New methods for simultaneous measurement of R2, R2', R2*, QSM, positive and negative susceptibility maps using mGESFIDE acquisition

학위논문 (석사)-- 서울대학교 대학원 : 공과대학 컴퓨터공학부, 2018. 8. 신영길.본 연구에서는 modified gradient-echo sampling of FID and echo (mGESFIDE) 신호를 이용하여 단 5분의 촬영 시간으로 R2, R2', R2*, 정량적 자화율 영상, 양의 자화율 영상, 음의 자화율 영상을 모두 획득할 수 있는 새로운 영상처리 방법을 제시한다. 먼저 본 연구에서는 mGESFIDE 신호를 라디오 주파수의 형태와 B1 자기장의 불균일성을 고려하여 보정한 새로운 와 영상 구성 방법을 제시한다. 다음으로 mGESFIDE 신호의 모든 메아리의 위상 값을 사용하여 국소 자기장 변화를 측정하는 새로운 방법도 제시한다. 이러한 방법의 유효성을 검증하기 위해서 인 비보(In vivo)의 뇌 영상을 촬영한 뒤 기존의 방법들과 비교를 한다. 본 연구에서 제안한 새로운 영상 처리 방법은 임상적 응용이 가능한 고속 영상법이 될 수 있을 것으로 기대된다.1. Introduction 1.1. Nuclear Magnetic Resonance 1.2. Bloch Equation 1.3. Image Formation 1.4. Pulse Sequence 1.5. Quantitative MRI 1.5.1. R2 and R2' mapping 1.5.2. Quantitative Susceptibility Mapping (QSM) 2. Proposed Methods 2.1. Introduction 2.2. Methods 2.2.1. mGESFIDE pulse sequence 2.2.2. Improved R2 and R2' estimation 2.2.3. Novel local field map estimation 2.2.4. Susceptibility sources separation 2.2.5. In vivo study 2.3. Results 3. Discussion and Conclusions 4. ReferencesMaste

Saccharomyces cerevisiae에서 사람 tissue transglutaminase inhibitor의 분리 정제

학위논문(석사)--서울대학교 대학원 :의학과 생화학전공,2001.Maste

Rheological behaviors of suspensions composed of alumina powders and polymeric binders

Maste

BIX01294 inhibits EGFR signaling in EGFR-mutant lung adenocarcinoma cells through the BCKDHA-mediated reduction of EGFR levels

BIX01294 (BIX), an inhibitor of G9a histone methyltransferase, has been reported to have antitumor activity against a variety of cancers. However, the molecular mechanisms underlying its anticancer effects, particularly against lung cancer, have remained unclear. Here, we report that BIX induces apoptotic cell death in EGFR-mutant non-small cell lung cancer (NSCLC) cells, but not in their wild type counterparts. Treatment with BIX resulted in a significant reduction of EGFR levels and inhibition of EGFR signaling only in the EGFR-mutant NSCLCs, leading to apoptosis. BIX also inhibited mitochondrial metabolic function and the cellular energy levels that are critical for maintaining the EGFR level. Further, BIX transcriptionally downregulated the branched-chain α-keto acid dehydrogenase (BCKDHA) transcripts that are essential for fueling the tricarboxylic acid (TCA) cycle. Interestingly, this BCKDHA downregulation was due to an inhibition of Jumanji-domain histone demethylases but not G9a histone methyltransferase. We observed that KDM3A, one of Jumanji-domain histone demethylases, epigenetically regulates the BCKDHA expression by binding to the BCKDHA gene promoter. BIX exposure also led to a significantly decreased EGFR level, causing apoptosis in EGFR-TKI (tyrosine kinase inhibitor)-resistant cell lines, that are dependent on EGFR signaling for survival. Taken together, our current data suggest that BIX triggers apoptosis only in EGFR-mutant NSCLCs via the inhibition of BCKDHA-mediated mitochondrial metabolic function

A Preclinical Study of Human Embryonic Stem Cell-Derived Mesenchymal Stem Cells for Treating Detrusor Underactivity by Chronic Bladder Ischemia

Background The therapeutic effects of human embryonic stem cell-derived multipotent mesenchymal stem cells (M-MSCs) were evaluated for detrusor underactivity (DUA) in a rat model with atherosclerosis-induced chronic bladder ischemia (CBI) and associated mechanisms. Methods Sixteen-week-old male Sprague?Dawley rats were divided into five groups (n?=?10). The DUA groups underwent 30 bilateral repetitions of endothelial injury to the iliac arteries to induce CBI, while the sham control group underwent a sham operation. All rats used in this study received a 1.25% cholesterol diet for 8 weeks. M-MSCs at a density of 2.5, 5.0, or 10.0?×?105 cells (250 K, 500 K, or 1000 K; K?=?a thousand) were injected directly into the bladder 7 weeks post-injury, while the sham and DUA group were treated only with vehicle (phosphate buffer solution). One week after M-MSC injection, awake cystometry was performed on the rats. Then, the bladders were harvested, studied in an organ bath, and prepared for histological and gene expression analyses. Results CBI by iliac artery injury reproduced voiding defects characteristic of DUA with decreased micturition pressure, increased micturition interval, and a larger residual volume. The pathological DUA properties were improved by M-MSC treatment in a dose-dependent manner, with the 1000 K group producing the best efficacy. Histological analysis revealed that M-MSC therapy reduced CBI-induced injuries including bladder fibrosis, muscular loss, and apoptosis. Transplanted M-MSCs mainly engrafted as vimentin and NG2 positive pericytes rather than myocytes, leading to increased angiogenesis in the CBI bladder. Transcriptomes of the CBI-injured bladders were characterized by the complement system, inflammatory, and ion transport-related pathways, which were restored by M-MSC therapy. Conclusions Single injection of M-MSCs directly into the bladder of a CBI-induced DUA rat model improved voiding profiles and repaired the bladder muscle atrophy in a dose-dependent manner

Small-sized mesenchymal stem cells with high glutathione dynamics show improved therapeutic potency in graft-versus-host disease

Small-sized mesenchymal stem cells with high glutathione dynamics show improved therapeutic potency in graft-versus-host diseas