Induction Motor Diagnosis in Variable Speed Drives

Several diagnostic techniques are presented for the detection of electrical fault in induction motor variable speed drives. These techinques are developed taking into account the impact of the control system on machine variables and non stationary operating conditions.

Non-Linear Analysis and Design of Synchronous Bearingless Multiphase Permanent Magnet Machines and Drives

A two-dimensional model to analyze the distribution of magnetic fields in the airgap of a PM electrical machines is studied. A numerical algorithm for non-linear magnetic analysis of multiphase surface-mounted PM machines with semi-closed slots is developed, based on the equivalent magnetic circuit method. By using a modular structure geometry, whose the basic element can be duplicated, it allows to design whatever typology of windings distribution. In comparison to a FEA, permits a reduction in computing time and to directly changing the values of the parameters in a user interface, without re-designing the model. Output torque and radial forces acting on the moving part of the machine can be calculated. In addition, an analytical model for radial forces calculation in multiphase bearingless Surface-Mounted Permanent Magnet Synchronous Motors (SPMSM) is presented. It allows to predict amplitude and direction of the force, depending on the values of torque current, of levitation current and of rotor position. It is based on the space vectors method, letting the analysis of the machine also during transients. The calculations are conducted by developing the analytical functions in Fourier series, taking all the possible interactions between stator and rotor mmf harmonic components into account and allowing to analyze the effects of electrical and geometrical quantities of the machine, being parametrized. The model is implemented in the design of a control system for bearingless machines, as an accurate electromagnetic model integrated in a three-dimensional mechanical model, where one end of the motor shaft is constrained to simulate the presence of a mechanical bearing, while the other is free, only supported by the radial forces developed in the interactions between magnetic fields, to realize a bearingless system with three degrees of freedom. The complete model represents the design of the experimental system to be realized in the laboratory.

Diagnosis and Fault detection in Electrical Machines and Drives based on Advanced Signal Processing Techniques

In the present thesis, a new methodology of diagnosis based on advanced use of time-frequency technique analysis is presented. More precisely, a new fault index that allows tracking individual fault components in a single frequency band is defined. More in detail, a frequency sliding is applied to the signals being analyzed (currents, voltages, vibration signals), so that each single fault frequency component is shifted into a prefixed single frequency band. Then, the discrete Wavelet Transform is applied to the resulting signal to extract the fault signature in the frequency band that has been chosen. Once the state of the machine has been qualitatively diagnosed, a quantitative evaluation of the fault degree is necessary. For this purpose, a fault index based on the energy calculation of approximation and/or detail signals resulting from wavelet decomposition has been introduced to quantify the fault extend. The main advantages of the developed new method over existing Diagnosis techniques are the following: - Capability of monitoring the fault evolution continuously over time under any transient operating condition; - Speed/slip measurement or estimation is not required; - Higher accuracy in filtering frequency components around the fundamental in case of rotor faults; - Reduction in the likelihood of false indications by avoiding confusion with other fault harmonics (the contribution of the most relevant fault frequency components under speed-varying conditions are clamped in a single frequency band); - Low memory requirement due to low sampling frequency; - Reduction in the latency of time processing (no requirement of repeated sampling operation).

Misregulation of the tumour suppressor gene CYLD drives hyperactivation of T cells leading to intestinal pathology

The tumour suppressor gene cyld is mutated in familial cylindromatosis, an autosomal-dominant condition that predisposes to multiple skin tumours. The deubiquitinase CYLD acts as a negative regulator of NF-κB signaling. To analyse the function of CYLD in vivo we used the CYLDex7/8 mice, which are characterized by loss of the full-length transcript and overexpression of a short splice variant of CYLD (sCYLD). In CYLDex7/8 mice the overexpression of sCYLD results in splenomegaly and lymphadenopathy. Additionally, the B cell population in spleen and lymph nodes is increased at the expense of T cells. Analysis of CYLDex7/8 T cells showed a significant reduction of CD4 single positive (SP) and CD8 SP T cells in the thymus and in the periphery. By investigating the impact of sCYLD in TCR signaling in thymocytes, we could demonstrate that sCYLD partially inhibited the activation of Zap70 and thereby negatively regulated TCR signaling. In vitro as well as in vivo we could show that CD4+ T cells displayed a hyperactive phenotype, proliferated to a better extent than WT cells and expressed high amounts of inflammatory cytokines such as IL-6 and IL-17A. Western Blots of steady state thymocytes and peripheral CD4+ T cells were performed, showing that the noncanonical pathway was highly upregulated visualized by the expression levels of RelB and p100 leading to a hyperactive phenotype of CD4+ T cells. In order to investigate the contribution of sCYLD in positive and negative selection in the thymus in vivo, the HY-TCR transgene (HYtg) was crossed to CYLDex7/8 mice. The analysis of CYLDex7/8 HYtg males revealed an increase in CD4+CD8+ DP as well as in CD8+ SP thymocytes, suggesting a less pronounced negative selection in CYLD mutant mice compared to HYtg control mice. Interestingly, the impaired negative selection in the thymus was accompanied by a strong colitis phenotype at early ages (4 weeks). Since medullary TECs (mTECs) play an important role in the late stage of T cell development by negatively selecting autoreactive thymocytes, the levels of mTECs in the medullary compartment was investigated. Of note, low numbers of mTECs were observed, combined with decreased expression levels of the mTEC markers UEA-1, keratin-5, claudin-3 and claudin-4. The reduction of mTECs in the medullary compartment could explain the inflammatory phenotype of CD4+ T cells in CYLDex7/8 mice leading to the severe intestinal pathology observed in these mice. Taken together, these results show an important role of sCYLD in T cell development and function as well as in NF-кB signaling of T cells.

Power Converters and Electric Drives for Smart Grid Applications

The present dissertation aims to explore, theoretically and experimentally, the problems and the potential advantages of different types of power converters for “Smart Grid” applications, with particular emphasis on multi-level architectures, which are attracting a rising interest even for industrial requests. The models of the main multilevel architectures (Diode-Clamped and Cascaded) are shown. The best suited modulation strategies to function as a network interface are identified. In particular, the close correlation between PWM (Pulse Width Modulation) approach and SVM (Space Vector Modulation) approach is highlighted. An innovative multilevel topology called MMC (Modular Multilevel Converter) is investigated, and the single-phase, three-phase and "back to back" configurations are analyzed. Specific control techniques that can manage, in an appropriate way, the charge level of the numerous capacitors and handle the power flow in a flexible way are defined and experimentally validated. Another converter that is attracting interest in “Power Conditioning Systems” field is the “Matrix Converter”. Even in this architecture, the output voltage is multilevel. It offers an high quality input current, a bidirectional power flow and has the possibility to control the input power factor (i.e. possibility to participate to active and reactive power regulations). The implemented control system, that allows fast data acquisition for diagnostic purposes, is described and experimentally verified.

Analysis and design of high performance multiphase electric drives for vehicle and aircraft applications

The first part of this thesis has focused on the construction of a twelve-phase asynchronous machine for More Electric Aircraft (MEA) applications. In fact, the aerospace world has found in electrification the way to improve the efficiency, reliability and maintainability of an aircraft. This idea leads to the aircraft a new management and distribution of electrical services. In this way is possible to remove or to reduce the hydraulic, mechanical and pneumatic systems inside the aircraft. The second part of this dissertation is dedicated on the enhancement of the control range of matrix converters (MCs) operating with non-unity input power factor and, at the same time, on the reduction of the switching power losses. The analysis leads to the determination in closed form of a modulation strategy that features a control range, in terms of output voltage and input power factor, that is greater than that of the traditional strategies under the same operating conditions, and a reduction in the switching power losses.

Sequential female assessment drives complex sexual selection on bower shape in a cichlid fish

In many animals, sexual selection on male traits results from female mate choice decisions made during a sequence of courtship behaviors. We use a bower-building cichlid fish, Nyassachromis cf. microcephalus, to show how applying standard selection analysis to data on sequential female assessment provides new insights into sexual selection by mate choice. We first show that the cumulative selection differentials confirm previous results suggesting female choice favors males holding large volcano-shaped sand bowers. The sequential assessment analysis reveals these cumulative differentials are the result of selection acting on different bower dimensions during the courtship sequence; females choose to follow males courting from tall bowers, but choose to engage in premating circling with males holding bowers with large diameter platforms. The approach we present extends standard selection analysis by partitioning the variances of increasingly accurate estimates of male reproductive fitness and is applicable to systems in which sequential female assessment drives sexual selection on male traits.

Cyclosporine A Drives a Th17‐and Th2‐Mediated Posttransplant Obliterative Airway Disease

Calcineurin-inhibitor refractory bronchiolitis obliterans (BO) represents the leading cause of late graft failure after lung transplantation. T helper (Th)2 and Th17 lymphocytes have been associated with BO development. Taking advantage of a fully allogeneic trachea transplantation model in mice, we addressed the pathogenicity of Th cells in obliterative airway disease (OAD) occurring in cyclosporine A (CsA)-treated recipients. We found that CsA prevented CD8+ T cell infiltration into the graft and downregulated the Th1 response but affected neither Th2 nor Th17 responses in vivo. In secondary mixed lymphocyte cultures, CsA dramatically decreased donor-specific IFN-γ production, enhanced IL-17 production and did not affect IL-13. As CD4+ depletion efficiently prevented OAD in CsA-treated recipients, we further explored the role of Th2 and Th17 immunity in vivo. Although IL-4 and IL-17 deficient untreated mice developed an OAD comparable to wild-type recipients, a single cytokine deficiency afforded significant protection in CsA-treated recipients. In conclusion, CsA treatment unbalances T helper alloreactivity and favors Th2 and Th17 as coexisting pathways mediating chronic rejection of heterotopic tracheal allografts.

Periosteal BMP2 activity drives bone graft healing

Bone graft incorporation depends on the orchestrated activation of numerous growth factors and cytokines in both the host and the graft. Prominent in this signaling cascade is BMP2. Although BMP2 is dispensable for bone formation, it is required for the initiation of bone repair; thus understanding the cellular mechanisms underlying bone regeneration driven by BMP2 is essential for improving bone graft therapies. In the present study, we assessed the role of Bmp2 in bone graft incorporation using mice in which Bmp2 has been removed from the limb prior to skeletal formation (Bmp2(cKO)). When autograft transplantations were performed in Bmp2cKO mice, callus formation and bone healing were absent. Transplantation of either a vital wild type (WT) bone graft into a Bmp2(cKO) host or a vital Bmp2(cKO) graft into a WT host also resulted in the inhibition of bone graft incorporation. Histological analyses of these transplants show that in the absence of BMP2, periosteal progenitors remain quiescent and healing is not initiated. When we analyzed the expression of Sox9, a marker of chondrogenesis, on the graft surface, we found it significantly reduced when BMP2 was absent in either the graft itself or the host, suggesting that local BMP2 levels drive periosteal cell condensation and subsequent callus cell differentiation. The lack of integrated healing in the absence of BMP2 was not due to the inability of periosteal cells to respond to BMP2. Healing was achieved when grafts were pre-soaked in rhBMP2 protein, indicating that periosteal progenitors remain responsive in the absence of BMP2. In contrast to the requirement for BMP2 in periosteal progenitor activation in vital bone grafts, we found that bone matrix-derived BMP2 does not significantly enhance bone graft incorporation. Taken together, our data show that BMP2 signaling is not essential for the maintenance of periosteal progenitors, but is required for the activation of these progenitors and their subsequent differentiation along the osteo-chondrogenic pathway. These results indicate that BMP2 will be among the signaling molecules whose presence will determine success or failure of new bone graft strategies.

Inflammasome-dependent IFN-γ drives pathogenesis in Streptococcus pneumoniae meningitis

The pathology associated with Streptococcus pneumoniae meningitis results largely from activation of immune-associated pathways. We systematically investigated the production of IFN subtypes, as well as their influence on pathology, in a mouse model of S. pneumoniae meningitis. Despite the occurrence of a mixed IFN type I/II gene signature, no evidence for production or involvement of type I IFNs in disease progression was found. In contrast, type II IFN (IFN-γ) was strongly induced, and IFN-γ(-/-) mice were significantly protected from severe disease. Using intracellular cytokine staining and targeted cell-depletion approaches, NK cells were found to be the dominant source of IFN-γ. Furthermore, production of IFN-γ was found to be dependent upon ASC and IL-18, indicating that an ASC-dependent inflammasome pathway was responsible for mediating IFN-γ induction. The influence of IFN-γ gene deletion on a range of processes known to be involved in bacterial meningitis pathogenesis was examined. Although neutrophil numbers in the brain were similar in infected wild-type and IFN-γ(-/-) mice, both monocyte recruitment and CCL2 production were less in infected IFN-γ(-/-) mice compared with infected wild-type controls. Additionally, gene expression of NO synthase was strongly diminished in infected IFN-γ(-/-) mice compared with infected controls. Finally, bacterial clearance was enhanced in IFN-γ(-/-) mice, although the underlying mechanism remains unclear. Together, these data suggest that inflammasome-dependent IFN-γ contributes via multiple pathways to pathology during S. pneumoniae meningitis.

Isolated autosomal dominant growth hormone deficiency: stimulating mutant GH-1 gene expression drives GH-1 splice-site selection, cell proliferation, and apoptosis

The majority of mutations that cause isolated GH deficiency type II (IGHD II) affect splicing of GH-1 transcripts and produce a dominant-negative GH isoform lacking exon 3 resulting in a 17.5-kDa isoform, which further leads to disruption of the GH secretory pathway. A clinical variability in the severity of the IGHD II phenotype depending on the GH-1 gene alteration has been reported, and in vitro and transgenic animal data suggest that the onset and severity of the phenotype relates to the proportion of 17.5-kDa produced. The removal of GH in IGHD creates a positive feedback loop driving more GH expression, which may itself increase 17.5-kDa isoform productions from alternate splice sites in the mutated GH-1 allele. In this study, we aimed to test this idea by comparing the impact of stimulated expression by glucocorticoids on the production of different GH isoforms from wild-type (wt) and mutant GH-1 genes, relying on the glucocorticoid regulatory element within intron 1 in the GH-1 gene. AtT-20 cells were transfected with wt-GH or mutated GH-1 variants (5'IVS-3 + 2-bp T->C; 5'IVS-3 + 6 bp T->C; ISEm1: IVS-3 + 28 G->A) known to cause clinical IGHD II of varying severity. Cells were stimulated with 1 and 10 mum dexamethasone (DEX) for 24 h, after which the relative amounts of GH-1 splice variants were determined by semiquantitative and quantitative (TaqMan) RT-PCR. In the absence of DEX, only around 1% wt-GH-1 transcripts were the 17.5-kDa isoform, whereas the three mutant GH-1 variants produced 29, 39, and 78% of the 17.5-kDa isoform. DEX stimulated total GH-1 gene transcription from all constructs. Notably, however, DEX increased the amount of 17.5-kDa GH isoform relative to the 22- and 20-kDa isoforms produced from the mutated GH-1 variants, but not from wt-GH-1. This DEX-induced enhancement of 17.5-kDa GH isoform production, up to 100% in the most severe case, was completely blocked by the addition of RU486. In other studies, we measured cell proliferation rates, annexin V staining, and DNA fragmentation in cells transfected with the same GH-1 constructs. The results showed that that the 5'IVS-3 + 2-bp GH-1 gene mutation had a more severe impact on those measures than the splice site mutations within 5'IVS-3 + 6 bp or ISE +28, in line with the clinical severity observed with these mutations. Our findings that the proportion of 17.5-kDa produced from mutant GH-1 alleles increases with increased drive for gene expression may help to explain the variable onset progression, and severity observed in IGHD II.