Tohoku University · 공학
유지 사이고 교수의 연구실은 생물학적 합성과 분자 신호 전달 메커니즘을 중심으로 한 다학제적 연구를 수행하고 있습니다. 특히 폴리하이드록시알카노산 공중합체의 미생물 합성 및 물리적·열적 특성 제어, EGFR 및 PDGF 수용체 간의 신호 교차 작용 메커니즘 규명이 핵심 연구 방향입니다. 또한 세포 내 신호 전달 경로에서 GSK3의 조절 메커니즘과 센서 배치 최적화 문제에 대한 수학적 알고리즘 개발도 함께 진행하고 있습니다. 이는 생물재료 개발과 의료 영상 진단, 생물의학적 신호 전달 이해에 응용됩니다.
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
Microbial synthesis of copolymers of [R]-3-hydroxybutyrate (3HB) and 4-hydroxybutyrate (4HB), P(3HB-co-4HB), by Alcaligenes eutrophus, Alcaligenes latus, and Comamonas acidovorans from various carbon sources has been studied. The copolyester compositions varied from 0 to 100 mol% 4HB, depending on the microorganism and the combination of carbon substrates supplied. The thermal and physical properties of compositions with 0–100 mol% 4HB were investigated. The copolyesters represented a wide varie
Previous studies showed that the epidermal growth factor receptor (EGFR) can be transactivated by platelet-derived growth factor (PDGF) stimulation and that EGFR transactivation is required for PDGF-stimulated cell migration. To investigate the mechanism for cross talk between the PDGF beta receptor (PDGFbetaR) and the EGFR, we stimulated rat aortic vascular smooth muscle cells (VSMC) with 20 ng of PDGF/ml. Transactivation of the EGFR, defined by receptor tyrosine phosphorylation, occurred with
Glycogen synthase kinase 3 (GSK3) was inhibited by 50% within 5 min when A431 cells were stimulated with epidermal growth factor (EGF). The inhibition was unaffected by rapamycin at concentrations which blocked the activation of p70 S6 kinase, and reversed by incubation with protein phosphatase-1. EGF stimulation of A431 cells inhibited GSK3 alpha and GSK3 beta to a similar extent, and inhibition was accompanied by phosphorylation of the tryptic peptides containing the serine residues phosphoryl
In this paper, the sparse sensor placement problem for least-squares estimation is considered, and the previous novel approach of the sparse sensor selection algorithm is extended. The maximization of the determinant of the matrix which appears in pseudo-inverse matrix operations is employed as an objective function of the problem in the present extended approach. The procedure for the maximization of the determinant of the corresponding matrix is proved to be mathematically the same as that of
Cardiac tamponade is usually a consequence of increased pericardial pressure with accumulation of pericardial effusion. Pericardial effusion may be caused by acute pericarditis, tumor, uremia, hypothyroidism, trauma, cardiac surgery, or other inflammatory/noninflammatory conditions. In this article we describe four scenarios illustrated by case reports where a small or apparently small pericardial effusion may produce cardiac tamponade. The first scenario illustrates how a small pericardial effu
