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In this paper, the tunable PIFA for the correction of impedance mismatch due to human hand effect has been developed. Metal-to-metal direct contact type RF MEMS switch has been used for tuning the resonance frequency of the capacitor loaded PIFA, which is piezoelectrically actuated with low actuation voltage. The characteristics of the tunable PIFA have been measured in the presence of phantom hand in order to show the feasibility for the correction of resonance frequency shift by the human hand effects. When the switch is in the on state, the resonant frequency of the PIFA shifted from 762 MHz to 690 MHz attributed to the phantom hand effect. By changing the switch status to the off state, the PIFA recovers its original resonant frequency with the phantom hand. The measured resonant frequency of the PIFA in the switch off state is 760 MHz with the phantom hand and the return loss at the resonant frequency is -22 dB.

Oxidative DNA damage is a known risk factor of lung cancer. The glutathione peroxidase (GPX) antioxidant enzyme that reduces hydrogen peroxide and lipid peroxides plays a significant role in protecting cells from the oxidative stress induced by reactive oxygen species. The aim of this case-control study was to investigate effects of oxidative stress and genetic polymorphisms of the GPX1 genes and the interaction between them in the carcinogenesis of lung cancer.Two hundreds patients with lung cancer and 200 age- and sex-matched controls were enrolled in this study. Every subject was asked to complete a questionnaire concerning their smoking habits and their environmental exposure to PAHs. The genotypes of the GPX1 and 8-oxoguanine glycosylase 1 (hOGG1) genes were examined and the concentrations of urinary 1-hydroxypyrene (1-OHP), 2-naphthol and 8-hydroxydeoxyguanosine (8-OH-dG) were measured.Cigarette smoking was a significant risk factor for lung cancer. The levels of urinary 8-OH-dG were higher in the patients (p0.001), whereas the urinary 1-OHP and 2-naphthol levels were higher in the controls. The GPX1 codon 198 polymorphism was associated with an increased risk of lung cancer. Individuals carrying the Pro/Leu or Leu/Leu genotype of GPX1 were at a higher risk for lung cancer (adjusted OR = 2.29). In addition, these individuals were shown to have high urinary 8-OH-dG concentrations compared to the individuals with the GPX1 Pro/Pro genotype. On the other hand, the polymorphism of the hOGG1 gene did not affect the lung cancer risk and the oxidative DNA damage.These results lead to a conclusion that individuals with the GPX1 Pro/Leu or Leu/Leu genotype would be more susceptible to the lung cancer induced by oxidative stress than those individuals with the Pro/Pro genotype.

To clarify the carcinogenicity of acetaldehyde when associated with ALDH (aldehyde dehydrogenase) 2 polymorphism, Aldh2 knock-out (Aldh2-/-) mice and their wild type (Aldh2+/+) mice were exposed to two different concentrations of acetaldehyde (125 ppm and 500 ppm) for two weeks. Aldh2-/- mice, which have the same genetic background as C57BL/6J (wild mice) except for the Aldh2 gene, were used as models of humans who lack ALDH2 activity. Urinary 8-hydroxydeoxyguanosine (8-OHdG) and plasma malondialdehyde (MDA) levels were measured as indicators of oxidative DNA damage and lipid peroxidation, respectively. At 125 ppm acetaldehyde exposure for 12 d, urinary 8-OHdG levels in Aldh2+/+ mice did not increase. However, urinary 8-OHdG levels in Aldh2-/- mice were slightly increased by the end of the exposure. On the other hand, plasma MDA levels did not increase in either Aldh2-/- orAldh2+/+ mice. At 500 ppm, urinary 8-OHdG levels in both Aldh2-/- and Aldh2+/+ mice significantly increased after 6 and 12 d, but there was no genetic difference. On the other hand, plasma MDA levels in Aldh2+/+ and Aldh2-/- mice did not increase at either 125 ppm or 500 ppm after two weeks of exposure. In conclusion, it is suspected that DNA was damaged by acetaldehyde inhalation, and that susceptibility to acetaldehyde varies according to Aldh2 genotype.

Objectives Mucin gene expression and mucin production are markedly increased in inflammatory airway disorders such as asthma, chronic bronchitis and rhinosinusitis. Cytokines, lipopolysaccharides and other inflammatory mediators such as prostaglandin and leukotriene are related to the secretion and production of mucin. However, the relationship of leukotrienes with mucin genes expression is not clear. The aim of this study is to evaluate MUC2/5AC gene expression and mucin secretion by the leukotriene receptor in human airway epithelial cells. Methods The effect of leukotriene D4 and the leukotriene receptor antagonist, pranlukast hydrate (ONO-1078) on the regulation of MUC2/5AC gene expression and mucin secretion were observed in human airway NCI-H292 epithelial cells. The mRNA levels of MUC2/5AC and the amount of mucin were determined by reverse transcription-polymerase chain reaction (RT-PCR) and immunoassay. Results Leukotriene D4 upregulated MUC2/5AC gene expression and mucin secretion in a dose dependent pattern. Pranlukast hydrate (ONO-1078, 100 μM) downregulated the leukotriene D4-induced MUC2/5AC gene expression and mucin secretion. Conclusion These results suggest that the leukotriene receptor system is one of the mechanisms related to MUC2/5AC gene expression and mucin secretion in the human airway epithelium.

Polycyclic aromatic hydrocarbons (PAHs), which are risk factors for lung cancer, have been reported to induce oxidative DNA damage. The paraoxonase (PON) plays a significant role in the detoxification of a variety of organophosphorous compounds, with paraoxonase-1 (PON1) being one of the endogenous free-radical scavenging systems in the human body. The aim of this case-control study was to investigate the effects of PAH exposure, oxidative stress and the Q192R polymorphism of PON1 genes, and their interactions in the carcinogenesis of lung cancer.One hundred and seventy seven lung cancer patients and 177 age- and sex-matched controls were enrolled in this study. Each subject was asked to complete a questionnaire concerning their smoking habits and environmental exposure to PAHs. The Q192R genotypes of the PON1 gene was examined, and the concentrations of urinary 1-hydroxypyrene (1-OHP), 2-naphthol and 8-hydroxydeoxyguanosine (8-OH-dG) measured.Cigarette smoking was found to be a significant risk factor for lung cancer. The urinary 8-OH-dG level was higher in the patients, whereas the urinary 1-OHP and 2-naphthol levels were higher in the controls. There was a significant correlation between the urinary levels of 8-OH-dG and 1-OHP in both the cases and controls. The PON1 polymorphism was associated with an increased risk of lung cancer. Individuals carrying the Q/Q genotype of the PON1 gene were found to be at higher risk of developing lung cancer. There was a significant correlation between the urinary levels of 8-OH-dG and 1-OHP in those with the PON1 Q/Q genotype.These results lead to the conclusion that PAHs would induce oxidative DNA damage, especially in individuals with the PON1 Q/Q genotype. Therefore, people with the PON1 Q/Q genotype would be more susceptible to lung cancer than those with the R/R or Q/R genotypes of the PON1 gene.

In recent years, organic compounds have been clarified as one of major root causes of the haze, and carbon and amine components are major of them to organize. Therefore, both two should be controlled simultaneously for preventing haze defects on photomask. It is well known that UV/O 3 treatment has a strong efficiency of removing organic matters 1 . For that reason, we have inserted it into our cleaning process, especially for EA.PSMs. And the surface variation of mask, after UV/O 3 treatment, has been confirmed by the change of surface free energy on it. And organic matters remaining on mask surface have been identified by Gas Chromatography Mass Spectrometry (GC MS) with two different sample preparation methods: Thermal Desorption (TD) and direct extraction. As a result of UV/O 3 treatment, we confirmed that it has an excellent removing efficiency of aromatic compounds and semi-volatile organics on mask surface. Finally, through the haze accelerating tests, we have known that conventional SPM/SC-1 cleaning with UV/ O 3 treatment has been having a much higher threshold energy value in terms of causing haze defects on masks about 20 times higher than that of the cleaning with just SPM/SC-1.

In this paper, three dimensional finite element method is used for the analysis of thin film bulk acoustic wave resonator (TFBAR) at 5 GHz. The TFBAR is placed on thin membrane after removal of substrate material for the suppression of loading effects and three different geometries (rectangular, polygonal and circular) are implemented and modeled. The size of fabricated TFBAR are from 100/spl times/100 /spl mu/m/sup 2/ to 200/spl times/200 /spl mu/m/sup 2/ and full-wave modeled results are compared with the measurement. It is found that the modeled and measured results agree within 1% in terms of series and parallel resonant frequencies. Furthermore, the different shapes of TFBAR revealed slightly different bandwidth characteristics, which is defined on frequency spacing between the series and parallel resonant frequencies. The another goal of this work is to study the variation of the size of resonator on how affects the performance of TFBAR. As the size of resonator increase, the electrical impedance of TFBAR decrease at the resonant frequencies and out of resonant frequencies. These phenomena contribute to improve the effects of the attenuations of TFBAR filter in stop-band to some degree.

We have chosen a combination of thermal treatment and hot D.I water rinsing as a part of methodologies to remove chemical residuals on mask surface. A new step of thermal treatment has been inserted in our standard manufacturing procedure for EAPSM. After thermal treatment, Ion Chromatography (IC) methods are used to confirm the surface cleanliness. As a result of our study, thermal treatment can considerably reduce residuals (e.g. ammonium, sulfuric and others) on mask surface. So, it could be suggested that the thermal treatment is an effective way to minimize residual ions. Also, in order to understand on haze source and mechanism, we investigated on artificial acceleration method for haze formation. We preceded haze acceleration test by using modified haze acceleration system (UV 172nm light). From the acceleration test, we found that humidity, irradiation energy, concentration of chemical residuals are dominant factors of haze formation.

We investigated the control of residual ions on the mask surface and the phase/transmission change rate by using thermal treatment after a conventional cleaning process. We hypothesized that the remaining sulfuric ions on the mask surface could combine with other ions and produce compounds during the thermal treatment. These compounds are easily removed by a hot D.I water rinse. Our study shows that the amount of remaining sulfuric ions is 250ng/mask when the mask has been thermally treated. The amount of sulfuric ions is substantially reduced compared to the results of other cleaning processes. Additionally we have found that the thermal treatment can be reduced varying the phase/trans value according to the cleaning cycle and the variation was stable even with a higher concentration of SC-1 solution.

In this paper, a new modeling methodology for thin film bulk acoustic resonators (TFBAR) is presented and the formulations for each lumped element in the model are also presented. The proposed model has three optimization variables which is half of the modified Butterworth-Van Dyke (MBVD) model, and as a result the curve fitting for the measured data is much faster and more accurate than any other conventional models. In addition, two types TFBAR ladder filters are designed and fabricated to analyze the effects of on-wafer inductor integration. Fabricated on-wafer spiral inductor reveals the Q-factor of 9 at 2 GHz and the inductor integrated filters have approximately 10 to 12 dB out-of-band rejection improvement compared to the original filters.

We determined expression levels of hepatic cytochrome P450 (CYP) 2E1, 2B1/2 and 4B1 enzymes in aldehyde dehydrogenase 2 (Aldh2) +/+ and Aldh2 −/− mice by immunoblotting assay following subchronic ethanol exposure for eight days. Using ethanol exposure, the protein expression levels of CYP2E1, 2B1/2 and 4B1 in Aldh2 +/+ mice were increased by factors of 2.61, 1.88 and 2.01 compared with Aldh2 +/+ mice that were not exposed to ethanol, respectively. On the other hand, in the Aldh2 −/− mice, CYP2E1, 2B1/2 and 4B1 protein expression levels after ethanol treatment were shown to be 1.99, 1.05 and 1.33 greater than those of Aldh2 −/− control mice, respectively. We also found an interesting fact in the present study; the Aldh2 −/− mice were shown to have higher CYP2E1 (by a factor of 4.19), 2B1/2 (by a factor of 2.89) and 4B1 (by a factor of 1.53) protein expression levels than Aldh2 +/+ mice despite the lack of ethanol treatment. These results suggest that CYP2E1, 2B1/2 and 4B1 play some role in ethanol metabolism and that Aldh2-deficient individuals may have higher levels of CYP2E1, 2B1/2 and 4B1 enzymes compared to Aldh2 wild-type individuals.

In Embedded Attenuated PSMs(Phase Shift Masks), chrome residues on MoSiON, especially at the edge of a pattern, should be decreasing the phase-shift effect and it must be also causing CD(critical dimension) variations in a wafer-process. Chrome residues on MoSiON are well known being generated at second level lithography or according to performance of cleaning process before it. In this paper, we investgated the influence of treatment on Cr surface during MoSiON etch process using CF4 plasma and proposed the optimum treatment procedure to reduce the Cr residues originated form re-deposition of carbon-contained polymers in CF4 plasma.

CYPs (cytochrome P450s) catalyze the conversion of numerous numbers of xenobiotics including carcinogens and drugs. CYPs can be involved in metabolic pathways of activation of procarcinogens and/or inactivation of carcinogens during the tumorigenic processes. Recently, increasing number of cancer tissues as well as normal tissues have been found to express a variety of CYPs. The local expression of CYPs in tumors appears to be very important for the management of cancers since CYPs expressed in tumors may be involved in activation and/or inactivation of anticancer drugs. The expression of CYPs in tumors may also convert endogenous substrates to metabolites that facilitate cancer development. In this review, we summarize the association of CYP expression in cancer tissues with carcinogenesis and cancer treatment.

As feature sizes of phase shift mask (PSM) have dropped below half-micron, resist adhesion have become a more critical issue, especially during second level lithography. Second writing process requires special consideration, because the resist's mechanical strength of resists on patterned chrome and patterned glass is smaller in comparison to that on the un-patterned chrome blank. If the adhesion strength is not sufficient to withstand the stress during subsequent processes, patterns will be damaged during second level lithography. Resists stress at pattern edges that subsequent processes, pattern will be damaged during second level lithography. Resist stress at pattern edges that weaken its adhesive property, together with the low mechanical strength of resists on glass, creates ample probability for the unwanted phenomenon in PSM process. In this paper, we investigate the effects of property and adhesive strength of resists on surfaces at different treatment before resist coating process, and observe the defects generation after different treatment.

Chromium compounds are carcinogenic to the human lung, although the detailed biochemical mechanism is still unclear. To understand the carcinogenic mechanism in cells exposed to low level hexavalent chromium, we measured the generation of reactive oxygen species (ROS) and 8-hydroxydeoxyguanosine (8-OH-dG), the transcription of hogg1, which encodes an 8-OH-dG repair protein, and NF-kappaB activation levels in the A549 human lung epithelial cell line after exposure to Cr (VI) at concentrations of 12.5 to 800 microM. In A549 cells, ROS levels and DNA binding by NF-kappaB increased in proportion to the concentration of Cr (VI). These increases were diminished by pretreatment with catalase, superoxide dismutase, or D-mannitol, but the levels of 8-OH-dG and expression of hogg1 did not change significantly with Cr (VI) exposure. These results suggest that the induction of ROS and the activation of NF-kappaB are important in the carcinogenic mechanism of Cr (VI), but it is unlikely that Cr (VI) concentrations below 800 microM increase 8-OH-dG levels or the expression of hogg1.

Now that the human genome has been sequenced, we consider that combinations of 3 to 10 million polymorphic loci scattered throughout the genome contribute to individual differences. Genetic polymorphism analysis is useful for the made-to-order medical treatment of patients and the prevention of disease onset in normal healthy individuals. Individually-tailored disease prevention based on findings such as genetic polymorphism analysis results can be grasped by the concept of evidence-based prevention (EBP). In this paper we outline cytochrome P450 (CYP) 1A1 and 2E1 polymorphism-related differences in metabolic activation of carcinogens in relation to the risk of lung cancer, and explain single nucleotide polymorphism (SNP). We also compare the reports to date on SNP types in CYP1A1 and CYP2E1 in relation to the risk of lung cancer with our study results, examine survival rates of lung cancer patients by CYP1A1 or CYP2E1 genotype and discuss the applicability of SNP research to EBP.

Background Mucus plays an important role in protecting human airway from external environments. Highly glycosylated mucin proteins are the major components of mucus, responsible for its viscoelastic properties. Excessive mucus is major manifestation of inflammatory respiratory diseases. Epigallocatechin-3-gallate (EGCG) is major component of green tea extract and known to provide numerous functions, such as anti-oxidant effect, anti-tumor effect, anti-diabetic effect and anti-inflammatory effect. But precise mechanisms are still unclear. Methods Using NCI-H292 human airway epithelial cells, we measured phorbol 12-myrisate 13-acetate (PMA)-induced MUC5B mRNA expression with the treatment of indicated doses of EGCG. We also measured PMA-induced MUC5B protein secretion with the treatment of indicated doses of EGCG using ELISA technique in NCI-H292 cells. To test the brief signaling pathways, we performed activation study of mitogen-activated protein kinase (MAPK) pathways, which is well-known to signaling the PMA-induced mucin gene over-expression, using Western blot technique in NCI-H292 cells. And then we performed in vivo study using ovalbumin-induced asthmatic mice model and control mice group. In ovalbumin-sensitized asthmatic mice model, EGCG was treated with indicated dose. And then ovalbumin was challenged and we sacrificed the mice. Tissue samples from the mice were stained with PAS (periodic acid-Schiff) for mucin distribution in bronchioles of each group. Immunocytochemical stain was performed using MUC5B specific antibody. MUC5B mRNA and protein level was measured using extracted lung tissues. Results PMA-induced MUC5B mRNA and protein level was significantly decreased after treatment of EGCG at all doses in NCI-H292 cells. PMA-induced phosphorylation of p38 MAPK was significantly decreased after treatment of EGCG at all doses in NCI-H292 cells. Results from in vivo studies showed that decreased bronchiolar mucin distribution in the group of pretreated with EGCG in asthmatic mice. MUC5B mRNA and protein levels were significantly decreased in the group of pretreated with EGCG in asthmatic mice. Conclusions PMA-induced MUC5B mRNA and protein over-expression in both NCI-H292 cells and extracted tissues from asthmatic mice were significantly decreased with the treatment of EGCG. We demonstrated that EGCG downregulates mucin gene expression through the MAPK signaling pathway in asthma.

Received April 15, 2015 Revised June 3, 2015 Accepted June 3, 2015 Address for correspondence Yong-Dae Kim, MD, PhD Department of OtorhinolaryngologyHead and Neck Surgery, College of Medicine, Yeungnam University, 170 Hyeonchung-ro, Nam-gu, Daegu 42415, Korea Tel +82-53-620-3781 Fax +82-53-628-7884 E-mail ydkim@med.yu.ac.kr Background and ObjectivesZZPolyinosinic-polycytidylic acid (Poly I:C) is structurally similar to double-stranded RNA, and is known to induce various inflammatory mediators and to cause inflammatory reactions in airway epithelial cells. However, the effect of Poly I:C on secretion of mucins in human airway epithelial cells has been very rarely reported. In this study, the effect and brief signaling pathway of Poly I:C on the expression of mucin genes were investigated in human airway epithelial cells. Materials and MethodZZIn mucin-producing human NCI-H292 airway epithelial cells and the primary cultures of normal human nasal epithelial cells, the effect and signaling pathway of Poly I:C on expression of mucin genes were investigated using reverse transcriptase-polymerase chain reaction, real-time PCR, enzyme immunoassay, and immunoblot analysis with specific inhibitors and small interfering RNA (siRNA) for mitogen-activated protein kinase (MAPK). ResultsZZPoly I:C induced the MUC5B expression, and activated the phosphorylation of ERK1/2 and p38 MAPK. U0126 (ERK1/2 MAPK inhibitor) and SB203580 (p38 MAPK inhibitor) inhibited the Poly I:C-induced MUC5B expression. In addition, the knockdown of ERK2 and p38 MAPK by siRNA significantly blocked the Poly I:C-induced MUC5B mRNA expression. ConclusionZZPoly I:C induces the MUC5B expression via ERK2 and p38 MAPK signaling pathways in human airway epithelial cells. Therefore, Poly I:C may play a role in the regulation of mucus hypersecretion through MAPK signaling pathways in the human airway epithelial cells. Korean J Otorhinolaryngol-Head Neck Surg 2015;58(9):615-21

현재 이과학 영역의 수술에서 출혈을 줄이기 위해 혈관 수 축작용이 있는 epinephrine을 수술부위에 국소주사 또는 점 막 도포의 형태로 널리 이용하고 있다. 허용 범위 용량 내의 epinephrine 사용은 그 자체가 심혈관계에 영향을 미쳐 심계항 진, 빈맥, 부정맥과 같은 부작용을 일으킬 수 있고, 과량 사용되거 나 혈관에 직접 주입될 경우 전신 흡수에 의한 심독성이 발 현되어 심근증, 폐부종, 심정지 등의 심각한 합병증이 일어날 수 있다. Epinephrine과 같은 catecholamine의 증가에 의한 심근 증은 1969년 지주막하출혈 환자에게서 처음 보고되었고, 크롬친화세포종 환자의 내인성 catecholamine 증가에 의한 심근증과 epinephrine을 국소주사한 후 발생한 심근증에 대 해 다수의 증례를 찾아볼 수 있으나, 이과학 영역의 수술에서 허용범위 용량 내의 epinephrine 국소주사 후 발생한 심근증 은 극히 드물다. 심근증 중 하나인 스트레스 유발성 심근증(stress induced cardiomyopathy, SCI)은 개별적인 관상동맥의 혈액 공급부위 와는 무관하게 수축기에 심기저부의 심근운동만 살아있고 심 첨부가 풍선처럼 부풀어 오르는 양상(apical ballooning)을 보 이는 심장질환으로, 갑작스런 감정적인 스트레스, 물리적 활동 의 증가, catecholamine의 갑작스런 증가 등이 원인으로 추정되 고 있으며, 급성 심근경색증의 진단기준에 부합하나, 관상 동 맥 조영술상 의미 있는 협착이나 폐쇄소견은 보이지 않는 질환 을 지칭한다. 이에 저자들은 수술 전 시행한 심전도 및 혈액검사에서 특이 소견을 보이지 않았던 환자에서 중이 수술 중 허용범위 내 용 량의 epinephrine을 피하주사 후 발생한 심근증 2예를 경험 하였기에 문헌고찰과 함께 보고하는 바이다. Two Case of Stress Induced Cardiomyopathy after Injection of Epinephrine during Middle Ear Surgery Hyung Gyun Na, Si-Youn Song, Yong-Dae Kim, and Chang Hoon Bae Department of Otorhinolaryngology-Head and Neck Surgery, College of Medicine, Yeungnam University, Daegu; and Center for Respiratory Disease, Yeungnam University Medical Center, Daegu, Korea

정상 선방세포와 조직학적으로 유사한 선방세포암(acinic cell carcinoma)은 1953년까지 병리학적으로 양성종양의 경과 를 보이는 선종(adenoma)으로 여겨졌다. 그러나, 그 이후 여러 보고에서 이 종양이 악성종양에서 관찰되는 잦은 재발과 주위 림프절 전이 및 원격전이를 일으키는 것으로 밝혀져 선방세포 암으로 불리게 되었다. 선방세포암은 췌장, 유방, 폐, 비인강과 타액선 등 다양한 부 위에서 발생하는 것으로 보고되며, 그 중 주타액선에서 주로 발생하고, 주타액선 중에서는 이하선에서 대부분 발생한다. 선방세포암이 악하선과 설하선에서 발생하는 경우는 드문 것 으로 알려져 있고, 그 중 설하선에 선방세포암이 발생한 경우 는 전 세계적으로 8예가 보고될 정도로 극히 드물며, 국내에는 아직 보고된 바가 없다. 또한, 저자들이 경험한 증례처럼 하 마종과 함께 선방세포암이 발견된 경우는 단 1예밖에 없다. 하 마종은 타액선관의 절단이나 파열에 의해 유출된 타액과 주변 결체 조직 간의 염증반응이나 타액선관의 부분적 폐쇄 등에 의한 타액선 상피조직의 증식에 의해 발생하는 것으로 알려져 있으며, 타액선 종양, 화농성 육아종, 타액관 결석, 혈관종, 림 프관종 등과 감별이 필요한 질환이다. 저자들은 최근 재발한 하마종 치료를 위해 우측 설하선 절 제술을 시행한 젊은 여자 환자에서 설하선에서 발생한 선방세 포암 1예를 경험하였기에 문헌 고찰과 함께 보고하는 바이다.

Received March 25, 2015 Revised May 8, 2015 Accepted May 17, 2015 Address for correspondence Yong-Dae Kim, MD, PhD Department of OtorhinolaryngologyHead and Neck Surgery, College of Medicine, Yeungnam University, 170 Hyeonchung-ro, Nam-gu, Daegu 705-703, Korea Tel +82-53-620-3781 Fax +82-53-628-7884 E-mail ydkim@med.yu.ac.kr Background and ObjectivesZZMulti-walled carbon nanotubes (MWCNT) are one of the most commonly used nanomaterials to date. Recent studies have demonstrated that MWCNT increase immune response and allergic inflammation in airway epithelial cells. However, the effects of MWCNT on mucin in human airway epithelial cells have not been reported. Therefore, in the present study, the effect of MWCNT on MUC16, MUC5AC, and MUC5B expressions were investigated in human airway epithelial cells. Subjects and MethodZZIn mucin-producing human NCI-H292 airway epithelial cells and primary cultures of normal nasal epithelial cells, the effects of MWCNT on MUC16, MUC5AC, and MUC5B expression were analyzed by reverse transcription polymerase chain reaction, real-time polymerase chain reaction, and enzyme-linked immunosorbent assay. ResultsZZIn human NCI-H292 airway epithelial cells, MWCNT significantly induced the expression MUC5AC and MUC5B mRNA and the production of MUC5AC and MUC5B protein. However, MWCNT did not induce the expression of MUC16 mRNA. In the primary cultures of normal nasal epithelial cells, MWCNT also induced the expression of MUC5AC and MUC5B mRNA and the production of MUC5AC and MUC5B proteins. ConclusionZZThe results of this study demonstrate that MWCNT induces MUC5AC and MUC5B expression in human airway epithelial cells. These findings provide important information about the biological role of MWCNT on mucus-secretion in human airway epithelial cells. Korean J Otorhinolaryngol-Head Neck Surg 2015;58(8):552-7

The cleaning of embedded-attenuated phase shift masks (EAPSMs) is one of the most important enabling capabilities in the production of high-quality masks. Particles are commonly generated during Cr and MoSiON etching using inductively coupled plasma (ICP) tools. The cleaning process of EAPSMs requires not only the removal of particles on the phase shifting layer (MoSiON) and glass, but also the ability to leave the phase and transmission properties intact. Megasonic cleaning is a technique commonly used for removing particles on the surfaces of photomasks. However, megasonic processes employing SC-1 chemistry (specifically ammonium hydroxide) cannot be applied to a MoSiON PSM. Chemical erosion of the alkali-soluble phase shifting layer will drive phase and transmission performance outside of customer specifications. Therefore, EAPSM cleaning must balance simultaneously the complete removal of particles with the prevention physical damage. For these reasons, the cleaning process requires a high degree of control. In this paper, a new cleaning method was applied to MoSiON-based masks utilizing megasonic cleaning because it had a little change on phase and transmission. Traditional SC-1 chemistry was not used at all. Results obtained through this method showed a little change on phase and transmission. The particles on glass also can be sufficiently removed using megasonic process with the dilute SC-1 chemistry. The cleaning technique for the fabrication of EAPSMs with no variation in phase and transmission after the cleaning process will be presented.

Urinary 1-hydroxypyrene (1-OHP) has been used as a biomarker for environmental polyaromatic hydrocarbon (PAH) exposure. However, it is known that there is an interindividual variability in metabolism of pyrene to 1-OHP depending on the activities of the metabolizing enzymes, especially cytochrome P450s (CYPs). In this study, we investigated the 1-hydroxylation of pyrene by 10 forms of cDNA-expressed human P450s in order to identify the principal isoforms of P450s that are involved in the major metabolic pathway of pyrene. The pyrene 1-hydroxylation activity was found to be the highest in CYP1A1 at both 0.5 and 50microM of pyrene, followed by CYP1B1 and 1A2, whereas other enzymes, including CYP2A6, 2C8, 2C9*1, 2C19, 2D6, 2E1, 3A4, and control microsomes, showed very low or undetectable rates of 1-hydroxylation. In conclusion, CYP1A1, 1B1, and 1A2 are major metabolizing enzymes in 1-hydroxylation of pyrene in vitro. This suggests that the individual difference of these enzymes must be included in epidemiological studies to evaluate PAH exposure using urinary 1-OHP.

Interleukin-1beta (IL-1beta) has been implicated in the pathogenesis of inflammatory diseases of the airway. In this study, we investigated the regulation of MUC2 and MUC5AC expression and of their regulatory mechanisms through cyclooxygenase-2 (COX-2) and prostaglandin E(2) (PGE(2)). Cells activated by IL-1beta showed increased COX-2, MUC2, and MUC5AC expressions at both the mRNA and protein levels. Mucin production was blocked by the selective COX-2 inhibitor NS398, and PGE(2) directly induced MUC2 and MUC5AC expression at both the mRNA and protein levels in a dose-dependent manner. These results suggest a role for PGE(2) in IL-1beta-induced mucin synthesis in NCI-H292 cells. To investigate the roles of molecules upstream of COX-2 in mucin regulation, we examined the role of mitogen-activated protein kinases (MAPKs). Cells activated by IL-1beta showed increased extracellular signal-regulated kinase (ERK)1/2 and p38 phosphorylation, and IL-1beta-induced MUC2 and MUC5AC production was blocked by the ERK pathway inhibitor PD98059 or the p38 inhibitor SB203580. The inhibition of both MAPKs reduced IL-1beta-induced COX-2 expression and PGE(2) synthesis. Furthermore, the addition of PGE(2) to cells overcame the inhibitory effects of both MAPK inhibitors in IL-1beta-induced mucin production. These results indicate that in human pulmonary epithelial cells, IL-1beta activates ERK or p38 to induce COX-2 production, which in turn induces MUC2 and MUC5AC production.

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-1beta (IL-1beta) 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-1beta. 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 (RARalpha), and inhibited by the specific RARalpha antagonist Ro 41-5253. Here, we demonstrate that the RARalpha antagonist can effectively inhibit IL-1beta-induced MUC2 and MUC5AC gene expression and reduce intracellular MUC5AC protein. Further investigation showed that the RARalpha antagonist also inhibited the stimulation of MUC2 and MUC5AC mRNA expression by tumor necrosis factor-alpha, LPS, and NE.

This study demonstrates for the first time the effects of IL-1beta on the regulation of protein production as well as MUC2 gene transcription in cultured human airway epithelial cells. The effect of IL-1beta on the regulation of MUC2 protein was determined by flow cytometric analysis. The expression level of MUC2 induced by IL-1beta increased in a dose-dependent manner. MUC2 transcripts were detected after 2 h of exposure to IL-1beta and reached maximal level after 8 h. Actinomycin D experiments indicated that the IL-1beta-mediated MUC2 expression was controlled by transcriptional regulation. Both RT-PCR and FACS analysis showed that budesonide concomitantly attenuated IL-1beta mediated MUC2 gene as well as protein production levels. Use of the glucocorticoid receptor antagonist, RU-486, restored the inhibitory effect of budesonide on the IL-1beta-mediated MUC2 protein as well as gene. The data suggest that IL-1beta up-regulates MUC2 gene by transcriptional regulation and that budesonide suppresses the IL-1beta-medicated MUC2 expression via decreased transcriptional activation.

편평상피세포암종(squamous cell carcinoma)은 두경부에 서 가장 흔히 발생하는 악성종양으로 흡연, 음주와 자외선 노 출 등이 원인이 된다. 그러나 침샘에 발생하는 경우는 매우 드물어 전체 침샘에 발생하는 악성 종양 중 1%도 되지 않으며, 대부분 이하선에 발생하는 것으로 알려져 있다. 침샘에서 편평상피세포암으로 진단되는 경우는 편평상피 세포를 일부 포함하는 고악성도 점액표피양암종(high grade mucoepidermoid carcinoma)과 피부 등의 다른 인접부위에 서 발생한 편평상피세포암의 직접적인 침윤, 다른 장기에 발 생한 편평상피세포암의 원격전이, 침샘 내 림프절로의 전이, 원 발성 편평상피세포암 등이 있다. 침샘 중에서도 악하선에 발생한 편평상피세포암종에 대한 보고는 매우 드물다. 또한, 지금까지 보고된 편평상피세포암 종의 증례들이 대부분 피부암의 직접적인 침습이나 악하선 내 림프절로 암종이 전이된 것들로 악하선에 발생한 원발성 편평 상피세포암종의 빈도는 더욱 드물 것으로 생각되며, 아직까지 국내에 보고된 바는 없다. 저자들은 수십 년간 지속된 악하선 종물이 최근 3~4개월 간 크기가 갑자기 증가하여 내원한 70세 여자 환자에서 악하 선의 원발성 편평상피세포암종 1예를 경험하였기에 문헌고찰 과 함께 보고하는 바이다.

Purpose: We present a case of acquired ocular motor apraxia accompanied with esotropia due to multiple brain infarcts. Case summary: A 59-year-old male was referred for diplopia that started 9 years before presentation and continued after multiple brain infracts including right cerebellum, right occipital lobe, medulla oblongata and inferior pons. At initial examination, his best corrected visual acuity was 20/22 in the right eye and 20/25 in the left eye and he had 12 prism diopter (PD) esotropia at distance and near in primary gaze with correction. His duction and version were normal; however, his horizontal saccade was notably decreased. Two years and 8 months after presentation, the patient had 15 PD esotropia at distance and near with correction. His duction and version were normal and vertical saccadic eye movements were observed. However, horizontal saccade disappeared. The patient also exhibited a distinguishing head thrust following the order for saccadic eye movement. He was diagnosed with an acquired ocular motor apraxia accompanied with esotropia. During the follow-up period the patient underwent bilateral recession of the medial rectus. The usual diplopia and his horizontal esodeviation improved to 3 PD of esotropia at distance. Conclusions: Multiple brain infarcts can result in an acquired ocular motor apraxia accompanied with esotropia. Varying types of ocular motor disorders should be considered in patients with a previous medical history of brain infarct. J Korean Ophthalmol Soc 2014;55(9):1396-1400

Objectives Delphinidin is one of the anthocyanidins. It is believed to have anti-inflammatory property including antioxidant, antiangiogenic, and anti-cancer properties. However, the anti-inflammatory effect of delphinidin in mucin-producing human airway epithelial cells has not been determined. Therefore, this study was conducted in order to investigate the effect and the brief signaling pathway of delphinidin in lipopolysaccharide (LPS)-induced MUC8 and MUC5B expression in human airway epithelial cells. Methods In mucin-producing human NCI-H292 airway epithelial cells and primary cultures of normal nasal epithelial cells, the reverse transcriptase-polymerase chain reaction (RT-PCR), real-time PCR, enzyme immunoassay were used for investigating the expressions of MUC8, MUC5, and Toll-like receptor 4 (TLR4), after LPS treatment and delphinidin treatment. And the signaling pathway of delphinidin on LPS-induced MUC8 and MUC5B expression was investigated using the RT-PCR, and immunoblot analysis. To confirm the involvement of TLR4 in LPS-induced MUC8 and MU5B expression, the cells were transfected with TLR4 siRNA. Results In NCI-H292 airway epithelial cells, LPS (100 ng/mL) significantly induced TLR4, MUC8, and MUC5B expression. TLR4 siRNA significantly blocked LPS-induced MUC8 and MUC5B mRNA expression. LPS (100 ng/mL) significantly activated the phosphorylation of extracellular signal related kinase (ERK) 1/2 and p38 mitogen-activated protein kinase (MAPK). Delphinidin (50 and 100 µM) inhibited LPS-induced TLR4, MUC8, and MUC5B expression and LPS-induced phosphorylation of ERK1/2 and p38 MAPK. In the primary cultures of normal nasal epithelial cells, delphinidin (50 and 100 µM) significantly inhibited LPS-induced TLR4, MUC8, and MUC5B gene expression. Conclusion These results suggest that delphinidin attenuates LPS-induced MUC8 and MUC5B expression through the TLR4-mediated ERK1/2 and p38 MAPK signaling pathway in human airway epithelial cells. These findings indicated that delphinidin may be a therapeutic agent for control of inflammatory airway diseases.

Received June 23, 2014 Revised July 23, 2014 Accepted July 24, 2014 Address for correspondence Yong-Dae Kim, MD, PhD Department of OtorhinolaryngologyHead and Neck Surgery, College of Medicine, Yeungnam University, 170 Hyeonchung-ro, Nam-gu, Daegu 705-802, Korea Tel +82-53-620-3781 Fax +82-53-628-7884 E-mail ydkim@med.yu.ac.kr Background and ObjectivesZZRoflumilast, a selective inhibitor of phosphodiesterase type 4, has an anti-inflammatory property. It has been used in the treatment of chronic inflammatory airway diseases such as chronic obstructive pulmonary disease and asthma. However, the effect of roflumilast on mucus secretion in inflammatory airway epithelial cells has not been reported. Therefore, this study was aimed at investigating the effects of roflumilast on the inflammatory mediator-induced MUC5AC and MUC5B expression in human airway epithelial cells. Materials and MethodZZIn human mucin-producing NCI-H292 airway epithelial cells and primary cultures of nasal epithelial cells, the effects of roflumilast on lipopolysaccharide (LPS)and phorbl-12-myrsitate-13-acetate (PMA)-induced MUC5AC and MUC5B expression were analyzed by reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay. ResultsZZRoflumilast attenuated LPS-induced MUC5AC and MUC5B mRNA and glycoprotein expression in NCI-H292 cells. And roflumilast attenuated PMA-induced MUC5AC and MUC5B mRNA and glycoprotein expression in NCI-H292 cells. In addition, roflumilast attenuated LPS and PMA-induced MUC5AC and MUC5B mRNA expression in the primary cultures of nasal epithelial cells. ConclusionZZThese results suggest that roflumilast attenuates MUC5AC and MUC5B expressions in airway epithelial cells. Roflumilast may be a potentially ideal therapeutic agent for the control of mucus-hypersecretion in treating chronic inflammatory airway diseases. Korean J Otorhinolaryngol-Head Neck Surg 2014;57(12):830-5

Background and Objectives MUC5AC and MUC5B are representative secretory mucin genes in the human airway. MUC5AC and MUC5B expression are increased by a variety of inflammatory mediators. Betulinic acid, a naturally occurring pentacyclic triterpenoid, is known to have an anti-inflammatory property. However, the effects of betulinic acid on mucin secretion of airway epithelial cells still have not been reported. Therefore, in this study, the effect of betulinic acid on inflammatory mediators-induced MUC5AC and MUC5B expression was investigated in human airway epithelial cells. Materials and Method In the mucin-producing human NCI-H292 airway epithelial cells, the effects of betulinic acid on interleukin-1β (IL-1β)-, lipopolysaccharide (LPS)-, and phorbol myristate acetate (PMA)-induced MUC5AC and MUC5B expression were analyzed by reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay. Results Betulinic acid attenuated IL-1β-, LPS- and PMA-induced MUC5B mRNA and glycoprotein expression in NCI-H292 cells. Betulinic acid did not attenuate IL-1β-, LPS- and PMA-induced MUC5AC mRNA and glycoprotein expression in NCI-H292 cells. Conclusion These results suggest that betulinic acid attenuates IL-1β-, LPS- and PMA-induced MUC5B expression in airway epithelial cells. Therefore, betulinic acid may modulate a control of mucus-hypersecretion in airway inflammatory disease. Korean J Otorhinolaryngol-Head Neck Surg 2014;57(8):526-32

Received September 4, 2013 Revised October 30, 2013 Accepted October 31, 2013 Address for correspondence Chang Hoon Bae, MD, PhD Department of OtorhinolaryngologyHead and Neck Surgery, College of Medicine, Yeungnam University, 170 Hyeonchung-ro, Nam-gu, Daegu 705-703, Korea Tel +82-53-620-3784 Fax +82-53-628-7884 E-mail baich@med.yu.ac.kr Background and ObjectivesZZTinnitus is a disease with high prevalence and a wide range of etiologies. Tinnitus has a lot of impact on the patients, causing psychological distress such as anxiety and depression. Type D personality is related to the negative emotions including to anxiety and depression. Therefore, the goal of this study was to understand the relationship between tinnitus and anxiety/depression/type D personality. Subjects and MethodZZNinety three patients with chronic subjective tinnitus, who visited the Department of Otorhinolaryngology-Head Neck Surgery in Yeungnam University Hospital from May, 2012 to October, 2012. The tinnitus patients were asked to complete a survey: regarding demographic data, otologic history, Beck Depression Inventory (BDI), Hamilton anxiety scale (HAM-A), type D personality scale 14 (DS-14), and tinnitus handicap inventory (THI). ResultsZZThe tinnitus patients had significantly higher levels of type D personality (58.1%). In the tinnitus patients, as the score of THI increased, the BDI and HAM-A scores increased. As the DS-14 score increased, the THI scores increased. ConclusionZZThese results suggest that the tinnitus patients have high prevalence of type D personality compared to that shown in the general population. And the handicap of tinnitus is related to anxiety, depression and type D personality. Korean J Otorhinolaryngol-Head Neck Surg 2014;57:22-6

서울대학교 의과대학 안과학교실, 분당서울대학교병원 안과, 서울대학교병원운영 서울특별시보라매병원 안과, 서울대학교병원 임상의학연구소 서울인공안구센터 Department of Ophthalmology, Seoul National University College of Medicine, Seoul, Korea Department of Ophthalmology, Seoul National University Bundang Hospital, Seongnam, Korea Department of Ophthalmology, Seoul Municipal Government–Seoul National University Boramae Medical Center, Seoul, Korea Seoul Artificial Eye Center, Seoul National University Hospital Clinical Research Institute, Seoul, Korea

We evaluated the distribution of nitric oxide (NO) in the rat nasal mucosa using nicotineamide adenosine dinucleotide phosphate (NADPH)-diaphorase histochemistry. The NADPH-diaphorase positive nerve fibers in the nasal mucosa were observed around blood vessels and submucosal glands and in sphenopalatine ganglions. Strong positive reactions for NADPH-diaphorase were observed in ganglions as compared with the other tissues. In septal and turbinate mucosa, positive reactions for NADPH-diaphorase were mainly seen in the anterior portion, and a few positive reactions were observed in the posterior portion. No positive reactions for NADPH-diaphorase were demonstrated in the sinus mucosa. These results suggest that NO may be related to regulation of blood flow, glandular secretion and neurotransmission, and also that NO may play an important role in the defence mechanism of the upper airway system against external environments.