As the number of coronavirus disease 2019 (COVID-19) patients increased rapidly, the Korean government decided to pay most of the related medical expenses with finances from the National Health Insurance (NHI). We aimed to document changes in NHI medical expenses during the COVID-19 pandemic period. We also sought to compare how Japan and Taiwan, neighboring countries with NHI systems, responded to COVID-19 and to discuss policy implications.

OBJECTIVES: A positive association between air pollution and both the incidence and prevalence of diabetes mellitus (DM) has been reported in some epidemiologic and animal studies, but little research has evaluated the relationship between air pollution and diabetic coma. Diabetic coma is an acute complication of DM caused by diabetic ketoacidosis or hyperosmolar hyperglycemic state, which is characterized by extreme hyperglycemia accompanied by coma. We conducted a time-series study with a generalized additive model using a distributed-lag non-linear model to assess the association between ambient air pollution (particulate matter less than 10 μm in aerodynamic diameter, nitrogen dioxide [NO2], sulfur dioxide, carbon monoxide, and ozone) and emergency department (ED) visits for DM with coma in Seoul, Korea from 2005 to 2009. METHODS: The ED data and medical records from the 3 years previous to each diabetic coma event were obtained from the Health Insurance Review and Assessment Service to examine the relationship with air pollutants. RESULTS: Overall, the adjusted relative risks (RRs) for an interquartile range (IQR) increment of NO2 was statistically significant at lag 1 (RR, 1.125; 95% confidence interval [CI], 1.039 to 1.219) in a single-lag model and both lag 0-1 (RR, 1.120; 95% CI, 1.028 to 1.219) and lag 0-3 (RR, 1.092; 95% CI, 1.005 to 1.186) in a cumulative-lag model. In a subgroup analysis, significant positive RRs were found for females for per-IQR increments of NO2 at cumulative lag 0-3 (RR, 1.149; 95% CI, 1.022 to 1.291). CONCLUSIONS: The results of our study suggest that ambient air pollution, specifically NO2, is associated with ED visits for diabetic coma.
Air Pollutants ; Air Pollution* ; Animals ; Carbon Monoxide ; Coma ; Diabetes Mellitus ; Diabetic Coma* ; Diabetic Ketoacidosis ; Emergencies* ; Emergency Service, Hospital* ; Female ; Humans ; Hyperglycemia ; Hyperglycemic Hyperosmolar Nonketotic Coma ; Incidence ; Insurance, Health ; Korea* ; Medical Records ; Nitrogen Dioxide ; Nonlinear Dynamics ; Prevalence ; Seoul* ; Sulfur Dioxide

OBJECTIVES: The goal of this study was to investigate the short-term effect of ambient air pollution on emergency department (ED) visits in Seoul for asthma according to patients’ prior history of allergic diseases. METHODS: Data on ED visits from 2005 to 2009 were obtained from the Health Insurance Review and Assessment Service. To evaluate the risk of ED visits for asthma related to ambient air pollutants (carbon monoxide [CO], nitrogen dioxide [NO₂], ozone [O₃], sulfur dioxide [SO₂], and particulate matter with an aerodynamic diameter <10 μm [PM₁₀]), a generalized additive model with a Poisson distribution was used; a single-lag model and a cumulative-effect model (average concentration over the previous 1-7 days) were also explored. The percent increase and 95% confidence interval (CI) were calculated for each interquartile range (IQR) increment in the concentration of each air pollutant. Subgroup analyses were done by age, gender, the presence of allergic disease, and season. RESULTS: A total of 33 751 asthma attack cases were observed during the study period. The strongest association was a 9.6% increase (95% CI, 6.9% to 12.3%) in the risk of ED visits for asthma per IQR increase in O₃ concentration. IQR changes in NO₂ and PM₁₀ concentrations were also significantly associated with ED visits in the cumulative lag 7 model. Among patients with a prior history of allergic rhinitis or atopic dermatitis, the risk of ED visits for asthma per IQR increase in PM₁₀ concentration was higher (3.9%; 95% CI, 1.2% to 6.7%) than in patients with no such history. CONCLUSIONS: Ambient air pollutants were positively associated with ED visits for asthma, especially among subjects with a prior history of allergic rhinitis or atopic dermatitis.
Air Pollutants ; Air Pollution* ; Asthma* ; Dermatitis, Atopic ; Emergencies* ; Emergency Service, Hospital* ; Humans ; Insurance, Health ; Korea ; Nitrogen Dioxide ; Ozone ; Particulate Matter ; Rhinitis, Allergic ; Seasons ; Seoul ; Sulfur Dioxide

Background : This study was designed to investigate gastrointestinal neuroendocrine tumors with an emphasis on their clinicopathological characteristics. Methods : Sixty-five cases were reviewed and classified as typical carcinoid (TC), atypical carcinoid (AC), large cell neuroendocrine carcinoma (LCNEC) and small cell carcinoma (SmCC). We performed immunohistochemistry to characterize the expression of the immunoreactivity for synaptophysin, chromogranin, gastrin, somatostatin, thyroid transcription factor-1, p53 and Ki-67. Results : Most commonly, the tumors were located in the rectum (54%), followed by the stomach (23%) and colon (9%). Histologically, the tumors were classified as 49 TCs, 4 ACs, 6 LCNECs and 6 SmCCs. Most tumors were stained positive for synaptophysin and/or chromogranin. Four LCNECs and one SmCC were p53-positive. The carcinoids revealed a low level (<5%) of reactivity for Ki-67, while > or =30% of the cells showed reactivity for Ki-67 in the majority of LCNECs and SmCCs. Six patients with metastatic carcinoids were older than those patients without metastasis (64 vs 48 years, respectively, p=0.004). Furthermore, the size of tumors was larger for the patients with metastatic carcinoids than for the patients with nonmetastatic carcinoids (2.3 vs 0.5 cm, respectively, p=0.005). Conclusion : Old age, large tumor size and muscle invasion are associated with high grade neuroendocrine tumor and lymph node metastasis for those patients with carcinoids.
Carcinoid Tumor ; Carcinoma, Neuroendocrine ; Carcinoma, Small Cell ; Colon ; Gastrins ; Gastrointestinal Tract ; Humans ; Immunohistochemistry ; Lymph Nodes ; Neoplasm Metastasis ; Neuroendocrine Tumors* ; Rectum ; Somatostatin ; Stomach ; Synaptophysin ; Thyroid Gland

BACKGROUND: The molecular events leading to the development of sporadic late-onset Alzheimer's disease (AD) have not been defined. A number of mechanism for the protective effects of non-steroidal anti-inflammatory drugs (NSAIDs) in AD have been proposed. We investigated the ibuprofen effect of global gene expression on the amyloid-beta25-35 (Abeta25-35)-stimulated human astrocytoma cell. METHODS: U373MG, a human astrocytoma cell line, was incubated with 25 microM of aggregated Abeta25-35 or aggregated Abeta25-35 plus 100 microM ibuprofen at 37degrees C for 24 hours. Cells treated with ibuprofen alone were used as the negative control. Differential gene expression analysis was carried out with the Illumina human whole genome microarray. Real-time reverse transcriptase polymerase chain reaction (RT-PCR) was also done to validate the gene expression changes. After Welch's t-test, the significant subset of outlier genes were identified by an expression change cut-off 1.5 fold, p<0.05. Kyoto Encyclopedia of Genes and Genomes database was used for cellular signaling pathway analysis. RESULTS: A total of 371 differentially expressed genes were identified from 16,692 detectable signals in Abeta25-35 peptide stimulated U373MG cells- 182 up-regulated genes with 21 biological pathways including biosynthesis of steroid, peroxisome proliferator-activated receptor signaling pathway and focal adhesion and 189 down-regulated genes with 14 biological pathways including transforming growth factor-beta signaling pathway, axon guidance and mitogen activated protein kinase signaling pathway. Ibuprofen suppressed the up-regulated expression of immunity/inflammation (especially, SERPINE1), signal pathway, metabolism and cancer-related genes. The expression of microarray data was confirmed by real-time RT-PCR. CONCLUSION: Aggregated Abeta25-35 induces expression of widespread transcriptional alterations, namely 21 functional groups 182 up-regulated genes and 14 functional groups 189 down-regulated genes in U373MG cells. Ibuprofen, a commonly used NSAID, suppressed Abeta25-35-induced increase of global changes in transcription of sets of genes especially immunity/inflammation, signal pathway, metabolism and cancer-related genes.
Alzheimer Disease ; Amyloid beta-Peptides ; Anti-Inflammatory Agents, Non-Steroidal ; Astrocytoma ; Axons ; Cell Line ; Focal Adhesions ; Gene Expression ; Genome ; Humans ; Ibuprofen ; Oligonucleotide Array Sequence Analysis ; Peptide Fragments ; Peroxisomes ; Protein Kinases ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction

PURPOSE: The association between liver enzymes and death from external causes has not been examined. We investigated the association between serum aminotransferase levels and external-cause mortality in a large prospective cohort study. MATERIALS AND METHODS: A total of 142322 subjects of 35-59 years of age who completed baseline examinations in 1990 and 1992 were enrolled. Mortalities were identified using death certificates. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were categorized into quintiles. Sub-distribution hazards ratios and 95% confidence intervals (CIs) were estimated using a competing risks regression model in which deaths from other causes were treated as competing risks. RESULTS: Of 8808 deaths, 1111 (12.6%) were due to external causes. Injury accounted for 256 deaths, and suicide accounted for 255. After adjusting for covariates, elevated ALT and AST were significantly associated with an increased risk of all external-cause mortalities, as well as suicide and injury. Sub-distribution hazards ratios (95% CIs) of the highest versus the lowest quintiles of serum ALT and AST were, respectively, 1.57 (1.26-1.95) and 1.45 (1.20-1.76) for all external causes, 2.73 (1.68-4.46) and 1.75 (1.15-2.66) for suicide, and 1.79 (1.10-2.90) and 1.85 (1.21-2.82) for injury. The risk of external-cause mortality was also significantly higher in the fourth quintile of ALT (21.6-27.5 IU/L) than in its first quintile. CONCLUSION: Elevated aminotransferase levels, even within the normal range, were significantly associated with increased risk of all external-cause mortalities, including suicide, and injury.
Adult ; Alanine Transaminase/*blood/metabolism ; Aspartate Aminotransferases/*blood/metabolism ; Female ; Humans ; Male ; Middle Aged ; *Mortality ; *Population Surveillance ; Proportional Hazards Models ; Prospective Studies ; Republic of Korea/epidemiology ; Risk

OBJECTIVES: Neurological soft signs have been regarded as endophenotypes associated with the genetic basis of schizophrenia. This study was to investigate the intra-familial correlations of the neurological soft signs according to their genetic loading. METHODS: Schizophrenic patients(N=14) were included, who had one parent with a family history of schizophrenia and the other without it. Genetic loading was determined by the patient's family history of schizophrenia using the Family Interview for Genetic Studies(FIGS). These parents were subdivided into two groups. The first group was designated as'presumed carriers'(N=9) of genetic loading, who had one or more schizophreic first- or second-degree relatives. The second group was designated as'presumed non-carriers'(N=11) of genetic loading, who had no schizophrenic first- or second-degree relatives. Normal controls(N=12) consisted of people without schizophrenic relatives. NSS were evaluated using the Neurological Evaluation Scale-Korean Version (NES-K), and the intra-familial correlations of NSS were tested using the Intra-Class Coefficients(ICC) method. RESULTS: The scores of Motor Coordination subdimension of NES-K were significantly correlated between the patients and their presumed carriers(ICC=.804, p=.016), but not significantly correlated between the patients and their presumed noncarriers. In other subdimensions of NES-K, no significant correlation were found between the patients and their parents regardless of the genetic loading. But, there were no statistically significant differences in the scores of Motor Coordination subdimension of NES-K between the patients and controls. CONCLUSION: This study did not prove that the neurological soft signs might be an endophenotype of schizophrenia that cosegregate with the genetic loading. The future study using more subjects than this would be needed.
Endophenotypes ; Genetic Load ; Humans ; Parents ; Schizophrenia

Autosomal dominant polycystic kidney disease (ADPKD) is a systemic disorder associated with various extrarenal complications. The major cardiovascular complications of ADPKD include valvulopathies and vascular ectasia. A 64-year-old man who was diagnosed with ADPKD seven years previously was admitted to our hospital for heart failure. Pelvic computed tomography revealed multiple variable-sized cysts in both kidneys. Transthoracic echocardiography showed enlargement of the left ventricle and left atrium. Severe mitral regurgitation and moderate aortic regurgitation with annuloaortic ectasia were observed. The left main coronary artery was dilated. The patient had various cardiovascular features associated with ADPKD.
Aortic Valve Insufficiency ; Coronary Vessels ; Dilatation, Pathologic ; Echocardiography ; Heart Atria ; Heart Failure ; Heart Ventricles ; Humans ; Kidney ; Middle Aged ; Mitral Valve Insufficiency ; Polycystic Kidney, Autosomal Dominant*

Humoral hypercalcemia of malignancy (HHM) is rarely associated with cholangiocarcinoma (CC), and represents dismal prognosis. A 63-year-old male was admitted for evaluation of an intrahepatic mass. He was diagnosed with HHM associated with locally advanced CC. As the tumor responded to the concurrent chemoradiotherapy with capecitabine and cisplatin, serum calcium level was normalized. However, according to the disease progression, he suffered recurrence of HHM and he expired approximately one year after initial diagnosis. A 68-year-old male who presented with abdominal pain was diagnosed with metastatic CC. After the eighth cycle of gemcitabine and cisplatin, progression of the disease was found with HHM. He was treated with the best supportive care, until his demise approximately one month after the diagnosis of HHM. We report on two cases of HHM associated with CC that demonstrate strong correlation between hypercalcemia and disease burden.
Abdominal Pain ; Calcium ; Chemoradiotherapy ; Cholangiocarcinoma ; Cisplatin ; Deoxycytidine ; Disease Progression ; Fluorouracil ; Humans ; Hypercalcemia ; Male ; Paraneoplastic Syndromes ; Parathyroid Hormone-Related Protein ; Prognosis ; Recurrence ; Capecitabine

SINE-VNTR-Alu (SVA) elements are present in hominoid primates and are divided into 6 subfamilies (SVA-A to SVA-F) and active in the human population. Using a bioinformatic tool, 22 SVA element-associated genes are identified in the human genome. In an analysis of genomic structure, SVA elements are detected in the 5' untranslated region (UTR) of HGSNAT (SVA-B), MRGPRX3 (SVA-D), HYAL1 (SVA-F), TCHH (SVA-F), and ATXN2L (SVA-F) genes, while some elements are observed in the 3'UTR of SPICE1 (SVA-B), TDRKH (SVA-C), GOSR1 (SVA-D), BBS5 (SVA-D), NEK5 (SVA-D), ABHD2 (SVA-F), C1QTNF7 (SVA-F), ORC6L (SVA-F), TMEM69 (SVA-F), and CCDC137 (SVA-F) genes. They could contribute to exon extension or supplying poly A signals. LEPR (SVA-C), ALOX5 (SVA-D), PDS5B (SVA-D), and ABCA10 (SVA-F) genes also showed alternative transcripts by SVA exonization events. Dominant expression of HYAL1_SVA appeared in lung tissues, while HYAL1_noSVA showed ubiquitous expression in various human tissues. Expression of both transcripts (TDRKH_SVA and TDRKH_noSVA) of the TDRKH gene appeared to be ubiquitous. Taken together, these data suggest that SVA elements cause transcript isoforms that contribute to modulation of gene regulation in various human tissues.
3' Untranslated Regions ; 5' Untranslated Regions ; Exons ; Gene Expression Profiling ; Genome, Human ; Genomics ; Humans ; Lung ; Organ Specificity ; Poly A ; Primates ; Protein Isoforms