Dong-Youn Kim

Signal Compensation for Analog Rotor Position Errors due to Nonideal Sinusoidal Encoder Signals

This paper proposes a compensation algorithm for the analog rotor position errors caused by nonideal sinusoidal encoder output signals including offset and gain errors. In order to achieve a much higher resolution, position sensors such as resolvers or incremental encoders can be replaced by sinusoidal encoders. In practice, however, the periodic ripples related to the analog rotor position are generated by the offset and gain errors between the sine and cosine output signals of sinusoidal encoders. In this paper, the effects of offset and gain errors are easily analyzed by applying the concept of a rotating coordinate system based on the dq transformation method. The synchronous d-axis signal component is used directly to detect the amplitude of the offset and gain errors for the proposed compensator. As a result, the offset and gain errors can be well corrected by three integrators located on the synchronous d-axis component. In addition, the proposed algorithm does not require any additional hardware and can be easily implemented by a simple integral operation. The effectiveness of the proposed algorithm is verified through several experimental results.

A Control Method for Power-Assist Devices using a BLDC Motor for Manual Wheelchairs

This paper proposes a new operation and control strategy for Power-Assisted Wheelchairs (PAW) using one brushless DC (BLDC) motor. The conventional electrical wheelchairs are too heavy and large for one person to move because they have two electric motor wheels. On the other hand, the proposed PAW system has a small volume and is easy to move due to the presence of a single wheel motor. Unlike the conventional electric wheelchairs, this structure for a PAW does not have a control joystick to reduce its weight and volume. To control the wheelchair without a joystick, a special control system and algorithm are needed for proper operation of the wheelchair. In the proposed PAW system uses only one sensor to detect the acceleration and direction of PAW’s movement. By using this sensor, speed control can be achieved. With a speed control system, there are three kinds of operations that can be done on the speed of a PAW: the increment of PAW speed by summing external force, the decrement of PAW speed by subtracting external force, and emergency breaking by evaluating the time duration of external force. The validity of the proposed algorithm is verified through experimental results.

Compensation of Current Offset Error in Half-Bridge PWM Inverter for Linear Compressor

This paper proposes a novel compensation algorithm of current offset error for single-phase linear compressor in home appliances. In a half-bridge inverter, current offset error may cause unbalanced DC-link voltage when the DC-link is comprised of two serially connected capacitors. To compensate the current measurement error, the synchronous reference frame transformation is used for detecting the measurement error. When an offset error occurs in the output current of the half-bridge inverter, the d-axis current has a ripple with frequency equal to the fundamental frequency. With the use of a proportional-resonant controller, the ripple component can be removed, and offset error can be compensated. The proposed compensation method can easily be implemented without much computation and additional hardware circuit. The validity of the proposed algorithm is verified through experimental results.

Sensorless control method of 3-Phase BLDC motor through the real time compensation of back-EMF constant

This paper proposes the novel sensorless control algorithm for 3-Phase BLDC motors with trapezoidal back-EMF. The proposed algorithms include both the new back-EMF estimation method by using the DC current model and a compensator for the electric parameter errors of the BLDC motor to improve performance of sensorless control more exactly. The back-EMF can be easily calculated from the electrical voltage equation. However, it has some errors at the commutation period. This error can be reduced by using the proposed sensorless control algorithm which is derived by using the mechanical and electrical equation simultaneously for the accurate estimation of the back-EMF. In this case, the back-EMF estimation is affected by the electric parameters. If the motor parameters have errors, there will be some errors of the estimated back-EMF. Therefore, a new algorithm is needed for parameter error compensation. Among the motor parameters, stator resistor and back-EMF constant are mainly affected by the temperature. Therefore, this paper proposes the new sensorless control algorithm with the real time compensation of the motor parameter variation according to temperature. The main attractive features of the proposed algorithm have the robustness to the parameter variation and the transient state, and the less torque ripple by using the DC-current model. The usefulness of the proposed sensorless control method is verified through the simulation.

Research of PWM Modulation for Regeneration Braking of BLDC Motor

This paper proposes a regeneration braking algorithm for Brushless DC (BLDC) motor system. The unipolar switching method has a limitation about the regeneration braking when the BLDC motor is operated in the low speed region. The proposed algorithm alternatively utilizes the unipolar and bipolar switching method to implement the regeneration braking for overall speed range. The bipolar switching method is used when the BLDC motor is operated in the low speed region. The switching transition point is determined by analyzing the unipolar and bipolar switching during the regeneration braking. The effectiveness of proposed algorithm is verified by using the experimental results.

G.P.234

Spinal muscular atrophy (SMA) is a heterogeneous neuromuscular disease of progressive degeneration of anterior horn motor neuron due to homozygous mutation of the survival motor neuron gene (SMN1). Recently, the difference in the SMN2 copy number is considered a critical factor influencing the severity of the disease. We present 2 patients of the same family diagnosed as late onset SMA, genetically confirmed to have homozygous deletion of exon 7 and 8 in SMN1 but showed marked intra-familial variability due to difference in the SMN2 copy number variation. A 43-year old female patient presented with progressive proximal limb weakness which started during high school but did not deteriorate until her age of 40. She visited our clinic at the age of 43 when she started to have difficulty in hiking. Her elder brother was also affected but remarkably more severe in weakness. He had running difficulties during high school but his limb weakness significantly deteriorated to lose independent ambulation since late teen. After nerve conduction study, needle electromyography, muscle imaging and genetic studies, SMN1 revealed the deletion of exon 7 and 8 to make genetic diagnosis of late onset type III SMA. We also measured copy number of SMN2 by MLPA method. Interestingly, SMN2 copy number inversely matched with the severity showing 4 copies with the proband, 3 copies with her brother. We clearly demonstrated the presence of phenotypic variability within the same family, clinically and neuro-radiologically, and it matched with the difference in SMN2 copy numbers. We suggest that SMN2 copy number may be a valuable tool to explain intra-familial variability of SMA severity, and to predict the prognosis with better precision.

G.P.260

Nemaline myopathy (NM) is a clinically heterogeneous congenital myopathy characterized by the presence of nemaline rods in the skeletal muscle fibers. We investigated the clinical variation and pathological features in Korean patients with NM. Thirteen patients were diagnosed through muscle biopsy. Six patients had the typical congenital type, which showed the motor development delay and hypotonia at birth. Six patients showed the mild childhood type with the gait disturbance. One patient had the intermediate congenital type, who needed mechanical ventilation. Regarding the distribution of weakness, five patients presented distal dominant weakness across the clinical type. High arched palates and feet deformity were observed. Equino varus deformity was identified in two patients. But, we could not find the cardiac muscle involvement. Typical nemaline rods were recognized on light microscopy with muscle biopsy from 11 patients. However, we could identify the nemaline filamentous aggregation in electro microscope (EM) from 2 patients. One of them showed a mitochondrial abnormality in EM. Type 1 fiber predominance was in all patients. The causative mutation form 8 patients was investigated, we found a missense heterozygous mutation in exon 1 of TPM3 gene (c.32T>A, p.Met11Lys). Seven patients showed negative results in ACTA1 gene. The thirteen patients in this study did not share much common feature except the dysmorphic appearance. The clinical diversity was prominent with the distribution of muscle weakness and the severity of respiratory dysfunction. This study showed the phenotypic heterogeneity of NM is not only with clinical features but also with pathological findings in our patient pool. Wider application of whole exome sequencing may help overcome the phenotypic and genotypic diversity in the diagnosis of NM.

G.P.267

Nebulin is a giant sarcomeric protein spanning whole length of thin filament, and its coding gene (NEB) mostly causes autosomal recessive nemaline myopathy. The NEB mutations may also cause distal nebulin myopathy with initial presentation of foot drop, and recent reports added another muscle disease of core-rod myopathy with double presentation of nemaline rods and cores. In this study, two patients with nemaline rods in muscle pathology were recruited, one of whom (patient 1) was the proband of a symptomatic sibling. Patient 1 initially presented with foot drop and has been a slow runner since childhood. His fourth elder brother also complained of foot drop and gait disturbance. Patient 2 had gait disturbance since age 5, and his ankle dorsiflexors were the most weak among all muscles. All the patients were still ambulant and never complained of respiratory restriction. Muscle CT scans revealed atrophy of anterior tibial muscles in both of patients. Muscle pathology additionally showed core lesions and mitochondrial abnormalities, as well as nemaline rods. Nemaline myopathy-causing genes were first excluded and then, whole exome sequencing and followed targeted sequencing were detected three novel mutations in NEB gene: one missense, one single bp deletion and del/ins mutations. One missense mutation was shared by all of them. This study represents the disease associated with novel NEB mutations marked by the presence of additional pathological features, as well as nemaline rods. Although mixed pathology has been already reported in core-rod myopathy with NEB mutations, muscle pathology in these patients is more characteristic, and clinical manifestation is much milder compared with the previous ones. This report suggests the expanded clinical and pathological spectrum of nebulin-associated myopathy with new genetic and pathologic features. Further, next genome sequencing might be helpful for searching mutations in big, huge-sized genes, such as NEB.

G.P.286

In silico prediction tools for genetic variation have now become the commodity in genetic analysis. Each tool utilizes their own algorithm to give us the results. Dysferlin (DYSF) is a transmembrane protein, crucial for sarcolemmal repair, and its recessive genetic defects bring about progressive muscular weakness either as Miyoshi distal myopathy or limb girdle muscular dystrophy 2B. The Leiden database lists one of the most corroborating data set on the pathogenicity of each genotype in the field of muscular dystrophy. In this study, we compared the in silico analysis results and the published pathogenicity of the dysferlin mutations listed on Leiden database. We suggest a new cut-off value that can be optimally used to test a new mutation with in silico tools. We used PROVEAN and SIFT online software to predict a possibly damaging mutation. This is a prediction tool used mainly to test the impact on the biological function of a protein by a missense mutation or amino acid substitution. We used the Leiden open variation database on dysferlin mutations and utilized the complete sequence variants data provided by the website. PROVEAN tool showed a remarkably better result to test dysferlin nonsense mutations than SIFT tool. On using PROVEAN tool for dysferlin missense mutation, we propose a new cut-off value of −5.365. Individualized cut-off values for other genes will expand the usefulness of in silico prediction tools.

P.12.9 Electrophysiological characterization of novel CLCN1 mutations found in Korean patients with myotonia congenita

Myotonia congenita is the most common non-dystrophic channelopathy of the skeletal muscle. It is characterized by clinical myotonia on voluntary contraction, accompanied by warm-up alleviation with repeated movements. Mutations of the chloride channel gene (CLCN1) are responsible for the disease. Both autosomal dominant and recessive inheritance patterns are reported, while recessive cases are more frequent. We analyzed 38 Korean patients with myotonia congenita. Twelve mutations were found and 8 of them were novel. Patch clamp recording revealed significant difference between mutated genes and WT in current density, current–voltage curve, and open probability. Noteworthy of them were 2 peculiar mutations, R47W and A298T, found together as compound heterozygotes in 6 patients. To our best knowledge, they have not been reported to cause any disease phenotype and R47W is even listed in dbSNP as minor allele. R47W is coded from exon 1 and located at N-terminal; A298T is from exon 8, the hotspot of CLCN1 mutation and reside in domain V. By electrophysiologic techniques we could successfully show the pathogenicity of CLCN1 mutations in Korean patients with myotonia congenita. Mild electrophysiological abberation of R47W may explain the paucity of its homozygous patients despite its relatively high allele frequency. However, compound heterozygosity of R47W with A298T disclosed typical electrophysiologic abnormality in myotonia congenita. Further study on heterodimeric interaction of chloride channel protein is warranted to better understand its function and abnormalities.