Search

Shaft voltage generated in electric vehicle (EV) motors is a critical issue as it can lead to motor performance degradation and damage, potentially resulting in vehicle fault and endangering the driver’s safety. To prevent such faults, a newly structured layered shield based on flexible printed circuit board (FPCB) has been proposed, and its effectiveness in reducing shaft voltage was experimentally verified when applied to a scaled-down traction motor. This study experimentally investigates the effect of the layered shield on shaft voltage reduction in an interior permanent magnet synchronous motor (IPMSM) type EV traction motor under various operating conditions. The results demonstrate that the application of the layered shield reduced shaft voltage by 80 % in high-voltage systems, significantly enhancing motor durability and preventing faults. This paper presents the effectiveness and applicability of the layered shield in addressing shaft voltage issues in EV traction motors, highlighting its potential to prevent motor faults that are directly related to driver safety.

Recently, the motor drive system of electric vehicles (EVs) has been increased to high voltage to enhance the output and efficiency of the motor. However, higher voltage exacerbates common-mode voltage (CMV), which is the main cause of bearing faults. Due to the CMV component, shaft voltage is generated in the motor, shortening the life of the bearing and, in severe cases, causing serious motor faults due to bearing damage. Therefore, it is very important to reduce the shaft voltage of the motor. This paper proposes a method for reducing shaft voltage by applying a shield ring with a novel structure to the stator part of the interior permanent magnet synchronous motor (IPMSM). First, the parasitic capacitance and shaft voltage equivalent circuit model of the IPMSM are analyzed. The effect of shaft voltage based on the material of the shield ring is then analyzed. In addition, changes in shaft voltage magnitude are analyzed according to the shape of the shield ring. Finally, the proposed method is verified through experiments.

Static eccentricity fault (SEF) primarily occurs due to external mechanical shocks and incorrect manufacturing processes. In the case of SEF condition, vibration and noise in the electric motor are generated due to unbalanced magnetic forces. Additionally, SEF conditions lead to an increase in the iron loss of motor due to the unbalanced air gap flux density. As iron loss increases, the temperature of the main part of the motor increases, which has a negative effect. Therefore, this paper presents a robust design optimization model where the characteristics of a six-phase interior permanent magnet synchronous motor (IPMSM) do not change drastically even when SEF occurs. First, magnetic flux density, iron loss, and efficiency according to the rotor shape are analyzed using the finite element method (FEM). Second, under identical stator structure conditions, characteristics derived from the finite element method (FEM) are verified through experiments analyzing different rotor shapes. Finally, robust design optimization is performed to ensure that the motor characteristics do not change drastically even when SEF occurs.

Objectives Real-time polymerase chain reaction is currently used as a confirmatory test for coronavirus disease 2019 (COVID-19). The test results are interpreted as positive, negative, or inconclusive, and are used only for a qualitative classification of patients. However, the test results can be quantitated using threshold count (Ct) values to determine the amount of virus present in the sample. Therefore, this study investigated the diagnostic usefulness of Ct results through various quantitative analyzes, along with an analysis of clinical and epidemiological characteristics. Methods Clinical and epidemiological data from 4,642 COVID-19 patients in April 2021 were analyzed, including the Ct values of the RNA-dependent RNA polymerase (RdRp), envelope (E), and nucleocapsid (N) genes. Clinical and epidemiological data (sex, age, underlying diseases, and early symptoms) were collected through a structured questionnaire. A correlation analysis was used to examine the relationships between variables. Results All 3 genes showed statistically significant relationships with symptoms and severity levels. The Ct values of the RdRp gene decreased as the severity of the patients increased. Moreover, statistical significance was observed for the presence of underlying diseases and dyspnea. Conclusion Ct values were found to be related to patients’ clinical and epidemiological characteristics. In particular, since these factors are closely related to symptoms and severity, Ct values can be used as primary data for predicting patients’ disease prognosis despite the limitations of this method. Conducting follow-up studies to validate this approach might enable using the data from this study to establish policies for preventing COVID-19 infection and spread.

Summary: The regulatory effect of non-coding large-scale structural variations (SVs) on proto-oncogene activation remains unclear. This study investigated SV-mediated gene dysregulation by profiling 3D cancer genome maps from 40 patients with colorectal cancer (CRC). We developed a machine learning-based method for spatial characterization of the altered 3D cancer genome. This revealed a frequent establishment of “de novo chromatin contacts” that can span multiple topologically associating domains (TADs) in addition to the canonical TAD fusion/shuffle model. Using this information, we precisely identified super-enhancer (SE)-hijacking and its clonal characteristics. Clonal SE-hijacking genes, such as TOP2B, are recurrently associated with cell-cycle/DNA-processing functions, which can potentially be used as CRC prognostic markers. Oncogene activation and increased drug resistance due to SE-hijacking were validated by reconstructing the patient’s SV using CRISPR-Cas9. Collectively, the spatial and clonality-resolved analysis of the 3D cancer genome reveals regulatory principles of large-scale SVs in oncogene activation and their clinical implications.

In this paper, parameter optimization of multi-layered interior permanent-magnet synchronous motors for electric vehicle propulsion is carried out to improve torque ripple and efficiency at low- and high-speed regions. First, we establish a torque ripple map based on d-q currents. The ripples of the d-q parameters and harmonics of the phase flux linkages are then analyzed to investigate the relationship between the torque ripple and the parameters. Second, we compose and analyze an iron loss map based on d-q currents, and then investigate the parameters that affect the harmonics of the flux density. In particular, because the high-speed region is highly vulnerable to iron loss, the parameters related to this tendency are also analyzed. Based on the analysis results, we develop a parameter optimization strategy that leads to an optimal design. To analyze the electro-magnetic performances of the motors, two- and three-dimensional finite elements analyses are carried out by employing sinusoidal and inverter-controlled currents, and the improvement achieved are demonstrated by the experimental validations on prototypes.

This paper proposes a method of eliminating common-mode voltage (CMV) and shaft voltage in dual three-phase motors using the carrier phase shift of space vector pulse width modulation (SVPWM). SVPWM for the dual three-phase motor is simply implemented using two traditional three-phase SVPWM structures. The representative work of the study is to eliminate the shaft voltage by applying the carrier phase shift method due to the cancellation of CMV. It was verified that the proposed method could reduce the shaft voltage with a simple technique, rather than applying a complex algorithm to reduce it. Also, the motor current and torque behaviors are analyzed to confirm that the proposed method does not affect the motor characteristics. The proposed method has been analyzed based on an equivalent circuit model and it has been verified through the experiment that the shaft voltage is simply eliminated by applying the proposed method.

The dynamic eccentricity fault (DEF) of the interior permanent magnet synchronous motor (IPMSM) is mainly caused by external mechanical shock. In the case of DEF, an unbalanced magnetic force occurs because the length of the air gap is not constant. Noise and vibration of the motor occur due to unbalanced magnetic force. In addition, since the length of the air gap is not constant, the distribution of magnetic flux density is distorted, and iron loss is increased. As the iron loss increases, the temperature rises, and an irreversible demagnetization fault (IDF) of the permanent magnet occurs due to overheating. Therefore, in this paper, the fault mechanism of IDF due to DEF of IPMSM for electric vehicle (EV) traction is analyzed. Initially, the magnetic flux density and iron loss characteristics according to the healthy condition and DEF condition are analyzed using the finite element method (FEM). Then, the detailed iron loss analysis is performed based on the phase current waveform measured through the load test of the motor. Finally, the fault mechanism of IDF due to DEF was verified through an electric-axle load test on a manufactured motor having eccentricity.

Abstract Circulating tumor DNA (ctDNA) may reveal dynamic tumor status during therapy. We conducted serial ctDNA analysis to investigate potential association with clinical outcome in metastatic colorectal cancer (mCRC) patients receiving chemotherapy. Tissue KRAS/NRAS wild-type mCRC patients were enrolled and treated with first-line cetuximab-containing chemotherapy. ctDNA isolated from plasma were analyzed by next generation sequencing (NGS) with 16 targeted gene panel. Among 93 patients, 84 (90.3%) had at least 1 somatic mutation in baseline ctDNA samples (average 2.74). Five patients with KRAS or NRAS hotspot mutation in the ctDNA showed significantly worse progression-free survival (PFS) (p = 0.029). Changes in average variant allele frequency (VAF) in ctDNA showed significant correlation with tumor size change at the time of first response evaluation (p = 0.020) and progressive disease (PD) (p = 0.042). Patients whose average VAF decreased below cutoff (

Analyzing cell-free DNA (cfDNA) as a source of circulating tumor DNA is useful for diagnosing or monitoring patients with cancer. However, the concordance between cfDNA within liquid biopsy and genomic DNA (gDNA) within tumor tissue biopsy is still under debate. To evaluate the concordance in a clinical setting, we enrolled 54 patients with metastatic colorectal cancer and analyzed their plasma cfDNA, gDNA from peripheral blood mononuclear cells (PBMC), and gDNA from available matched tumor tissues using ultra-deep sequencing targeting 10 genes (38-kb size) recurrently mutated in colorectal cancer. We first established a highly reliable cut-off value using reference material. The sensitivity of detecting KRAS hotspot mutations in plasma was calculated as 100%, according to digital droplet PCR. We could selectively detect clinically important somatic alterations with a variant allele frequency as low as 0.18%. We next compared somatic mutations of the 10 genes between cfDNA and genomic DNA from tumor tissues and observed an overall 93% concordance rate between the two types of samples. Additionally, the concordance rate of patients with the time interval between liquid biopsy and tumor tissue biopsy within 6 months and no prior exposure to chemotherapy was much higher than those without. The patients with KRAS mutant fragments in plasma had poor prognosis than those without the mutant fragments (33 months vs. 63 months; p

Cancer tissues have characteristic DNA methylation profiles compared with their corresponding normal tissues that can be utilized for cancer diagnosis with liquid biopsy. Using a genome-scale DNA methylation approach, we sought to identify a panel of DNA methylation markers specific for cell-free DNA (cfDNA) from patients with colorectal cancer (CRC). By comparing DNA methylomes between CRC and normal mucosal tissues or blood leukocytes, we identified eight cancer-specific methylated loci (ADGRB1, ANKRD13, FAM123A, GLI3, PCDHG, PPP1R16B, SLIT3, and TMEM90B) and developed a five-marker panel (FAM123A, GLI3, PPP1R16B, SLIT3, and TMEM90B) that detected CRC in liquid biopsies with a high sensitivity and specificity with a droplet digital MethyLight assay. In a set of cfDNA samples from CRC patients (n = 117) and healthy volunteers (n = 60), a panel of five markers on the platform of the droplet digital MethyLight assay detected stages I–III and stage IV CRCs with sensitivities of 45.9% and 95.7%, respectively, and a specificity of 95.0%. The number of detected markers was correlated with the cancer stage, perineural invasion, lymphatic emboli, and venous invasion. Our five-marker panel with the droplet digital MethyLight assay showed a high sensitivity and specificity for the detection of CRC with cfDNA samples from patients with metastatic CRC.

Poly(ADP-ribose) polymerase inhibitors have been shown dramatic responses in patients with BRCAness. However, clinical studies have been limited to breast cancer patients with germline mutations. Here, we describe a patient with metastatic breast cancer who had a rare BRCA1 somatic mutation (BRCA1 c.4336G>T (p.E1446*)) detected by cell-free DNA analysis after failing standard therapies. This tier III variant of unknown significance was predicted to be a pathogenic variant in our assessment, leading us to consider off-label treatment with olaparib. The patient responded well to olaparib for several months, with a decrease in allele frequency of this BRCA1 somatic mutation in cell-free DNA. Olaparib resistance subsequently developed with an increase in the allele frequency and new BRCA1 reversion mutations. To our knowledge, this is the first report confirming BRCA1 c.4336G>T (p.E1446*) as a mutation sensitive to olaparib in breast cancer and describing the dynamic changes in the associated mutations using liquid biopsy. [ABSTRACT FROM AUTHOR]

Purpose Circulating tumor DNA (ctDNA) is emerging as a valuable non-invasive tool to identify tumor heterogeneity and tumor burden. This study investigated ctDNA dynamics in metastatic colorectal cancer patients treated with regorafenib. Materials and Methods In this prospective biomarker study, plasma cell-free DNA (cfDNA) samples obtained at baseline, at the first response evaluation after 2 cycles of treatment, and at the time of progressive disease were sequenced using a targeted nextgeneration sequencing platform which included 106 genes. Results A total of 285 blood samples from 110 patients were analyzed. Higher baseline cfDNA concentration was associated with worse progression-free survival (PFS) and overall survival (OS). After 2 cycles of treatment, variant allele frequency (VAF) in the majority of ctDNA mutations decreased with a mean relative change of -31.6%. Decreases in the VAF of TP53, APC, TCF7L2, and ROS1 after 2 cycles of regorafenib were associated with longer PFS. We used the sum of VAF at each time point as a surrogate for the overall ctDNA burden. A reduction in sum (VAF) of = 50% after 2 cycles was associated with longer PFS (6.1 vs. 2.7 months, p=0.002), OS (11.3 vs. 5.9 months, p=0.001), and higher disease control rate (86.3% vs. 51.1%, p < 0.001). VAF of the majority of the ctDNA mutations increased at the time of disease progression, and VAF of BRAF increased markedly. Conclusion Reduction in ctDNA burden as estimated by sum (VAF) could be used to predict treatment outcome of regorafenib. [ABSTRACT FROM AUTHOR]

Purpose RNA editing generates protein diversity by altering RNA sequences in coding regions without changing the overall DNA sequence. Adenosine-to-inosine (A-to-I) RNA editing events have recently been reported in some types of cancer, but they are rare in human colorectal cancer (CRC). Therefore, this study was conducted to identify diverse RNA editing in CRC. Materials and Methods We compared transcriptome data of 39 CRC samples and paired adjacent tissues from The Cancer Genome Atlas database to identify RNA editing patterns in CRC, focusing on canonical A-to-I RNA edits in coding sequence regions. We investigated nonsynonymous RNA editing patterns by comparing tumor and normal tissue transcriptome data. Results The number of RNA edits varied from 12 to 42 per sample. We also observed that hypoand hyper-RNA editing patterns were distinguishable within the samples. We found 10 recurrent nonsynonymous RNA editing candidates in nine genes (PDLIM, NEIL1, SRP9, GLI1, APMAP, IGFBP7, ZNF358, COPA, and ZNF587B) and validated some by Sanger sequencing and the inosine chemical erasing assay. We further showed that editing at these positions was performed by the adenosine deaminase acting on RNA 1 enzyme. Most of these genes are hypoedited in CRC, but editing of GLI1 was increased in cancer tissues compared with normal tissues. Conclusion Our results show that nonsynonymous RNA editing patterns can be used to identify CRC patients and could serve as novel biomarkers for CRC. [ABSTRACT FROM AUTHOR]