• Tuberculosis and Respiratory Diseases
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• v.84 no.1
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• pp.1-12
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• 2021

Mycobacterium tuberculosis has infected more than two billion individuals worldwide, of whom 5%-10% have clinically active disease and 90%-95% remain in the latent stage with a reservoir of viable bacteria in the macrophages for extended periods of time. The tubercle bacilli at this stage are usually called dormant, non-viable, and/or non-culturable microorganisms. The patients with latent bacilli will not have clinical pictures and are not infectious. The infections in about 2%-23% of the patients with latent status become reactivated for various reasons such as cancer, human immunodeficiency virus infection, diabetes, and/or aging. Many studies have examined the mechanisms involved in the latent state of Mycobacterium and showed that latency modified the expression of many genes. Therefore, several mechanisms will change in this bacterium. Hence, this study aimed to briefly examine the genes involved in the latent state as well as the changes that are caused by Mycobacterium tuberculosis. The study also evaluated the relationship between the functions of these genes.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.16
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• pp.7111-7115
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• 2015

Background: The aim of the meta-analysis was to derive a more precise assessment of the association between p16 promoter methylation and thyroid cancer risk. Materials and Methods: The PubMed, Web of Science databases and Chinese CNKI were searched for relevant articles. Ultimately, seventeen case-control studies were included with a total of 804 thyroid cancer cases and 487 controls analysis by R Software (R version 3.1.2) including meta. Crude odds ratios with 95% confidence intervals were calculated using the random-effects model which were used to assess the strength of relationship between p16 methylation and lung carcinogenesis. Funnel plots were carried out to evaluate publication bias. Results: The meta-analysis results showed that the frequency of p16 promoter methylation in cancer tissue/blood was significantly higher than that normal tissue/blood (OR=5.46, 95%CI 3.12-9.55, P<0.0001) by random effects model with small heterogeneity. Conclusions: Thus, p16 promoter methylation may be associated with thyroid cancer risk.

• Journal of Nutrition and Health
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• v.24 no.5
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• pp.431-441
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• 1991

To investigate the influence of age and dietary fat level on the immune function and the growing potential of the fibroblast cells, male rats of 2 month, 6 month and 30 month of age were fed either 6% or 30% fat diet for 16 weeks. The weight of thymus decreased linearly with increasing age. And this age-dependent degeneration of thymus was delayed in rats fed low fat diets. The blastogenesis of spleen lymphocytes to PHA, ConA, and PWM was decreased with increasing age, however, no effect of dietary fat level was observed. The age-related decline in ratios of PHA/ConA response may suggest that T suppressor cell activity increases with age. In cell culture system, lung fibroblast cells from 30M rats showed lower plating efficiency. longer doubling time. and shorter cumulative doubling potential than those from 2M or 6M animals. Also. the morphology of fibroblasts from 30M rats was tended to be rouned rather than flattened and more variable in size and being generally larger. wherease those from 2M and 6M rats were uniform in size and adhered tightly to the culture vessel in ordered arrays. Therefore fibroblast cell culture system tried in this study reflects the changes of cellular aging.

• Journal of Sasang Constitutional Medicine
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• v.20 no.2
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• pp.98-110
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• 2008

1. Objectives The purpose of this study is to prove the anti-aging effects of Sipyimigwanjung-tang. 2. Methods The SD rats used in this experiment were 6, 18 and 36 weeks old. A part of the 36weeks was grown to 52 and 68 weeks at labarotary. Each age group was again divided into three groups. These 15 groups consisted of 6 rats each. One group was given no treatment, another group was dosed 200 ${\mu}l$ of normal saline daily, and the last group was dosed 200 ${\mu}l$ of 1% Sipyimigwanjung-tang(SYG) and saline mixture. At the conclusion of the experiment, the age groups were relabelled accordingly(10w, 22w, 40w, 52w and 68w). After 4 weeks, the tissue of liver, heart, spleen, lung, kidney and brain was biopsied in order to measure the SOD, GSH, MDA. 3. Results and Conclusions In liver, the activity of the SOD of 52w-SYG was significantly increased than that of 10w, 22w and 40w-SYG, the level of the GSH of 40w-SYG was significantly increased than that of the normal group, the activity of the catalase of 68w-SYG was significantly increased than that of the normal and control group, the level of the MDA of 52w-SYG and 68w-SYG was significantly decreased than that of the normal and control groups. In heart, the level of the GSH of 22w-SYG was significantly increased than that of the normal and control group. In spleen, the level of the GSH of 52w-SYG was significantly increased than that of the normal and control group. In lung, the level of the GSH of 52w-SYG was significantly increased than that of the normal group and the level of 68w-SYG was significantly increased than that of the normal and control group. In kidney, the level of the GSH of 10w-SYG was significantly increased than that of the normal group. In brain, the level of the GSH of 68w-SYG was significantly increased than that of the normal and control group. The SYG inhibited the histology degeneration of brain tissue. These results suggest that oral administration of SYG (Sipyimigwanjung-tang) decoction has anti-aging effects in aged rats.

• Journal of Radiation Protection and Research
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• v.34 no.2
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• pp.49-54
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• 2009

Mitochondrial DNA (mtDNA) deletion is a well-known marker for oxidative stress and aging and also contributes to their unfavorable effects in cultured cells and animal tissues. This study was conducted to investigate the effect of ionizing radiation (IR) on mtDNA deletion and the involvement of reactive oxygen species (ROS) in this process in human lung fibroblast (IMR-90) cells. Young IMR-90 cells at population doubling (PD) 39 were irradiated with $^{137}Cs$ $\gamma$-rays and the intracellular ROS level was determined by 2',7'-dichlorofluorescein diacetate (DCFH-DA) and mtDNA common deletion (4977bp) was detected by nested PCR. Old cells at PD 55 and $H_2O_2$-treated young cells were compared as the positive control. IR increased the intracellular ROS level and mtDNA 4977 bp deletion in IMR-90 cells dose-dependently. The increases of ROS level and mtDNA deletion were also observed in old cells and $H_2O_2$-treated young cells. To confirm the increased ROS level is essential for mtDNA deletion in irradiated cells, the effects of N-acetylcysteine (NAC) on IRinduced ROS and mtDNA deletion were examined. 5 mM NAC significantly attenuated the IR-induced ROS increase and mtDNA deletion. These results suggest that IR induces the mtDNA deletion and this process is mediated by ROS in IMR-90 cells.

• Journal of Chest Surgery
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• v.50 no.3
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• pp.153-162
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• 2017

Background: The mesenchymal-epithelial transition factor (MET) receptor can be overexpressed in solid tumors, including small cell lung cancer (SCLC). However, the molecular mechanism regulating MET stability and turnover in SCLC remains undefined. One potential mechanism of MET regulation involves the C-terminus of Hsp70-interacting protein (CHIP), which targets heat shock protein 90-interacting proteins for ubiquitination and proteasomal degradation. In the present study, we investigated the functional effects of CHIP expression on MET regulation and the control of SCLC cell apoptosis and invasion. Methods: To evaluate the expression of CHIP and c-Met, which is a protein that in humans is encoded by the MET gene (the MET proto-oncogene), we examined the expression pattern of c-Met and CHIP in SCLC cell lines by western blotting. To investigate whether CHIP overexpression reduced cell proliferation and invasive activity in SCLC cell lines, we transfected cells with CHIP and performed a cell viability assay and cellular apoptosis assays. Results: We found an inverse relationship between the expression of CHIP and MET in SCLC cell lines (n=5). CHIP destabilized the endogenous MET receptor in SCLC cell lines, indicating an essential role for CHIP in the regulation of MET degradation. In addition, CHIP inhibited MET-dependent pathways, and invasion, cell growth, and apoptosis were reduced by CHIP overexpression in SCLC cell lines. Conclusion: C HIP is capable of regulating SCLC cell apoptosis and invasion by inhibiting MET-mediated cytoskeletal and cell survival pathways in NCI-H69 cells. CHIP suppresses MET-dependent signaling, and regulates MET-mediated SCLC motility.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.27 no.2
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• pp.1-13
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• 2014

Objective : The purpose of this study is to understand conspicuous features of geroderma with visceral manifestation theory(臟象論). Methods : We categorized skin aging into wrinkles, hyperpigmentation, dry skin and face flush. After investigating the reason, histological changes and mechanism of each classification in western medicine, we interpreted them according to the malfunction of five viscera(五臟) in Korean medicine. Result : The results are as follows. 1. Pathologic change of dermis and subcutaneous fat makes wrinkles. We consider wrinkles as the malfunction of the spleen(脾). 2. Irregular synthesis and disproportion of melanin makes hyperpigmentation. We consider hyperpigmentation as the malfunction of the liver(肝). 3. Dry skin is attributed to a subtle disorder of epidermal maturation. We consider dry skin as the malfunction of the lung(肺). 4. Facial flush is detected in rosacea and menopausal hot flush, which are both related with blood vessel abnormality. We consider facial flush as the malfunction of the heart(心) Conclusion : We interpreted the pathologic changes and mechanism of skin aging in western medicine as the decrease of five viscera(五臟) in visceral manifestation theory(臟象論) of Korean medicine. Further studies are needed to apply these hypothesis to clinical diagnosis and treatment.

• Korean Journal of Applied Biomechanics
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• v.30 no.1
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• pp.93-101
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• 2020

Objective: The purpose of this study was to differences of foot plantar pressure balance and lung capacity according to cervical posture in adults. Method: The subjects consisted of 33 adults in their 20s and 50s who use M centers in B-gu and H-gu, B-City, and they measured foot plantar pressure balance and lung capacity according to cervical posture (cervical normal curvature posture, cervical flexural posture) in adults. Results: In this study, the difference of foot plantar pressure balance according to cervical posture were analyzed. In the difference between left and right foot pressure balance. It was 1.50% increased in the cervical flexural posture than in the cervical normal curvature posture, and a statistically significant difference was observed. In the difference between the anterior and posterior foot pressure balance. It was 4.28% increased in the cervical flexural posture than in the cervical normal curvature posture, and a statistically significant difference was observed. The difference of lung capacity according to cervical posture were analyzed. In the PEF, It was 58.63 l/min decreased in the cervical flexural posture than in the cervical normal curvature posture, and a statistically significant difference was observed. In the FEV1, It was 0.15 ℓ decreased in the cervical flexural posture than in the cervical normal curvature posture, and a statistically significant difference was observed. Conclusion: The results of this study suggest that had a positive effect on differences of foot plantar pressure balance and lung capacity at cervical normal curvature posture in adults. In future research, itis believed that research on the elderly who have collapsed the normal curvature posture due to aging, as well as teenagers whose normal curvature posture due to the use of smartphones, will contribute to the balance of foot pressure and improvement of the right cervical habits. In future studies, it is also believed that it will be necessary to measure lung capacity after performing exercise according to the cervical posture, thereby providing sufficient oxygen during exercise to enhance the persistence and efficiency of the movement.

• Journal of Life Science
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• v.24 no.8
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• pp.837-842
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• 2014

The purpose of this study was to investigate the effect of Brunfelsia grandiflora ethanol extract (BGEE) on the induction of autophagy via regulation of SIRT1 expression and p53 activation in a human lung fibroblast cell line, IMR 90. BGEE at a concentration of $5{\mu}g/ml$ or more exhibited a cytotoxic effect on IMR 90 cells. For the first time, this study showed that BGEE induces autophagy in normal human lung fibroblasts. BGEE also increased the expression level of beclin-1 at $2.5{\mu}g/ml$ or less and Atg7 at $5{\mu}g/ml$, both of which are known to be involved in the induction of autophagy. In addition, BGEE modulated the expression of other proteins related to autophagy in normal human lung fibroblasts. The expression levels of p53 and p-p53, an active form of p53, were decreased in the presence of BGEE at a noncytotoxic concentration. In contrast, the expression level of SIRT1 was increased in human lung fibroblasts treated with BGEE at a noncytotoxic concentration. Moreover, SA-${\beta}$-Gal staining, an aging marker, was reduced in the normal human lung fibroblasts treated with BGEE. These findings suggest that BGEE promotes the induction of autophagy and antiaging through the modulation of p53 and SIRT1 in human lung fibroblasts.

• Journal of Life Science
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• v.32 no.4
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• pp.310-317
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• 2022

Recently, interest in the harmful factors of particulate matter (PM), a major component of air pollution, has been increasing. In particular, PM_2.5 with a diameter of less than 2.5 ㎛ is well known to induce oxidative stress accompanied by autophagy in human lung epithelial cells. However, studies on whether PM_2.5 increases autophagy under oxidative stress and whether this process is reactive oxygen species (ROS)-dependent are insufficient. Therefore, in this study, we investigated whether PM_2.5 promotes autophagy through the generation of ROS in human alveolar epithelial A594 cells. According to our results, cells co-treated with PM_2.5 and hydrogen peroxide (H₂O₂) showed a lower cell viability than cells treated with each alone, which was associated with increased total and mitochondrial ROS production. The co-treatment of PM_2.5 and H₂O₂ also increased autophagy induction, which was confirmed through Cyto-ID staining, and the expression of autophagy biomarker proteins increased. However, when ROS generation was artificially blocked by N-acetyl-L-cysteine pretreatment, the reduction in cell viability and induction of autophagy by PM_2.5 and H₂O₂ co-treatment were markedly attenuated. Therefore, the present results suggest that PM_2.5-induced ROS generation may play a critical role in autophagy induction in A549 cells.