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WoS SCOPUS Document Type Document Title Abstract Authors Affiliation ResearcherID (WoS) AuthorsID (SCOPUS) Author Email(s) Journal Name JCR Abbreviation ISSN eISSN Volume Issue WoS Edition WoS Category JCR Year IF JCR (%) FWCI FWCI Update Date WoS Citation SCOPUS Citation Keywords (WoS) KeywordsPlus (WoS) Keywords (SCOPUS) KeywordsPlus (SCOPUS) Language Publication Stage Publication Year Publication Date DOI JCR Link DOI Link WOS Link SCOPUS Link
Article Atomic-scale operando observation of oxygen diffusion during topotactic phase transition of a perovskite oxide Topotactic phase transition of perovskite oxides enables fast, reversible oxygen transport with minimal volume change, which is advantageous for applications in solid oxide fuel cells. However, the oxygen-diffusion mechanism remains elusive due to the lack of direct atomic-scale observations. Here, we report operando atomic-scale observation and simulation revealing the diffusion mechanism during the topotactic transition of perovskite SrFeO3 to brownmillerite SrFeO2.5. Hyper-stoichiometric brownmillerite phase containing excess oxygen emerges at the phase boundary facilitates oxygen diffusion; oxygen diffuses predominantly along the FeO4 tetrahedral chains via sequential modification of oxygen coordination between FeO(4 )and FeO5. A steady-state oxygen diffusion is attained through interstitialcy diffusion across the fast-diffusion channels, which accommodates excess oxygen at the interstitial sites between SrO columns. The flexibility of multivalent Fe ions in accommodating various oxygen coordination and the rigidity of Sr lattice framework embracing excess oxygen are key to the fast, anisotropic oxygen diffusion. Xing, Yaolong; Kim, Inhwan; Kang, Kyeong Tae; Park, Bumsu; Wang, Zhen; Kim, Jong Chan; Jeong, Hu Young; Choi, Woo Seok; Lee, Jaekwang; Oh, Sang Ho Sungkyunkwan Univ, Dept Energy Sci, Suwon 16419, South Korea; Pusan Natl Univ, Dept Phys, Busan 46241, South Korea; Sungkyunkwan Univ, Dept Phys, Suwon 16419, South Korea; Kyungpook Natl Univ, Dept Phys, Daegu 41566, South Korea; CEMES CNRS, F-31055 Toulouse, France; Ulsan Natl Inst Sci & Technol, Sch Mat Sci & Engn, Ulsan 44919, South Korea; Korea Inst Energy Technol KENTECH, KENTECH Inst Energy Mat & Devices, Dept Energy Engn, Naju 58330, South Korea ; Choi, Woo Seok/G-8783-2014; Jeong, Hu/H-4413-2016; Oh, Sang Ho/AAG-1891-2020; Xing, Yaolong/MXJ-9903-2025 57220044509; 57226310158; 56002123900; 57199406153; 57209967922; 24293021400; 56463365400; 14031133800; 55888626200; 57558169000 choiws@skku.edu;jaekwangl@pusan.ac.kr;shoh@kentech.ac.kr; MATTER MATTER-US 2590-2393 2590-2385 5 9 SCIE MATERIALS SCIENCE, MULTIDISCIPLINARY 2022 18.9 4.8 1.08 2025-06-25 18 16 FUEL-CELL CATHODE; REDOX REACTIONS; TEMPERATURE; DYNAMICS; POINTS high-resolution transmission electron microscopy; in situ transmission electron microscopy; MAP1: Discovery; oxygen diffusion; perovskite oxide; solid oxide fuel cell; topotactic phase transition Atoms; Diffusion in gases; Iron compounds; Perovskite; Solid oxide fuel cells (SOFC); Strontium compounds; Atomic scale; Excess oxygen; High-resolution transmission electron microscopy; In-situ transmission electron microscopies; MAP1: discovery; Operando; Oxygen diffusion; Perovskite oxides; Solid-oxide fuel cell; Topotactic phase transition; High resolution transmission electron microscopy English 2022 2022-09-07 10.1016/j.matt.2022.06.013 바로가기 바로가기 바로가기 바로가기
Meeting Abstract Diffuse splenic 18F-FDG uptake and peripheral blood lymphocyte monocyte ratio for prognosis prediction in patients with diffuse large B- cell lymphoma Kim, K.; Kim, S.; Kim, S. Pusan Natl Univ, Busan, South Korea; Kyungpook Natl Univ, Busan, South Korea EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING EUR J NUCL MED MOL I 1619-7070 1619-7089 49 SUPPL 1 SCIE RADIOLOGY, NUCLEAR MEDICINE & MEDICAL IMAGING 2022 9.1 4.8 0 English 2022 2022-09 바로가기 바로가기
Review Dissecting exosome inhibitors: therapeutic insights into small-molecule chemicals against cancer Intensive research in the field of cancer biology has revealed unique methods of communication between cells through extracellular vesicles called exosomes. Exosomes are released from a broad spectrum of cell types and serve as functional mediators under physiological or pathological conditions. Hence, blocking the release of exosome bio carriers may prove useful for slowing the progression of certain types of cancers. Therefore, efforts are being made to develop exosome inhibitors to be used both as research tools and as therapies in clinical trials. Thus, studies on exosomes may lead to a breakthrough in cancer research, for which new clinical targets for different types of cancers are urgently needed. In this review, we briefly outline exosome inhibitors and discuss their modes of action and potential for use as therapeutic tools for cancer. Cancer: Blocking vesicle release from tumors Understanding how cells produce and release exosomes, nano-sized membrane-bound vesicles containing biological molecules, holds promise for developing new cancer therapies. Tumors release exosomes that remodel the nearby environment to promote cancer growth, suppress the immune response and induce drug resistance. Although some aspects of exosomes have been studied, little attention has been paid to exosome inhibitors and how they work. Moon-Chang Baek at Kyungpook National University in Daegu, South Korea, and co-workers have reviewed exosome inhibitors and possible applications to cancer, reporting that several compounds, such as pantethine, suppress exosome production and others, such as sulfisoxazole and macitentan, suppress exosome release. They report that inhibiting exosome release can prevent tumor cells from purging anti-cancer drugs, thus increasing drug accumulation and efficacy. This review highlights new options for alternative therapies for many types of cancer. Kim, Jong Hyun; Lee, Chan-Hyeong; Baek, Moon-Chang Daegu Catholic Univ, Sch Med, Dept Biochem, Daegu 42472, South Korea; Kyungpook Natl Univ, Sch Med, Dept Mol Med, CMRI,Exosome Convergence Res Ctr, Daegu 41944, South Korea 59087238700; 57189904697; 7006013097 mcbaek@knu.ac.kr; EXPERIMENTAL AND MOLECULAR MEDICINE EXP MOL MED 1226-3613 2092-6413 54 11 SCIE BIOCHEMISTRY & MOLECULAR BIOLOGY;MEDICINE, RESEARCH & EXPERIMENTAL 2022 12.8 4.8 2.68 2025-06-25 62 67 EXTRACELLULAR VESICLES; INTERCELLULAR-COMMUNICATION; LIPID RAFTS; BIOGENESIS; CANNABIDIOL; RELEASE; CELLS; MICROVESICLES; SYNTENIN; TRIGGERS Exosomes; Extracellular Vesicles; Humans; Neoplasms; action potential; cancer research; exosome; human; review; metabolism; neoplasm English 2022 2022-11 10.1038/s12276-022-00898-7 바로가기 바로가기 바로가기 바로가기
Review Effect of chromatin modifiers on the plasticity and immunogenicity of small-cell lung cancer Tumor suppressor genes (TSGs) are often involved in maintaining homeostasis. Loss of tumor suppressor functions causes cellular plasticity that drives numerous types of cancer, including small-cell lung cancer (SCLC), an aggressive type of lung cancer. SCLC is largely driven by numerous loss-of-function mutations in TSGs, often in those encoding chromatin modifiers. These mutations present a therapeutic challenge because they are not directly actionable. Alternatively, understanding the resulting molecular changes may provide insight into tumor intervention strategies. We hypothesize that despite the heterogeneous genomic landscape in SCLC, the impacts of mutations in patient tumors are related to a few important pathways causing malignancy. Specifically, alterations in chromatin modifiers result in transcriptional dysregulation, driving mutant cells toward a highly plastic state that renders them immune evasive and highly metastatic. This review will highlight studies in which imbalance of chromatin modifiers with opposing functions led to loss of immune recognition markers, effectively masking tumor cells from the immune system. This review also discusses the role of chromatin modifiers in maintaining neuroendocrine characteristics and the role of aberrant transcriptional control in promoting epithelial-to-mesenchymal transition during tumor development and progression. While these pathways are thought to be disparate, we highlight that the pathways often share molecular drivers and mediators. Understanding the relationships among frequently altered chromatin modifiers will provide valuable insights into the molecular mechanisms of SCLC development and progression and therefore may reveal preventive and therapeutic vulnerabilities of SCLC and other cancers with similar mutations. Kirk, Nicole A.; Kim, Kee-Beom; Park, Kwon-Sik Univ Virginia, Dept Microbiol Immunol & Canc Biol, Sch Med, Charlottesville, VA 22908 USA; Kyungpook Natl Univ, Sch Life Sci, KNU Creat Biores Grp BK21 4, Daegu 41566, South Korea 57219279893; 58136893800; 25958774500 kp5an@virginia.edu; EXPERIMENTAL AND MOLECULAR MEDICINE EXP MOL MED 1226-3613 2092-6413 54 12 SCIE BIOCHEMISTRY & MOLECULAR BIOLOGY;MEDICINE, RESEARCH & EXPERIMENTAL 2022 12.8 4.8 0.17 2025-06-25 4 4 EPITHELIAL-MESENCHYMAL TRANSITION; DEATH-LIGAND 1; INTEGRIN-ASSOCIATED PROTEIN; LONG NONCODING RNA; MALIGNANT-TRANSFORMATION; ANTIGEN PRESENTATION; PROMOTES METASTASIS; TUMOR-DEVELOPMENT; STEM-CELLS; E-CADHERIN Chromatin; Epithelial-Mesenchymal Transition; Humans; Lung Neoplasms; Mutation; Small Cell Lung Carcinoma; azacitidine; transcription factor EZH2; trichostatin A; antigen recognition; cancer immunotherapy; carcinogenesis; cell function; cell plasticity; chromatin; disease predisposition; epigenetics; epithelial mesenchymal transition; gene control; gene mutation; gene silencing; homeostasis; human; immune evasion; immune system; immunogenicity; metastasis; neuroendocrine system; nonhuman; protein function; Review; small cell lung cancer; transcription regulation; tumor cell; tumor growth; tumor microenvironment; chromatin; genetics; lung tumor; metabolism; mutation; small cell lung cancer English 2022 2022-12 10.1038/s12276-022-00905-x 바로가기 바로가기 바로가기 바로가기
Article Hypermethylation of PDX1, EN2, and MSX1 predicts the prognosis of colorectal cancer Despite numerous observations regarding the relationship between DNA methylation changes and cancer progression, only a few genes have been verified as diagnostic biomarkers of colorectal cancer (CRC). To more practically detect methylation changes, we performed targeted bisulfite sequencing. Through co-analysis of RNA-seq, we identified cohort-specific DNA methylation markers: CpG islands of the intragenic regions of PDX1, EN2, and MSX1. We validated that these genes have oncogenic features in CRC and that their expression levels are increased in correlation with the hypermethylation of intragenic regions. The reliable depth of the targeted bisulfite sequencing data enabled us to design highly optimized quantitative methylation-specific PCR primer sets that can successfully detect subtle changes in the methylation levels of candidate regions. Furthermore, these methylation levels can divide CRC patients into two groups denoting good and poor prognoses. In this study, we present a streamlined workflow for screening clinically significant differentially methylated regions. Our discovery of methylation markers in the PDX1, EN2, and MSX1 genes suggests their promising performance as prognostic markers and their clinical application in CRC patients. Cancer: Mapping malignant modifications An experimental strategy for detecting patterns of DNA modification reveals gene-specific alterations associated with worse outcomes in colorectal cancer patients. Many genomic regions undergo a process of chemical modification called methylation, which can strongly affect the expression of nearby genes. Many cancers exhibit abnormal methylation, and South Korean researchers led by Tae-You Kim of Seoul National University and Lark Kyun Kim of Yonsei University College of Medicine, Seoul, have developed a strategy for identifying such tumor-specific modifications. They identified a trio of genes that undergo excessive methylation in colorectal cancer, and show that this 'signature' is associated with more advanced metastatic tumors and shorter overall survival. The results from this study could give clinicians an additional diagnostic tool, and highlight the potential utility of performing such methylation profiling in other cancer types. Lee, Yeongun; Dho, So Hee; Lee, Jiyeon; Hwang, Ji-Hyun; Kim, Minjung; Choi, Won-Young; Lee, Jin-Young; Lee, Jongwon; Chang, Woochul; Lee, Min Young; Choi, Jungmin; Kim, Tae-You; Kim, Lark Kyun Yonsei Univ, Gangnam Severance Hosp, Grad Sch Med Sci, Severance Biomed Sci Inst,Coll Med,Brain Korea 21, Seoul, South Korea; Yonsei Univ, Grad Sch, Interdisciplinary Program Integrated OMICS Biomed, Seoul, South Korea; Yonsei Univ, Coll Life Sci & Biotechnol, Dept Biochem, Seoul, South Korea; Korea Univ, Dept Biomed Sci, Coll Med, Seoul, South Korea; Pusan Natl Univ, Coll Educ, Dept Biol Educ, Busan, South Korea; Kyungpook Natl Univ, Coll Pharm, Vessel Organ Interact Res Ctr MRC, Res Inst Pharmaceut Sci, Daegu, South Korea; Seoul Natl Univ, Grad Sch Convergence Sci & Technol, Canc Res Inst,Seoul Natl Univ Hosp, Dept Mol Med & Biopharmaceut Sci,Dept Internal Me, Seoul, South Korea ; Lee, Jae-Sung/A-5236-2015; Choi, Wonyoung/LMP-4209-2024; Kim, Byung/L-6884-2019 57455107100; 58352388800; 57211588445; 57340230300; 57220051662; 56147288900; 57190498084; 57201265002; 12797539700; 15119890400; 56589214500; 7407123459; 55747965100 kimty@snu.ac.kr;lkkim@yuhs.ac; EXPERIMENTAL AND MOLECULAR MEDICINE EXP MOL MED 1226-3613 2092-6413 54 2 SCIE BIOCHEMISTRY & MOLECULAR BIOLOGY;MEDICINE, RESEARCH & EXPERIMENTAL 2022 12.8 4.8 1.57 2025-06-25 17 17 INTRAGENIC DNA METHYLATION; GENES; DEMETHYLATION; BIOMARKERS; PCR Biomarkers, Tumor; Colorectal Neoplasms; CpG Islands; DNA Methylation; Humans; MSX1 Transcription Factor; Oncogenes; transcription factor MSX1; transcription factor PDX 1; MSX1 protein, human; transcription factor MSX1; tumor marker; adult; aged; Article; bisulfite sequencing; colorectal cancer; CpG island; DNA methylation; EN2 gene; female; gene expression; human; major clinical study; male; methylation specific polymerase chain reaction; MSX1 gene; PDX1 gene; tumor-related gene; colorectal tumor; genetics; metabolism; oncogene English 2022 2022-02 10.1038/s12276-022-00731-1 바로가기 바로가기 바로가기 바로가기
Editorial Material In situ/operando structural tracking of Ni-Fe LDH Deciphering in situ structure of layer double hydroxides (LDHs) and their corresponding mechanism of oxygen evolution reaction (OER) is essential to further development of LDH-based OER catalysts. In this issue of Chem Catalysis, Ko et al. demonstrated a scalable syn-thesis of ultrathin Ni-Fe LDH nanostructure, its chemical oxidation process, and its catalytic mechanism by in situ/operando spectros-copies, paving a solid pathway to potential practical application of LDH-based Kim, Byeongyoon; Chio, Sang-Il; Lee, Kwangyeol Korea Univ, Dept Chem, Seoul 02841, South Korea; Korea Univ, Res Inst Nat Sci, Seoul 02841, South Korea; Kyungpook Natl Univ, Dept Chem, Daegu 41566, South Korea; Kyungpook Natl Univ, Green Nano Mat Res Ctr, Dept Hydrogen & Renewable Energy, Daegu 41566, South Korea Kim, Byeongyoon/T-3659-2018; Lee, Kwangyeol/A-9269-2010 55532693200; 56167600800; 8510322900 sichoi@knu.ac.kr;kylee1@korea.ac.kr; MATTER MATTER-US 2590-2393 2590-2385 5 10 SCIE MATERIALS SCIENCE, MULTIDISCIPLINARY 2022 18.9 4.8 1.33 2025-06-25 5 5 English 2022 2022-10-05 10.1016/j.matt.2022.08.022 바로가기 바로가기 바로가기 바로가기
Article In vivo detection of hydrogen sulfide in the brain of live mouse: application in neuroinflammation models Purpose Hydrogen sulfide (H2S) plays important roles in brain pathophysiology. However, nuclear imaging probes for the in vivo detection of brain H2S in living animals have not been developed. Here, we report the first nuclear imaging probe that enables in vivo imaging of endogenous H2S in the brain of live mice. Methods Utilizing a bis(thiosemicarbazone) backbone, a fluorescent ATSM-FITC conjugate was synthesized. Its copper complex, Cu(ATSM-FITC) was thoroughly tested as a biosensor for H2S. The same ATSM-FITC ligand was quantitatively labeled with [Cu-64]CuCl2 to obtain a radioactive [Cu-64][Cu(ATSM-FITC)] imaging probe. Biodistribution and positron emission tomography (PET) imaging studies were performed in healthy mice and neuroinflammation models. Results The Cu(ATSM-FITC) complex reacts instantly with H2S to release CuS and becomes fluorescent. It showed excellent reactivity, sensitivity, and selectivity to H2S. Endogenous H2S levels in living cells were successfully detected by fluorescence microscopy. Exceptionally high brain uptake of [Cu-64][Cu(ATSM-FITC)] (> 9% ID/g) was observed in biodistribution and PET imaging studies. Subtle changes in brain H2S concentrations in live mice were accurately detected by quantitative PET imaging. Due to its dual modality feature, increased H2S levels in neuroinflammation models were characterized at the subcellular level by fluorescence imaging and at the whole-body scale by PET imaging. Conclusion Our biosensor can be readily utilized to study brain H2S function in live animal models and shows great potential as a novel imaging agent for diagnosing brain diseases. Nam, Bora; Lee, Woonghee; Sarkar, Swarbhanu; Kim, Jae-Hong; Bhise, Abhinav; Park, Hyun; Kim, Jung Young; Huynh, Phuong Tu; Rajkumar, Subramani; Lee, Kiwoong; Ha, Yeong Su; Cho, Seong Hwan; Lim, Jeong Eun; Kim, Kyung Won; Lee, Kyo Chul; Suk, Kyoungho; Yoo, Jeongsoo Kyungpook Natl Univ, Sch Med, Brain Korea 21 Four KNU Convergence Educ Program, Dept Mol Med, Daegu 41944, South Korea; Kyungpook Natl Univ, Sch Med, Brain Korea 21 Four KNU Convergence Educ Program, Dept Pharmacol, Daegu 41944, South Korea; Korea Inst Radiol & Med Sci, Div Appl RI, Seoul 01812, South Korea Kim, Kyunghoon/AGO-0079-2022; Sarkar, Swarbhanu/GOG-8975-2022; Bhise, Abhinav/MVY-6473-2025 57222734356; 55881469700; 36603493100; 55926599800; 57210174595; 56175671100; 7601371677; 56829091800; 57224804062; 57222365137; 36720940600; 57731910400; 57732661800; 57733158200; 42661704100; 7005114595; 8215136400 yooj@knu.ac.kr; EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING EUR J NUCL MED MOL I 1619-7070 1619-7089 49 12 SCIE RADIOLOGY, NUCLEAR MEDICINE & MEDICAL IMAGING 2022 9.1 4.8 1.52 2025-06-25 12 11 Imaging agent; Hydrogen sulfide; Gasotransmitter; Neuroinflammation ALZHEIMERS-DISEASE; FLUORESCENT-PROBES; H2S; COPPER; BETA; METABOLISM; INHIBITORS; STRATEGY; SULFUR; TOOLS Gasotransmitter; Hydrogen sulfide; Imaging agent; Neuroinflammation Animals; Brain; Coordination Complexes; Copper; Fluorescein-5-isothiocyanate; Fluorescent Dyes; Hydrogen Sulfide; Ligands; Mice; Neuroinflammatory Diseases; Organometallic Compounds; Thiosemicarbazones; Tissue Distribution; ascorbic acid; copper complex; cystathionine beta synthase; cysteine; dithiothreitol; fluorescein isothiocyanate; glutathione; homocysteine; hydrogen peroxide; hydrogen sulfide; lipopolysaccharide; mercaptoethanol; methylene blue; n,n dimethylaniline; nitrogen derivative; peroxynitrite; reactive oxygen metabolite; sodium chloride; sulfur derivative; thiosemicarbazone derivative; coordination compound; copper; fluorescent dye; ligand; organometallic compound; thiosemicarbazone derivative; animal experiment; animal model; animal tissue; Article; blood brain barrier; brain; brain tissue; carbon nuclear magnetic resonance; chemical structure; controlled study; cytotoxicity; embryo; enzyme activity; ex vivo study; female; fluorescence; fluorescence imaging; fluorescence intensity; fluorescence microscopy; HEK293 cell line; HeLa cell line; high performance liquid chromatography; histopathology; human; human cell; in vivo study; lipophilicity; male; mass spectrometry; molecular probe; mouse; MTT assay; nervous system inflammation; nonhuman; positron emission tomography; precipitation; proton nuclear magnetic resonance; quantitative analysis; quantum yield; radioactivity; radiochemistry; radiolabeling; rat; thin layer chromatography; ultraviolet visible spectroscopy; whole body imaging; animal; brain; diagnostic imaging; tissue distribution English 2022 2022-10 10.1007/s00259-022-05854-1 바로가기 바로가기 바로가기 바로가기
Article Incidence rate and factors associated with the development of secondary cancers after radioiodine therapy in differentiated thyroid cancer: a multicenter retrospective study Purpose The objective of this study was to estimate the incidence of secondary cancers and the factors associated with their development among patients who underwent radioiodine therapy (RIT) with differentiated thyroid cancer. Methods We retrospectively collected medical records for patients who underwent first RIT between January 1, 2000, and December 31, 2005, from seven tertiary hospitals in South Korea after total thyroidectomy for differentiated thyroid cancer. Cancer incidence and calculated standardized rate ratio were compared with Korean cancer incidence data. The association between the development of secondary cancers and various parameters was analyzed by Cox-proportional hazard regression. Results A total of 3106 patients were included in this study. Mean age at the time of diagnosis of thyroid cancer was 45.7 +/- 13.3 years old, and 2669 (85.9%) patients were female. The follow-up period was 11.9 +/- 4.6 (range, 1.2-19.6) years. A total of 183 secondary cancers, which included 162 solid and 21 hematologic cancers, occurred in 173 patients (5.6%). There was no significant difference between solid cancer incidence in our study population who underwent RIT and the overall Korean population, but the incidence of hematologic cancers and total cancer in our study was significantly higher compared with that of the Korean population. A multivariate analysis identified independent prognostic factors for the development of secondary cancer including age at 1st RIT, male, and total cumulative dose over 200 mCi. Conclusion We need to assess the risk benefit for patients who receive over 200 mCi of a total cumulative dose. Hong, Chae Moon; Shin, Ji-Yeon; Kim, Byeong Il; Song, Ho-Chun; Yoon, Joon-Kee; Won, Kyoung Sook; Kim, Seong-Min; Cho, Ihn Ho; Jeong, Shin Young; Lee, Sang-Woo; Lee, Jaetae Kyungpook Natl Univ, Sch Med, Dept Nucl Med, 130 Dongdeok Ro, Daegu 41944, South Korea; Kyungpook Natl Univ, Dept Prevent Med, Sch Med, Daegu, South Korea; Korea Atom Energy Res Inst, Dept Nucl Med, Seoul, South Korea; Chonnam Natl Univ, Sch Med, Dept Nucl Med, Gwangju, South Korea; Ajou Univ, Dept Nucl Med & Mol Imaging, Sch Med, Suwon, South Korea; Keimyung Univ, Dept Nucl Med, Sch Med, Daegu, South Korea; Chungnam Natl Univ, Sch Med, Dept Nucl Med, Daejeon, South Korea; Yeungnam Univ, Sch Med, Dept Nucl Med, Daegu, South Korea lee, sangwoo/KUD-1906-2024; Lee, Sang-Jun/A-3892-2015 37050876700; 55567961600; 57337367500; 7404037329; 7403587745; 7005951440; 57203773014; 7102561891; 36164032500; 57196249819; 7601451907 jaetae@knu.ac.kr; EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING EUR J NUCL MED MOL I 1619-7070 1619-7089 49 5 SCIE RADIOLOGY, NUCLEAR MEDICINE & MEDICAL IMAGING 2022 9.1 4.8 1.66 2025-06-25 12 12 Thyroid cancer; Secondary cancer; Radioiodine therapy; Radiation RADIOACTIVE IODINE THERAPY; 2ND PRIMARY MALIGNANCY; ATOMIC-BOMB SURVIVORS; RISK; GUIDELINES; NATIONWIDE; CARCINOMA; PAPILLARY; LEUKEMIA; NODULES Radiation; Radioiodine therapy; Secondary cancer; Thyroid cancer Adenocarcinoma; Adult; Female; Hematologic Neoplasms; Humans; Incidence; Infant; Iodine Radioisotopes; Male; Middle Aged; Neoplasms, Second Primary; Retrospective Studies; Thyroid Neoplasms; Thyroidectomy; fluorodeoxyglucose f 18; radioactive iodine; radioactive iodine; adult; Article; bladder cancer; brain cancer; breast cancer; cancer incidence; cancer patient; cancer prognosis; cancer screening; cancer surgery; colorectal cancer; controlled study; differentiated thyroid cancer; female; follow up; hematologic malignancy; Hodgkin disease; human; kidney cancer; Korean (people); larynx cancer; leukemia; lip cancer; liver cancer; low iodine diet; lung cancer; major clinical study; male; medical record review; metastasis; middle aged; mouth cancer; multicenter study; nonhodgkin lymphoma; ovary cancer; pancreas cancer; pharynx cancer; positron emission tomography-computed tomography; proportional hazards model; prostate cancer; radioisotope therapy; retrospective study; risk factor; solid malignant neoplasm; South Korea; standardized incidence ratio; stomach cancer; tertiary care center; thyroid follicular carcinoma; thyroid papillary carcinoma; total thyroidectomy; uterine cervix cancer; uterus cancer; adenocarcinoma; clinical trial; hematologic disease; incidence; infant; second cancer; thyroid tumor; thyroidectomy English 2022 2022-04 10.1007/s00259-021-05608-5 바로가기 바로가기 바로가기 바로가기
Article Phospholipase D2 controls bone homeostasis by modulating M-CSF-dependent osteoclastic cell migration and microtubule stability Phospholipase D2 (PLD2), a signaling protein, plays a central role in cellular communication and various biological processes. Here, we show that PLD2 contributes to bone homeostasis by regulating bone resorption through osteoclastic cell migration and microtubule-dependent cytoskeletal organization. Pld2-deficient mice exhibited a low bone mass attributed to increased osteoclast function without altered osteoblast activity. While Pld2 deficiency did not affect osteoclast differentiation, its absence promoted the migration of osteoclast lineage cells through a mechanism involving M-CSF-induced activation of the PI3K-Akt-GSK3 beta signaling pathway. The absence of Pld2 also boosted osteoclast spreading and actin ring formation, resulting in elevated bone resorption. Furthermore, Pld2 deletion increased microtubule acetylation and stability, which were later restored by treatment with a specific inhibitor of Akt, an essential molecule for microtubule stabilization and osteoclast bone resorption activity. Interestingly, PLD2 interacted with the M-CSF receptor (c-Fms) and PI3K, and the association between PLD2 and c-Fms was reduced in response to M-CSF. Altogether, our findings indicate that PLD2 regulates bone homeostasis by modulating osteoclastic cell migration and microtubule stability via the M-CSF-dependent PI3K-Akt-GSK3 beta axis. Bone disease: Possible treatment to rebalance bone remodeling A signaling protein that regulates bone resorption may prove a useful target in treating skeletal conditions such as osteoporosis and rheumatoid arthritis. Bone is synthesized by cells called osteoblasts, while osteoclasts trigger bone resorption, keeping the skeleton healthy. Imbalances in this recycling process are common in bone disorders. Je-Young Choi and Hyun-Ju Kim at Kyungpook National University in Daegu, South Korea, and co-workers demonstrated that phospholipase D2 (PLD2), a membrane protein, directly regulates bone resorption in mice. Mice without the Pld2 gene had increased osteoclast activity, resulting in low bone mass. The absence of PLD2 promotes the migration of osteoclasts via a particular signaling pathway. This increased the organization of microtubules, polymers that help form the cytoskeleton. The results suggest that regulating PLD2 activity could form the basis of a future treatment method. Kim, Hyun-Ju; Lee, Dong-Kyo; Jin, Xian; Che, Xiangguo; Ryu, Sung Ho; Choi, Je-Yong Kyungpook Natl Univ, Korea Mouse Phenotyping Ctr, Cell & Matrix Res Inst,Sch Med, Dept Biochem & Cell Biol,BK21 Plus KNU Biomed Con, Daegu 41944, South Korea; Pohang Univ Sci & Technol, Dept Life Sci, Pohang 37673, South Korea Choi, Je-Yong/AAR-7334-2021 57208650339; 57216603928; 57204810645; 54792660600; 7402110894; 7501391068 biohjk@knu.ac.kr;jechoi@knu.ac.kr; EXPERIMENTAL AND MOLECULAR MEDICINE EXP MOL MED 1226-3613 2092-6413 54 8 SCIE BIOCHEMISTRY & MOLECULAR BIOLOGY;MEDICINE, RESEARCH & EXPERIMENTAL 2022 12.8 4.8 1.28 2025-06-25 11 13 SEALING ZONE; DIFFERENTIATION; RESORPTION; PODOSOME; ORGANIZATION; GLUCOCORTICOIDS; ACTIVATION; MECHANISMS; MATURATION; CYTOKINE Animals; Bone Resorption; Cell Differentiation; Cell Movement; Glycogen Synthase Kinase 3 beta; Homeostasis; Macrophage Colony-Stimulating Factor; Mice; Microtubules; Osteoclasts; Phosphatidylinositol 3-Kinases; Phospholipase D; Proto-Oncogene Proteins c-akt; actin; colony stimulating factor 1; glycogen synthase kinase 3beta; phosphatidylinositol 3 kinase; phospholipase D2; protein kinase B; colony stimulating factor 1; glycogen synthase kinase 3beta; phosphatidylinositol 3 kinase; phospholipase D; phospholipase D2; protein kinase B; acetylation; animal cell; animal tissue; Article; bone homeostasis; bone mass; cell differentiation; cell function; cell migration; controlled study; enzyme deficiency; gene deletion; homeostasis; microtubule; microtubule acetylation; microtubule stability; mouse; musculoskeletal system parameters; nonhuman; osteoblast; osteoclast; osteolysis; Pld2 gene; protein function; protein protein interaction; signal transduction; animal; cell motion; homeostasis; metabolism; microtubule; osteolysis English 2022 2022-08 10.1038/s12276-022-00820-1 바로가기 바로가기 바로가기 바로가기
Article Second primary malignancy risk in thyroid cancer and matched patients with and without radioiodine therapy analysis from the observational health data sciences and informatics Purpose Risk of second primary malignancy (SPM) after radioiodine (RAI) therapy has been continuously debated. The aim of this study is to identify the risk of SPM in thyroid cancer (TC) patients with RAI compared with TC patients without RAI from matched cohort. Methods Retrospective propensity-matched cohorts were constructed across 4 hospitals in South Korea via the Observational Health Data Science and Informatics (OHDSI), and electrical health records were converted to data of common data model. TC patients who received RAI therapy constituted the target group, whereas TC patients without RAI therapy constituted the comparative group with 1:1 propensity score matching. Hazard ratio (HR) by Cox proportional hazard model was used to estimate the risk of SPM, and meta-analysis was performed to pool the HRs. Results Among a total of 24,318 patients, 5,374 patients from each group were analyzed (mean age 48.9 and 49.2, women 79.4% and 79.5% for target and comparative group, respectively). All hazard ratios of SPM in TC patients with RAI therapy were = 30 years). The HR within the target group was not significantly higher (< 1) in patients who received over 3.7 GBq of I-131 compared with patients who received less than 3.7 GBq of I-131 based on 95% CI. Conclusion There was no significant difference of the SPM risk between TC patients treated with I-131 and propensity-matched TC patients without I-131 therapy. Kim, Seok; Bang, Ji-In; Boo, Dachung; Kim, Borham; Choi, In Young; Ko, SooJeong; Yoo, Ie Ryung; Kim, Kwangsoo; Kim, Junmo; Joo, YoungHwan; Ryoo, Hyun Gee; Paeng, Jin Chul; Park, Jung Mi; Jang, Woncheol; Kim, Byungwon; Chung, Yangha; Yang, Dongyoon; Yoo, Sooyoung; Lee, Ho-Young Seoul Natl Univ, Bundang Hosp, Off eHlth Res & Business, 173rd St, Seongnam Si 436707, South Korea; CHA Univ, CHA Bundang Med Ctr, Dept Nucl Med, Seongnam, South Korea; Catholic Univ Korea, Coll Med, Dept Med Informat, Seoul, South Korea; Catholic Univ Korea, Dept Biomed & Hlth Sci, Seoul, South Korea; Catholic Univ Korea, Seoul St Marys Hosp, Coll Med, Dept Radiol,Div Nucl Med, Seoul, South Korea; Seoul Natl Univ Hosp, Transdisciplinary Dept Med & Adv Technol, Seoul, South Korea; Seoul Natl Univ, Med Res Ctr, Med Big Data Res Ctr, Seoul, South Korea; Seoul Natl Univ, Interdisciplinary Program Bioengn, Seoul, South Korea; Seoul Natl Univ Hosp, Biomed Res Inst, Seoul, South Korea; Seoul Natl Univ, Coll Med, Dept Nucl Med, Seoul, South Korea; Seoul Natl Univ Hosp, Dept Nucl Med, Seoul, South Korea; Soonchunhyang Univ, Bucheon Hosp, Dept Nucl Med, Gyeonggido, South Korea; Seoul Natl Univ, Dept Stat, Seoul, South Korea; Kyungpook Natl Univ, Dept Stat, Daegu, South Korea; Seoul Natl Univ, Bundang Hosp, Dept Nucl Med, Off eHlth Res & Business, 166 Gumi Ro, Seongnam Si 436707, South Korea ; Ryoo, Hyun Gee/GQH-2802-2022 55351915400; 56504705800; 57265979100; 57490465500; 25959506000; 57210809196; 7005731891; 57210575084; 57561492000; 57561689300; 57209471079; 6602895031; 57075244000; 8865884800; 57205674498; 57562077200; 57562077300; 8426359900; 56237826800 yoosoo0@snubh.org;debobkr@snubh.org; EUROPEAN JOURNAL OF NUCLEAR MEDICINE AND MOLECULAR IMAGING EUR J NUCL MED MOL I 1619-7070 1619-7089 49 10 SCIE RADIOLOGY, NUCLEAR MEDICINE & MEDICAL IMAGING 2022 9.1 4.8 2.77 2025-06-25 18 20 Thyroid cancer; Iodine-131; Neoplasm; Second primary; Risk; Common data model; Observational study RADIOACTIVE IODINE THERAPY; I-131 TREATMENT; NATIONWIDE; CARCINOMA; SURVIVAL; SURVEILLANCE; GUIDELINES; PREDICTORS; DIAGNOSIS Common data model; Iodine-131; Neoplasm, Second primary; Observational study; Risk; Thyroid cancer Adult; Data Science; Female; Humans; Informatics; Iodine Radioisotopes; Middle Aged; Neoplasms, Second Primary; Retrospective Studies; Thyroid Neoplasms; iodine 131; Iodine-131; radioactive iodine; adolescent; adult; aged; Article; cancer patient; cancer risk; cancer staging; child; cohort analysis; controlled study; female; human; infant; major clinical study; meta analysis; newborn; observational study; retrospective study; second cancer; South Korea; thyroid cancer; thyroidectomy; information science; middle aged; second cancer; thyroid tumor English 2022 2022-08 10.1007/s00259-022-05779-9 바로가기 바로가기 바로가기 바로가기
Article SMP30-mediated synthesis of vitamin C activates the liver PPARα/FGF21 axis to regulate thermogenesis in mice The vitamin-C-synthesizing enzyme senescent marker protein 30 (SMP30) is a cold resistance gene in Drosophila, and vitamin C concentration increases in brown adipose tissue post-cold exposure. However, the roles of SMP30 in thermogenesis are unknown. Here, we tested the molecular mechanism of thermogenesis using wild-type (WT) and vitamin C-deficient SMP30-knockout (KO) mice. SMP30-KO mice gained more weight than WT mice without a change in food intake in response to short-term high-fat diet feeding. Indirect calorimetry and cold-challenge experiments indicated that energy expenditure is lower in SMP30-KO mice, which is associated with decreased thermogenesis in adipose tissues. Therefore, SMP30-KO mice do not lose weight during cold exposure, whereas WT mice lose weight markedly. Mechanistically, the levels of serum FGF21 were notably lower in SMP30-KO mice, and vitamin C supplementation in SMP30-KO mice recovered FGF21 expression and thermogenesis, with a marked reduction in body weight during cold exposure. Further experiments revealed that vitamin C activates PPAR alpha to upregulate FGF21. Our findings demonstrate that SMP30-mediated synthesis of vitamin C activates the PPAR alpha/FGF21 axis, contributing to the maintenance of thermogenesis in mice. Metabolism: Vitamin C synthesis enzyme linked to heat production An enzyme involved in vitamin C synthesis also mediates the ability of mice to generate heat in response to cold exposures. Hae Young Chung from Pusan National University in Busan, South Korea, and colleagues showed that mice without a working version of this enzyme, known as SMP30, do not lose weight under cold conditions. That's because they cannot burn brown fat to create heat through a process called thermogenesis. The researchers detailed how vitamin C, whether produced naturally by SMP30-related signaling in mouse tissues or given via dietary supplement, triggers the activation of signaling molecules and growth factors necessary for thermogenesis. Since humans cannot synthesize their own vitamin C, and thus cannot take advantage of this heat-generating and fat-burning pathway, these findings may help explain a common cause of weight gain and obesity. Lee, Bonggi; An, Hye Jin; Kim, Dae Hyun; Lee, Min-Kyeong; Jeong, Hyeon Hak; Chung, Ki Wung; Go, Younghoon; Seo, Arnold Y.; Kim, Il Yong; Seong, Je Kyung; Yu, Byung Pal; Lee, Jaewon; Im, Eunok; Lee, In-Kyu; Lee, Myung-Shik; Yamada, Ken-ichi; Chung, Hae Young Pukyong Natl Univ, Dept Food Sci & Nutr, Busan, South Korea; Pusan Natl Univ, Coll Pharm, Dept Pharm, Busan 46241, South Korea; Pusan Natl Univ, Mol Inflammat Res Ctr Ageing Intervent MRCA, Busan 46241, South Korea; Pukyong Natl Univ, Dept Smart Green Technol Engn, Busan 48513, South Korea; Korea Inst Oriental Med, Korean Med Applicat Ctr, Daegu, South Korea; Howard Hughes Med Inst, Janelia Res Campus, Ashburn, VA USA; Seoul Natl Univ, Coll Vet Med, Res Inst Vet Sci, Lab Dev Biol & Genom, Seoul, South Korea; Seoul Natl Univ, Coll Vet Med, BK21 Plus Program Creat Vet Sci, Seoul, South Korea; Seoul Natl Univ, Korea Mouse Phenotyping Ctr KMPC, Seoul, South Korea; Seoul Natl Univ, Program Canc Biol, Interdisciplinary Program Bioinformat, Seoul, South Korea; Seoul Natl Univ, BIOMAX Inst, Seoul, South Korea; Univ Texas Hlth Sci Ctr San Antonio, Dept Physiol, San Antonio, TX 78229 USA; Kyungpook Natl Univ, Dept Internal Med, Sch Med, Daegu, South Korea; Yonsei Univ, Coll Med, Severance Biomed Sci Inst, Seoul, South Korea; Yonsei Univ, Coll Med, Dept Internal Med, Seoul, South Korea; Kyushu Univ, Dept Biofunct Sci, Fukuoka, Japan Lee, Jaewon/N-9064-2013; Lee, Myung/C-9606-2011; Lee, In-Kyu/AAR-6374-2021; Kim, Yong/L-8289-2019 57190990292; 55632415100; 57192665807; 57208016160; 57447943800; 38361189500; 55455882000; 11339208300; 55477678500; 7004962796; 7402092685; 56377510700; 55206707700; 36071537600; 7409119483; 55541058200; 57218539812 hyjung@pusan.ac.kr; EXPERIMENTAL AND MOLECULAR MEDICINE EXP MOL MED 1226-3613 2092-6413 54 11 SCIE BIOCHEMISTRY & MOLECULAR BIOLOGY;MEDICINE, RESEARCH & EXPERIMENTAL 2022 12.8 4.8 0.69 2025-06-25 6 7 ASCORBIC-ACID; BODY-TEMPERATURE; WEIGHT-LOSS; BROWN FAT; ADIPOCYTES; DEFICIENCY; FGF21; HEALTHY; SMP30; COLD Adipose Tissue, Brown; Animals; Ascorbic Acid; Calcium-Binding Proteins; Intracellular Signaling Peptides and Proteins; Liver; Mice; Mice, Inbred C57BL; Mice, Knockout; PPAR alpha; Thermogenesis; Vitamins; ascorbic acid; fibroblast growth factor 21; peroxisome proliferator activated receptor alpha; regucalcin; ascorbic acid; calcium binding protein; fibroblast growth factor 21; peroxisome proliferator activated receptor alpha; Ppara protein, mouse; Rgn protein, mouse; signal peptide; vitamin; adipose tissue; animal experiment; animal model; animal tissue; Article; ascorbic acid deficiency; body weight gain; body weight loss; C57BL 6 mouse; cohort analysis; cold exposure; controlled study; energy expenditure; food intake; human; indirect calorimetry; knockout mouse; lipid diet; male; mouse; nonhuman; pilot study; protein expression; protein function; synthesis; thermogenesis; upregulation; vitamin supplementation; wild type mouse; animal; brown adipose tissue; C57BL mouse; genetics; liver; metabolism; thermogenesis English 2022 2022-11 10.1038/s12276-022-00888-9 바로가기 바로가기 바로가기 바로가기
Article The parametric hurricane rainfall model with moisture and its application to climate change projections The parametric hurricane rainfall model (PHRaM), firstly introduced in 2007, has been widely used to forecast and quantify tropicalcyclone-induced rainfall (TC rainfall). The PHRaM is much more computationally efficient than global climate models, but PHRaM cannot be effectively utilized in the context of climate change because it does not have any parameters to capture the increase of tropospheric water vapor under the warming world. This study develops a new model that incorporates tropospheric water vapor to the PHRaM framework, named as the PHRaM with moisture (PHRaMM). The PHRaMM is trained to best fit the TC rainfall over the western North Pacific (WNP) unlike the PHRaM trained with the TCs over the continental US. The PHRaMM reliably simulates radial profile of TC rainfall and spatial distribution of accumulated rainfall during landfall in the present climate with the better prediction skills than existing statistical and operational numerical models. Using the PHRaMM, we evaluated the impacts of TC intensity and environmental moisture increase on TC rainfall change in a future climate. An increased TC intensity causes TC rainfall to increase in the inner-core region but to decrease in the outer region, whereas an increased environmental moisture causes the TC rainfall to increase over the entire TC area. According to the both effects of increased TC intensity and environmental moisture, the PHRaMM projected that the WNP TC rainfall could increase by 4.61-8.51% in the inner-core region and by 17.96-20.91% over the entire TC area under the 2-K warming scenario. Kim, Dasol; Park, Doo-Sun R.; Nam, Chaehyeon C.; Bell, Michael M. Univ Florida, Dept Geog, Gainesville, FL 32611 USA; Kyungpook Natl Univ, Dept Earth Sci Educ, Daegu, South Korea; Colorado State Univ, Dept Atmospher Sci, Ft Collins, CO 80523 USA ; Park, Doo-Sun/U-9448-2019; Bell, Michael/B-1144-2009; Kim, Dasol/GWR-1499-2022 56420697800; 37117659000; 56662775300; 57212816521 dsrpark@knu.ac.kr; NPJ CLIMATE AND ATMOSPHERIC SCIENCE NPJ CLIM ATMOS SCI 2397-3722 5 1 SCIE METEOROLOGY & ATMOSPHERIC SCIENCES 2022 9 4.8 1.13 2025-06-25 15 15 VERTICAL WIND SHEAR; ENVIRONMENTAL-CONDITIONS; TROPICAL CYCLONES; STORM MOTION; ASYMMETRIES; INTENSITY; FORECASTS; LANDFALL; RISK United States; climate change; climate modeling; hurricane event; precipitation intensity; scenario analysis English 2022 2022-11-04 10.1038/s41612-022-00308-9 바로가기 바로가기 바로가기 바로가기
Review Understanding the molecular basis of anorexia and tissue wasting in cancer cachexia Cancer cachexia syndrome is a major cause of morbidity and mortality in cancer patients in the advanced stage. It is a devastating disorder characterized by nutritional impairment, weakness, and wasting, and it affects treatment success and quality of life. Two major symptoms of cancer cachexia are anorexia and weight loss. Weight loss in cachexia is not reversed through increased food intake, suggesting that anorexia and weight loss in cancer patients are regulated by independent molecular mechanisms. Although the wasting phenotype mostly occurs in skeletal muscle and adipose tissue, other organs, such as the brain, liver, pancreas, heart, and gut, are also involved in cachexia. Thus, cachexia is a multiorgan syndrome. Although the molecular basis of cancer cachexia-induced weight loss is known, the mechanism underlying anorexia is poorly understood. Here, we highlight our recent discovery of a new anorexia mechanism by which a tumor-derived humoral factor induces cancer anorexia by regulating feeding-related neuropeptide hormones in the brain. Furthermore, we elucidated the process through which anorexia precedes tissue wasting in cachexia. This review article aims to provide an overview of the key molecular mechanisms of anorexia and tissue wasting caused by cancer cachexia. Cancer: When tumors cause weight loss Tumors can release factors that cause anorexia and weight loss in cancer patients, negatively impacting quality of life and treatment success. Patients with this condition, known as cachexia, can lose their appetite and be unable to gain weight even if they eat more. Although cancer cachexia directly causes the death of up to 20% of cancer patients, the mechanisms are poorly understood. Eunbyul Yeom and Kweon Yu at The Korea Research Institute of Bioscience and Biotechnology, Daejon, South Korea have reviewed the causes of cancer cachexia, highlighting their recent discovery that tumors produce a signaling molecule that induces anorexia by disrupting hunger signaling in the brain. Improving our understanding of the mechanisms underlying cancer cachexia may help in development of treatments. Yeom, Eunbyul; Yu, Kweon KRIBB, Dis Target Struct Res Ctr, Metab & Neurophysiol Res Grp, Daejeon 34141, South Korea; Kyungpook Natl Univ, Coll Nat Sci, Sch Life Sci, Daegu 41566, South Korea; Kyungpook Natl Univ, Sch Life Sci, FOUR KNU Creat BioRes Grp BK21, Daegu 41566, South Korea; UST, Dept Funct Genom, Daejeon, South Korea 56058004100; 7403385545 kweonyu@kribb.re.kr; EXPERIMENTAL AND MOLECULAR MEDICINE EXP MOL MED 1226-3613 2092-6413 54 4 SCIE BIOCHEMISTRY & MOLECULAR BIOLOGY;MEDICINE, RESEARCH & EXPERIMENTAL 2022 12.8 4.8 2.17 2025-06-25 53 53 FOOD-INTAKE; SKELETAL-MUSCLE; ENERGY-EXPENDITURE; ADIPOSE-TISSUE; MURINE MODEL; WEIGHT-LOSS; BODY-MASS; CYTOKINES; METABOLISM; MECHANISMS Adipose Tissue; Anorexia; Cachexia; Humans; Neoplasms; Quality of Life; activin; adenosine triphosphate; growth differentiation factor 15; immunoglobulin enhancer binding protein; interleukin 1; interleukin 6; myostatin; neuropeptide; proopiomelanocortin; somatomedin; transforming growth factor beta; tumor necrosis factor; uncoupling protein 1; adipose tissue; anorexia; cachexia; cell function; clinical feature; cytokine release; food intake; glucose intolerance; heart disease; human; multiple organ failure; muscle atrophy; nonhuman; protein secretion; protein synthesis; regulatory mechanism; Review; skeletal muscle; anorexia; complication; genetics; neoplasm; quality of life English 2022 2022-04 10.1038/s12276-022-00752-w 바로가기 바로가기 바로가기 바로가기
Article Pharmacological actions of dieckol on modulation of platelet functions and thrombus formation via integrin αIIbβ3 and cAMP signaling Background and purpose: Dieckol is a phlorotannin that can be found in seaweeds, particularly in Eisenia bicyclis (brown algae) and is known to have anti-oxidant, anti-inflammatory, and anti-microbial properties. It also possesses anti-thrombotic and pro-fibrinolytic activities; however, the mechanistic aspects of anti-platelet and anti-thrombotic activity are yet to be explored.& nbsp;Study design and methodology: We investigated the pharmacological effects of dieckol on the modulation of platelet functions using human, rat, and mice models. Inhibitory effects of dieckol on platelet aggregation were assessed using platelet-rich plasma and washed platelets, followed by measurement of dense granule secretions, fibrinogen binding to integrin alpha IIb beta 3, fibronectin adhesion assay, platelet spreading on immobilized fibrinogen, and clot retraction. Cyclic nucleotide signaling events were evaluated, such as cyclic-AMP production followed by vasodilator-stimulated phosphoprotein (VASP) stimulation. The in vivo anti-thrombotic potential was evaluated in mice using an acute pulmonary thromboembolism model and tail bleeding assay.& nbsp;Results: Dieckol markedly inhibited platelet aggregation and granule secretion; furthermore, it down-regulated integrin alpha IIb beta 3-mediated inside-out and outside-in signaling events, including platelet adhesion, spreading, and clot retraction, whereas it upregulated the cAMP-PKA-VASP pathway. Dieckol-treated mice significantly survived the thrombosis than vehicle treated mice, without affecting hemostasis. Histological examinations of lungs revealed minimum occluded vasculature in dieckol-treated mice.& nbsp;Conclusion: Dieckol possesses strong anti-platelet and anti-thrombotic properties and is a potential therapeutic drug candidate to treat and prevent platelet-related cardiovascular disorders. Irfan, Muhammad; Kwon, Tae-Hyung; Kwon, Hyuk-Woo; Rhee, Man Hee Kyungpook Natl Univ, Coll Vet Med, Dept Vet Med, Daegu 41566, South Korea; Univ Illinois, Coll Dent, Dept Oral Biol, Chicago, IL 60612 USA; Chuncheon Bio Ind Fdn, Chunchon 24232, South Korea; Far East Univ, Dept Biomed Lab Sci, Eumseong 27601, South Korea; Kyungpook Natl Univ, Coll Vet Med, Lab Physiol & Cell Signaling, Daegu 41566, South Korea Irfan, Muhammad/AAY-1961-2021; Rhee, Man/O-5705-2016 57223918800; 55419730800; 55200547400; 57211035357 rheemh@knu.ac.kr; PHARMACOLOGICAL RESEARCH PHARMACOL RES 1043-6618 1096-1186 177 SCIE PHARMACOLOGY & PHARMACY 2022 9.3 4.9 1.03 2025-06-25 7 9 Anti-platelet; Cyclic-AMP; Dieckol; Thrombosis; VASPSer-157 EISENIA-BICYCLIS; PROTEIN-KINASE; BROWN ALGA; PHOSPHORYLATION; INHIBITION; PHLOROTANNINS; GINSENOSIDES; ACTIVATION; MECHANISMS; ADHESION Anti-platelet; Cyclic-AMP; Dieckol; Integrin α<sub>IIb</sub>β<sub>3</sub>; Thrombosis; VASP<sup>Ser−157</sup> Animals; Benzofurans; Blood Platelets; Fibrinogen; Hemostasis; Mice; Platelet Aggregation; Platelet Glycoprotein GPIIb-IIIa Complex; Rats; Thrombosis; antithrombocytic agent; cyclic AMP; dieckol; fibrinogen; integrin alpha2bbeta3; lymphocyte antigen; mitogen activated protein kinase; phosphatidylinositol 3 kinase; phosphoprotein; plant medicinal product; protein kinase B; unclassified drug; benzofuran derivative; dieckol; fibrinogen; fibrinogen receptor; animal experiment; animal model; animal tissue; antiplatelet activity; antithrombotic activity; Article; blood clot retraction; blood clotting; controlled study; down regulation; drug mechanism; drug protein binding; Eisenia bicyclis; enzyme phosphorylation; human; lung embolism; mouse; nonhuman; rat; thrombocyte adhesion; thrombocyte aggregation; thrombocyte aggregation inhibition; thrombocyte function; thrombocyte rich plasma; thrombosis; upregulation; animal; hemostasis; metabolism; thrombocyte; thrombosis English 2022 2022-03 10.1016/j.phrs.2022.106088 바로가기 바로가기 바로가기 바로가기
Article Using eye-tracking to examine the role of first and second language glosses This study employs eye-tracking to investigate how first (L1) and second language (L2) glosses affect lexical uptake and reading behaviors in L2 learners of English. The study also explores the relationship between lexical uptake and reading behaviors as a function of gloss type. To investigate this, 81 Korean university students were asked to read a baseline passage with no gloss or the same passage with glosses in the study's L1 (Korean) or L2 (English). Their eye movements were recorded with an eye tracker as they read, and they were subsequently asked to respond to two vocabulary tests. Analyses of eye-tracking data and vocabulary test scores revealed that the presence or absence of L1 and L2 glosses might produce differences in lexical uptake and dissimilar attentional mechanisms. For instance, the study found that L1 and L2 glosses failed to significantly enhance the acquisition of visual word forms, whereas both types of glosses were significantly effective in consolidating form-meaning associations. Additionally, correlation analyses indicated that the relationship between reading behaviors and lexical acquisition might differ depending on gloss type. Ultimately, our findings provide a more comprehensive picture of L1 and L2 gloss effects, and have significant implications for L2 pedagogy. Kang, Hyeonah; Kweon, Soo-Ok; Choi, Sungmook Univ Arizona, Tucson, AZ 85721 USA; POSTECH, Pohang, South Korea; Kyungpook Natl Univ, Daegu, South Korea ; Kang, Hyeonah/JXW-8125-2024 57217042210; 37067465400; 56124260900 sungmookchoi@knu.ac.kr; LANGUAGE TEACHING RESEARCH LANG TEACH RES 1362-1688 1477-0954 26 6 SSCI EDUCATION & EDUCATIONAL RESEARCH;LINGUISTICS 2022 4.2 4.9 4.63 2025-06-25 18 21 attention; eye-tracking; form-meaning mappings; glossing; incidental vocabulary acquisition; visual word form acquisition INCIDENTAL VOCABULARY ACQUISITION; READING-COMPREHENSION; LEXICAL KNOWLEDGE; WORD MEANINGS; LANGUAGE; CONTEXT; EXPLICIT; L1 attention; eye-tracking; form–meaning mappings; glossing; incidental vocabulary acquisition; visual word form acquisition English 2022 2022-11 10.1177/1362168820928567 바로가기 바로가기 바로가기 바로가기
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