http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Noise reduction method for PHMR bridge sensor by resistance compensator
byeonghwa Lim,Jaehoon Lee,Changyeop Jeon,Cheol Gi Kim 한국자기학회 2021 한국자기학회 학술연구발표회 논문개요집 Vol.31 No.1
MR sensors are of great interest in industrial and medical applications due to their high sensitivity, portable size, and low cost. However, the noise of the MR sensor limits the sensitivity and requires complex signal processing, which limits the utilization of the sensor. To utilize the MR sensor effectively, it is necessary to increase the sensitivity of the sensor and reduce the noise. For this purpose, a self-balancing bridge type sensor with integrated resistance compensator for noise reduction in the frequency range from 0.5 Hz to 200 Hz has been devised. The proposed resistance compensator integrated with the self-bridge sensor architecture adjusted the offset voltage compensation at the Wafer level and significantly improved the sensor noise level. As a result, we achieved the lowest noise of 3.34nV/√Hz at about 100Hz. It was also confirmed that thermal drift was significantly reduced through offset voltage compensation. Therefore, the developed sensor can be used in various industrial and medical applications.
임병화(Byeonghwa Lim),김철기(CheolGi Kim) 한국자기학회 2020 韓國磁氣學會誌 Vol.30 No.5
Biomedical convergence technology based on magnetic technology has been potential ranges from expensive medical equipment such as MRI and MEG that can be used in large hospitals to laboratory-level equipment such as molecular diagnostic equipment, and simple devices that can be used by individuals such as immunochromatography. Until now, they are active in various fields in the field of disease diagnosis. Diagnosis technology using magnetic sensors and magnetic nanoparticles shows the possibility of developing small, portable equipment with diagnostic capabilities comparable to those of medical equipment used in hospitals. In addition to such disease diagnosis, various studies are being conducted as a next-generation biomedical technology such as manipulation of cell location and remote control of nerve cells. This paper briefly summarizes the previously described studies and introduces recent research trends in molecules(microscopic), cells(mesoscopic), organs and bodies(macroscopic) studies.
Lim, Sangyong,Yun, Jiae,Yoon, Hyunjin,Park, Chehwee,Kim, Boowon,Jeon, Byeonghwa,Kim, Dongho,Ryu, Sangryeol Oxford University Press 2007 Nucleic acids research Vol.35 No.6
<P>The global regulator Mlc is a repressor of several genes and operons that are involved in sugar uptake and metabolism. A <I>Salmonella enterica</I> serovar Typhimurium <I>mlc</I> mutant showed reduced levels of invasion and cytotoxicity compared to the wild-type, and exhibited reduced expression levels of <I>hilD</I>, <I>hilA</I> and <I>invF</I>, which are regulatory genes in the <I>Salmonella</I> pathogenicity island 1 (SPI1). However, the effects of Mlc on <I>hilD</I> expression and bacterial invasiveness were not seen in the <I>hilE</I> mutant, and <I>hilE</I> expression was increased in the <I>mlc</I> mutant, which suggests that Mlc exerts positive effects on the expression of SPI1 genes by reducing the expression of HilE, which is known to down-regulate the expression of SPI1 genes through direct interaction with HilD. We found that the two known promoters of <I>hilE</I> were not modulated by Mlc, and we identified a third promoter, designated P3, which was repressed by Mlc. The gel mobility shift assay and footprinting analysis revealed that Mlc repressed <I>hilE</I> in a direct manner by binding to two distinct sites in the <I>hilE</I> P3 promoter region. The specific down-regulation of <I>hilD</I> observed in the presence of Mlc regulon-inducible sugars, such as glucose and mannose, could not be detected in the <I>mlc</I> mutant. Based on these results, we propose that Mlc functions to sense the availability of sugars and is linked to virulence gene regulation by its ability to control <I>hilE</I> expression in <I>Salmonella</I>.</P>