According to previous survey, about two million of people were expected to suffer from toxic effects due to humidifier disinfectant (HD), regardless of healing or not. Extremely small group are recognized as HDs’ victims. Up to now, previous research tried to focus on interstitial fibrosis on terminal bronchiole because it is specific finding, compared with other diseases. To figure out overall effects from HDs, we recommend adverse outcome pathways (AOPs) as new approach. Reactive oxygen species (ROS) generation, decreased T-cell and pro-inflammatory cytokine release from macrophage could be key events between the exposure to HDs and diseases. ROS generation, decreased cell and pro-inflammatory cytokine release from macrophage could be cause of interstitial fibrosis, pneumonia and many other diseases such as asthma, allergic rhinitis, allergic dermatitis, fetal death, premature baby, autoimmune disease, hepatic toxicity, renal toxicity, cancer, and so on. We predict potential disease candidate by AOPs. We can validate the real risk of the adverse outcome by epidemiologic and toxicologic study using big data such as National Health Insurance data and AOPs knowledge base. Application of these kinds of new methods can find the potential disease list from the exposure to HD.
Asthma ; Autoimmune Diseases ; Bronchioles ; Dermatitis ; Fetal Death ; Fibrosis ; Humidifiers* ; Knowledge Bases ; Macrophages ; National Health Programs ; Pneumonia ; Reactive Oxygen Species ; Rhinitis, Allergic ; T-Lymphocytes

According to previous survey, about two million of people were expected to suffer from toxic effects due to humidifier disinfectant (HD), regardless of healing or not. Extremely small group are recognized as HDs’ victims. Up to now, previous research tried to focus on interstitial fibrosis on terminal bronchiole because it is specific finding, compared with other diseases. To figure out overall effects from HDs, we recommend adverse outcome pathways (AOPs) as new approach. Reactive oxygen species (ROS) generation, decreased T-cell and pro-inflammatory cytokine release from macrophage could be key events between the exposure to HDs and diseases. ROS generation, decreased cell and pro-inflammatory cytokine release from macrophage could be cause of interstitial fibrosis, pneumonia and many other diseases such as asthma, allergic rhinitis, allergic dermatitis, fetal death, premature baby, autoimmune disease, hepatic toxicity, renal toxicity, cancer, and so on. We predict potential disease candidate by AOPs. We can validate the real risk of the adverse outcome by epidemiologic and toxicologic study using big data such as National Health Insurance data and AOPs knowledge base. Application of these kinds of new methods can find the potential disease list from the exposure to HD.
Asthma ; Autoimmune Diseases ; Bronchioles ; Dermatitis ; Fetal Death ; Fibrosis ; Humidifiers ; Knowledge Bases ; Macrophages ; National Health Programs ; Pneumonia ; Reactive Oxygen Species ; Rhinitis, Allergic ; T-Lymphocytes

Several studies showed that the inflammatory and fibrotic responses induced by polyhexamethylene guanidine phosphate (PHMG-p) were similar to those observed for idiopathic pulmonary fibrosis in South Korea in 2011. “Omic” technologies can be used to understand the mechanisms underlying chemical-induced diseases. Studies to determine the toxicity of chemicals may facilitate understanding of the mechanisms underlying the development of pulmonary fibrosis at a molecular level; thus, such studies may provide information about the toxic characteristics of various substances. In this review, we have outlined the cellular and molecular mechanisms underlying idiopathic pulmonary fibrosis and described pulmonary fibrosis induced by various chemicals, including bleomycin, paraquat, and PHMG-p, based on the results of studies performed to date.
Bleomycin ; Epithelial Cells ; Guanidine ; Idiopathic Pulmonary Fibrosis ; Korea ; MicroRNAs ; Paraquat ; Pulmonary Fibrosis

Several studies showed that the inflammatory and fibrotic responses induced by polyhexamethylene guanidine phosphate (PHMG-p) were similar to those observed for idiopathic pulmonary fibrosis in South Korea in 2011. “Omic” technologies can be used to understand the mechanisms underlying chemical-induced diseases. Studies to determine the toxicity of chemicals may facilitate understanding of the mechanisms underlying the development of pulmonary fibrosis at a molecular level; thus, such studies may provide information about the toxic characteristics of various substances. In this review, we have outlined the cellular and molecular mechanisms underlying idiopathic pulmonary fibrosis and described pulmonary fibrosis induced by various chemicals, including bleomycin, paraquat, and PHMG-p, based on the results of studies performed to date.
Bleomycin ; Epithelial Cells ; Guanidine ; Idiopathic Pulmonary Fibrosis ; Korea ; MicroRNAs ; Paraquat ; Pulmonary Fibrosis*

Carcinoembryonic antigen(CEA) in blood and CSF was reported to be increased in cases of nervous system neoplasms by some investigators. To evaluate the oncological diagnostic value of CEA in the neurosurgical conditions, this study has been performed on 24 nervous system neoplasms and 8 non-nervous system as well as 49 controls. In addition, alpha-fetoprotein was also measured on the same conditions because of its close oncologic nature and recent diagnostic application on the general surgical conditions. The CEA concentration in blood and CSF were determined by CEA Radioimmunoassay kit, and the alpha-fetoprotein in blood and CSF were determined by GammaDab kit. The result showed that concentration of CEA and alpha-fetoprotein was higher and seemed to diagnostic in Extra-CNS neoplasma. In nerovous system, however, these were the lower than we expected, although were higher than control. Moreever, these levels were not unique on same oncologic condition and rather somewhat variable. From these results, increased concentration of these itself may be considered suggestive of existence of nervous system neoplasm, but it does mean neither degree of malignancy nor its origin.
alpha-Fetoproteins* ; Carcinoembryonic Antigen* ; Central Nervous System ; Humans ; Nervous System Neoplasms ; Radioimmunoassay ; Research Personnel

OBJECTIVES: Aromatase inhibitors that block estrogen synthesis are a proven first-line hormonal therapy for postmenopausal breast cancer. Although it is known that standardized extract of Ginkgo biloba (EGb761) induces anti-carcinogenic effects like the aromatase inhibitors, the effects of EGb761 on steroidogenesis have not been studied yet. Therefore, the effects of EGb761 on steroidogenesis and aromatase activity was studied using a H295R cell model, which was a good in vitro model to predict effects on human adrenal steroidogenesis. METHODS: Cortisol, aldosterone, testosterone, and 17β-estradiol were evaluated in the H295R cells by competitive enzyme-linked immunospecific assay after exposure to EGb761. Real-time polymerase chain reaction were performed to evaluate effects on critical genes in steroid hormone production, specifically cytochrome P450 (CYP11/17/19/21) and the hydroxysteroid dehydrogenases (3β-HSD2 and 17β-HSD1/4). Finally, aromatase activities were measured with a tritiated water-release assay and by western blotting analysis. RESULTS: H295R cells exposed to EGb761 (10 and 100 μg/mL) showed a significant decrease in 17β-estradiol and testosterone, but no change in aldosterone or cortisol. Genes (CYP19 and 17β-HSD1) related to the estrogen steroidogenesis were significantly decreased by EGb761. EGb761 treatment of H295R cells resulted in a significant decrease of aromatase activity as measured by the direct and indirect assays. The coding sequence/ Exon PII of CYP19 gene transcript and protein level of CYP19 were significantly decreased by EGb761. CONCLUSIONS: These results suggest that EGb761 could regulate steroidogenesis-related genes such as CYP19 and 17β-HSD1, and lead to a decrease in 17β-estradiol and testosterone. The present study provides good information on potential therapeutic effects of EGb761 on estrogen dependent breast cancer.
Adrenocortical Carcinoma* ; Aldosterone ; Anticarcinogenic Agents ; Aromatase Inhibitors ; Aromatase* ; Blotting, Western ; Breast Neoplasms ; Clinical Coding ; Cytochrome P-450 Enzyme System ; Estrogens ; Exons ; Ginkgo biloba* ; Humans* ; Hydrocortisone ; Hydroxysteroid Dehydrogenases ; In Vitro Techniques ; Real-Time Polymerase Chain Reaction ; Testosterone ; Therapeutic Uses

Sturge-Weber syndrome was rare. But reported from 1860. We present a typical case of Sturge-Weber syndrome in a child and discussed the symptoms, signs, and pathological finding of various examinations in neurosurgical field such as plain x-ray, 4-vessel angiography, CT scan, EEG, IQ test, exophthamometry, opthalmometry, and fundoscopy. We find marked abnormality and asymmetry in that examination.
Angiography ; Child ; Electroencephalography ; Humans ; Sturge-Weber Syndrome* ; Tomography, X-Ray Computed

No abstract available.
Imaging, Three-Dimensional ; Magnetic Resonance Angiography*

OBJECTIVES: In order to identify the possibility of slender bitterling (SB) (Acheilognathus yamatsutae) being used as a test species for estrogenic endocrine disrupting chemicals (EEDCs), we carried out the cloning and sequence characterization of the estrogen receptor (ER). METHODS: The ER from a slender bitterling was obtained by reverse transcriptase-polymerase chain reaction (RT-PCR), 5'- and 3'-rapid amplification of cDNA ends (5'-RACE and 3'-RACE) and T-vector cloning. The expression of ER mRNA was also analyzed in six tissues (brain, liver, kidney, gill, gonad, and intestines) by real-time PCR. RESULTS: We obtained an ER from the slender bitterling. The SB ER cDNA was 2189 base pairs (bp) in length and contained a 1707 bp open reading frame that encoded 568 amino acid residues. The SB ER amino acid sequence clustered in a monophyletic group with the ERalpha of other fish, and was more closely related to zebrafish ERalpha (88% identity) than to the ERalpha of other fish. The SB ER cDNA was divided into A/B, C, D, E and F domains. The SB ER has conserved important sequences for ER functions, such as the DNA binding domain (D domain), which are consistent with those of other teleosts. CONCLUSIONS: The ER of the slender bitterling could provide basic information in toxicological studies of EEDCs in the slender bitterling.
Amino Acid Sequence ; Animals ; Base Pairing ; Clone Cells ; Cloning, Molecular ; Cloning, Organism ; DNA ; DNA, Complementary ; Endocrine Disruptors ; Estrogen Receptor alpha ; Estrogens ; Gills ; Gonads ; Kidney ; Liver ; Open Reading Frames ; RNA, Messenger ; Zebrafish

OBJECTIVES: Marijuana is one of the most frequently abused drug in Korea and its adverse health effects are controversial. p53 is known to be crucial in regulating the DNA damage responses, and adverse effects can occur when it is regulated by marijuana smoke. We evaluated a role of p53 on genotoxic effect and apoptosis in lung cancer cells exposed to marijuana smoke condensates (MSCs). METHODS: The p53-related genotoxicity and apoptosis of MSCs were evaluated using in vitro bioassay, viz., comet assay, cytokinesis-block micronucleus assay and apoptosis assay. We used two cell lines with differential p53 expression (p53-wildtype (WT) H460 and p53-null H1299). RESULTS: MSCs significantly increased DNA breakages and chromosomal changes in p53-WT H460 and p53-null H1299 cells. The genotoxicity induced by MSCs in p53-null H1299 cells showed greater sensitivity than p53-WT H460 cells. Moreover, MSCs showed a significant increase in reactive oxygen species production and apoptosis. The apoptotic responses induced by MSCs were higher in p53-WT H460 cells than in p53-null H1299 cells. Significantly increased mRNA expression or apoptosis related genes, including p53, caspase-3, and Bax/Bcl-2 ratio were observed in the p53-WT H460 cells exposed to MSCs. CONCLUSIONS: These results suggest that MSCs induce DNA/chromosomal damages and apoptosis in human lung cancer cells and p53 plays an important role in the cellular response to MSCs. The present study may have border implications for our understanding of pulmonary diseases.
Apoptosis ; Biological Assay ; Cannabis ; Caspase 3 ; Cell Line ; Comet Assay ; DNA ; DNA Damage ; Humans ; Korea ; Lung Diseases ; Lung Neoplasms ; Micronucleus Tests ; Reactive Oxygen Species ; RNA, Messenger ; Smoke ; Tumor Suppressor Protein p53