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

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

Safety assurance of a high voltage controller for an industrial robotic system

Due to the risk of discharge sparks and ignition, there are strict rules concerning the safety of high voltage electrostatic systems used in industrial painting robots. In order to assure that the system fulfils its safety requirements, formal verification is an important tool to supplement traditional testing and quality assurance procedures. The work in this paper presents formal verification of the most important safety functions of a high voltage controller. The controller has been modelled as a finite state machine, which was formally verified using two different model checking software tools; Simulink Design Verifier and RoboTool. Five safety critical properties were specified and formally verified using the two tools. Simulink was chosen as a low-threshold entry point since MathWorks products are well known to most practitioners. RoboTool serves as a software tool targeted towards model checking, thus providing more advanced options for the more experienced user. The comparative study and results show that all properties were successfully verified. The verification times in both tools were in the order of a few minutes, which was within the acceptable time limit for this particular application

BOD1 Is Required for Cognitive Function in Humans and <i>Drosophila</i>

Here we report a stop-mutation in the BOD1 (Biorientation Defective 1) gene, which co-segregates with intellectual disability in a large consanguineous family, where individuals that are homozygous for the mutation have no detectable BOD1 mRNA or protein. The BOD1 protein is required for proper chromosome segregation, regulating phosphorylation of PLK1 substrates by modulating Protein Phosphatase 2A (PP2A) activity during mitosis. We report that fibroblast cell lines derived from homozygous BOD1 mutation carriers show aberrant localisation of the cell cycle kinase PLK1 and its phosphatase PP2A at mitotic kinetochores. However, in contrast to the mitotic arrest observed in BOD1-siRNA treated HeLa cells, patient-derived cells progressed through mitosis with no apparent segregation defects but at an accelerated rate compared to controls. The relatively normal cell cycle progression observed in cultured cells is in line with the absence of gross structural brain abnormalities in the affected individuals. Moreover, we found that in normal adult brain tissues BOD1 expression is maintained at considerable levels, in contrast to PLK1 expression, and provide evidence for synaptic localization of Bod1 in murine neurons. These observations suggest that BOD1 plays a cell cycle-independent role in the nervous system. To address this possibility, we established two Drosophila models, where neuron-specific knockdown of BOD1 caused pronounced learning deficits and significant abnormalities in synapse morphology. Together our results reveal novel postmitotic functions of BOD1 as well as pathogenic mechanisms that strongly support a causative role of BOD1 deficiency in the aetiology of intellectual disability. Moreover, by demonstrating its requirement for cognitive function in humans and Drosophila we provide evidence for a conserved role of BOD1 in the development and maintenance of cognitive features

Determination of hydroxyl groups in biorefinery resources via quantitative 31P NMR spectroscopy

The analysis of chemical structural characteristics of biorefinery product streams (such as lignin and tannin) has advanced substantially over the past decade, with traditional wet-chemical techniques being replaced or supplemented by NMR methodologies. Quantitative 31P NMR spectroscopy is a promising technique for the analysis of hydroxyl groups because of its unique characterization capability and broad potential applicability across the biorefinery research community. This protocol describes procedures for (i) the preparation/solubilization of lignin and tannin, (ii) the phosphitylation of their hydroxyl groups, (iii) NMR acquisition details, and (iv) the ensuing data analyses and means to precisely calculate the content of the different types of hydroxyl groups. Compared with traditional wet-chemical techniques, the technique of quantitative 31P NMR spectroscopy offers unique advantages in measuring hydroxyl groups in a single spectrum with high signal resolution. The method provides complete quantitative information about the hydroxyl groups with small amounts of sample (~30 mg) within a relatively short experimental time (~30-120 min)

Glycomic Characterization of Induced Pluripotent Stem Cells Derived from a Patient Suffering from Phosphomannomutase 2 Congenital Disorder of Glycosylation (PMM2-CDG)

PMM2-CDG, formerly known as congenital disorder of glycosylation-Ia (CDG-Ia), is caused by mutations in the gene encoding phosphomannomutase 2 (PMM2). This disease is the most frequent form of inherited CDG-diseases affecting protein N-glycosylation in human. PMM2-CDG is a multisystemic disease with severe psychomotor and mental retardation. In order to study the pathophysiology of PMM2-CDG in a human cell culture model, we generated induced pluripotent stem cells (iPSCs) from fibroblasts of a PMM2-CDG-patient (PMM2-iPSCs). Expression of pluripotency factors and in vitro differentiation into cell types of the three germ layers was unaffected in the analyzed clone PMM2-iPSC-C3 compared with nondiseased human pluripotent stem cells (hPSCs), revealing no broader influence of the PMM2 mutation on pluripotency in cell culture. Analysis of gene expression by deep-sequencing did not show obvious differences in the transcriptome between PMM2-iPSC-C3 and nondiseased hPSCs. By multiplexed capillary gel electrophoresis coupled to laser induced fluorescence detection (xCGE-LIF) we could show that PMM2-iPSC-C3 exhibit the common hPSC N-glycosylation pattern with high-mannose-type N-glycans as the predominant species. However, phosphomannomutase activity of PMM2-iPSC-C3 was 27% compared with control hPSCs and lectin staining revealed an overall reduced protein glycosylation. In addition, quantitative assessment of N-glycosylation by xCGE-LIF showed an up to 40% reduction of high-mannose-type N-glycans in PMM2-iPSC-C3, which was in concordance to the observed reduction of the Glc3Man9GlcNAc2 lipid-linked oligosaccharide compared with control hPSCs. Thus we could model the PMM2-CDG disease phenotype of hypoglycosylation with patient derived iPSCs in vitro. Knock-down of PMM2 by shRNA in PMM2-iPSC-C3 led to a residual activity of 5% and to a further reduction of the level of N-glycosylation. Taken together we have developed human stem cell-based cell culture models with stepwise reduced levels of N-glycosylation now enabling to study the role of N-glycosylation during early human development