Biomedical subjects

Ho Kim

Publications and source records attributed to Ho Kim.

At least 19 recordsLinked to original sources

PubMed2003

Thyrotropin-mediated repression of class II trans-activator expression in thyroid cells: involvement of STAT3 and suppressor of cytokine signaling.

It has been suggested that class I and class II MHC are contributing factors for numerous diseases including autoimmune thyroid diseases, type 1 diabetes, rheumatoid arthritis, Alzheimer's disease, and multiple sclerosis. The class II trans-activator (CIITA), which is a non-DNA-binding regulator of class II MHC transcription, regulates the constitutive and inducible expression of the class I and class II genes. FRTL-5 thyroid cells incubated in the presence of IFN-gamma have a significantly higher level of cell surface rat MHC class II RTI.B. However, the IFN-gamma-induced RT1.B expression was suppressed significantly in cells incubated in the presence of thyrotropin. Thyrotropin (TSH) represses IFN-gamma-induced CIITA expression by inhibiting type IV CIITA promoter activity through the suppression of STAT1 activation and IFN regulatory factor 1 induction. This study found that TSH induces transcriptional activation of the STAT3 gene through the phosphorylation of STAT3 and CREB activation. TSH induces SOCS-1 and SOCS-3, and TSH-mediated SOCS-3 induction was dependent on STAT3. The cell line stably expressing the wild-type STAT3 showed a higher CIITA induction in response to IFN-gamma and also exhibited TSH repression of the IFN-gamma-mediated induction of CIITA. However, TSH repression of the IFN-gamma-induced CIITA expression was not observed in FRTL-5 thyroid cells, which stably expresses the dominant negative forms of STAT3, STAT3-Y705F, and STAT3-S727A. This report suggests that TSH is also engaged in immunomodulation through signal cross-talk with the cytokines in thyroid cells.

Animals↗

PubMed2003

RET/PTC (rearranged in transformation/papillary thyroid carcinomas) tyrosine kinase phosphorylates and activates phosphoinositide-dependent kinase 1 (PDK1): an alternative phosphatidylinositol 3-kinase-independent pathway to activate PDK1.

Thyroid cancers are a leading cause of death due to endocrine malignancies. RET/PTC (rearranged in transformation/papillary thyroid carcinomas) gene rearrangements are the most frequent genetic alterations identified in papillary thyroid carcinoma. Although the oncogenic potential of RET/PTC is related to intrinsic tyrosine kinase activity, the substrates for this enzyme are yet to be identified. In this report, we show that phosphoinositide-dependent kinase 1 (PDK1), a pivotal serine/threonine kinase in growth factor-signaling pathways, is a target of RET/PTC. RET/PTC and PDK1 colocalize in the cytoplasm. RET/PTC phosphorylates a specific tyrosine (Y9) residue located in the N-terminal region of PDK1. Y9 phosphorylation of PDK1 by RET/PTC requires an intact catalytic kinase domain. The short (iso 9) and long forms (iso 51) of the RET/PTC kinases (RET/PTC1 and RET/PTC3) induce Y9 phosphorylation of PDK1. Moreover, Y9 phosphorylation of PDK1 by RET/PTC does not require phosphatidylinositol 3-kinase or Src activity. RET/PTC-induced phosphorylation of the Y9 residue results in increased PDK1 activity, decrease of cellular p53 levels, and repression of p53-dependent transactivation. In conclusion, RET/PTC-induced tyrosine phosphorylation of PDK1 may be one of the mechanisms by which it acts as an oncogenic tyrosine kinase in thyroid carcinogenesis.

3-Phosphoinositide-Dependent Protein Kinases↗

PubMed2003

The lag-effect pattern in the relationship of particulate air pollution to daily mortality in Seoul, Korea.

To assess differences in the lag-effect pattern in the relationship between particulate matter less than 10 microm in aerodynamic diameter (PM(10)) and cause-specific mortality in Seoul, Korea, from January 1995 to December 1999, we performed a time-series analysis. We used a generalized additive Poisson regression model to control for time trends, temperature, humidity, air pressure, and the day of the week. The PM(10) effect was estimated on the basis of the time-series models using the 24-h means and the quadratic distributed-lag models using a cumulative 6-day effect. One interquartile range increase in the 6-day cumulative mean of PM(10) (43.12 microg/m(3)) was associated with an increase in non-accidental deaths [3.7%, 95% confidence interval (CI): 2.1, 5.4], respiratory disease (13.9%, 95% CI: 6.8, 21.5), cardiovascular disease (4.4%, 95% CI: -1.0, 9.0), and cerebrovascular disease (6.3%, 95% CI: 2.3, 10.5). We found the following patterns in the disease-specific lag-effect window: respiratory mortality was more affected by air pollution level on the day of death, whereas cardiovascular deaths were more affected by the previous day's air pollution level. Cerebrovascular deaths were simultaneously associated with the air pollution levels of the same day and the previous day. The patterns in the lag effect from the distributed-lag models were similar to those of a series of time-series models with 24-h means. These results contribute to our understanding of how exposure to air pollution causes adverse health effects.

Adolescent↗

PubMed2003

CR6-interacting factor 1 interacts with Gadd45 family proteins and modulates the cell cycle.

The Gadd45 family of proteins includes Gadd45alpha, MyD118/Gadd45beta, and CR6/OIG37/Gadd45gamma. These proteins play important roles in maintaining genomic stability and in regulating the cell cycle. This study reports the cloning of a novel protein called CR6-interacting factor 1 (CRIF1) which interacts with Gadd45alpha, MyD118/Gadd45beta, and CR6/OIG37/Gadd45gamma. CRIF1 binds specifically to the Gadd45 family proteins, as determined by an in vitro glutathione S-transferase pull-down assay and an in vivo mammalian cell two-hybrid assay along with coimmunoprecipitation assays. CRIF1 mRNA is highly expressed in the thyroid gland, heart, lymph nodes, trachea, and adrenal tissues. CRIF1 localizes exclusively to the nucleus and colocalizes with Gadd45gamma. Recombinant CRIF1 inhibits the histone H1 kinase activity of immunoprecipitated Cdc2-cyclin B1 and Cdk2-cyclin E, and the inhibitory effects were additive with Gadd45 proteins. Overexpression of CRIF1 increases the percentage of cells in G1, decreases the percentage of cells in S phase, and suppresses growth in NIH3T3 cells. The down-regulation of endogenous CRIF1 by the transfection of the small interfering RNA duplexes resulted in the inactivation of Rb by phosphorylation and decreased the G1 phase cell populations. Expression of CRIF1 is barely detectable in adrenal adenoma and papillary thyroid cancer and much lower than in adjacent normal tissue. The results presented here suggest that CRIF1 is a novel nuclear protein that interacts with Gadd45 and may play a role in negative regulation of cell cycle progression and cell growth.

3T3 Cells↗

PubMed2003

Genetic effects on urinary 1-hydroxypyrene levels in a Korean population.

Urinary 1-hydroxypyrene (1-OHP) has been used as a biomarker for assessing the level of exposure to environmental carcinogenic polycyclic aromatic hydrocarbons (PAHs). In order to perform the appropriate biological monitoring for examining the level of exposure to PAHs, this study investigated whether or not genetic polymorphisms of the metabolic enzymes, which might be involved in the metabolism of pyrene, affected the urinary 1-OHP levels in a population of 661 Koreans (male, 63%; female, 37%; mean age, 36.5 +/- 11.1 years) who were not occupationally exposed to PAHs. Urinary 1-OHP was detected in 76% of the subjects (range 0.001-3.8 micro g/l). Among the physical and lifestyle factors, cigarette-smoking was found to be associated with the urinary 1-OHP levels (P < 0.05). After adjusting for these factors, we found that the GSTT1 genotypes affected the urinary 1-OHP levels, i.e. the GSTT1 present subjects had approximately 1.5 times the urinary 1-OHP level than the GSTT1 null subjects (P < 0.05). In the case of the subjects who were also GSTM1 null, this trend became stronger, i.e. the GSTT1 present subjects had approximately 2 times the urinary 1-OHP level (P < 0.01). However, the genetic polymorphism of the other metabolic enzymes, cytochrome P-450 (CYP)1A1, CYP1B1 and GSTM1 alone, did not affect the urinary 1-OHP level. Therefore, this study suggests that the GSTT1 genetic polymorphism has the potential to affect the biological monitoring of PAHs with urinary 1-OHP, and might act as a genetic factor in PAH-related toxicity.

Adult↗

PubMed2003

Regulation of the phosphatidylinositol 3-kinase, Akt/protein kinase B, FRAP/mammalian target of rapamycin, and ribosomal S6 kinase 1 signaling pathways by thyroid-stimulating hormone (TSH) and stimulating type TSH receptor antibodies in the thyroid gland.

Thyroid-stimulating hormone (TSH) regulates the growth and differentiation of thyrocytes by activating the TSH receptor (TSHR). This study investigated the roles of the phosphatidylinositol 3-kinase (PI3K), PDK1, FRAP/mammalian target of rapamycin, and ribosomal S6 kinase 1 (S6K1) signaling mechanism by which TSH and the stimulating type TSHR antibodies regulate thyrocyte proliferation and the follicle activities in vitro and in vivo. The TSHR immunoprecipitates exhibited PI3K activity, which was higher in the cells treated with either TSH or 8-bromo-cAMP. TSH and cAMP increased the tyrosine phosphorylation of TSHR and the association between TSHR and the p85alpha regulatory subunit of PI3K. TSH induced a redistribution of PDK1 from the cytoplasm to the plasma membrane in the cells in a PI3K- and protein kinase A-dependent manner. TSH induced the PDK1-dependent phosphorylation of S6K1 but did not induce Akt/protein kinase B phosphorylation. The TSH-induced S6K1 phosphorylation was inhibited by a dominant negative p85alpha regulatory subunit or by the PI3K inhibitors wortmannin and LY294002. Rapamycin inhibited the phosphorylation of S6K1 in the cells treated with either TSH or 8-bromo-cAMP. The stimulating type TSHR antibodies from patients with Graves disease also induced S6K1 activation, whereas the blocking type TSHR antibodies from patients with primary myxedema inhibited TSH- but not the insulin-induced phosphorylation of S6K1. In addition, rapamycin treatment in vivo inhibited the TSH-stimulated thyroid follicle hyperplasia and follicle activity. These findings suggest an interaction between TSHR and PI3K, which is stimulated by TSH and cAMP and might involve the downstream S6K1 but not Akt/protein kinase B. This pathway may play a role in the TSH/stimulating type TSH receptor antibody-mediated thyrocyte proliferation in vitro and in the response to TSH in vivo.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed2003

Activation of signal transducer and activator of transcription 3 by oncogenic RET/PTC (rearranged in transformation/papillary thyroid carcinoma) tyrosine kinase: roles in specific gene regulation and cellular transformation.

Thyroid papillary carcinomas are characterized by RET/PTC (rearranged in transformation/papillary thyroid carcinoma) rearrangements that result in fusion of the tyrosine kinase domain of the RET receptor to the N-terminal sequences encoded by heterologous genes. This thyroid-specific rearrangement causes aberrant expression of RET/PTC and results in constitutive ligand-independent activation of RET kinase. However, it is unclear how RET/PTC activates the specific signaling pathways for cellular transformation. In this study, we show that RET/PTC associates with signal transducer and activator of transcription 3 (STAT3) and activates it by the specific phosphorylation of the tyrosine 705 residue. Activation of STAT3 requires the intrinsic kinase activity of RET/PTC; Janus tyrosine kinase and c-Src kinase are not involved in the RET/PTC-mediated activation of STAT3. RET/PTC-induced activation of STAT3 induces the STAT3-responsive genes, vascular endothelial growth factor, cyclin D1, and intercellular adhesion molecule 1. In addition, RET/PTC-mediated cellular transformation and proliferation of transformed cells require tyrosine 705 phosphorylation of STAT3 in NIH3T3 cells. We conclude that STAT3 activation by the RET/PTC tyrosine kinase is one of the critical signaling pathways for the regulation of specific genes, such as cyclin D1, vascular endothelial growth factor, and intercellular adhesion molecule 1, and for cellular transformation.

Carcinoma, Papillary↗

PubMed2003

Ischemic stroke associated with decrease in temperature.

BACKGROUND: Some studies suggest low temperatures can affect mortality, especially deaths associated with circulatory and respiratory conditions. METHODS: We investigated the association between ischemic stroke onset and decrease in temperature in 545 patients over a 3-year period (January 1998 to December 2000) in Incheon, Korea. We used a case-crossover study design to assess changes in the risk of ischemic stroke during a brief hazard period after exposure to decrease in temperature. For each subject, the case period was matched to 2 control periods exactly 1 week before and after onset of the ischemic stroke. RESULTS: Decreased ambient temperature was associated with risk of acute ischemic stroke. The strongest effect was seen on day after exposure to cold weather. The odds ratio (OR) for an interquartile range decrease in temperature was 2.9 (95% confidence interval [CI] = 1.5-5.3). The risk period was 24-48 hours after cold exposure. Risk estimates associated with decreased temperature were greater in the winter than in the summer. Women, persons greater than 65 years of age, nonobese persons, and those with previous hypertension or hypercholesterolemia were more susceptible to cold-induced ischemic stroke. CONCLUSIONS: These results suggest that stroke occurrence rises with decreasing temperature, and that even a moderate decrease in temperature can increase the risk of ischemic stroke. Susceptible people should take steps to protect themselves from cold, especially in the winter.

Age Factors↗

PubMed2003

CXC chemokine receptor 4 expression and function in human anaplastic thyroid cancer cells.

Anaplastic thyroid carcinomas (ATCs) are highly aggressive, extremely lethal human cancers with poor therapeutic response. Chemokines are a superfamily of small cytokine-like proteins that induce, through their interaction with G protein-coupled receptors, cytoskeletal rearrangement, firm adhesion to endothelial cells, and directional migration. In this study, we characterized the expression of CXC chemokine receptor 4 (CXCR4) and analyzed its functions in ARO cells, a human ATC cell. The normal primary cultured thyroid cells and ATC cell lines expressed CXCR4 and stromal cell-derived factor (SDF)-1 alpha transcripts, detected by RT-PCR. Fluorescence activated cell sorting analysis of CXCR4 expression in normal and ATC cells showed that ARO cells expressed significant levels of CXCR4. FRO, NPA, and normal thyroid cells did not express membrane CXCR4, as determined by fluorescence activated cell sorting analysis. To identify the functional role of CXCR4 in ARO cells, we treated ARO cells with SDF-1 alpha and analyzed the signaling pathways, cellular migration, and proliferation. SDF-1alpha enhanced the migration but did not affect the proliferation of ARO cells or activate the Janus kinase/signal transducer and activator of transcription signaling pathways. However, SDF-1 alpha/CXCR4 activation resulted in phosphorylation of the p70S6 kinase and its target protein, ribosomal S6 protein, and also activation of the ERK1/ERK2 signaling pathways. Furthermore, SDF-1 alpha/CXCR4- mediated activation of the p70S6 kinase and phosphorylation of the S6 protein were inhibited by treatment with an mTOR/FRAP inhibitor. The specificity of the CXCR4-mediated migration of ARO cells was demonstrated by the dose-dependent inhibition of migration by neutralizing anti-CXCR4. The ATC cells, FRO and NPA, which do not express CXCR4, did not demonstrate significant SDF-1 alpha-mediated migration in vitro. In addition, the CXCR4-mediated migration of ARO cells was inhibited by treatment with pertussis toxin (a Gi-protein inhibitor) and PD 98059 (a mitogen-activated ERK kinase inhibitor) but not by LY294002 and wortmanin, phosphatidylinositol 3-kinase inhibitors. These findings suggest that a subset of ATC cells expresses functional CXCR4, which may be important in tumor cell migration and local tumor invasion.

Carcinoma↗

PubMed2003

Gadd45gamma expression is reduced in anaplastic thyroid cancer and its reexpression results in apoptosis.

Anaplastic thyroid carcinomas are a highly aggressive and extremely lethal form of human cancer, but the biological characteristics related to their aggressive nature are not understood. Moreover, Gadd45 family proteins have been implicated in a variety of growth-regulatory mechanisms, including DNA replication and repair, G(2)/M checkpoint control, and apoptosis. In this study we found that Gadd45gamma RNA was present at significantly lower levels in anaplastic cancer cells, compared with normal primary cultured thyrocytes. In addition, the adenovirus-mediated reexpression of Gadd45gamma significantly inhibited the proliferation of anaplastic thyroid carcinoma cells, ARO, FRO, and NPA cells, which was attributed to apoptosis. Furthermore, the adenovirus-mediated delivery of Gadd45gamma gene in anaplastic thyroid cancer resulted in the inhibition of tumor growth in vivo. This in vitro and in vivo activity of the adenovirus-mediated transduction of CR6/Gadd45gamma, on anaplastic thyroid cancer cell growth suppression, was reminiscent of the effects of p53. This study demonstrates that the Gadd45gamma gene has potential use as a candidate gene for gene therapy in anaplastic thyroid cancer.

Adenoviridae↗

PubMed2003

Infant susceptibility of mortality to air pollution in Seoul, South Korea.

OBJECTIVE: Susceptibility of target populations to air pollution is an important issue, because air pollution policies and standards should be based on the susceptibilities of those at particular risk. To evaluate which age group is more susceptible to the adverse health effects of air pollution, we compared the effects of air pollution on mortality among postneonates, those aged 2 to 64 years, and those over 65 years of age. DESIGN: Daily counts of total and respiratory death along with daily levels of meteorological variables and air pollutants were analyzed using generalized additive Poisson regression. The relative risks (RR) of mortality for interquartile changes of the levels of particulate matter <10 micro m (PM(10)) were calculated on the same day. RESULTS: For postneonates, the RR of total mortality for an interquartile change (42.9 micro g/m(3)) in PM(10) (RR: 1.142; 95% confidence interval [CI]: 1.096-1.190) was greatest among age groups. Next were the elderly over 65 years of age (RR: 1.023; 95% CI: 1.022-1.024). Regarding respiratory mortality, RR for an interquartile change of PM(10) in postneonates (RR: 2.018; 95% CI: 1.784-2.283) was also greater than those in the other groups. CONCLUSIONS: These results agree with the hypothesis that infants are most susceptible to PM(10) in terms of mortality, particularly respiratory mortality.

Adolescent↗

PubMed2002

Statin inhibits interferon-gamma-induced expression of intercellular adhesion molecule-1 (ICAM-1) in vascular endothelial and smooth muscle cells.

Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, known as statins, are widely used for primary and secondary prevention of coronary artery atherosclerosis. Pathogenesis of atherosclerosis is multistep processes where transendothelial migration of various leukocytes including monocytes is a crucial step. Interferon-gamma (IFN-gamma) contributes in this process by activating macrophages and T-lymphocytes, and by inducing adhesion molecules in vascular endothelial and smooth muscle cells. In this study we investigated the expression of intercellular cell adhesion molecule-1 (ICAM-1) in transformed endothelial cell line ECV304 cells as influenced by lovastatin, tumor necrosis factor-alpha (TNF-alpha) and IFN-gamma. Results show that lovastatin suppresses expression of ICAM-1 by inhibiting the IFN-gamma-induced extracellular signal-regulated kinase (ERK) p44/p42-STAT1 signaling pathway. In cells treated with lovastatin and IFN-gamma, ICAM-1 was expressed at a lower level than in cells treated with IFN-gamma alone. However, lovastatin does not reduce TNF-alpha induced expression of ICAM-1. A similar result was observed in cells treated with the MEKK inhibitor PD98059 and IFN-gamma. Cis-acting DNA sequence elements were identified in the 5'-flanking region of the ICAM-1 promoter that mediate inhibition by lovastatin; these sequences map to the IFN-gamma activated site which also binds the STAT1 homodimer. However, lovastatin did not inhibit IFN-gamma-mediated induction of the Y701 phosphorylated form of STAT1. But lovastatin does inhibit the IFN-gamma-mediated phosphorylation of ERK1/ERK2 (T202/Y204) and S727 phosphorylation of STAT1. TNF-alpha does not induce phosphorylation of ERK1/ERK2 and S727 in ECV304 and smooth muscle cells. The results provide the evidences that statins may have beneficial effects by inhibiting IFN-gamma action in atherosclerotic process

Animals↗

PubMed2002

Identification of radiation-specific responses from gene expression profile.

The responses to ionizing radiation (IR) in tumors are dependent on cellular context. We investigated radiation-related expression patterns in Jurkat T cells with nonsense mutation in p53 using cDNA microarray. Expression of 2400 genes in gamma-irradiated cells was distinct from other stimulations like anti-CD3, phetohemagglutinin (PHA) and concanavalin A (ConA) in unsupervised clustering analysis. Among them, 384 genes were selected for their IR-specific changes to make 'RadChip'. In spite of p53 status, every type of cells showed similar patterns in expression of these genes upon gamma-radiation. Moreover, radiation-induced responses were clearly separated from the responses to other genotoxic stress like UV radiation, cisplatin and doxorubicin. We focused on two IR-related genes, phospholipase Cgamma2 (PLCG2) and cytosolic epoxide hydrolase (EPHX2), which were increased at 12 h after gamma-radiation in RT-PCR. TPCK could suppress the induction of these two genes in either of Jurkat T cells and PBMCs, which might suggest the transcriptional regulation of PLCG2 and EPHX2 by NF-kappaB upon gamma-radiation. From these results, we could identify the IR-specific genes from expression profiling, which can be used as radiation biomarkers to screen radiation exposure as well as probing the mechanism of cellular responses to ionizing radiation.

Apoptosis↗

PubMed2002

Gradient echo magnetic resonance imaging in the prediction of hemorrhagic vs ischemic stroke: a need for the consideration of the extent of leukoariosis.

BACKGROUND: Multifocal signal loss lesion (MSLL) on gradient echo magnetic resonance imaging (GE-MRI) may reflect bleeding-prone microangiopathy. However, MSLLs are also known to be associated with leukoariosis; leukoariosis is commonly associated with occlusive-type vascular lesions. OBJECTIVE: To determine whether MSLL on GE-MRI is significantly associated with the type of stroke--intracerebral hemorrhagic (ICH) stroke more often than an ischemic stroke (infarction)--regardless of the extent of leukoariosis. PATIENTS AND METHODS: We studied 91 patients who had an acute stroke and were admitted to the Department of Neurology, Seoul National University Hospital, Seoul, South Korea, from March 1, 1997, to July 31, 1998. These patients underwent both conventional MRI and GE-MRI. The GE-MRI was used to count MSLLs. We also counted lacunae and classified leukoariosis (none or mild and advanced). Multiple logistic regression analysis was used to test for MSLL-leukoariosis interaction association with the type of stroke (ICH over infarction) and to evaluate the relative contribution of an MSLL--adjusted for age, sex, and lacunae--in discriminating the type of stroke. RESULTS: The association between MSLL and ICH statistically significantly differed by leukoariosis (P =.003 for MSLL-leukoariosis interaction term). The MSLL count on GE-MRI was significantly associated with the type of stroke (ICH over infarction; odds ratio, 2.46; 95% confidence interval, 1.38-4.39) when leukoariosis was classified as none or mild. When leukoariosis was classified as advanced, there was a decrease in the odds ratio of MSLL to 0.99 (95% confidence interval, 0.94-1.04). CONCLUSIONS: Our findings indicate that MSLL on GE-MRI is a predictor of ICH vs infarction in patients with no or mild leukoariosis, but not in patients with advanced leukoariosis. Therefore, in the evaluation of GE-MRI for a bleeding-prone microangiopathy, the extent of leukoariosis should be considered.

Adult↗

PubMed2002

Association of air pollution with school absenteeism due to illness.

OBJECTIVE: To assess the association of air pollution and school absenteeism among elementary students. DESIGN: Time-series analysis of air pollution and school absenteeism data with controlling for long-term trends, seasonality, day of the week, and holiday as well as meteorologic variables. SETTING: School absenteeism data for the period from March 2, 1996, to December 22, 1999, were collected from student attendance reports of one elementary school in Seoul, Korea. MAIN OUTCOME MEASURES: The number of daily illness-related absences was analyzed against the daily levels of air pollution by generalized additive Poisson regression. The relative risks of absenteeism for air pollution exposure of interquartile ranges (the range from the lowest 25% of the value to the lowest 75% of the value) on absenteeism were calculated on the same day. RESULTS: Exposure to air pollutants such as particulate matter of 10 micro m or less in aerodynamic diameter (PM(10)), sulfur dioxide, and ozone, was associated with illness-related absenteeism. The estimated relative risks were 1.06 (95% confidence interval, 1.04-1.09) per 42.1- micro g/m( 3) increase in PM(10), 1.09 (95% confidence interval, 1.07-1.12) per 5.68-part per billion increase in sulfur dioxide, and 1.08 (95% confidence interval, 1.06-1.11) per 15.94-part per billion increase in ozone. There was no significant relationship between nitrogen dioxide level and illness-related absenteeism. CONCLUSION: Air pollution is associated with illness-related absences among elementary students.

Absenteeism↗

PubMed2002

Poly(dimethylsiloxane) microchip for precolumn reaction and micellar electrokinetic chromatography of biogenic amines.

We have demonstrated that precolumn derivatization and capillary electrophoresis separation on a poly(dimethylsiloxane) (PDMS) microchip can be realized as efficient as those on glass microchips. In an optimized condition of micellar electrokinetic chromatography (MEKC), using 25 mM sodium borate buffer (pH 10.0) with 25 mM sodium dodecyl sulfate (SDS) and 5% v/v methanol, the electroosmotic flow in an oxidized PDMS microchip is stabilized within 3% for days. By employing a fluorometric derivatization with o-phthaldialdehyde (OPA) in an optimally designed reaction chamber, four most important biogenic amines occurring in foods, histamine, tyramine, putrescine, and tryptamine, are quantitatively determined in less than 1 min at the levels applicable to real samples. The migration behaviors of anionic OPA-derivatized biogenic amines under the MEKC conditions are analyzed, and it has been found that under our separation conditions, the electrophoretic mobility of the SDS micelles is significantly greater than those of the anions in the aqueous phase. The channel manifold in a PDMS substrate is fabricated using replica molding against a thick photoresist, SU-8, pattern generated by photolithography. The plate with the microchannel pattern is strongly, irreversibly bonded to another PDMS plate by using a new bonding technique, which employs surface oxidation by corona discharge generated from a cheap, handy source, Tesla coil.

Biogenic Amines↗

PubMed2002

Air pollution and asthma among children in Seoul, Korea.

BACKGROUND: As information about the health risks associated with air pollution has become available, attention has focused increasingly on susceptible persons such as children and persons with preexisting respiratory diseases, such as asthma. METHODS: We investigated the association between outdoor air pollution and asthma attacks among children under 15 years of age in Seoul, Korea. We estimated the relative risks of hospitalization associated with an interquartile range (IQR) increase in pollutant concentrations and used time series analysis of the counts by means of the generalized additive Poisson model. RESULTS: The estimated relative risk of hospitalization for asthma was 1.07 (95% confidence interval [CI] = 1.04-1.11) for particulate matters less than or equal to 10 microm in aerodynamic diameter (IQR = 40.4 microg/m3); 1.11 (95% CI = 1.06-1.17) for sulfur dioxide (IQR = 4.4 ppb); 1.15 (95% CI = 1.10-1.20) for nitrogen dioxide (IQR = 14.6 ppb); 1.12 (95% CI = 1.07-1.16) for ozone (IQR = 21.7 ppb); and 1.16 (95% CI = 1.10-1.22) for carbon monoxide (IQR = 1.0 ppm). CONCLUSIONS: These findings support the hypothesis that air pollution at levels below the current standards of Korea is harmful to sensitive subjects such as asthmatic children.

Adolescent↗

PubMed2002

Air pollution: a new risk factor in ischemic stroke mortality.

BACKGROUND AND PURPOSE: Air pollution is known to be associated with cardiovascular disease, but little is known about the occurrence of stroke in relation to air pollution. We investigated the association between acute stroke mortality and air pollution over a 7-year period (January 1991 through December 1997) in Seoul, Korea. METHODS: A generalized additive model was used to regress daily stroke death counts for each air pollutant, controlling for time trends, day of the week, and meteorological influences such as temperature, relative humidity, and atmospheric pressure. Ischemic and hemorrhagic stroke deaths were examined separately. RESULTS: The effects of air pollutants on ischemic stroke mortality were statistically significant, whereas this was not the case for hemorrhagic stroke mortality. We observed estimated relative risks of 1.03 (95% CI, 1.00 to 1.06) and 1.04 (95% CI, 1.01 to 1.08) for ischemic stroke mortality for each interquartile range increase in total suspended particulates and sulfur dioxide concentrations on the same day. We also found significantly increased relative risks of 1.04 (95% CI, 1.01 to 1.07) for nitrogen dioxide with a 1-day lag, of 1.06 (95% CI, 1.02 to 1.09) for carbon monoxide with a 1-day lag, and of 1.06 (95% CI, 1.02 to 1.10) for ozone with a 3-day lag for each interquartile range increase. CONCLUSIONS: These findings indicate that air pollutants are significantly associated with ischemic stroke mortality, which suggests an acute pathogenetic process in the cerebrovascular system induced by air pollution.

Air Pollution↗