Objectives: The purpose of our study was to investigate medical care utilization behavior and the conceptions of disease treatment among spine disease patients.Summary of Literature Review: Analyzing the medical care utilization behavior and conceptions of disease treatment among spine disease patients is important. Materials and Methods: A survey was administered to 500 first-time patients who visited the spine center of a tertiary educational hospital from May 2017 to August 2019. Results: A total of 479 valid responses were analyzed. A minority of patients (16.1%) visited the tertiary educational hospital without having previously visited a private hospital. Spinal procedures and surgery were considered negatively by 52.6% of respondents, and 14.8% of patients reported negative perceptions of orthopedic drugs. Conclusions Extensive efforts will be required to improve unreasonable medical utilization behavior by changing patients’ incorrect knowledge and beliefs about hospitals, diseases, and treatments.

Osteoporotic fractures (OFs) are critical hard outcomes of osteoporosis and are characterized by decreased bone strength induced by low bone density and microarchitectural deterioration in bone tissue. Most OFs cause acute pain, hospitalization, immobilization, and slow recovery in patients and are associated with increased mortality. A variety of genetic studies have suggested associations of genetic variants with the risk of OF. Genome-wide association studies have reported various single-nucleotide polymorphisms and copy number variations (CNVs) in European and Asian populations. To identify CNV regions associated with OF risk, we conducted a genome-wide CNV study in a Korean population. We performed logistic regression analyses in 1,537 Korean subjects (299 OF cases and 1,238 healthy controls) and identified a total of 8 CNV regions significantly associated with OF (p < 0.05). Then, one CNV region located on chromosome 20q13.12 was selected for experimental validation. The selected CNV region was experimentally validated by quantitative polymerase chain reaction. The CNV region of chromosome 20q13.12 is positioned upstream of a family of long non-coding RNAs, LINC01260. Our findings could provide new information on the genetic factors associated with the risk of OF.
Acute Pain ; Asian Continental Ancestry Group ; Bone and Bones ; Bone Density ; DNA Copy Number Variations ; Genome-Wide Association Study ; Hospitalization ; Humans ; Immobilization ; Logistic Models ; Mortality ; Osteoporosis ; Osteoporotic Fractures* ; Polymerase Chain Reaction ; Real-Time Polymerase Chain Reaction ; RNA, Long Noncoding

BACKGROUND: Until recently, genome-wide association study (GWAS)-based findings have provided a substantial genetic contribution to type 2 diabetes mellitus (T2DM) or related glycemic traits. However, identification of allelic heterogeneity and population-specific genetic variants under consideration of potential confounding factors will be very valuable for clinical applicability. To identify novel susceptibility loci for T2DM and glycemic traits, we performed a two-stage genetic association study in a Korean population. METHODS: We performed a logistic analysis for T2DM, and the first discovery GWAS was analyzed for 1,042 cases and 2,943 controls recruited from a population-based cohort (KARE, n=8,842). The second stage, de novo replication analysis, was performed in 1,216 cases and 1,352 controls selected from an independent population-based cohort (Health 2, n=8,500). A multiple linear regression analysis for glycemic traits was further performed in a total of 14,232 nondiabetic individuals consisting of 7,696 GWAS and 6,536 replication study participants. A meta-analysis was performed on the combined results using effect size and standard errors estimated for stage 1 and 2, respectively. RESULTS: A combined meta-analysis for T2DM identified two new (rs11065756 and rs2074356) loci reaching genome-wide significance in CCDC63 and C12orf51 on the 12q24 region. In addition, these variants were significantly associated with fasting plasma glucose and homeostasis model assessment of beta-cell function. Interestingly, two independent single nucleotide polymorphisms were associated with sex-specific stratification in this study. CONCLUSION: Our study showed a strong association between T2DM and glycemic traits. We further observed that two novel loci with multiple diverse effects were highly specific to males. Taken together, these findings may provide additional insights into the clinical assessment or subclassification of disease risk in a Korean population.
Blood Glucose ; Cohort Studies ; Diabetes Mellitus, Type 2* ; Fasting ; Genetic Association Studies ; Genome-Wide Association Study* ; Homeostasis ; Humans ; Linear Models ; Male ; Polymorphism, Single Nucleotide ; Population Characteristics

No abstract available.
Diabetes Mellitus, Type 2* ; Genome-Wide Association Study*

BACKGROUND AND OBJECTIVES: Ten to twenty percent of children with Kawasaki disease (KD) do not respond to initial intravenous immunoglobulin (IVIG) treatment. If untreated, approximately 15% to 25% of KD patients have complications. The aim of this study was to find useful predictors of responsiveness to initial IVIG treatment in KD. SUBJECTS AND METHODS: We retrospectively reviewed medical records of 91 children diagnosed with KD at Myong Ji Hospital from March 2012 to April 2014. Before and after (24 hours to 36 hours) IVIG treatment, the following laboratory data were obtained: hemoglobin (Hb) level, white blood cell count, proportion of neutrophil, lymphocyte and eosinophil, platelet count, erythrocyte sedimentation rate (ERS), C-reactive protein (CRP), creatine kinase (CK), creatine kinase MB (CK-MB), and N-terminal pro-brain natriuretic peptide (NT-proBNP). Subjects were then divided into two groups: IVIG-responsive or IVIG-resistant. RESULTS: Of 91 patients, 11 (12%) required retreatment. By univariate analysis, before-IVIG laboratory parameters of white blood cell count, % neutrophil, ERS, CRP, sodium, CK, CK-MB, and NT-proBNP were significantly different between IVIG-responsive and IVIG-resistant patient groups. In the after-IVIG laboratory parameters, Hb level, white blood cell count, % neutrophil, % lymphocyte, CRP, CK, CK-MB, and NT-pro-BNP were significantly different between the two groups. While the mean-differences were not statistically significant, fractional change (FC)-CRP and FC-% neutrophil showed significant difference. By multivariate analysis, FC-CRP was confirmed to be an independent predictor for initial IVIG resistance. CONCLUSION: Fractional change-C-reactive protein might be a useful and important value for predicting initial IVIG resistance in KD patients.
Blood Sedimentation ; C-Reactive Protein ; Child ; Creatine Kinase ; Eosinophils ; Humans ; Immunization, Passive* ; Immunoglobulins ; Immunoglobulins, Intravenous ; Leukocyte Count ; Lymphocytes ; Medical Records ; Mucocutaneous Lymph Node Syndrome* ; Multivariate Analysis ; Neutrophils ; Platelet Count ; Retreatment ; Retrospective Studies ; Risk Factors ; Sodium

The carcinoid tumors of middle ear are very rare, however, more than 50 cases including 2 cases in Korea have been reported since 1980. A 36-year-old male had been managed under the diagnostic impression of hemotympanum due to head trauma in 2005; he revisited our clinic after 8 years with sudden facial paralysis and external auditory canal mass. Canal wall down mastoidectomy and tympanoplasty were performed and pathologic results revealed a carcinoid tumor of the middle ear. A facial paralysis of this patient was cured after the treatment.
Adult ; Carcinoid Tumor* ; Craniocerebral Trauma ; Ear Canal ; Ear, Middle* ; Facial Paralysis* ; Humans ; Korea ; Male ; Tympanoplasty

Liver enzyme elevations, as an indicator of liver function, are widely associated with metabolic diseases. Genome-wide population-based association studies have identified a genetic susceptibility to liver enzyme elevations and their related traits; however, the genetic architecture in childhood remains largely unknown. We performed a genome-wide association study to identify new genetic loci for liver enzyme levels in a Korean childhood cohort (n = 484). We observed three novel loci (rs4949718, rs80311637, and rs596406) that were multiply associated with elevated levels of alanine transaminase and aspartate transaminase. Although there are some limitations, including genetic power, additional replication and functional characterization will support the clarity on the genetic contribution that the ST6GALNAC3, ADAMTS9, and CELF2 genes have in childhood liver function.
Alanine Transaminase ; Aspartate Aminotransferases ; Child ; Cohort Studies ; Genetic Loci ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Humans ; Liver ; Metabolic Diseases

Hypertension is the major factor of most death and high blood pressure (BP) can lead to stroke, myocardial infarction and cardiac failure. Moreover, hypertension is strongly correlated with body mass index (BMI). Although the exact causes of hypertension are still unclear, some of genetic loci were discovered from genome-wide association study (GWAS). Therefore, it is essential to study genetic variation for finding more genetic factor affecting hypertension. The purpose of our study is to conduct a CNV association study for hypertension-related traits, BP and BMI, in Korean individuals. We identified 2,206 CNV regions from 3,274 community-based Korean participants using the Affymetrix Genome-Wide Human SNP Array 6.0 platform and performed a logistic regression analysis of CNVs with two hypertension-related traits, BP and BMI. Moreover, the 4,692 participants in an independent cohort were selected for respective replication analyses. GWAS of CNV identified two loci encompassing previously known hypertension-related genes: LPA (lipoprotein) on 6q26, and JAK2 (Janus kinase 2) on 9p24, with suggestive p-values (0.0334 for LPA and 0.0305 for JAK2). These two positive findings, however, were not evaluated in the replication stage. Our result confirmed the conclusion of CNV study from the WTCCC suggesting weak association with common diseases. This is the first study of CNV association study with BP and BMI in Korean population and it provides a state of CNV association study with common human diseases using SNP array.
Blood Pressure ; Body Mass Index ; Coat Protein Complex I ; Cohort Studies ; Genetic Loci ; Genetic Variation ; Genome-Wide Association Study ; Heart Failure ; Humans ; Hypertension ; Logistic Models ; Myocardial Infarction ; Phosphotransferases ; Stroke

Protein arginine methylation is important for a variety of cellular processes including transcriptional regulation, mRNA splicing, DNA repair, nuclear/cytoplasmic shuttling and various signal transduction pathways. However, the role of arginine methylation in protein biosynthesis and the extracellular signals that control arginine methylation are not fully understood. Basic fibroblast growth factor (bFGF) has been identified as a potent stimulator of myofibroblast dedifferentiation into fibroblasts. We demonstrated that symmetric arginine dimethylation of eukaryotic elongation factor 2 (eEF2) is induced by bFGF without the change in the expression level of eEF2 in mouse embryo fibroblast NIH3T3 cells. The eEF2 methylation is preceded by ras-raf-mitogen-activated protein kinase kinase (MEK)-extracellular signal-regulated kinase (ERK1/2)-p21(Cip/WAF1) activation, and suppressed by the mitogen-activated protein kinase (MAPK) inhibitor PD98059 and p21(Cip/WAF1) short interfering RNA (siRNA). We determined that protein arginine methyltransferase 7 (PRMT7) is responsible for the methylation, and that PRMT5 acts as a coordinator. Collectively, we demonstrated that eEF2, a key factor involved in protein translational elongation is symmetrically arginine-methylated in a reversible manner, being regulated by bFGF through MAPK signaling pathway.
Animals ; Arginine ; Cell Dedifferentiation ; Cyclin-Dependent Kinase Inhibitor p21/genetics/metabolism ; Elongation Factor 2 Kinase/*metabolism ; Fibroblast Growth Factor 2/*metabolism ; Fibroblasts/*metabolism/pathology ; Flavonoids/pharmacology ; MAP Kinase Signaling System/drug effects/genetics ; Methylation ; Mice ; Mitogen-Activated Protein Kinases/antagonists & inhibitors ; Myofibroblasts/pathology ; NIH 3T3 Cells ; Protein Methyltransferases/*metabolism ; Protein-Arginine N-Methyltransferases/*metabolism ; RNA, Small Interfering/genetics

Protein arginine methylation is important for a variety of cellular processes including transcriptional regulation, mRNA splicing, DNA repair, nuclear/cytoplasmic shuttling and various signal transduction pathways. However, the role of arginine methylation in protein biosynthesis and the extracellular signals that control arginine methylation are not fully understood. Basic fibroblast growth factor (bFGF) has been identified as a potent stimulator of myofibroblast dedifferentiation into fibroblasts. We demonstrated that symmetric arginine dimethylation of eukaryotic elongation factor 2 (eEF2) is induced by bFGF without the change in the expression level of eEF2 in mouse embryo fibroblast NIH3T3 cells. The eEF2 methylation is preceded by ras-raf-mitogen-activated protein kinase kinase (MEK)-extracellular signal-regulated kinase (ERK1/2)-p21(Cip/WAF1) activation, and suppressed by the mitogen-activated protein kinase (MAPK) inhibitor PD98059 and p21(Cip/WAF1) short interfering RNA (siRNA). We determined that protein arginine methyltransferase 7 (PRMT7) is responsible for the methylation, and that PRMT5 acts as a coordinator. Collectively, we demonstrated that eEF2, a key factor involved in protein translational elongation is symmetrically arginine-methylated in a reversible manner, being regulated by bFGF through MAPK signaling pathway.
Animals ; Arginine ; Cell Dedifferentiation ; Cyclin-Dependent Kinase Inhibitor p21/genetics/metabolism ; Elongation Factor 2 Kinase/*metabolism ; Fibroblast Growth Factor 2/*metabolism ; Fibroblasts/*metabolism/pathology ; Flavonoids/pharmacology ; MAP Kinase Signaling System/drug effects/genetics ; Methylation ; Mice ; Mitogen-Activated Protein Kinases/antagonists & inhibitors ; Myofibroblasts/pathology ; NIH 3T3 Cells ; Protein Methyltransferases/*metabolism ; Protein-Arginine N-Methyltransferases/*metabolism ; RNA, Small Interfering/genetics