Non-linear MPC for winding loss optimised torque control of anisotropic PMSM

For a non-linear anisotropic permanent magnet synchronous machine (PMSM), a prediction model for model predictive control (MPC) considering effects like cross-coupling and saturation is developed in a straight forward procedure. The objective of the designed MPC is either tracking of reference currents or torque tracking. Both approaches use the projected fast gradient method (PFGM) as optimisation algorithm. The latter approach makes look-up-tables for current references obsolete and additionally minimises winding losses. This two approaches are compared in a simulation study with a state of the art PI controller

Ein Verfahren zur lexikographischen modellprädiktiven Regelung mit der Anwendung auf eine permanenterregte Synchronmaschine

Bei der konventionellen Drehmomentregelung von Permanentmagneterregten Synchronmaschinen (PSM) werden Solldrehmomente unter der Berücksichtigung von Leistungsverlusten durch statische Kennfelder in Sollströme überführt. Dieses Vorgehen ist dynamisch suboptimal, interdependent und stark maschinenabhängig. Diese Arbeit widmet sich der Frage: Wie kann ein Model Predictive Controller (MPC) entworfen werden, durch welchen die Ziele Drehmomenterreichung und Verlustminimierung simultan optimiert werden und wie können die gesteigerten Anforderungen in der Elektromobilität durch diesen Ansatz erfüllt werden? Hierfür wird die Beschreibung des Regelziels im MPC als multikriterielles lexikographisches Optimierungsproblem (LOP) formuliert, was einer strengen Priorisierung der beiden Regelziele entspricht. Um diesen Ansatz für echtzeitfähige Systeme tauglich zu machen, wird für die Integration des LOP in den MPC eine neue Methode vorgeschlagen, die beide Regelziele in eine Gütefunktion transformiert. Die Anforderungen der Elektromobilität werden im MPC durch die Berücksichtigung der Nichtlinearität des magnetischen Kreises – insbesondere Sättigung, Reluktanz und Kreuzverkopplung – sowie exakter Spannungs- und Strombegrenzung berücksichtigt. Durch die neue zugeschnittene Methode wird die mittlere Berechnungszeit des LOP deutlich verringert und gleichzeitig das Regelergebnis verbessert. Die Analyse der Potentiale dieses Ansatzes erfolgt im Vergleich mit einem PI-Zustandsregler durch die Untersuchung der jeweils erzielbaren Regelergebnisse in anwendungsnahen Szenarien. Bei der Anwendung der Regler auf die Kompensation von Getriebeschwingungen im Antriebsstrang eines Elektrofahrzeugs zeigt das vorgeschlagene Verfahren zusätzliche Potentiale für schnelle dynamische Vorgänge an den Betriebsgrenzen

IFN regulatory factor 4 controls post-ischemic inflammation and prevents chronic kidney disease

Ischemia reperfusion injury (IRI) of the kidney results in interferon regulatory factor 4 (IRF4)–mediated counter-regulation of the acute inflammatory response. Beyond that, IRF4 exerts important functions in controlling the cytokine milieu, T-cell differentiation, and macrophage polarization. The latter has been implicated in tissue remodeling. It therefore remains elusive what the role of IRF4 is in terms of long-term outcome following IRI. We hypothesized that an inability to resolve chronic inflammation in Irf4−/− mice would promote chronic kidney disease (CKD) progression. To evaluate the effects of IRF4 in chronic upon acute injury in vivo, a mouse model of chronic injury following acute IRI was employed. The expression of Irf4 increased within 10 days after IRI in renal tissue. Both mRNA and protein levels remained high up to 5 weeks upon IRI, suggesting a regulatory function in the chronic phase. Mice deficient in IRF4 display increased tubular cell loss and defective clearance of infiltrating macrophages. These phenomena were associated with increased expression of pro-inflammatory macrophage markers together with reduced expression of alternatively activated macrophage markers. In addition, IRF4-deficient mice showed defective development of alternatively activated macrophages. Hints of a residual M1 macrophage signature were further observed in human biopsy specimens of patients with hypertensive nephropathy vs. living donor specimens. Thus, IRF4 restricts CKD progression and kidney fibrosis following IRI, potentially by enabling M2 macrophage polarization and restricting a Th1 cytokine response. Deteriorated alternative macrophage subpopulations in Irf4−/− mice provoke chronic intrarenal inflammation, tubular epithelial cell loss, and renal fibrosis in the long course after IRI in mice. The clinical significance of these finding for human CKD remains uncertain at present and warrants further studies

Treatment delay of bone tumours, compilation of a sociodemographic risk profile: A retrospective study

<p>Abstract</p> <p>Background</p> <p>Bone tumours are comparatively rare tumours and delays in diagnosis and treatment are common. The purpose of this study was to analyse sociodemographic risk factors for bone tumour patients in order to identify those at risk of prolonged patients delay (time span from first symptoms to consultation), professional delay (from consultation to treatment) or symptom interval (from first symptoms to treatment). Understanding these relationships might enable us to shorten time to diagnosis and therapy.</p> <p>Methods</p> <p>We carried out a retrospective analysis of 265 patients with bone tumours documenting sociodemographic factors, patient delay, professional delay and symptom interval. A multivariate explorative Cox model was performed for each delay.</p> <p>Results</p> <p>Female gender was associated with a prolonged patient delay. Age under 30 years and rural living predisposes to a prolonged professional delay and symptom interval.</p> <p>Conclusion</p> <p>Early diagnosis and prompt treatment are required for successful management of most bone tumour patients. We succeeded in identifying the histology independent risk factors of age under 30 years and rural habitation for treatment delay in bone tumour patients. Knowing about the existence of these risk groups age under 30 years and female gender could help the physician to diagnose bone tumours earlier. The causes for the treatment delays of patients living in a rural area have to be investigated further. If the delay initiates in the lower education of rural general physicians, further training about bone tumours might advance early detection. Hence the outcome of patients with bone tumours could be improved.</p

Maternal and fetal genetic effects on birth weight and their relevance to cardio-metabolic risk factors.

Birth weight variation is influenced by fetal and maternal genetic and non-genetic factors, and has been reproducibly associated with future cardio-metabolic health outcomes. In expanded genome-wide association analyses of own birth weight (n = 321,223) and offspring birth weight (n = 230,069 mothers), we identified 190 independent association signals (129 of which are novel). We used structural equation modeling to decompose the contributions of direct fetal and indirect maternal genetic effects, then applied Mendelian randomization to illuminate causal pathways. For example, both indirect maternal and direct fetal genetic effects drive the observational relationship between lower birth weight and higher later blood pressure: maternal blood pressure-raising alleles reduce offspring birth weight, but only direct fetal effects of these alleles, once inherited, increase later offspring blood pressure. Using maternal birth weight-lowering genotypes to proxy for an adverse intrauterine environment provided no evidence that it causally raises offspring blood pressure, indicating that the inverse birth weight-blood pressure association is attributable to genetic effects, and not to intrauterine programming.The Fenland Study is funded by the Medical Research Council (MC_U106179471) and Wellcome Trust