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Objectives Doxycycline is commonly used in medicine for its bacteriostatic antimicrobial properties. Recent studies have reported that doxycycline also has anti-inflammatory effects. Matrix metalloproteinase (MMP)-9 has been found to be involved in the physiological and pathological process of inflammatory airway disease. Phorbol 12-myristate 13-acetate (PMA), a protein kinase C activator, is known to stimulate the expression of MMP and mucin genes in the airway and intestinal epithelial cells. Therefore, the effects and signal pathways of doxycycline on PMA-induced MUC5B expression dependent MMP-9 in human airway epithelial cells were investigated. Methods In human NCI-H292 airway epithelial cells, MUC5B and MMP-9 mRNA expression, MUC5B protein expression, and MMP-9 protein activity after the treatment with PMA, MMP-9 or doxycycline were determined by reverse transcriptase-polymerase chain reaction, enzyme immunoassay, gelatin zymography, and Western blot analysis. Results PMA increased MMP-9 and MUC5B expression. MMP-9 increased MUC5B expression. Doxycycline inhibited PMA-induced MUC5B expression, and PMA-induced MMP-9 mRNA expression and protein activity. Doxycycline inhibited phosphorylation of p38 induced by PMA and MMP-9. Conclusion The results of this study suggest that doxycycline inhibited PMA-induced MUC5B mRNA expression and protein production through the MMP-9 and p38 pathways in human NCI-H292 airway epithelial cells.

Garlic has been shown to have antimicrobial, hypolipidemic, antithrombotic, antitumor and immunostimulatory properties. The medicinal effects of garlic are derived from the flavonoid and organosulfur components. Diallyl disulfide (DADS), an organosulfur, is the main component responsible for the diverse biological effects of garlic. However, the effects of DADS on mucin gene expression in airway epithelial cells have not been reported to date. Therefore, this study was performed to investigate the effects and brief signaling pathway of DADS associated with MUC5B expression in NCI-H292 epithelial cells using RT-PCR, ELISA, western blot, immunocytochemistry and cell transfection with siRNA. DADS induced MUC5B expression and activated the phosphorylation of ERK1/2 MAPK. In addition, U0126 inhibited DADS-induced MUC5B expression and DADS-activated phosphorylation of ERK1/2 MAPK. Moreover, the immunopositive cells for MUC5B protein did not appear after treatment of DADS with U0126, and the knockdown of ERK2 MAPK by ERK2 MAPK siRNA significantly blocked DADS-induced MUC5B mRNA expression. However, DADS did not activate the phosphorylation of p38 MAPK, and SB203580 did not inhibit DADS-induced MUC5B expression. This is the first study to show that DADS-induced MUC5B expression appears to be regulated by activation of the ERK2 MAPK signaling pathway in human NCI-H292 airway epithelial cells. Copyright © 2011 John Wiley & Sons, Ltd.

So far, previous works with respect to evaluating program contents have concentrated on the implementation of general educational content evaluation. In terms of the efforts required to solve problems, however, there are a few evaluation methods on educational programming language contents. Therefore, we propose new evaluation criteria for educational programming language contents. The detailed research contents can be summarized as follows. First, we analyze existing works and propose naval evaluation criteria for educational programming language contents. Second, the new evaluation criteria is verified by teachers who use Visual Basic educational contents via questionaries. Also, a program content is experimented via the evaluation criteria. Finally, it is expected that our proposed evaluation criteria for educational programming language contents can be used to evaluate newly developed educational programming language contents and to design its evaluation plans.

Rapid identification of enteropathogenic bacteria in stool samples is critical for clinical diagnosis and antimicrobial therapy. In this study, we describe the development of an approach that couples multiplex PCR with hybridization to a DNA microarray, to allow the simultaneous detection of the 10 pathogens. The microarray was synthesized with 20-mer oligonucleotide probes that were designed to be specific for virulence-factor genes of each strain. The detection limit for genomic DNA from a single strain was approximately 10 fg. In the presence of heterogeneous non-target DNA, the detection sensitivity of the array decreased to approximately 100 fg. We did not observe any non-specific hybridization. In addition, we successfully used this oligonucleotide-based DNA microarray to identify the causative agents in clinical stool samples from patients with food-borne enteritis.

A benign pleomorphic adenoma is the most common tumor of the salivary glands. This tumor has the potential to metastasize to bone, the head and neck region, visceral organs and skin. Although there a few reports about a benign pleomorphic adenoma metastasizing to the maxillary sinus in the paranasal sinuses, there are no reports about a metastatic benign pleomorphic adenoma in the sphenoid sinus. We report here on a case of a benign pleomorphic adenoma of the soft palate that metastasized to the sphenoid sinus, and we briefly review the relevant clinical literature.

BackgroundMacrolides are known to have anti-inflammatory, immunomodulatory, and tissue reparative effects. The purpose of this study was to determine the effect of macrolides (erythromycin [EM] and roxithromycin [RXM]) on the differentiation of fibroblasts into myofibroblasts and extracellular matrix accumulation in transforming growth factor (TGF) beta1–induced nasal polyp–derived fibroblasts (NPDFs) and to determine if NADPH oxidase (Nox) 4 and reactive oxygen species (ROS) are involved in the aforementioned processes.MethodsNasal polyps of six patients (three women and three men; 32.3 ± 5.2 years of age) were acquired during surgery and NPDFs were isolated from surgical tissues. NPDFs were pretreated with macrolides for 2 hours before differentiation induction by TGF-beta1. The mRNA expressions of alpha-smooth muscle actin (SMA), collagen types I and III, and Nox4 were determined by reverse-transcription–polymerase chain reaction, and the expression of alpha-SMA protein was determined by immunocytochemical staining. The amount of total collagen production was analyzed by SirCol collagen dye-binding assay. ROS activity was measured by nitroblue tetrazolium reduction assay and was visualized by fluorescent microscopy.ResultsIn TGF-beta1–induced NPDFs, EM, and RXM significantly inhibited expressions of alpha-SMA and collagen types I and III mRNA and reduced alpha-SMA and collagen protein levels at concentrations of 5 and 10 μg/mL. EM and RXM also inhibited TGF-β1–induced ROS production and Nox4 mRNA expression at the same concentrations.ConclusionThese results suggest the possibility that EM and RXM may play an important role in inhibiting the development of nasal polyps through their antioxidant effect.

The aim of this study was to evaluate effects of EEG patterns induced by three types ((1) resting mode(control group), (2) light massage mode, (3) strong massage mode in the electrical chair-massager for 15 minutes) in a sample of 16 healthy adults. Changes in anxiety and stress were assessed, and electroencephalogram was recorded. Anxiety scores(STAI: State Anxiety Inventory, VAS: Visual Analog Scale) decreased in all groups. For anxiety scores, the strong massage group showed the greatest decrease in stress. All groups also showed an increase in delta and theta activity, but only strong massage group showed a signigicant difference. All groups showed a decrease in alpha activity. Also, EEG changes in two groups except a control group showed a decrease in beta activity.

Urinary hippuric acid (HA) has been widely used as a biological marker of occupational exposure to toluene, although it is no longer valid for low levels of toluene exposure. Toluene exposure is known to induce oxidative DNA damage and the metabolism is affected by genetic polymorphisms of some metabolizing enzymes. Therefore, genetic polymorphisms of these metabolizing enzymes must be considered in the evaluation of oxidative stress caused by toluene exposure. We evaluated the relationship between urinary 8-hydroxydeoxyguanosine (8-OHdG), a marker of oxidative DNA damage, and urinary HA in individuals without occupational exposure to toluene and characterized the possible roles of GSTM1, GSTT1, and aldehyde dehydrogenase 2 (ALDH2) genotypes in the relationships between these markers. In this study, we enrolled 92 healthy Koreans. Urinary HA and 8-OHdG levels were measured and the correlations between them were statistically tested according to the GSTM1, GSTT1, and ALDH2 genotypes. HA did not significantly correlate with urinary 8-OHdG in overall subjects. However, the correlation between them showed a statistical significance in individuals with GSTM1-null, GSTT1-null, and ALDH2 *2/*2 genotypes (r = 0.766, p < 0.01). This study shows that the relationship between urinary HA and 8-OHdG concentration is modified by genetic polymorphisms of some metabolizing enzymes such as GSTM1, GSTT1, and ALDH2.

Leptin, an adipocyte-secreted hormone that regulates food intake and metabolic response, has been recently reported to increase in the serum during inflammatory airway disease associated with mucus-hypersecretion. We investigated the effects of leptin on mucin expression in human airway epithelial cells and the signaling pathways. The expression of the leptin receptor was evaluated in human nasal mucosa and NCI-H292 cells. Leptin-induced expression of major respiratory mucins in NCI-H292 cells was analyzed. Mutant leptin, which acts as a receptor antagonist, and specific inhibitors of extracellular signal-regulated kinase (ERK1/2), p38 and Janus kinase-2 (JAK2)/signal transducer and activator of transcription-3 (STAT3) were used. Leptin receptors were expressed in the nasal mucosa and NCI-H292 cells. Treatment with leptin significantly increased the expression of MUC5AC and MUC5B in NCI-H292 cells; these effects were blocked by mutant leptin. The cells activated by leptin showed increased ERK1/2, p38, and STAT3 phosphorylation. Leptin-induced MUC5B expression was blocked by the ERK1/2 and p38 pathway inhibitors, but not by the JAK2/STAT3 pathway inhibitor. Leptin might significantly contribute to the production of major gel-forming mucins by direct stimulation of airway epithelial cells and the activation of leptin receptors coupled with the activation of ERK1/2 or p38, but not the JAK2/STAT3 pathway.

This study examines the relationship between urinary arsenic concentration and urinary 8-hydroxydeoxyguanosine (8-OHdG) concentrations, an index of oxidative DNA damage, among women who live near abandoned metal mines. The sample consisted of 165 residents living near two abandoned metal mines located in Chungbuk Province. Demographic characteristics as well as environmental factors relevant to arsenic exposure were collected through interviews, and urinary arsenic concentrations and urinary 8-OHdG concentrations of the research subjects were measured. The collected data were subsequently analyzed using the statistics program SPSS 12.0. T he geometric average of urinary arsenic concentrations among the research subjects was 5.65 μg/g creatinine. In a correlation analysis between urinary arsenic and 8-OHdG concentrations, the correlation coefficient was significant (p

Since 2005, Cyber home learning systems(CHLS) have been run with the purpose of clearing up the regional disparity and reducing the private education cost. At this point, it is necessary to have the analysis on the satisfaction and effectiveness awareness of the CHLS. The goal of this paper is to suggest an evaluation model for satisfaction and pedagogical effectiveness of CHLS and to support the management of satisfaction and effectiveness awareness of the CHLS for the low-income bracket children. Our major contributions can be summarized as follows: First, we present an evaluation model of satisfaction and effectiveness awareness of the CHLS for the low-income bracket children. Second, we survey the satisfaction, effectiveness awareness and improvement facts from the students who divided according to their sex, residence area and classes and compare with suggesting evaluation models. This paper is to find the measurement of the satisfaction and effectiveness awareness of the CHLS for the low-income bracket children. Furthermore, we can use this model as a material to balance the education opportunity, which is the purpose of CHLS, and abolish the education differentials.Keywords:Cyber Home Learning System, Distance Learning, e-Learning, Effectiveness, Satisfaction, Low-income Family

Environmental dietary carcinogens and genetic polymorphisms in metabolic enzymes have been reported to be the risk factors for gastric cancer. This study was undertaken to investigate the effects of the diet, the N-acetyltransferase (NAT) 2 acetylation status and their interaction on gastric cancer risk. The study population consisted of 471 gastric cancer patients and 471 age- and sex-matched control subjects. NAT2 genotypes were identified using single-nucleotide primer extension reaction methods. Thirty-one alleles related to 12 polymorphism sites were assayed in this study. Significantly increased odds ratios were observed in former smokers (OR = 2.39, 95% CI = 1.57-3.62), heavy drinkers (OR = 1.28, 95% CI = 1.06-1.55) and individuals who eat well-done meat (OR = 1.24, 95% CI = 1.09-1.41). The odds ratios (95% CI) for high intake of kimchi, stews and soybean paste were 3.27 (2.44-4.37), 1.96 (1.50-2.58) and 1.63 (1.24-2.14), respectively. The NAT2 genotype alone was not associated with gastric cancer risk. A significant gene-environment interaction was observed between environmental carcinogens and NAT2 genotypes. The odds ratios for kimchi, stews and soybean paste were higher in slow/intermediate acetylators than in rapid acetylators. The odds ratios for slow/intermediate acetylators were 2.28 (95% CI: 1.29-4.04) for light smokers and 3.42 (95% CI: 2.06-5.68) for well-done meat intake. The NAT2 acetylator genotype may be an important modifier of the effects of environmental factors on gastric cancer risk.

Background Glutaredoxins (GRX)-1 is glutathione-dependent oxidoreductase. However, the role of these enzymes remains unknown in airway inflammatory diseases. Therefore, we aimed to establish the expression pattern of GRX-1 in the nasal polyps (NPs) and to assess the regulatory mechanisms associated with GRX-1 expression in interleukin (IL)-1beta-treated airway epithelial cells. Methods The expression of GRX-1 in NPs and normal nasal mucosa were analyzed by reverse-transcription polymerase chain reaction and immunohistochemical staining. IL-1beta–induced reactive oxygen species (ROS) formation and GRX-1 expression in the airway epithelial cells was determined by flow cytometry and immunoassay. Results The expression level of GRX-1 in NPs was significantly higher than in the normal nasal mucosa (p < 0.05). GRX-1 was highly expressed in the surface epithelial cells and the submucosal glandular cells in the NPs. IL-1beta increased the intracellular ROS formation and GRX-1 expression in airway epithelial cells. The inhibition of IL-1beta–induced ROS production by N-acetyl-cystein, an ROS scavenger, reduced GRX-1 expression. Diphenyleneiodonium and apocynin, NADPH oxidase inhibitors, did not abolish IL-1beta–induced ROS ormation and GRX-1 expression, whereas budesonide attenuated it. Conclusion High GRX-1 expression in NPs might be a primary de ense against chronic in lammatory oxidative stress in nasal mucosa. IL-1beta–induced up-regulation o GRX-1 in airway epithelial cells is probably mediated by ROS. Glucocorticoids can regulate IL-1beta–induced ROS ormation and GRX-1 expression.

In this study, 1-hydroxypyrene (1-OHP)-imprinted TiO 2 gel films were prepared by spin coating. Incorporation of the template molecules and their removal were confirmed by UV–vis absorption spectra measurements. Guest selectivity of the 1-OHP-imprinted TiO 2 film was estimated to be 1.6, 1.9, and 1.4 against benzoic acid (BA), 1-naphthol (1-NA), and 4-(phenylazo)benzoic acid (4-PABA)-imprinted TiO 2 film, respectively. The 1-OHP-imprinted films demonstrated greater binding to 1-OHP than the reference imprinted films. Similar results were obtained with the BA, 1-NA, and 4-PABA-imprinted films, and their guest selectivity against the reference imprinted films amounted to 1.2–3.1 times greater. This result suggests that the binding cavity of the imprinted TiO 2 gel matrices discriminates between molecular size, shape, and functional groups. Although much improvement is still needed, this imprinting process is a simple, useful, and less time-consuming way to prepare discriminative receptor cavities.

The mechanism of the adverse health effects of ambient particulate matter on humans has not been well-investigated despite many epidemiologic association studies. Measurement of personal exposure to particulate pollutants and relevant biological effect markers are necessary in order to investigate the mechanism of adverse health effects, particularly in fragile populations considered to be more susceptible to the effects of pollutants.We measured personal exposure to PM(2.5) and examined oxidative stress using urinary malondialdehyde three times in 51 preschoolers and 38 elderly subjects. A linear mixed-effects model was used to estimate PM(2.5) effects on urinary MDA levels.Average personal exposure of the children and elderly to PM(2.5) was 80.5 +/- 29.9 and 20.7 +/- 12.7 mug/m(3), respectively. Mean urinary MDA level in the children and the elderly was 3.6 +/- 1.9 and 4.0 +/- 1.6 mumol/g creatinine. For elderly subjects the PM(2.5) level was significantly associated with urinary MDA after adjusting for age, sex, BMI, passive smoking, day-care facility site, alcohol consumption, cigarette smoking, and medical history (heart disease, hypertension and bronchial asthma). However, there was no significant relationship for children.The elderly were more susceptible than young children to oxidative stress as a result of ambient exposure to PM(2.5). Identification of oxidative stress induced by PM(2.5) explains the mechanism of adverse health effects such as cardiovascular or respiratory diseases, particularly in the elderly.

Escherichia coli (E. coli) and Staphylococcus aureus (S. aureus) release extracellular vesicles (EVs). E. coli-derived and S. aureus-derived EVs are associated with neutrophilic respiratory inflammation. In neutrophilic respiratory inflammation of human, expression of mucin is increased in airway epithelial cells and is associated with increased morbidity and mortality of the affected patients. However, no study on the effects of EVs on expression of mucin genes has been reported in airway epithelial cells. Therefore, this study was conducted in order to examine the effects and the brief signaling pathways of E. coli-derived and S. aureus-derived EVs on MUC5AC expression in human airway epithelial cells.In mucin-producing human NCI-H292 airway epithelial cells and primary cultures of normal nasal epithelial cells, the effects and signaling pathways of E. coli-derived and S. aureus-derived EVs on MUC5AC expression were examined using reverse transcription-polymerase chain reaction (RT-PCR), real-time PCR, enzyme immunoassay, and immunoblot analysis with several specific inhibitors and small interfering RNA (siRNA).E. coli-derived and S. aureus-derived EVs induced MUC5AC expression. E. coli-derived and S. aureus-derived EVs significantly activated phosphorylation of extracellular signal related kinase 1/2 (ERK1/2) mitogen-activated protein kinase (MAPK) and p38 MAPK. ERK1/2 MAPK inhibitor, p38 MAPK inhibitor, ERK1/2 MAPK siRNA, and p38 MAPK siRNA significantly blocked E. coli-derived and S. aureus-derived EVs induced MUC5AC messenger RNA (mRNA) expression.The results of this study suggest that E. coli-derived and S. aureus-derived EVs induced MUC5AC expression via ERK1/2 and p38 MAPK signaling pathways in human airway epithelial cells.

Objectives Excessive production of mucus results in plugging of the airway tract, which can increase morbidity and mortality in affected patients. In patients with diabetes, inflammatory airway disease appears with more frequent relapse and longer duration of symptoms. However, the effects of high glucose (HG) on the secretion of mucin in inflammatory respiratory diseases are not clear. Therefore, this study was conducted in order to investigate the effect and the brief signaling pathway of HG on MUC5B expression in human airway epithelial cells. Methods The effect and signaling pathway of HG on MUC5B expression were investigated using reverse transcriptase-polymerase chain reaction (RT-PCR), real-time PCR, enzyme immunoassay, and immunoblot analysis with specific inhibitors and small interfering RNA. Results HG increased MUC5B expression and epidermal growth factor receptor (EGFR) expression, and activated the phosphorylation of EGFR and p38 mitogen-activated protein kinase (MAPK). Pretreatment with EGFR inhibitor significantly attenuated the HG-induced phosphorylation of p38 MAPK, and pretreatments with p38 inhibitor or EGFR inhibitor significantly attenuated HG-induced MUC5B expression. In addition, knockdown of p38 MAPK by p38 MAPK siRNA significantly blocked HG-induced MUC5B expression. Conclusion These findings suggest that HG induces MUC5B expression via the sequential activations of the EGFR/p38 MAPK signaling pathway in human airway epithelial cells.

Objectives/Hypothesis: Among the airway mucin genes, the MUC4 gene is an important gene in its response to inflammatory diseases of the upper airway. However, the expression and regulation of the MUC4 gene in the nasal polyps remains unclear. Study Design: The purpose of this study was to evaluate the expression of MUC4 mRNA and synthesis of mucin glycoprotein in the nasal polyps before and after treatment with a topical steroid in vivo and in vitro. Methods: Nasal polyps were obtained from 20 patients with chronic rhinosinusitis and were subsequently cultured. The level of MUC4 mRNA was measured by reverse-transcription polymerase chain reaction, and the amount of the MUC4 mucin glycoprotein was estimated by the enzyme-linked immunosorbent assay method. Results: The expression of MUC4 mRNA was found to be significantly higher in the nasal polyps than in the inferior turbinate (P < .05). The addition of interleukin (IL)-1β and lipopolysaccharide (LPS) increased the expression of MUC4 mRNA and mucin glycoprotein synthesis in cultured nasal polyp epithelial cells. Treatment with glucocorticoid inhibited the expression of MUC4 mRNA in the nasal polyps; it also inhibited the expression of IL-1β and LPS-induced MUC4 mRNA and mucin glycoprotein synthesis in cultured nasal polyp epithelial cells. The inhibitory effects of glucocorticoid were restored by treatment with a glucocorticoid receptor antagonist (RU-486). Conclusions: These results suggest that the MUC4 gene is expressed in the nasal polyps and that glucocorticoid can control the expression of the MUC4 gene and mucin glycoprotein synthesis.

This paper proposed a new modular inverse algorithm based on the right-shifting binary Euclidean algorithm. For an n-bit numbers, the number of operations for the proposed algorithm is reduced about 61.3% less than the classical binary extended Euclidean algorithm. The proposed algorithm implementation shows substantial reduction in computation time over Galois field GF(p).

Insect and birds in nature flap their wings to generate fluid dynamic forces that are required for locomotion. To develop a feasible flapping MAV, it is of crucially important to study the fundamental relations between flapping motion and thrust generation. In this paper, the onset conditions of the thrust generation of a heaving flat plate is investigated using a Lattice-Boltzmann method. For a fixed heaving amplitude of h/C

This study aimed to clarify the variation of urinary excretion of 1-hydroxypyrene, which is a major metabolite of pyrene, in relation to lifestyle, including factors such as diet and smoking. The study subjects were 251 workers (male: 196, female: 55, mean age: 44.3) who were not occupationally exposed to PAHs. Urine specimens were collected from 8:00 a.m. to 11:00 a.m. and their 1-hydroxypyrene concentrations were determined by HPLC. A questionnaire was distributed in order to learn gross aspects of the subjects' lifestyles, i.e., smoking, alcohol consumption, coffee/black tea intake, and dietary habits. Multiple linear regression analysis revealed that cigarette consumption most strongly affected the 1-hydroxypyrene level in urine, followed by dietary balance. The urinary 1-hydroxypyrene concentrations of smokers were about 2 times higher than those of non-smokers. Subjects who ate more meat and/or fish excreted 1.5-2 times more 1-hydroxypyrene in urine than those who ate more vegetables.

This paper presented a low power design of a 32bit block cypher processor reduced from the original 128bit architecture. The primary purpose of this research is to evaluate physical implementation results rather than theoretical aspects. The data path and diffusion function of the processor were reduced to accommodate the smaller hardware size. As a running example demonstrating the design approach, we employed a modified ARIA algorithm having four S-boxes. The proposed 32bit ARIA processor comprises 13,893 gates which is 68.25% smaller than the original 128bit structure. The design was synthesized and verified based on the standard cell library of the MagnaChip`s 0.35um CMOS Process. A transistor level power simulation shows that the power consumption of the proposed processor reduced to 61.4mW, which is 9.7% of the original 128bit design. The low power design of the block cypher Processor would be essential for improving security of battery-less wireless sensor networks or RFID.

Acetaldehyde production during ethanol metabolism has been implicated as an important link between oxidative stress and cell damage, which suggests that oxidative stress caused by ethanol exposure may be more severe in aldehyde dehydrogenase 2 (ALDH2)-deficient individuals than in those with wild-type ALDH2. We evaluated the activities of the major antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), in liver tissue isolated from Aldh2 +/+ and Aldh2 –/ –m ice that were exposed to ethanol. The activities of CAT and GPx were significantly increased by ethanol treatment in Aldh2 +/+ mice (3.33-fold and 1.65-fold, respectively). The mean activity of SOD in Aldh2 +/+ mice was 1.46-fold that in the Aldh2 +/+ control group, but the difference was not statistically significant. In Aldh2 –/ –m ice, the activities of SOD and CAT were decreased and that of GPx was slightly increased after ethanol exposure, but the differences were not significant. We postulate that antioxidant enzyme expression after ethanol consumption may differ according to the intracellular level of acetaldehyde or free radicals, whic hi nt urn depends on the activity of ALDH2. These results suggest that the greater toxicity of ethanol in Aldh2 –/– mice than in Aldh2 +/+ mice may be due to decreased antioxidant enzyme

Inhalation of cadmium can lead to development of inflammatory airway diseases such as acute pulmonary edema and chronic obstructive pulmonary disease. In inflammatory airway diseases, expression of mucins is increased, which leads to increased morbidity and mortality of the affected patients. However, no study on the effect of cadmium on expression of mucin genes in airway epithelial cells has been reported. Therefore, this study was conducted in order to investigate the effect and the brief signaling pathway of cadmium on expression of mucin genes in human airway epithelial cells.In mucin-producing human NCI-H292 airway epithelial cells and primary cultures of normal nasal epithelial cells, the effect and signaling pathway of cadmium on expression of mucin genes were investigated using reverse transcription-polymerase chain reaction (RT-PCR), real-time PCR, enzyme immunoassay, and immunoblot analysis with several specific inhibitors and small interfering RNA (siRNA).Cadmium increased mucin 8 (MUC8) expression and Toll-like receptor (TLR) 4 messenger RNA (mRNA) expression. Cadmium significantly activated phosphorylation of extracellular signal related kinase 1/2 (ERK1/2) mitogen-activated protein kinase (MAPK) and p38 MAPK. ERK1/2 MAPK inhibitor, p38 MAPK inhibitor, TLR4 siRNA, ERK1/2 MAPK siRNA, and p38 MAPK siRNA significantly blocked cadmium-induced MUC8 mRNA expression. TLR4 siRNA significantly blocked cadmium-activated phosphorylation of ERK1/2 MAPK and p38 MAPK.The results of this study suggest for the first time that cadmium induces MUC8 expression via TLR4-mediated ERK1/2 and p38 MAPK signaling pathway in human airway epithelial cells.

Drinking water is a main source of human exposure to arsenic. Hence, the determination of arsenic in groundwater is essential to assess its impact on public health. Here, we report arsenic levels in the groundwater of 722 sites covering all six major provinces of Korea. Water was sampled in two occasions (summer, 722 sites and winter, 636 sites) and the arsenic levels were measured with highly sensitive inductively coupled plasma-mass spectrometry method (limit of detection, 0.1 μg/l) to encompass the current drinking water standard (10 μg/l). Seasonal variation was negligible, but the geographical difference was prominent. Total arsenic in groundwater ranged from 0.1 to 48.4 μg/l. A 88.0-89.0% of sites were2.0 μg/l and the remaining ones generally did not exceed 10 μg/l (6.4-7.0%, 2.0-4.9 μg/l; 2.4-3.0%, 5.0-9.9 μg/l). However, some areas (1.0-9.2%) exhibited10 μg/l. Notably, urinary arsenic excretion of people around these regions was markedly higher compared with non-contaminated areas (5 μg/l) (79.7±5.2 μg/g (N=122) vs 68.4±5.4 μg/g (N=65) creatinine, P=0.052). All stratified analysis also revealed higher urinary excretion, where a statistically significant difference was noted for non-smokers (85.9±12.7 vs 54.0±6.3, P=0.030), suggesting that arsenic-contaminated groundwater may contribute to its systemic exposure.

Introduction Recent studies have suggested that a few genes are associated with Hg metabolism in the human body. The aims of this study were to define the potential modifying effects of Single-Nucl...

In this paper, a fully wafer-level packaged RF MEMS switch has been demonstrated, which has low operation voltage, using a piezoelectric actuator. The piezoelectric actuator was designed to operate at low actuation voltage for application to advanced mobile handsets. The dc contact type RF switch was packaged using the wafer-level bonding process. The CPW transmission lines and piezoelectric actuators have been fabricated on separate wafers and assembled together by the wafer-level eutectic bonding process. A gold and tin composite was used for eutectic bonding at a low temperature of 300 °C. Via holes interconnecting the electrical contact pads through the wafer were filled completely with electroplated copper. The fully wafer-level packaged RF MEMS switch showed an insertion loss of 0.63 dB and an isolation of 26.4 dB at 5 GHz. The actuation voltage of the switch was 5 V. The resonant frequency of the piezoelectric actuator was 38.4 kHz and the spring constant of the actuator was calculated to be 9.6 N m−1. The size of the packaged SPST (single-pole single-through) switch was 1.2 mm × 1.2 mm including the packaging sealing rim. The effect of the proposed package structure on the RF performance was characterized with a device having CPW through lines and vertical feed lines excluding the RF switches. The measured packaging loss was 0.2 dB and the return loss was 33.6 dB at 5 GHz.

The number of fatalities in Japan attributable to lung cancer exceeded 50000 in 2001. It is socially desirable that various markers, which can be utilized for the prevention of lung cancer, be established. We believe that smoking or exposure to carcinogens in air induces mutations in bronchial and alveolar epithelia, leading to the development of lung cancer. It would be useful to have markers of individual differences in susceptibility to chemical carcinogen-induced lung cancer 1) to identify genetic polymorphisms of enzymes metabolizing chemical carcinogens and 2) to investigate the expression of enzymes metabolizing chemical carcinogens. In this paper, we review CYP expression in the bronchial epithelium. CYP1, CYP2 and CYP3 are expressed in the bronchial epithelium. We also show the relationship between the genetic polymorphisms of cytochrome P450 (CYP) and a person's susceptibility to chemical carcinogen-induced lung cancer. We demonstrate the relationship between cigarette consumption and the CYP expression profile in the bronchial epithelium. To maintain and promote public health, we must apply evidence, such as CYP polymorphisms and CYP profiles to disease prevention and also to aggressively advance evidence-based prevention (EBP) of lung cancer.

The mixing effect is studied by comparing rotating and oscillating stirrers in the micro channel. The cases of Re

Highly miniaturized RF bandpass filter using a thin-film bulk acoustic wave resonator (TFBAR) is designed and fabricated for 5-GHz-band application. The topology of the fabricated filter is based on a ladder-type configuration that has a common trimming inductor connected concurrently with two shunt TFBARs and the trimming inductor is directly connected to the ground. The role of unit the TFBAR's physical characteristics such as the size and thickness of the TFBAR determine the performance of the TFBAR filter, including the effect of the electrical impedance-matching characteristics of the TFBAR filter. The shape of the fabricated TFBARs are tetragons with unparallel sides and the sizes of resonator are smaller than 70/spl times/70 /spl mu/m/sup 2/ to ensure the ranges of impedance-matched filter performance. The insertion loss and bandwidth of fabricated TFBAR filters are less than 2.8 dB and 160 MHz at 3 dB. The out-of-band rejection is over 30 dB. The actual size of filter is smaller than 700/spl times/600 /spl mu/m/sup 2/, including signal and ground pad sizes.

Unlike most empirical studies on the administered protection measures that dealt with the developed countries, the present study reveals the relationship between macroeconomic variables and the number of investigations of antidumping duties in Korea. The unit root tests show that it is not unrealistic to assume that all concerned variables are integrated of order one. Johansen's cointegration test shows that there is a long run equilibrium relationship between antidumping duties and real GDP growth rate. The error correction model reveals that protection measures such as antidumping duties lead to slowdown in the overall economic activities in Korea.

In order to consider the effect of Karman vortex for mixing, mixing indices are calculated for 4 models of micro channel flows driven from the combinations of a circular cylinder and a oscillating stirrer. And their results are compared to that of a simple straight micro channel flow(model I). The mixing rate is improved 5.5 times by Karman vortex (model II) and 11.0 times by the stirrer(model III) respectively. In case of successive mixing by the cylinder and the stirrer(model IV), of shortening the channel length for the complete mixing as well as 1.37 times improvement of mixing efficiency then model III. And then, variation of mixing indices are much stable comparing with the others. Thus, it is found that the Karman vortex plays a good role as a pre-mixing method. The D2Q9 Lattice Boltzmann methods are used.

Despite the availability of 3D CAD systems, the designers in shipyards still use 2D CAD systems because of the need to produce drawings rapidly and a shortage of labor. The shipyard spends much time and labor analyzing the design information contained in 2D drawings and creating 3D model for the downstream processes. The design information is represented by symbols that are well known among designers in shipyard. Symbols are expressed by meaningless geometric shapes. These shapes are recognized to have meanings by analysis of experienced and knowledgeable designers. We propose a method for automatic recognition of 2D symbols and the extraction of design information from the midship drawings. The shape and rationale of 2D symbols used in ship design have been analyzed, and symbols have been classified according to the analysis. Based on the classified symbols, the developed system recognizes the symbols expressed in 2D drawings. The extracted design information is assorted by design rationales. The meaningless geometric shape is translated into the design information including designer's intents. The extracted design data can be applied to the design process in shipyards, and the 3D ship model can be automatically created.

Nitropyrenes (NPs) present in diesel and gasoline emissions are mutagenic and carcinogenic in experimental animals. Nitro-reduction of 1-NP causes oxidative stress. It is unclear whether 8-hydroxydeoxyguanosine (8-OH-dG) is produced from 1-NP and whether it contributes to the carcinogenic activity of 1-NP. In this study, we measured the level of reactive oxygen species (ROS) in cultured human lung epithelial cells after exposure to 1-NP and the intracellular level of 8-OH-dG and expression level of the 8-OH-dG repair enzymes. As results, 1-NP induced the generation of 8-OH-dG via ROS, but 8-OH-dG repair enzymes prevented an increase of 8-OH-dG formation in cellular DNA of the A549 cell line below 250 microM of 1-NP. These data suggest that 1-NP can induce oxidative DNA damage by generation of ROS, which may play a role in the carcinogenesis induced by 1-NP. These data also suggest that individuals with impaired DNA repair enzymes might be more susceptible to lung cancer induced by 1-NP.

SRT division schemes are presented based on a redundant number operand format aiming high speed operation. The proposed SRT division method based on a redundant binary adder (RBA) and one based on a recoded binary signed digit adder (RBSDA) show a 33% and 50% speed improvement, respectively. The time complexity of the proposed division based on redundant number is O(n); importantly, the redundant number based design is easy to implement due to its structural regularity.

This study was designed to investigate the relationship between environmental exposure to polycyclic aromatic hydrocarbons (PAHs) and oxidative stress, and to evaluate the effects of cigarette smoking and the genetic polymorphisms of CYP1A1, CYP2E1, GSTM1, NAT2 and UGT1A6 on the relationship. The subjects of this study were 105 healthy Korean males without occupational exposure to PAHs. The 8-hydroxydeoxyguanosine (8-OHdG) level in leukocytes, and urinary 1-hydroxypyrene (1-OHP) and 2-naphthol concentrations, were measured by high-performance liquid chromatography. Genetic polymorphisms of CYP1A1, CYP2E1, GSTM1, NAT2 and UGT1A6 were identified by PCR and PCR-RFLP methods. The 8-OHdG level showed a significant correlation with the 1-OHP concentration in all subjects (p

Several epidemiological studies have reported an association between environmental pollution and various health conditions in individuals residing in industrial complexes. To evaluate the effects of pollution from industrial complex on human health, we performed a pooled analysis of environmental epidemiologic monitoring data for residents living near national industrial complexes in Korea. The respiratory and allergic symptoms and the prevalence of acute and chronic diseases, including cancer, were used as the outcome variables for health effects. Multiple logistic regression analysis was used to analyze the relationship between exposure to pollution from industrial complexes and health conditions. After adjusting for age, sex, smoking status, occupational exposure, level of education, and body mass index, the residents near the industrial complexes were found to have more respiratory symptoms, such as cough (odds ratio [OR], 1.18; 95% confidence interval [CI], 1.06 to 1.31) and sputum production (OR, 1.13; 95% CI, 1.03 to 1.24), and symptoms of atopic dermatitis (OR, 1.10; 95% CI, 1.01 to 1.20). Among residents of the industrial complexes, the prevalence of acute eye disorders was approximately 40% higher (OR, 1.39; 95% CI, 1.04 to 1.84) and the prevalence of lung and uterine cancer was 3.45 times and 1.88 times higher, respectively, than those among residents of the control area. This study showed that residents living in the vicinity of industrial complexes have a high risk of acute and chronic diseases including respiratory and allergic conditions. These results can be used as basic objective data for developing health management measures for individuals residing near industrial complexes.

There have been few studies on the association between vitamin D levels and gastric cancer in Asian populations, but no studies have been performed on the interactions between vitamin D intake and polymorphisms in the vitamin D pathway. The effects of vitamin D intake, vitamin D related genetic polymorphisms, and their association with the incidence of gastric cancer were investigated in a hospital case-control study, including 715 pairs of newly diagnosed gastric cancer patients and controls matched for age and sex. Correlations between vitamin D intake and plasma vitamin D concentrations were also assessed in a subset of subjects. No statistically significant difference was observed in the dietary intake of vitamin D between the patients and controls, nor were there any evident associations between vitamin D intake and risk of gastric cancer in multivariate analyses. Vitamin D intake significantly correlated with the circulating 25-hydroxyvitamin D levels, but not with the active form of the vitamin, 1,25-dihydroxyvitamin D. There were no statistically significant interactions between vitamin D intake, and VDR or TXNIP polymorphisms. This study suggests that dietary vitamin D intake is not associated with gastric cancer risk, and the genetic polymorphisms of vitamin D-related genes do not modulate the effect of vitamin D with respect to gastric carcinogenesis.

Purpose: High-fat (HF) feeding induces hypothalamic leptin resistance via the activation of toll-like receptor 4 (TLR4). TLR4 deficiency confers resistance to diet-induced obesity. Udenafil, an anti-impotence drug, inhibits TLR4 in airway epithelial cells in vitro. In this study, we evaluated whether udenafil suppressed the hypothalamic expression of TLR4 and reduced body weight. Materials and Methods: The hypothalamic expression of TLR4, phosphodiesterase 5 (PDE5), nuclear factor-κB (NF-κB), and myeloid differentiation primary response gene 88 (Myd88) was analyzed by real-time polymerase chain reaction after treating mice for 2 days with udenafil (0, 12, 120, or 600 μg/d). Furthermore, the hypothalamic expression of TLR4, pro-opiomelanocortin (POMC), and neuropeptide Y (NPY) was analyzed after 9 days’ treatment with udenafil and/or leptin. We also measured body weight and food intake following 9 days of udenafil and/or leptin treatment in control- and HF-fed mice. Results: Udenafil suppressed hypothalamic TLR4 mRNA expression dose-dependently. The changes were associated with decreased PDE5, NF-κB, and Myd88 expression. Udenafil treatment for 9 days reduced body weight and caloric intake in HF-fed mice. This may have been associated with the suppression of NPY expression that was elevated by HF feeding. POMC expression was not affected by udenafil. However, udenafil did not augment the effects of leptin on the reduction of body weight and caloric intake in HF-fed mice. Conclusions: These results suggested that udenafil reduced body weight by suppressing hypothalamic TLR4 mRNA expression in HF-fed mice and the combination effect of udenafil and leptin was additive rather than synergistic.

The use of a GnRH agonist (GnRHa) in central precocious puberty (CPP) is known to slow puberty progression, subsequently prevent early menarche, and attenuate the height loss caused by advanced skeletal maturation. But enhancing the final height has been so controversial that an additional approach has been used. We investigated the menarcheal age and near final height (NFH) in girls with CPP treated with GnRHa (N = 61) or GnRHa combined GH (N = 24). GnRHa was started at 8.1 ± 0.7 yr and administered for 2.1 ± 1.0 years. GH was used for 2.1 ± 1.1 yr in subjects with a short predicted adult height (PAH). Menarche occurred at 11.6 ± 0.8 yr of age, which was 15.7 ± 6.4 mo after GnRHa discontinuation. PAH increased significantly from 152.0 ± 7.2 cm to 158.8 ± 5.6 cm during treatment, and the NFH (159.7 ± 4.8 cm) was taller than the midparental height (157.8 ± 3.4 cm). The combined treatment group showed a greater height increment during treatment. Younger age, taller height at the start of treatment, taller parental height and longer duration of treatment were the factors influencing NFH. In conclusion, GnRHa treatment in girls with CPP could improve NFH and delay menarche close to the general population. If GnRHa combined with GH is used in girls with CPP and a short midparental height, it would improve the NFH to a value similar to that in the general population.

Proinflammatory cytokines, lipopolysaccharide (LPS), and neutrophil elastase (NE) have been implicated in the induction of hypersecretion of respiratory mucus. In this study, we demonstrated that interleukin-1 β (IL-1 β) increased MUC2 and MUC5AC mRNA levels 2- to 3-fold in a time- and dose-dependent manner in NCI-H292 cells. In contrast, MUC5B mRNA was not significantly changed. A transcription inhibitor blocked the stimulation of MUC2 and MUC5AC gene expression by IL-1 β. A translation inhibitor did not interfere with the induction of MUC2 mRNA expression, whereas stimulation of MUC5AC mRNA was blocked, suggesting de novo protein synthesis is required for the stimulation of MUC5AC mRNA. We previously reported that induction of MUC2, MUC5AC, and MUC5B gene expressions by retinoic acid is mediated by the retinoic acid receptor (RAR α) , and inhibited by the specific RAR α antagonist Ro 41-5253. Here, we demonstrate that the RAR α antagonist can effectively inhibit IL-1 β -induced MUC2 and MUC5AC gene expr...

β-Glucan is found in the cell walls of fungi, bacteria, and some plant tissues, and is detected by the innate immune system. Furthermore, this recognition is known to worsen respiratory symptoms in patients with allergic and inflammatory airway diseases. However, the means by which β-glucan affects the secretion of major mucins by human airway epithelial cells has not been elucidated. Therefore, in this study, the effect and signaling pathway of β-glucan on mucins MUC4 and MUC5B were investigated in human airway epithelial cells.In NCI-H292 cells and human normal nasal epithelial cells, the effect and signaling pathway of β-glucan on MUC4 and MUC5B expression were investigated using reverse transcriptase-polymerase chain reaction (RT-PCR), real-time PCR, enzyme immunoassay, and immunoblot analysis with specific inhibitors and small interfering RNA (siRNA).β-Glucan increased MUC4 and MUC5B expression and activated the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). SB203580 (a p38 MAPK inhibitor) and pyrrolidine dithiocarbamate (PDTC; a NF-κB inhibitor) inhibited β-glucan-induced MUC4 and MUC5B expression. In addition, siRNA knockdown of p38 MAPK blocked β-glucan-induced MUC4 and MUC5B mRNA expression and β-glucan-activated phosphorylation of NF-κB. Furthermore, Toll-like receptor 4 (TLR4) mRNA expression was increased by β-glucan, and siRNA knockdown of TLR4 blocked β-glucan-induced MUC4 and MUC5B mRNA expression and β-glucan-activated phosphorylation of p38 MAPK and NF-κB.These results demonstrate that in human airway epithelial cells β-glucan induces MUC4 and MUC5B expression via the TLR4-p38 MAPK-NF-κB signaling pathway.

Background Among a variety of inflammatory mediators, visfatin is a proinflammatory adipocytokine associated with inflammatory reactions in obesity, metabolic syndrome, chronic inflammatory disease, and autoimmune disease. However, the biological role of visfatin in secretion of major mucins in human airway epithelial cells has not been reported. Therefore, this study was conducted in order to investigate the effect and the brief signaling pathway of visfatin on MUC8 and MUC5B expression in human airway epithelial cells. Results Visfatin significantly induced MUC8 and MUC5B expression. Visfatin significantly activated phosphorylation of p38 MAPK. Treatment with SB203580 (p38 MAPK inhibitor) and knockdown of p38 MAPK by siRNA significantly blocked visfatin-induced MUC8 and MUC5B expression.Visfatin significantly increased ROS formation. Treatment with SB203580 significantly attenuated visfatin-induced ROS formation. Treatment with NAC (ROS scavenger) and DPI (NADPH oxidase inhibitor) significantly attenuated visfatin-induced MUC8 and MUC5B expression. However, treatment with NAC and DPI did not attenuate visfatin-activated phosphorylation of p38 MAPK. Visfatin significantly activated the phosphorylation of NF-κB. Treatment with PDTC (NF-κB inhibitor) significantly attenuated visfatin-induced MUC8 and MUC5B expression. Conclusions These results suggest that visfatin induces MUC8 and MUC5B expression through p38 MAPK/ROS/NF-κB signaling pathway in human airway epithelial cells.