A5003356554- Islamic Finance and Communication
- Mast cells and histamine
- Gastrointestinal Tumor Research and Treatment
- Synthesis and Catalytic Reactions
- Cardiovascular Disease and Adiposity
- Phosphodiesterase function and regulation
- Synthesis of β-Lactam Compounds
- Cardiac Structural Anomalies and Repair
- Cardiovascular Health and Disease Prevention
- Helicobacter pylori-related gastroenterology studies
- Cardiovascular Function and Risk Factors
- NF-κB Signaling Pathways
- Blood Pressure and Hypertension Studies
- Physics of Superconductivity and Magnetism
- Immune Cell Function and Interaction
- Heart Failure Treatment and Management
- Color perception and design
- Mechanical Circulatory Support Devices
- Textile materials and evaluations
- Engineering Applied Research
- Superconductivity in MgB2 and Alloys
- melanin and skin pigmentation
- Superconducting Materials and Applications
- Acute Myocardial Infarction Research
Otsuka (Japan)
2024
Osaka Metropolitan University
2024
Tohoku University
2004-2021
In assessing the effects of smoking cessation on endothelial function, low-flow-mediated constriction (L-FMC) may provide complementary information to flow-mediated dilation (FMD). However, value total (FMTD), an index that incorporates L-FMC into FMD, remains underreported. We aimed evaluate effect as assessed by FMD and FMTD, clarify its associated clinical factors. enrolled 118 consecutive current smokers without previous coronary artery disease (72.9% were men; age: 59 ± 11 years) who...
For a future design of fusion power plant, concept remountable SC magnet is proposed to improve cost performance. In this butt jointing HT_C used as method and contact force can be obtained from electromagnetic indu
Abstract Purpose: Gastrointestinal stromal tumor (GIST), the most common mesenchymal with KIT or PDGFRA driver mutations, is typically treated tyrosine kinase inhibitors (TKI). However, resistance to TKIs due secondary mutations a challenge in advanced GISTs. In addition, there are currently no effective therapies for several other molecular subtypes, such as succinate dehydrogenase–deficient Therefore, novel therapeutic strategies needed. Experimental Design: To address this need, we tested...
<div>AbstractPurpose:<p>Gastrointestinal stromal tumor (GIST), the most common mesenchymal with <i>KIT</i> or <i>PDGFRA</i> driver mutations, is typically treated tyrosine kinase inhibitors (TKI). However, resistance to TKIs due secondary mutations a challenge in advanced GISTs. In addition, there are currently no effective therapies for several other molecular subtypes, such as succinate dehydrogenase–deficient Therefore, novel therapeutic strategies...
<p>Supplementary Fig. S3. Antagonistic effect of cilostamide on the anticancer activity OPB-171775</p>
<p>Supplementary Fig. S5. Flow cytometric analysis of cell cycle arrest and death induced by OPB-171775</p>
<p>Supplementary Fig. S5. Flow cytometric analysis of cell cycle arrest and death induced by OPB-171775</p>
<p>Supplementary Fig. S2. Coexpression of PDE3A and SLFN12 as sensitivity factors for OPB-171775</p>
<p>Supplementary Fig. S2. Coexpression of PDE3A and SLFN12 as sensitivity factors for OPB-171775</p>
<div>AbstractPurpose:<p>Gastrointestinal stromal tumor (GIST), the most common mesenchymal with <i>KIT</i> or <i>PDGFRA</i> driver mutations, is typically treated tyrosine kinase inhibitors (TKI). However, resistance to TKIs due secondary mutations a challenge in advanced GISTs. In addition, there are currently no effective therapies for several other molecular subtypes, such as succinate dehydrogenase–deficient Therefore, novel therapeutic strategies...
<p>Supplementary Fig. S1. PDE3A mRNA expression in PDX tumors and <i>in vivo</i> efficacy of OPB-171775</p>
<p>Supplementary Fig. S1. PDE3A mRNA expression in PDX tumors and <i>in vivo</i> efficacy of OPB-171775</p>
<p>Supplementary Fig. S3. Antagonistic effect of cilostamide on the anticancer activity OPB-171775</p>
<p>Supplementary Fig. S6. Effects of OPB-171775 on cell cycle and its combination with imatinib in GIST</p>
<p>Supplementary Fig. S4. GCN2 phosphorylation and downstream signaling induced by OPB-171775.</p>
<p>Supplementary Fig. S4. GCN2 phosphorylation and downstream signaling induced by OPB-171775.</p>
<p>Supplementary Fig. S6. Effects of OPB-171775 on cell cycle and its combination with imatinib in GIST</p>