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Dental Treatment of Shell Teeth Associated with Osteogenesis Imperfecta: a Case Report
Hanbyeol Kim,Hyuntae Kim,Ji-Soo Song,Teo Jeon Shin,Hong-Keun Hyun,Young-Jae Kim,Jung-Wook Kim,Ki-Taeg Jang Asia Association for Disability and Oral Health 2023 International Journal of Disability and Oral Healt Vol.19 No.1
Kim Hanbyeol,Kim Hyo Keun,Hong Dawon,Kim Minsu,Jang Sein,Yang Chul-Su,Yoon Seokhyun 한국유전학회 2023 Genes & Genomics Vol.45 No.7
Background Single-cell RNA-seq enabled microscopic studies on tissue microenvironment of many diseases. Inflammatory bowel disease, an autoimmune disease, is involved with various dysfunction of immune cells, for which single-cell RNA-seq may provide us a deeper insight into the causes and mechanism of this complex disease. Objective In this work, we used public single-cell RNA-seq data to study tissue microenvironment around ulcerative colitis, an inflammatory bowel disease causing chronic inflammation and ulcers in large intestine. Methods Since not all the datasets provide cell-type annotations, we first identified cell identities to select cell populations of our interest. Differentially expressed genes and gene set enrichment analysis was then performed to infer the polarization/activation state of macrophages and T cells. Cell-to-cell interaction analysis was also performed to discover distinct interactions in ulcerative colitis. Results Differentially expressed genes analysis of the two datasets confirmed the regulation of CTLA4, IL2RA, and CCL5 genes in the T cell subset and regulation of S100A8/A9, CLEC10A genes in macrophages. Cell-to-cell interaction analysis showed CD4+ T cells and macrophages interact actively to each other. We also identified IL-18 pathway activation in inflammatory macrophages, evidence that CD4+ T cells induce Th1 and Th2 differentiation, and also found that macrophages regulate T cell activation through different ligand-receptor pairs, viz. CD86-CTL4, LGALS9-CD47, SIRPA-CD47, and GRN-TNFRSF1B. Conclusion Analysis of these immune cell subsets may suggest novel strategies for the treatment of inflammatory bowel disease.
( Hanbyeol Kim ),( In Ho Kwon ),( Junho Cho ),( Ha Young Park ),( Woon Hyung Yeo ),( Kyung Hye Park ),( June Yeop Lee ) 대한응급의학회 2014 대한응급의학회 학술대회초록집 Vol.2014 No.2
Intramural esophageal dissection (IED) can be described as a laceration between the mucosa and submucosa of the esophagus. It usually caused by rapidly increased intraesophageal pressure We report a case of IED which occurred after performing an esophagogastroduodenoscopy (EDGS). A 38-year-old male was transferred to the emergency department from a local clinic with suspicion of tracheoesophageal fistula (T-E fistula). He complained epigastric are pain, nausea and vomiting from 5 days ago. So he had been performed EGDS to find cause of epigastric area pain in the local clinic. And a pus secreting hole was found during performing EGDS that suspected as T-E fistula. Initial vital signs were stable and he complained acutely aggravated epigastric are pain after EGDS but had no tenderness on his abdomen. We could found air shade in the mediastinum just next to the trachea. We performed Chest computerized tomography (CT) and esophagography in order to evaluate T-E fistula or injury of the esophagus. Chest CT and esophagography showed presentation of a true and false lumen within the esophagus. The diagnosis of Intramural esophageal dissection was made based on chest CT and esophagography. We consulted to the thoracic surgeon, and primary repair of esophageal mucosa was done. Patient was discharged on POD #11 without complication. Most common causes of IED are iatrogenic causes such as standard endoscopy and endoscopic intervention. It has high incidence in the elderly women and the people who have bleeding tendency. Emergency physicians should consider IED in the case of epigastric area pain that has occured after endoscopy.
FAST ANDROID IMPLIMENTATION OF MONTE CARLO SIMULATION FOR PRICING EQUITY-LINKED SECURITIES
HANBYEOL JANG,HYUNDONG KIM,SUBEOM JO,HANRIM KIM,SERI LEE,JUWON LEE,JUNSEOK KIM 한국산업응용수학회 2020 Journal of the Korean Society for Industrial and A Vol.24 No.1
In this article, we implement a recently developed fast Monte Carlo simulation (MCS) for pricing equity-linked securities (ELS), which is most commonly issued autocallable structured financial derivative in South Korea, on the mobile platform. The fast MCS is based on Brownian bridge technique. Although mobile platform devices are easy to carry around, mobile platform devices are slow in computation compared to desktop computers. Therefore, it is essential to use a fast algorithm for pricing ELS on the mobile platform. The computational results demonstrate the practicability of Android application implementation for pricing ELS.
Hanbyeol Kim,Sang Yoon Park,Suena Ji,Jin Won Cho 한국당과학회 2012 한국당과학회 학술대회 Vol.2012 No.1
β-O-linked N-acetylglucosamine(O-GlcNAc) is dynamic post-translational modification in nucleus and cytosol and it is regulated by O-GlcNAc transferase(OGT) and O-GlcNAcase. Many proteins, such as transcription factors, enzymes, cytoskeletal proteins, ribosomal proteins and chaperones have been identified to be modified with O-GlcNAc. O-GlcNAc modification modifies at their Ser/Thr residues and affects their functions. The hexosamine biosynthesis pathway takes about 5% of glucose in total glucose flux, and it’s final product is UDP-GlcNAc, which is source of O-GlcNAc modification. O-GlcNAc modification is reported to involve in skeletal muscle metabolism and development process. We studied whether O-GlcNAc modification is involved in differentiation in myoblast C2C12 cell. We observed that total O-GlcNAc modification level was dynamically changed during myogenesis. After treatment NButGT, we observed that myogenin expression level decreased. Using RT PCR, we found that mRNA level of myogenin decrease after treatment NButGT. And we found that the promoter activity of myogenin decreases after NButGT using reporter gene assay. For finding the promoter region affected O -GlcNAc , we did reporter gene assay using shorter length promoter and found at least 169 base pair upstream region of myogenin is affected by O-GlcNAc. And using this region, we found that Mef2c protein can be important transcription factor regulated by O-GlcNAc using avidin-biotin complex DNA binding assay. We confirm that Mef2c is O-GlcNAcylated using immunoprecipitation and we found several O-GlcNAcylated sites on Mef2c using mass spectrometry. Based on the result, we made the Mef2c point mutants converted from Serine, Threonine of O-GlcNAcylated sites to Alanine. Additionally, we found O-GlcNAc modification could regulate DNA binding affinity and transcriptional complex formation.
Hanbyeol Kim,HoJung Seo,SangYoon Park,Jin Won Cho 한국당과학회 2013 한국당과학회 학술대회 Vol.2013 No.1
β-O-linked N-acetylglucosamine(O-GlcNAc) is dynamic post-translational modification in nucleus and cytosol and it is regulated by O-GlcNAc transferase(OGT) and O-GlcNAcase. Many proteins, such as transcription factors, enzymes, cytoskeletal proteins, ribosomal proteins and chaperones have been identified to be modified with O-GlcNAc. O-GlcNAc modification modifies at their Ser/Thr residues and affects their functions. The hexosamine biosynthesis pathway takes about 5% of glucose in total glucose flux, and it’s final product is UDP-GlcNAc, which is source of O-GlcNAc modification. O-GlcNAc modification is reported to involve in skeletal muscle metabolism and development process. We studied whether O-GlcNAc modification is involved in differentiation in myoblast C2C12 cell. We observed that total O-GlcNAc modification level was dynamically changed during myogenesis. After treatment NButGT, we observed that myogenin expression level decreased. Using RT PCR, we found that mRNA level of myogenin decrease after treatment NButGT. And we found that the promoter activity of myogenin decreases after NButGT using reporter gene assay. For finding the promoter region affected O-GlcNAc , we did reporter gene assay using shorter length promoter and found at least 169 base pair upstream region of myogenin is affected by O-GlcNAc. And using this region, we found that Mef2c protein can be important transcription factor regulated by O-GlcNAc using avidin-biotin complex DNA binding assay. We confirm that Mef2c is O-GlcNAcylated using immunoprecipitation and we found several O-GlcNAcylated sites on Mef2c using mass spectrometry. Based on the result, we made the Mef2c point mutants converted from Serine, Threonine of O-GlcNAcylated sites to Alanine. Additionally, we found O-GlcNAc modification could regulate DNA binding affinity and transcriptional complex formation.