병원 근로자들의 고용형태에 따른 직무 스트레스와 삶의 질의 관계

전은숙,이강숙,이선영,유재희,홍아름 大韓産業醫學會 2009 대한직업환경의학회지 Vol.21 No.1

목적 본 연구는 병원에 종사하는 정규직 비정규직 근로자의 직무스트레스와 삶의 질 수준을 파악하고 직무스트레스와 삶의 질과의 관련성 및 삶의 질에 영향을 미치는 요인을 규명하기위해 수행되었다 방법 자기기입형 설문조사를 실시하였으며 정규직 172명 비정규직 189명이 최종 분석하였다 일반적 특성과 한국인 직무스트레스 측정도구-단축형 (Korean occupational stress scale short form) 삶의 질 측정을 위한 도구 WHOQOL-BREF를 사용하였다 결과 정규직에 비해 비정규직에서 직무스트레스 수준이 높았다 정규직은 직무요구도와 직장문화의 항목에서 비정규직은 직무자율성 직무불안정성 보상부적절의 항목에서 직무스트레스 요인이 유의하게 많았다 삶의 질수준은 정규직 근로자에서 유의하게 높았으며 심리적 영역 사회적 영역 생활환경 영역에서 비정규직보다 유의하게 높은 수준을 보였다 결론 정규직과 비정규직 근로자의 직무스트레스 요인과 삶의 질 수준은 달랐다 고용형태를 막론하고 직무스트레스는 삶의 질에 부정적인 영향을 미치고 있었으며 비정규직은 직장문화로 인한 스트레스 요인이 많을수록 삶의 질이 낮았다 따라서 병원근로자의 삶의 질 향상을 위하여 적절한 관리 혹은 프로그램이 제공되어야 할 것이며 특히 비정규직 근로자의 직무스트레스를 일으키는 요인들에 대한 적절한 관리가 필요할 것이다 Objective This study was conducted to evaluate the relationship between job stress and quality of life for hospital workers by type of employment Methods Data were obtained for 361 workers in a large hospital 172 of whom were categorized as typical workers defined by permanent employee and 189 of whom were categorized as atypical workers defined by fixed term contraction Job stress was assessed using the Korean Occupational Stress Scale Short Form and the World Health Organization Quality of Life-BREF Questionnaire Results Atypical workers had significantly higher scores for job related stress in the domains Of insufficient control over work job insecurity and lack of reward in the workplace compared with typical workers who had higher scores for stress in the domains of job demands and occupational climate Test scores also indicated that typical workers had a significantly better quality of life than atypical workers especially in terms of mental health social relationships and environment Conclusion These findings suggested that factors contributing to job-related stress were different between typical and atypical hospital and typical workers are likely to have a better quality of life

Structural and Electrical Properties of EOT HfO₂ (<1 nm) Grown on InAs by Atomic Layer Deposition and Its Thermal Stability

Kang, Yu-Seon,Kang, Hang-Kyu,Kim, Dae-Kyoung,Jeong, Kwang-Sik,Baik, Min,An, Youngseo,Kim, Hyoungsub,Song, Jin-Dong,Cho, Mann-Ho American Chemical Society 2016 ACS APPLIED MATERIALS & INTERFACES Vol.8 No.11

<P>We report on-changes in the structural, interfacial, and electrical characteristics of sub-1 nm equivalent oxide thickness (EOT) HfO2 grown on InAs by atomic layer deposition. When the HfO2 film was deposited on an InAs substrate at a temperature of 300 degrees C, the HfO2 was in an amorphous phase with an sharp interface, an EOT of 0.9 nm, and low preexisting interfacial defect states. During post deposition annealing (PDA) at 600 degrees C, the HfO2 was transformed from an amorphous to a single crystalline orthorhombic phase, which minimizes the interfacial lattice mismatch below 0.8%. Accordingly, the HfO2 dielectric after the PDA had a dielectric constant of similar to 24 because of the permittivity of the well-ordered orthorhombic HfO2 structure. Moreover, border traps were reduced by half than the as-grown sample due to a reduction in bulk defects in HfO2 dielectric during the PDA. However, in terms of other electrical properties, the characteristics of the PDA-treated sample were degraded compared to the as-grown sample, with EOT values of 1.0 run and larger interfacial defect states (D-it) above 1 x 10(14) cm(-2) eV(-1). X-ray photoelectron spectroscopy data indicated that the diffusion of In atoms from the InAs substrate into the HfO2 dielectric during the PDA at 600 degrees C resulted in the development of substantial midgap states.</P>

Cks1 regulates human hepatocellular carcinoma cell progression through osteopontin expression

Kang, Yu-Seon,Jeong, Eun-Jeong,Seok, Hyun-Jeong,Kim, Seon-Kyu,Hwang, Jin-Seong,Choi, Mu Lim,Jo, Dong-Gyu,Kim, Yuna,Choi, Jinhyeon,Lee, Yeo-Jin,Jung, Eunsun,Min, Jeong-Ki,Han, Tae-Su,Kim, Jang-Seong Elsevier 2019 Biochemical and biophysical research communication Vol.508 No.1

<P><B>Abstract</B></P> <P>Precise cell cycle regulation is critical to prevent aberrant cell proliferation and cancer progression. Cks1 was reported to be an essential accessory factor for SCF<SUP>Skp2</SUP>, the ubiquitin ligase that targets p27<SUP>Kip1</SUP> for proteasomal degradation; these actions drive mammalian cell transition from G1 to S phase. In this study, we investigated the role played by Cks1 in the growth and progression of human hepatocellular carcinoma (HCC) cells. Silencing Cks1 expression abrogated osteopontin (OPN) expression in a p27<SUP>Kip1</SUP>-dependent manner in Huh7 HCC cells. OPN increased the proliferation, migration and invasion of Huh7 cells. Pharmacological inhibitor studies demonstrated that ERK1/2 signaling is responsible mainly for Cks1-mediated OPN expression. Cks1 appears to regulate ERK1/2 signaling through the expression of dual-specificity phosphatase 16 (DUSP16) because both Cks1 knockdown, which leads to DUSP16 upregulation, and DUSP16 overexpression decreased ERK1/2 phosphorylation and the resulting OPN expression. The same is true for the Cks1-mediated increases in p27<SUP>Kip1</SUP>, suggesting that Cks1 regulates OPN expression through activating ERK1/2 signaling either by suppressing DUSP16 expression or by a p27<SUP>Kip1</SUP>-dependent mechanism. Cks1 and OPN expression levels were significantly higher, but DUSP16 expression levels were significantly lower in HCC tissues than in normal liver tissues. Both Cks1 and OPN expression were negatively correlated with DUSP16 expression, whereas Cks1 expression was positively correlated with OPN expression. Moreover, combined panels for the expression levels of Cks1, DUSP16 and OPN showed significant prognostic power for the risk assessment of HCC patient overall survival. In conclusion, our data propose a novel function for Cks1 as a tumor promoter through the expression of the strongly oncogenic protein OPN in HCC.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Cks1 promotes OPN expression in human HCC cells. </LI> <LI> The Cks1-mediated upregulation of DUSP16 or p27<SUP>Kip1</SUP> decreased OPN expression. </LI> <LI> DUSP16- or p27<SUP>Kip1</SUP>-mediated ERK1/2 inactivation is responsible for OPN abrogation. </LI> <LI> Cks1, DUSP16 and OPN may be a useful prognostic biomarker panel for HCC patients. </LI> </UL> </P>

Effects of Nitrogen Incorporation in HfO₂ Grown on InP by Atomic Layer Deposition: An Evolution in Structural, Chemical, and Electrical Characteristics

Kang, Yu-Seon,Kim, Dae-Kyoung,Kang, Hang-Kyu,Jeong, Kwang-Sik,Cho, Mann-Ho,Ko, Dae-Hong,Kim, Hyoungsub,Seo, Jung-Hye,Kim, Dong-Chan American Chemical Society 2014 ACS APPLIED MATERIALS & INTERFACES Vol.6 No.6

<P>We investigated the effects of postnitridation on the structural characteristics and interfacial reactions of HfO<SUB>2</SUB> thin films grown on InP by atomic layer deposition (ALD) as a function of film thickness. By postdeposition annealing under NH<SUB>3</SUB> vapor (PDN) at 600 °C, an InN layer formed at the HfO<SUB>2</SUB>/InP interface, and ionized NH<SUB><I>x</I></SUB> was incorporated in the HfO<SUB>2</SUB> film. We demonstrate that structural changes resulting from nitridation of HfO<SUB>2</SUB>/InP depend on the film thickness (i.e., a single-crystal interfacial layer of <I>h</I>-InN formed at thin (2 nm) HfO<SUB>2</SUB>/InP interfaces, whereas an amorphous InN layer formed at thick (>6 nm) HfO<SUB>2</SUB>/InP interfaces). Consequently, the tetragonal structure of HfO<SUB>2</SUB> transformed into a mixture structure of tetragonal and monoclinic because the interfacial InN layer relieved interfacial strain between HfO<SUB>2</SUB> and InP. During postdeposition annealing (PDA) in HfO<SUB>2</SUB>/InP at 600 °C, large numbers of oxidation states were generated as a result of interfacial reactions between interdiffused oxygen impurities and out-diffused InP substrate elements. However, in the case of the PDN of HfO<SUB>2</SUB>/InP structures at 600 °C, nitrogen incorporation in the HfO<SUB>2</SUB> film effectively blocked the out-diffusion of atomic In and P, thus suppressing the formation of oxidation states. Accordingly, the number of interfacial defect states (<I>D</I><SUB>it</SUB>) within the band gap of InP was significantly reduced, which was also supported by DFT calculations. Interfacial InN in HfO<SUB>2</SUB>/InP increased the electron-barrier height to ∼0.6 eV, which led to low-leakage-current density in the gate voltage region over 2 V.</P><P><B>Graphic Abstract</B> <IMG SRC='http://pubs.acs.org/appl/literatum/publisher/achs/journals/content/aamick/2014/aamick.2014.6.issue-6/am4049496/production/images/medium/am-2013-049496_0014.gif'></P><P><A href='http://pubs.acs.org/doi/suppl/10.1021/am4049496'>ACS Electronic Supporting Info</A></P>

Defect States below the Conduction Band Edge of HfO₂ Grown on InP by Atomic Layer Deposition

Kang, Yu-Seon,Kim, Dae-Kyoung,Kang, Hang-Kyu,Cho, Sangwan,Choi, Sungho,Kim, Hyoungsub,Seo, Jung-Hye,Lee, Jouhahn,Cho, Mann-Ho American Chemical Society 2015 The Journal of Physical Chemistry Part C Vol.119 No.11

<P>The electronic structure and nature of the defect states below the conduction band edge of an HfO<SUB>2</SUB> gate dielectric grown on InP substrate prepared by atomic layer deposition was examined using X-ray photoelectron spectroscopy (XPS), X-ray absorption spectroscopy (XAS), and density functional theory (DFT). When the HfO<SUB>2</SUB> dielectric was deposited on an InP substrate with an abrupt interface, the resulting HfO<SUB>2</SUB> develops a tetragonal (<I>t</I>) structure, which minimizes the interfacial lattice mismatch. The O <I>K</I>-edge absorption features and DFT calculations indicated that additional structural distortion occurred by a <I>q</I> = −2 charged O vacancy (VO<SUP>–2</SUP>) in the <I>t</I>-HfO<SUB>2</SUB>. The electronic structure and the charge-transition levels of <I>t</I>-HfO<SUB>2</SUB> with VO<SUP>–2</SUP> were assigned based on a second derivative analysis of O <I>K</I>-edge features; 12 distinct pre-edge defect states below the Hf 5d conduction band edge were evident when the degeneracies resulting from Jahn–Teller splitting and crystal field splitting were removed. No changes in the electronic structure near valence band edge by VO<SUP>–2</SUP> were observed in XPS valence spectra. Moreover, O vacancies in <I>t</I>-HfO<SUB>2</SUB> lead to substantial midgap states caused by interstitial elemental In or P in the <I>t</I>-HfO<SUB>2</SUB> due to the enhanced out-diffusion of elemental In or P through O vacancies. We conclude that both the defect states near the CBE and the midgap states could be controlled by the incorporation of nitrogen into the HfO<SUB>2</SUB> using a thermal NH<SUB>3</SUB> treatment.</P><P><B>Graphic Abstract</B> <IMG SRC='http://pubs.acs.org/appl/literatum/publisher/achs/journals/content/jpccck/2015/jpccck.2015.119.issue-11/jp511666m/production/images/medium/jp-2014-11666m_0010.gif'></P>

Multiple Gastrointestinal Stromal Tumors: Clinicopathologic and Genetic Analysis of 12 Patients

Kang, Dae Young,Park, Cheol Keun,Choi, Jong Sang,Jin, So Young,Kim, Hyun Jung,Joo, Mee,Kang, Mi Seon,Moon, Woo Sung,Yun, Ki Jung,Yu, Eun Sil,Kang, Haeyun,Kim, Kyoung-Mee Lippincott Williams Wilkins, Inc. 2007 The American journal of surgical pathology Vol.31 No.2

Multiple gastrointestinal stromal tumors (GISTs) are extremely rare and usually associated with type 1 neurofibromatosis and familial GIST. The aim of this study was to investigate the clinical, phenotypic, and genetic characteristics of multiple GISTs to gain insights into their underlying pathogenesis and clinical behavior. Forty-seven paraffin blocks of multiple GISTs from 12 patients were analyzed. Genomic DNA was extracted from the tumor and normal mucosa and mutations for 4 exons of KIT gene and 3 exons of PDGFRA gene were determined. Among 12 patients with multiple GISTs, 5 were sporadic, 2 were familial with germline mutations of KIT gene, and 5 were associated with type 1 neurofibromatosis. All but 1 sporadic and familial multiple GISTs showed mutations of KIT gene shared by the same mutation on each GIST mass within a patient. But in 1 sporadic case, different types of KIT mutations were observed. Two familial multiple GIST cases showed diffuse involvement of the gastrointestinal tract with diffuse hyperplasia of interstitial cell of Cajal. Multiple GISTs associated with type 1 neurofibromatosis were located in the jejunum and harbored no mutations of KIT or PDGFRA. Different types of KIT gene mutation found in our case raise a possibility that recurrence of GISTs within a gastrointestinal tract may have a chance to be a rare occurrence of multiple primary GISTs instead of true recurrence. Multiple GISTs show unique clinical, phenotypic, and genotypic characteristics that are dependent on the particular underlying mechanisms, but the overall prognosis is favorable regardless of the numbers or phenotype of GISTs.

DUSP1 induces paclitaxel resistance through the regulation of p-glycoprotein expression in human ovarian cancer cells

Kang, Yu-Seon,Seok, Hyun-Jeong,Jeong, Eun-Jeong,Kim, Yuna,Yun, Seok-Joong,Min, Jeong-Ki,Kim, Sun Jin,Kim, Jang-Seong Elsevier 2016 Biochemical and biophysical research communication Vol.478 No.1

<P><B>Abstract</B></P> <P>The heterogeneity and genetic instability of ovarian cancer cells often lead to the development of drug resistance, closely related with the increased cancer-related mortality. In this study, we investigated the role of dual-specificity phosphatase 1 (DUSP1) in the development of the resistance in human ovarian cancer cells against paclitaxel. Overexpression of DUSP1 in HeyA8 human ovarian cancer cells (HeyA8-DUSP1) up-regulated the expression of the drug efflux pump, p-glycoprotein. Consequently, HeyA8-DUSP1 cells are highly resistant to paclitaxel, with the resistance comparable to that of a multi-drug resistance cell line (HeyA8-MDR). Moreover, over expression of DUSP1 significantly increased the activation of p38 MAPK, leaving the activation of ERK1/2 and JNK1/2 unaffected. Pharmacological suppression of p38 MAPK activity prevents the up-regulation of p-glycoprotein expression and the consequent resistance against paclitaxel in HeyA8-DUSP1 cells. By contrast, HeyA8-MDR cells expressed a significantly higher level of DUSP1, but treatment with small interference RNA against DUSP1 significantly suppressed the expression of p-glycoprotein and the resistance against paclitaxel in HeyA8-MDR cells. Ectopic expression of MKK3, an upstream activator of p38 MAPK, significantly up-regulated the expression of p-glycoprotein and increased the consequent resistance against paclitaxel in HeyA8 cells. Collectively, these data indicated that DUSP1 may induce the resistance against paclitaxel through the p38 MAPK-mediated overexpression of p-glycoprotein in human ovarian cancer cells.</P> <P><B>Highlights</B></P> <P> <UL> <LI> DUSP1 induces Pgp expression and paclitaxel resistance in ovarian cancer cells. </LI> <LI> DUSP1 mediates p38 MAPK activation leading to Pgp-mediated paclitaxel resistance. </LI> <LI> Inhibition of DUSP1 or p38 MAPK reverses Pgp-mediated paclitaxel resistance. </LI> <LI> DUSP1-p38 MAPK-Pgp axis is a novel mechanism for paclitaxel resistance. </LI> </UL> </P>

프리저브드용 불두화에 대한 글리콜 최적 처리 조건 구명

유선영(Seon-Young Yu),박수민(Su-Min Park),정호용(Ho-Yong Jeong),강기오(Ki-O Kang),강성선(Sung-Seon Kang),허북구(Buk-Gu Heo),박윤점(Yun-Jum Park) 한국원예학회 2011 한국원예학회 학술발표요지 Vol.2011 No.5

Leptin-promoted cilia assembly is critical for normal energy balance.

Han, Yu Mi,Kang, Gil Myoung,Byun, Kyunghee,Ko, Hyuk Wan,Kim, Joon,Shin, Mi-Seon,Kim, Hyun-Kyong,Gil, So Young,Yu, Ji Hee,Lee, Bonghee,Kim, Min-Seon American Society for Clinical Investigation 2014 The Journal of clinical investigation Vol.124 No.5

<P>The majority of mammalian cells have nonmotile primary cilia on their surface that act as antenna-like sensory organelles. Genetic defects that result in ciliary dysfunction are associated with obesity in humans and rodents, which suggests that functional cilia are important for controlling energy balance. Here we demonstrated that neuronal cilia lengths were selectively reduced in hypothalami of obese mice with leptin deficiency and leptin resistance. Treatment of N1 hypothalamic neuron cells with leptin stimulated cilia assembly via inhibition of the tumor suppressors PTEN and glycogen synthase kinase 3β (GSK3β). Induction of short cilia in the hypothalamus of adult mice increased food intake and decreased energy expenditure, leading to a positive energy balance. Moreover, mice with short hypothalamic cilia exhibited attenuated anorectic responses to leptin, insulin, and glucose, which indicates that leptin-induced cilia assembly is essential for sensing these satiety signals by hypothalamic neurons. These data suggest that leptin governs the sensitivity of hypothalamic neurons to metabolic signals by controlling the length of the cell's antenna.</P>

수술 전 선행화학요법을 시행한 난소의 원발성 악성 혼합성 뮬러리안종양

강명선 ( Kang Myeong Seon ),김석모 ( Kim Seog Mo ),최호선 ( Choe Ho Seon ),이유경 ( Lee Yu Gyeong ) 대한산부인과학회 2004 Obstetrics & Gynecology Science Vol.47 No.2

Objective : This study was perfomed to evaluate the expression of MAGE gene and human papillomavirus (HPV) 16, 18 type in patients with cervical neoplasia using in exfoliated cervical cells. Methods : The expression of common MAGE gene (MAGE 1 to 6) in cervical scraps was studied by reverse-transcription plymerase chain reaction (RT-PCR) in 12 normal control patient and 48 patients with abnormal cytologic results. In all 60 patients, colposcopic directed biopsy and HPV test by polymerase chain reaction (PCR) was done. Results : The pathologic results of 60 patients was 12 cervicitis, 37 cervical intraepithelial neoplasis (14 LSIL, 23 HSIL), and 11 invasive squamous cell carcinomas. No expression of common MAGE gene was detected in 12 cervical scraps of cervicitis. The common MAGE gene of LSIL, HSIL and invasive squamous cell carcinomas was expressed in two (14.3%), seventeen (73.9%), ten (90.9%) respectively. HPV type 16 or 18 was detected in 1 cervicitis, 5 LSIL, 20 HSIL and 10 invasive squamous cell carcinoma. In 51 patients (85%), the HPV test result and the common MAGE gene expression showed coincident results. Conclusion : This result suggests common MAGE gene might be potential tumor marker in cervical neoplasia and adjuvant test of the Papanicolaou smear.