Active vibration control of rotating machines

Second order matrix equations arise in the description of real dynamical systems. Traditional modal control approaches utilise the eigenvectors of the undamped system to diagonalise the system matrices. Any remaining off-diagonal terms in the modal damping matrix are discarded. A regrettable automatic consequence of this action is the destruction of any notion of the skew-symmetry in the damping. The methods presented in this thesis use the `Lancaster Augmented Matrices' (LAMs) allowing state space representations of the second order systems. `Structure preserving transformations' (SPTs) are used to manipulate the system matrices whilst preserving the structure within the LAMs. Utilisation of the SPTs permits the diagonalisation of the system mass, damping and stiffness matrices for non-classically damped systems. Thus a modal control method is presented in this thesis which exploits this diagonalisation. The method introduces independent modal control in which a separate modal controller is designed in modal space for each individual mode or pair of modes. The modal displacements and velocities for the diagonalised systems are extracted from the physical quantities using first order SPT-based filters. Similarly the first order filters are used to translate the modal force into the physical domain. Derivation of the SPT-filters is presented together with a method by which one exploits the non-uniqueness of the diagonalising filters such that initially unstable filters are stabilised. In the context of active control of rotating machines, standard optimal controller methods enable a trade-off to be made between (weighted) mean-square vibrations and (weighted) mean-square control forces, or in the case of a machines controlled using magnetic bearings the currents injected into the magnetic bearings. One shortcoming of such controllers for magnetic bearings is that no concern is devoted to the voltages required. In practice, the voltage available imposes a strict limitation on the maximum possible rate of change of control force (force slew rate). This thesis presents a method which removes the aforementioned existing shortcomings of traditional optimal control. Case studies of realistic rotor systems are presented to illustrate the modal control and control force rate penalisation methods. The system damping matrices of the case studies contain skew-symmetric components due to gyroscopic forces typical of rotating machines. The SPT-based modal control method is used to decouple the non-classically damped equations of motion into n single degree of freedom systems. Optimal modal controllers are designed independently in the modal space such that the modal state, modal forces and modal force rates are weighted as required. The SPT-based modal control method is shown to yield superior results to the conventional notion of independent modal space control according to reasonable assessment

Active vibration control of rotating machines

Second order matrix equations arise in the description of real dynamical systems. Traditional modal control approaches utilise the eigenvectors of the undamped system to diagonalise the system matrices. Any remaining off-diagonal terms in the modal damping matrix are discarded. A regrettable automatic consequence of this action is the destruction of any notion of the skew-symmetry in the damping. The methods presented in this thesis use the `Lancaster Augmented Matrices' (LAMs) allowing state space representations of the second order systems. `Structure preserving transformations' (SPTs) are used to manipulate the system matrices whilst preserving the structure within the LAMs. Utilisation of the SPTs permits the diagonalisation of the system mass, damping and stiffness matrices for non-classically damped systems. Thus a modal control method is presented in this thesis which exploits this diagonalisation. The method introduces independent modal control in which a separate modal controller is designed in modal space for each individual mode or pair of modes. The modal displacements and velocities for the diagonalised systems are extracted from the physical quantities using first order SPT-based filters. Similarly the first order filters are used to translate the modal force into the physical domain. Derivation of the SPT-filters is presented together with a method by which one exploits the non-uniqueness of the diagonalising filters such that initially unstable filters are stabilised. In the context of active control of rotating machines, standard optimal controller methods enable a trade-off to be made between (weighted) mean-square vibrations and (weighted) mean-square control forces, or in the case of a machines controlled using magnetic bearings the currents injected into the magnetic bearings. One shortcoming of such controllers for magnetic bearings is that no concern is devoted to the voltages required. In practice, the voltage available imposes a strict limitation on the maximum possible rate of change of control force (force slew rate). This thesis presents a method which removes the aforementioned existing shortcomings of traditional optimal control. Case studies of realistic rotor systems are presented to illustrate the modal control and control force rate penalisation methods. The system damping matrices of the case studies contain skew-symmetric components due to gyroscopic forces typical of rotating machines. The SPT-based modal control method is used to decouple the non-classically damped equations of motion into n single degree of freedom systems. Optimal modal controllers are designed independently in the modal space such that the modal state, modal forces and modal force rates are weighted as required. The SPT-based modal control method is shown to yield superior results to the conventional notion of independent modal space control according to reasonable assessment

Modal Control of Vibration in Rotating Machines and Other Generally Damped Systems

Second order matrix equations arise in the description of real dynamical systems. Traditional modal control approaches utilise the eigenvectors of the undamped system to diagonalise the system matrices. A regrettable consequence of this approach is the discarding of residual off-diagonal terms in the modal damping matrix. This has particular importance for systems containing skew-symmetry in the damping matrix which is entirely discarded in the modal damping matrix. In this paper a method to utilise modal control using the decoupled second order matrix equations involving non-classical damping is proposed. An example of modal control successfully applied to a rotating system is presented in which the system damping matrix contains skew-symmetric components

Modal Control of Vibration in Rotating Machines and Other Generally Damped Systems

Second order matrix equations arise in the description of real dynamical systems. Traditional modal control approaches utilise the eigenvectors of the undamped system to diagonalise the system matrices. A regrettable consequence of this approach is the discarding of residual o-diagonal terms in the modal damping matrix. This has particular importance for systems containing skew-symmetry in the damping matrix which is entirely discarded in the modal damping matrix. In this paper a method to utilise modal control using the decoupled second order matrix equations involving nonclassical damping is proposed. An example of modal control sucessfully applied to a rotating system is presented in which the system damping matrix contains skew-symmetric components

Inherited variation in immune genes and pathways and glioblastoma risk

To determine whether inherited variations in immune function single-nucleotide polymorphisms (SNPs), genes or pathways affect glioblastoma risk, we analyzed data from recent genome-wide association studies in conjunction with predefined immune function genes and pathways. Gene and pathway analyses were conducted on two independent data sets using 6629 SNPs in 911 genes on 17 immune pathways from 525 glioblastoma cases and 602 controls from the University of California, San Francisco (UCSF) and a subset of 6029 SNPs in 893 genes from 531 cases and 1782 controls from MD Anderson (MDA). To further assess consistency of SNP-level associations, we also compared data from the UK (266 cases and 2482 controls) and the Mayo Clinic (114 cases and 111 controls). Although three correlated epidermal growth factor receptor (EGFR) SNPs were consistently associated with glioblastoma in all four data sets (Mantel–Haenzel P values = 1 × 10−5 to 4 × 10−3), independent replication is required as genome-wide significance was not attained. In gene-level analyses, eight immune function genes were significantly (minP < 0.05) associated with glioblastoma; the IL-2RA (CD25) cytokine gene had the smallest minP values in both UCSF (minP = 0.01) and MDA (minP = 0.001) data sets. The IL-2RA receptor is found on the surface of regulatory T cells potentially contributing to immunosuppression characteristic of the glioblastoma microenvironment. In pathway correlation analyses, cytokine signaling and adhesion–extravasation–migration pathways showed similar associations with glioblastoma risk in both MDA and UCSF data sets. Our findings represent the first systematic description of immune genes and pathways that characterize glioblastoma risk

Combining Asian and European genome-wide association studies of colorectal cancer improves risk prediction across racial and ethnic populations

Polygenic risk scores (PRS) have great potential to guide precision colorectal cancer (CRC) prevention by identifying those at higher risk to undertake targeted screening. However, current PRS using European ancestry data have sub-optimal performance in non-European ancestry populations, limiting their utility among these populations. Towards addressing this deficiency, we expand PRS development for CRC by incorporating Asian ancestry data (21,731 cases; 47,444 controls) into European ancestry training datasets (78,473 cases; 107,143 controls). The AUC estimates (95% CI) of PRS are 0.63(0.62-0.64), 0.59(0.57-0.61), 0.62(0.60-0.63), and 0.65(0.63-0.66) in independent datasets including 1681-3651 cases and 8696-115,105 controls of Asian, Black/African American, Latinx/Hispanic, and non-Hispanic White, respectively. They are significantly better than the European-centric PRS in all four major US racial and ethnic groups (p-values < 0.05). Further inclusion of non-European ancestry populations, especially Black/African American and Latinx/Hispanic, is needed to improve the risk prediction and enhance equity in applying PRS in clinical practice

Genome-wide association analysis implicates dysregulation of immunity genes in chronic lymphocytic leukaemia

Several chronic lymphocytic leukaemia (CLL) susceptibility loci have been reported; however, much of the heritable risk remains unidentified. Here we perform a meta-analysis of six genome-wide association studies, imputed using a merged reference panel of 1,000 Genomes and UK10K data, totalling 6,200 cases and 17,598 controls after replication. We identify nine risk loci at 1p36.11 (rs34676223, P=5.04 × 10−13), 1q42.13 (rs41271473, P=1.06 × 10−10), 4q24 (rs71597109, P=1.37 × 10−10), 4q35.1 (rs57214277, P=3.69 × 10−8), 6p21.31 (rs3800461, P=1.97 × 10−8), 11q23.2 (rs61904987, P=2.64 × 10−11), 18q21.1 (rs1036935, P=3.27 × 10−8), 19p13.3 (rs7254272, P=4.67 × 10−8) and 22q13.33 (rs140522, P=2.70 × 10−9). These new and established risk loci map to areas of active chromatin and show an over-representation of transcription factor binding for the key determinants of B-cell development and immune response

Pleiotropic Associations of Risk Variants Identified for Other Cancers With Lung Cancer Risk: The PAGE and TRICL Consortia

BackgroundGenome-wide association studies have identified hundreds of genetic variants associated with specific cancers. A few of these risk regions have been associated with more than one cancer site; however, a systematic evaluation of the associations between risk variants for other cancers and lung cancer risk has yet to be performed.MethodsWe included 18023 patients with lung cancer and 60543 control subjects from two consortia, Population Architecture using Genomics and Epidemiology (PAGE) and Transdisciplinary Research in Cancer of the Lung (TRICL). We examined 165 single-nucleotide polymorphisms (SNPs) that were previously associated with at least one of 16 non–lung cancer sites. Study-specific logistic regression results underwent meta-analysis, and associations were also examined by race/ethnicity, histological cell type, sex, and smoking status. A Bonferroni-corrected P value of 2.5×10–5 was used to assign statistical significance.ResultsThe breast cancer SNP LSP1 rs3817198 was associated with an increased risk of lung cancer (odds ratio [OR] = 1.10; 95% confidence interval [CI] = 1.05 to 1.14; P = 2.8×10–6). This association was strongest for women with adenocarcinoma (P = 1.2×10–4) and not statistically significant in men (P = .14) with this cell type (P het by sex = .10). Two glioma risk variants, TERT rs2853676 and CDKN2BAS1 rs4977756, which are located in regions previously associated with lung cancer, were associated with increased risk of adenocarcinoma (OR = 1.16; 95% CI = 1.10 to 1.22; P = 1.1×10–8) and squamous cell carcinoma (OR = 1.13; CI = 1.07 to 1.19; P = 2.5×10–5), respectively.ConclusionsOur findings demonstrate a novel pleiotropic association between the breast cancer LSP1 risk region marked by variant rs3817198 and lung cancer risk

Genome-wide association analysis implicates dysregulation of immunity genes in chronic lymphocytic leukaemia

Several chronic lymphocytic leukaemia (CLL) susceptibility loci have been reported; however, much of the heritable risk remains unidentified. Here we perform a meta-analysis of six genome-wide association studies, imputed using a merged reference panel of 1,000 Genomes and UK10K data, totalling 6,200 cases and 17,598 controls after replication. We identify nine risk loci at 1p36.11 (rs34676223, P=5.04 × 10−13), 1q42.13 (rs41271473, P=1.06 × 10−10), 4q24 (rs71597109, P=1.37 × 10−10), 4q35.1 (rs57214277, P=3.69 × 10−8), 6p21.31 (rs3800461, P=1.97 × 10−8), 11q23.2 (rs61904987, P=2.64 × 10−11), 18q21.1 (rs1036935, P=3.27 × 10−8), 19p13.3 (rs7254272, P=4.67 × 10−8) and 22q13.33 (rs140522, P=2.70 × 10−9). These new and established risk loci map to areas of active chromatin and show an over-representation of transcription factor binding for the key determinants of B-cell development and immune response