RIFEL - Ripple and Electromagnetic Fields in Electric Vehicles

The electrical system in an electrified vehicle consists of high voltage (HV) components interacting in a complex way. The switching interaction in the power electronics results in ripple causing electromagnetic fields, disturbing other electronics and degradation of components. An overview of this can first be obtained when a physical system is built which could lead to unintentional over- or under dimensioning of HV components. This lack of information within the electrical system can lead to late verifications in the project causing substantial cost if changes are needed. This project aims at improving early evaluation of new concepts, create tools and build the necessary competence for a virtual system model that includes the key HV components: battery, electrical motor and power electronics, a simple load along with cable and connectors. This virtual model shall be able to simulate voltage and current ripple generated by the power electronics, initially in a frequency range up to 100 kHz. Results from the simulations shall be presented both in time and frequency domain as well as be expressed in RMS values for easier comparison to measured results. Some of the more important findings are briefly summarised below;For the high voltage battery, the electrical characteristics up to a frequency of roughly 1000 Hz was well determined using an impedance spectroscopy instrument at cell level and then multiplied by the numbers of cells.\ua0 However for finding the impedance behaviour for frequencies above 1000 Hz, the determination must be done on the battery pack level since bus bars and other component in the complete battery pack will be dominating in this frequency range. From measurements of differential mode impedance in high voltage cables it is found that it is important that the mutual inductance between the centre conductor and shield is included in the model to describe cable impedance below 10 kHz properly.The control of the inverter is very important for the overall behaviour and in this project SVM was used which has been shown to give the lowest current and voltage ripple of the traditional switching schemes. And for the machine model, the temperature variations must be taken into account since the machine parameters has been found to vary with ~20 % over the specified temperature range.The system model is found to agree well with rig measurements well up to 1 MHz with regards to both currents and voltages at the DC and AC sides. Furthermore, measurements in a real car match those in the rig. For time domain simulations, it was decided to use Ansys Simplorer since it can handle the inverter and the electrical machine simulations very well and for frequency domain simulations, it was decided to use LTspice since it is freeware, has support for AC-sweeps, improved switching compared to other SPICE-simulators, and is easy to use.Magnetic field simulations have been calculated and compared to measurements in the driveline rig at Chalmers. It was a good match across the investigated frequency range 10 Hz to 100 kHz.In this project, only internally developed component models were considered. To expand the functionality of the system modelling tool, international interface standards such as the Functional Mockup Interface (FMI) need to be investigated. Consequently, it would be a good idea to include additional automotive OEMs as well as suppliers and software vendors in future research collaborations

Class-switched marginal zone B cells in spleen have relatively low numbers of somatic mutations

The vast majority of rodent splenic marginal zone (MZ)-B cells are naive IgM(+) cells. A small fraction of these MZ-B cells carry mutated V-genes, and represent IgM(+) memory MZ-B cells. Here we reveal further heterogeneity of B cells with a MZ-B cell phenotype, by providing evidence for the existence of class-switched memory MZ-B cells in the rat. In essence, we observed IGHV5 encoded Cgamma transcripts, among FACS-purified MZ-B cells, defined as HIS24(low)HIS57(bright) cells. Furthermore, we found that most IgG encoding transcripts are mutated. There is no significant difference in IGHV5 repertoire and subclass usage of these IgG encoding transcripts collected from B cells with a MZ-B cell phenotype and B cells with a follicular (FO) B cell phenotype. However, the IGHV5 genes encoding for IgG antibodies of MZ-B cells exhibited significantly fewer mutations, compared to those with a FO-B cell phenotype. In one rat we found a clonally related set of IgG encoding sequences, of which one was derived from the MZ-B cell fraction and the other from the FO-B cell fraction. We speculate that these two subpopulations of class-switched B cells are both descendants from naive FO-B cells and are generated in germinal centers. Class-switched memory cells with a MZ-B cell phenotype may provide the animal with a population of IgG memory cells that can respond rapidly to blood-borne pathogens

Safety and efficacy of fluoxetine on functional outcome after acute stroke (AFFINITY): a randomised, double-blind, placebo-controlled trial

Background Trials of fluoxetine for recovery after stroke report conflicting results. The Assessment oF FluoxetINe In sTroke recoverY (AFFINITY) trial aimed to show if daily oral fluoxetine for 6 months after stroke improves functional outcome in an ethnically diverse population. Methods AFFINITY was a randomised, parallel-group, double-blind, placebo-controlled trial done in 43 hospital stroke units in Australia (n=29), New Zealand (four), and Vietnam (ten). Eligible patients were adults (aged ≥18 years) with a clinical diagnosis of acute stroke in the previous 2–15 days, brain imaging consistent with ischaemic or haemorrhagic stroke, and a persisting neurological deficit that produced a modified Rankin Scale (mRS) score of 1 or more. Patients were randomly assigned 1:1 via a web-based system using a minimisation algorithm to once daily, oral fluoxetine 20 mg capsules or matching placebo for 6 months. Patients, carers, investigators, and outcome assessors were masked to the treatment allocation. The primary outcome was functional status, measured by the mRS, at 6 months. The primary analysis was an ordinal logistic regression of the mRS at 6 months, adjusted for minimisation variables. Primary and safety analyses were done according to the patient's treatment allocation. The trial is registered with the Australian New Zealand Clinical Trials Registry, ACTRN12611000774921. Findings Between Jan 11, 2013, and June 30, 2019, 1280 patients were recruited in Australia (n=532), New Zealand (n=42), and Vietnam (n=706), of whom 642 were randomly assigned to fluoxetine and 638 were randomly assigned to placebo. Mean duration of trial treatment was 167 days (SD 48·1). At 6 months, mRS data were available in 624 (97%) patients in the fluoxetine group and 632 (99%) in the placebo group. The distribution of mRS categories was similar in the fluoxetine and placebo groups (adjusted common odds ratio 0·94, 95% CI 0·76–1·15; p=0·53). Compared with patients in the placebo group, patients in the fluoxetine group had more falls (20 [3%] vs seven [1%]; p=0·018), bone fractures (19 [3%] vs six [1%]; p=0·014), and epileptic seizures (ten [2%] vs two [<1%]; p=0·038) at 6 months. Interpretation Oral fluoxetine 20 mg daily for 6 months after acute stroke did not improve functional outcome and increased the risk of falls, bone fractures, and epileptic seizures. These results do not support the use of fluoxetine to improve functional outcome after stroke

Intestinal IgA synthesis: Localization and requirements for IgA class switch recombination

Production of IgA at mucosal surfaces is one of the most striking features of the mucosal immune system. Despite that IgA was first discovered in the 1950’s and secretory IgA described in gut secretions and breast milk in the mid 1960’s we still have limited information about the sites and exact requirements for IgA class switch recombination. The aim of this thesis work was to investigate potential locations for induction of T-independent IgA responses using CD40 deficient mice as a model. Furthermore, as germ free mice have very poor IgA levels in the gut lamina propria (LP) we investigated whether this is because of a lack of IgA CSR at the inductive sites or whether the commensal flora is involved in maintaining IgA plasma cells at the effector site in the LP itself. Finally we used new ways of assessing the development of T-dependent IgA responses during oral immunizations using NP-hapten-conjugated cholera toxin as our oral immunogen. CD40-/- mice have very low levels of serum IgG, are unable to form GC and as a consequence, cannot respond to TD antigens. However, we found that CD40-/- mice hosted near normal levels of IgA plasma cells in the gut LP, indicating that IgA CSR was intact and could occur in the absence of GC-formations and CD40-signalling. The ongoing controversy between researchers claiming evidence for two types of IgA CSR processes in the gut; one TD in the organized gut associated lymphoid system (GALT), and another pathway dependent on the commensal flora and ongoing in the non-organized LP itself, prompted us to investigate these theories in more detail using CD40-/- mice and molecular markers for IgA CSR. We found no evidence for IgA CSR in the gut LP and that IgA CSR was restricted to the GALT and the Peyer’s patches (PP), in particular. In support of this notion, we observed clonally related Ig heavy chain variable sequences in widely separated segments of small intestinal biopsies, suggesting a common source rather than a disseminated process in the non-organized gut tissue. In addition, analyzing the GL7int cells for molecular markers of IgA CSR clearly showed that the cells could undergo IgA CSR despite not being derived from histologically detectable GCs. Therefore, we believe that the main pathway for CD40-independent IgA CSR is via the PPs, as in WT mice, and that the IgA CSR precedes the GC-stage where somatic hypermutations are introduced. Furthermore, studies in germ free mice revealed that GCs were present and IgA CSR was ongoing in the PPs, despite the lack of commensal gut microflora. Therefore, we hypothesize that the effector site, the lamina propria, is deficient in supporting IgA responses. Finally, we studied TD IgA responses at a molecular level during oral immunizations using NP-CT conjugates as antigen. We found that repeated oral immunization generated affinity matured and clonally selected IgA responses originating from the GALT. Three immunizations generated 15% antigen specific IgA plasma cells in the LP, distributed evenly thoughout the intestine. In conclusion, we have provided evidence that TI IgA CSR occurs exclusively in the GALT prior to SHM in GCs. IgA CSR activity was never found in the non-organized LP, and peritoneal cavity B-cells do not significantly contribute to LP IgA plasma cells. Additionally, we show that the induction of IgA CSR is intact in GF mice, but subsequent IgA plasma cell development appears to be impaired, resulting in a 90% reduction in gut IgA plasma cells in the small and large intestine. Finally we show that TD IgA responses are efficiently generated in the GALT and that the responses early on undergo mutational selection events that result in high affinity IgA plasma cells seeding the gut LP