarity for homologous recombination to occur has been identified as the major barrier to interspecies transfer of chromosomal DNA in bacteria. In this study we determined if regions of high DNA similarity between the genomes of the indigenous bacteria in the GIT of rats and feed introduced DNA could lead to homologous recombination and acquisition of antibiotic resistance genes. Results: Plasmid DNA with two resistance genes (nptII and aadA) and regions of high DNA similarity to 16S rRNA and 23S rRNA genes present in a broad range of bacterial species present in the GIT, where constructed and added to standard rat feed. Six rats, with a normal microbiota, were fed DNA containing pellets daily over four days before sampling of the microbiota from the different GI compartments (stomach, small intestine, cecum and colon). In addition, two rats were included as negative controls. Antibiotic resistant colonies growing on selective media were screened for recombination with feed introduced DNA by PCR targeting unique sites in the putatively recombined regions. Conclusions: The analyses showed that extensive ingestion of DNA (100 \ub5g plasmid) per day did not lead to increased proportions of kanamycin resistant bacteria, nor did it produce detectable transformants among the aerobic microbiota examined for 6 rats (detection limit <1 transformant per 1.1 x 108 cultured bacteria). The key methodological challenges to HGT detection in animal feedings trials are identified and discussed

    An international parentage and identification panel for the domestic cat (Felis catus)

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    Seventeen commercial and research laboratories participated in two comparison tests under the auspices of the International Society for Animal Genetics to develop an internationally tested, microsatellite-based parentage and identification panel for the domestic cat (Felis catus). Genetic marker selection was based on the polymorphism information content and allele ranges from seven random-bred populations (n = 261) from the USA, Europe and Brazil and eight breeds (n = 200) from the USA. Nineteen microsatellite markers were included in the comparison test and genotyped across the samples. Based on robustness and efficiency, nine autosomal microsatellite markers were ultimately selected as a single multiplex ‘core’ panel for cat identification and parentage testing. Most markers contained dinucleotide repeats. In addition to the autosomal markers, the panel included two gender-specific markers, amelogenin and zinc-finger XY, which produced genotypes for both the X and Y chromosomes. This international cat parentage and identification panel has a power of exclusion comparable to panels used in other species, ranging from 90.08% to 99.79% across breeds and 99.47% to 99.87% in random-bred cat populations

    CDK1 is a synthetic lethal target for KRAS mutant tumours.

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    Activating KRAS mutations are found in approximately 20% of human cancers but no RAS-directed therapies are currently available. Here we describe a novel, robust, KRAS synthetic lethal interaction with the cyclin dependent kinase, CDK1. This was discovered using parallel siRNA screens in KRAS mutant and wild type colorectal isogenic tumour cells and subsequently validated in a genetically diverse panel of 26 colorectal and pancreatic tumour cell models. This established that the KRAS/CDK1 synthetic lethality applies in tumour cells with either amino acid position 12 (p.G12V, pG12D, p.G12S) or amino acid position 13 (p.G13D) KRAS mutations and can also be replicated in vivo in a xenograft model using a small molecule CDK1 inhibitor. Mechanistically, CDK1 inhibition caused a reduction in the S-phase fraction of KRAS mutant cells, an effect also characterised by modulation of Rb, a master control of the G1/S checkpoint. Taken together, these observations suggest that the KRAS/CDK1 interaction is a robust synthetic lethal effect worthy of further investigation

    A Gain-of-Function Germline Mutation in Drosophila ras1 Affects Apoptosis and Cell Fate during Development

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    The RAS/MAPK signal transduction pathway is an intracellular signaling cascade that transmits environmental signals from activated receptor tyrosine kinases (RTKs) on the cell surface and other endomembranes to transcription factors in the nucleus, thereby linking extracellular stimuli to changes in gene expression. Largely as a consequence of its role in oncogenesis, RAS signaling has been the subject of intense research efforts for many years. More recently, it has been shown that milder perturbations in Ras signaling during embryogenesis also contribute to the etiology of a group of human diseases. Here we report the identification and characterization of the first gain-of-function germline mutation in Drosophila ras1 (ras85D), the Drosophila homolog of human K-ras, N-ras and H-ras. A single amino acid substitution (R68Q) in the highly conserved switch II region of Ras causes a defective protein with reduced intrinsic GTPase activity, but with normal sensitivity to GAP stimulation. The ras1R68Q mutant is homozygous viable but causes various developmental defects associated with elevated Ras signaling, including cell fate changes and ectopic survival of cells in the nervous system. These biochemical and functional properties are reminiscent of germline Ras mutants found in patients afflicted with Noonan, Costello or cardio-facio-cutaneous syndromes. Finally, we used ras1R68Q to identify novel genes that interact with Ras and suppress cell death

    Live-Cell Microscopy Reveals Small Molecule Inhibitor Effects on MAPK Pathway Dynamics

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    Oncogenic mutations in the mitogen activated protein kinase (MAPK) pathway are prevalent in human tumors, making this pathway a target of drug development efforts. Recently, ATP-competitive Raf inhibitors were shown to cause MAPK pathway activation via Raf kinase priming in wild-type BRaf cells and tumors, highlighting the need for a thorough understanding of signaling in the context of small molecule kinase inhibitors. Here, we present critical improvements in cell-line engineering and image analysis coupled with automated image acquisition that allow for the simultaneous identification of cellular localization of multiple MAPK pathway components (KRas, CRaf, Mek1 and Erk2). We use these assays in a systematic study of the effect of small molecule inhibitors across the MAPK cascade either as single agents or in combination. Both Raf inhibitor priming as well as the release from negative feedback induced by Mek and Erk inhibitors cause translocation of CRaf to the plasma membrane via mechanisms that are additive in pathway activation. Analysis of Erk activation and sub-cellular localization upon inhibitor treatments reveals differential inhibition and activation with the Raf inhibitors AZD628 and GDC0879 respectively. Since both single agent and combination studies of Raf and Mek inhibitors are currently in the clinic, our assays provide valuable insight into their effects on MAPK signaling in live cells

    Essential Role of Cdc42 in Ras-Induced Transformation Revealed by Gene Targeting

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    The ras proto-oncogene is one of the most frequently mutated genes in human cancer. However, given the prevalence of activating mutations in Ras and its association with aggressive forms of cancer, attempts to therapeutically target aberrant Ras signaling have been largely disappointing. This lack of progress highlights the deficiency in our understanding of cellular pathways required for Ras-mediated tumorigenesis and suggests the importance of identifying new molecular pathways associated with Ras-driven malignancies. Cdc42 is a Ras-related small GTPase that is known to play roles in oncogenic processes such as cell growth, survival, invasion, and migration. A pan-dominant negative mutant overexpression approach to suppress Cdc42 and related pathways has previously shown a requirement for Cdc42 in Ras-induced anchorage-independent cell growth, however the lack of specificity of such approaches make it difficult to determine if effects are directly related to changes in Cdc42 activity or other Rho family members. Therefore, in order to directly and unambiguously address the role of Cdc42 in Ras-mediated transformation, tumor formation and maintenance, we have developed a model of conditional cdc42 gene in Ras-transformed cells. Loss of Cdc42 drastically alters the cell morphology and inhibits proliferation, cell cycle progression and tumorigenicity of Ras-transformed cells, while non-transformed cells or c-Myc transformed cells are largely unaffected. The loss of Cdc42 in Ras-transformed cells results in reduced Akt signaling, restoration of which could partially rescues the proliferation defects associated with Cdc42 loss. Moreover, disruption of Cdc42 function in established tumors inhibited continued tumor growth. These studies implicate Cdc42 in Ras-driven tumor growth and suggest that targeting Cdc42 is beneficial in Ras-mediated malignancies

    Expression of B-RAF V600E in Type II Pneumocytes Causes Abnormalities in Alveolar Formation, Airspace Enlargement and Tumor Formation in Mice

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    Growth factor induced signaling cascades are key regulatory elements in tissue development, maintenance and regeneration. Perturbations of these cascades have severe consequences, leading to developmental disorders and neoplastic diseases. As a major function in signal transduction, activating mutations in RAF family kinases are the cause of human tumorigenesis, where B-RAF V600E has been identified as the prevalent mutant. In order to address the oncogenic function of B-RAF V600E, we have generated transgenic mice expressing the activated oncogene specifically in lung alveolar epithelial type II cells. Constitutive expression of B-RAF V600E caused abnormalities in alveolar epithelium formation that led to airspace enlargements. These lung lesions showed signs of tissue remodeling and were often associated with chronic inflammation and low incidence of lung tumors. The inflammatory cell infiltration did not precede the formation of the lung lesions but was rather accompanied with late tumor development. These data support a model where the continuous regenerative process initiated by oncogenic B-RAF-driven alveolar disruption provides a tumor-promoting environment associated with chronic inflammation
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