• 한국엔터테인먼트산업학회논문지
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• 제14권7호
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• pp.609-621
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• 2020

본 연구는 의료기관의 환경요인을 매개로 의료기관 종사자들의 라이프 스타일에 따른 조직몰입이 진료비 삭감률에 미치는 영향이 무엇인지 알아보기 위한 연구로 전라도에 있는 의료기관 종사자 300명을 대상으로 설문조사하였다. 본 연구의 결과는 다음과 같다. 첫째, 인구사회학적 특성에 따른 조직 몰입도는 연령, 학력, 성별, 결혼, 직종, 소득과 근무 연수에서 유의한 차이를 보였다. 둘째, 인구사회학적 특성에 따른 환경요인은 결혼, 근무 연수, 병원유형에서 유의한 차이를 보였다. 셋째, 입원삭감률은 직종, 근무 연수 병원유형에서, 외래삭감률은 연령, 결혼, 직종, 근무 연수, 병원유형에서 유의한 차이를 보였다 넷째, 조직몰입, 환경요인, 삭감률의 상관관계를 알아 본 결과 입원 삭감률과 외래 삭감률은 정적 상관이 유의하게 있는 것으로 나타났다. 다섯째, 조직몰입과 환경요인을 동시에 투입하여 입원삭감률에 미치는 영향을 살펴본 결과 조직몰입과 입원삭감률에서 환경요인이 부분매개, 외래삭감률은 조직몰입과 외래삭감률에서 환경요인이 완전매개 하는 것으로 나타났다. 본 연구로 의료기관의 효율적인 운영방안과 효과적인 인력관리를 위한 기초자료를 제공하고자 한다

• Journal of Preventive Medicine and Public Health
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• 제46권2호
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• pp.82-88
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• 2013

Objectives: Unprotected leisure time exposure to ultraviolet radiation from the sun or artificial tanning beds is the most important environmental risk factor for melanoma, a malignant skin cancer with increasing incidences over the past decades. The aim of the present study was to assess the impact of skin health information provided by several sources and different publishing issues on knowledge, risk perception, and sun protective behavior of sunbathers. Methods: A cross-sectional questionnaire survey was conducted among Austrian residents (n=563) spending leisure time outdoors in August 2010. Results: Print media, television, and family were perceived as the most relevant sources of information on skin health, whereas the source physician was only ranked as fourth important source. Compared to other sources, information provided by doctors positively influenced participants' knowledge on skin risk and sun protective behavior resulting in higher scores in the knowledge test (p=0.009), higher risk perception (p<0.001), and more sun protection (p<0.001). Regarding gender differences, internet was more often used by males as health information source, whereas females were more familiar with printed information material in general. Conclusions: The results of this survey put emphasis on the demand for information provided by medical professionals in order to attain effective, long-lasting promotion of photoprotective habits.

• Molecules and Cells
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• 제25권2호
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• pp.253-257
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• 2008

Acrolein is a highly electrophilic ${\alpha},{\beta}$-unsaturated aldehyde present in a number of environmental sources, especially cigarette smoke. It reacts strongly with the thiol groups of cysteine residues by Michael addition and has been reported to inhibit nuclear $factor-{\kappa}B$ ($NF-{\kappa}B$) activation by lipopolysaccharide (LPS). The mechanism by which it inhibits $NF-{\kappa}B$ is not clear. Toll-like receptors (TLRs) play a key role in sensing microbial components and inducing innate immune responses, and LPS-induced dimerization of TLR4 is required for activation of downstream signaling pathways. Thus, dimerization of TLR4 may be one of the first events involved in activating TLR4-mediated signaling pathways. Stimulation of TLR4 by LPS activates both myeloid differential factor 88 (MyD88)- and TIR domain-containing adapter inducing $IFN{\beta}$ (TRIF)-dependent signaling pathways leading to activation of $NF-{\kappa}B$ and IFN-regulatory factor 3 (IRF3). Acrolein inhibited $NF-{\kappa}B$ and IRF3 activation by LPS, but it did not inhibit $NF-{\kappa}B$ or IRF3 activation by MyD88, inhibitor ${\kappa}B$ kinase $(IKK){\beta}$, TRIF, or TNF-receptor-associated factor family member-associated $NF-{\kappa}B$ activator (TANK)-binding kinase 1 (TBK1). Acrolein inhibited LPS-induced dimerization of TLR4, which resulted in the down-regulation of $NF-{\kappa}B$ and IRF3 activation. These results suggest that activation of TLRs and subsequent immune/inflammatory responses induced by endogenous molecules or chronic infection can be modulated by certain chemicals with a structural motif that enables Michael addition.

• Environmental Analysis Health and Toxicology
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• 제21권3호
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• pp.229-238
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• 2006

Although, mercury (Hg) is not a naturally abundant element in the environment, residues frequently occur in many environmental compartments because of widespread contamination from industrial and agricultural practices. This research evaluated Hg-B concentrations of general population who was not occupationally exposed. And also evaluates the association between life factor and health effect with Hg-B concentration of general adult through interrelationship estimation and index about kidney function and oxidative damage that appeared by questionnaire survey and medical examination. Average concentration of Hg-B was 3.19 $\mu$g/L (ND$\sim$8.64 $\mu$g/L), and persons who exceed mercury exposure level (5 $\mu$g/L) presented in WHO (1990) appeared by 16 (7.0%). High-risk group (smoking and meat main intake group) had significantly higher Hg-B concentration than low-risk group (non-smoking and vegetable diet main intake group) (p < 0.05, low-risk group: 3.30 $\mu$g/L (ND$\sim$8.64 $\mu$g/L), high-risk group: 4.27 $\mu$g/L (ND$\sim$7.84 $\mu$g/L).

• Asian Pacific Journal of Cancer Prevention
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• 제16권18호
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• pp.8533-8539
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• 2016

Background: B-cell chronic lymphocytic leukemia B (B-CLL), the most common type of leukemia, may be caused by apoptosis deficiency in the body. Adipose tissue-derived mesenchymal stem cells (AD-MSCs) as providers of pro-apoptotic molecules such as tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), can be considered as an effective anti-cancer therapy candidate. Therefore, in this study we assessed the role of tumor necrosis factor-producing mesenchymal stem cells oin apoptosis of B-CLL cells resistant to fludarabine-based chemotherapy. Materials and Methods: In this study, after isolation and culture of AD-MSCs, a lentiviral LeGO-iG2-TRAIL-GFP vector containing a gene producing the ligand pro-apoptotic with plasmid PsPAX2 and PMDG2 virus were transfected into cell-lines to generate T293HEK. Then, T293HEK cell supernatant containing the virus produced after 48 and 72 hours was collected, and these viruses were transduced to reprogram AD-MSCs. Apoptosis rates were separately studied in four groups: group 1, AD-MSCs-TRAIL; group 2, AD-MSCs-GFP; group 3, AD-MSCs; and group 4, CLL. Results: Observed apoptosis rates were: group 1, $42{\pm}1.04%$; group 2, $21{\pm}0.57%$; group 3, $19{\pm}2.6%$; and group 4, % $0.01{\pm}0.01$. The highest rate of apoptosis thus occurred ingroup 1 (transduced TRAIL encoding vector). In this group, the average medium-soluble TRAIL was 72.7pg/m and flow cytometry analysis showed a pro-apoptosis rate of $63{\pm}1.6%$, which was again higher than in other groups. Conclusions: In this study we have shown that tumor necrosis factor (TNF) secreted by AD-MSCs may play an effective role in inducing B-CLL cell apoptosis.

• 대한예방의학회:학술대회논문집
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• 대한예방의학회 2005년도 제57차 추계 학술대회 연제집
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• pp.372-372
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• 2005

• 동의생리병리학회지
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• 제26권2호
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• pp.160-165
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• 2012

Osteoporotic fracture became a serious social problem, which related with mortality and morbidity in old age population. Osteoclast which is responsible for bone resorption is originated from hematopoietic cell line and plays a key role osteoporotic bone loss. Cynanchum wilfordii (Asclepiadaceae) roots have been used in Korean folk medicine for the treatment of diabetes mellitus and aging progression. Also, recent studies have shown that the extract and fractions of Cynanchi Wilfordii Radix have various pharmacological actions including scavenging free radicals, enhancing immunity, reducing high serum cholesterol, and anti-tumor activity. However, the effect of extract of Cynanchi Wilfordii Radix in osteoclast differentiation had not been reported. Thus, we evaluated the effect of Cynanchi Wilfordii Radix on receptor activator of nuclear factor-${\kappa}B$ ligand (RANKL)-induced osteoclast differentiation. Through our study, we found that Cynanchi Wilfordii Radix significantly inhibited osteoclast differentiation induced by RANKL. Cynanchi Wilfordii Radix suppressed the activation of p38 pathway and $NF{\kappa}B$ in bone marrow macrophages (BMMs) treated with RANKL. Also, Cynanchi Wilfordii Radix significantly inhibited the mRNA expression of c-Fos, tartrate-resistant acid phosphatase (TRAP), osteoclast-associated receptor (OSCAR), nuclear factor of activated T cells (NFAT)c1 and cathepsin K in BMMs treated with RANKL. Particularly, Cynanchi Wilfordii Radix inhibited the protein expression of c-fos and NFATc1. Taken together, our results demonstrated that Cynanchi Wilfordii Radix may be useful treatment option of bone-related disease such as osteoporosis leads to fracture of bone and rheumatoid arthritis.

• 한국의사학회지
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• 제31권2호
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• pp.53-62
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• 2018

It is known that the development of medical science is influenced by various social environmental factors. Historically, Chinese Medicine developed the most during the Song Yuan dynasty, and the reason for this was known to be due to socio-political factors. According to recent studies, however, this period also had severe changes in climate and environment. Therefore, this study was conducted under the premise that this change in climate and environment influenced medical development. When looking at the coldness of the 11th~12th century and data indicating warming before and after this period, the Song Yuan dynasty went through drastic periods of climate change. Therefore, diseases related to heat such as bubonic plague, measles, and malaria were common. Furthermore, due to occasional wars during the Song Yuan dynasty, social unrest was aggravated and infectious diseases spread due to land development and environmental pollution. As the health of people were threatened due to these factors, the printing and distribution of medical text were encouraged, and during this process, the great 4 doctors of Jin-Yuan appeared. The reason why they studied cures for infectious diseases due to heat was related to climatic environment change. The development in medical science is closely related to socio-political factors, however the change in climatic environments are inevitably related to disease emergence as well. Therefore, it should always be taken into consideration as an important factor that promotes development in medical science.

• Parasites, Hosts and Diseases
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• 제58권3호
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• pp.217-227
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• 2020

Trichomonas vaginalis causes inflammation of the prostate and has been detected in tissues of prostate cancers (PCa), prostatitis and benign prostatic hyperplasia. Obesity is a risk factor for PCa and causes a chronic subclinical inflammation. This chronic inflammation further exacerbates adipose tissue inflammation as results of migration and activation of macrophages. Macrophages are the most abundant immune cells in the PCa microenvironment. M2 macrophages, known as Tumor-Associated Macrophages, are involved in increasing cancer malignancy. In this study, conditioned medium (TCM) of PCa cells infected with live trichomonads contained chemokines that stimulated migration of the mouse preadipocytes (3T3-L1 cells). Conditioned medium of adipocytes incubated with TCM (ATCM) contained Th2 cytokines (IL-4, IL-13). Macrophage migration was stimulated by ATCM. In macrophages treated with ATCM, expression of M2 markers increased, while M1 markers decreased. Therefore, it is suggested that ATCM induces polarization of M0 to M2 macrophages. In addition, conditioned medium from the macrophages incubated with ATCM stimulates the proliferation and invasiveness of PCa. Our findings suggest that interaction between inflamed PCa treated with T. vaginalis and adipocytes causes M2 macrophage polarization, so contributing to the progression of PCa.

• Molecules and Cells
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• 제41권7호
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• pp.695-702
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• 2018

The inner ear is a complex sensory organ responsible for hearing and balance. Formation of the inner ear is dependent on tight regulation of spatial and temporal expression of genes that direct a series of developmental processes. Recently, epigenetic regulation has emerged as a crucial regulator of the development of various organs. However, what roles higher-order chromatin organization and its regulator molecules play in inner ear development are unclear. CCCTC-binding factor (CTCF) is a highly conserved 11-zinc finger protein that regulates the three-dimensional architecture of chromatin, and is involved in various gene regulation processes. To delineate the role of CTCF in inner ear development, the present study investigated inner ear-specific Ctcf knockout mouse embryos (Pax2-Cre; $Ctcf^{fl/fl}$). The loss of Ctcf resulted in multiple defects of inner ear development and severely compromised otic neurogenesis, which was partly due to a loss of Neurog1 expression. Furthermore, reduced Neurog1 gene expression by CTCF knockdown was found to be associated with changes in histone modification at the gene's promoter, as well as its upstream enhancer. The results of the present study demonstrate that CTCF plays an essential role in otic neurogenesis by modulating histone modification in the Neurog1 locus.