• Annals of Occupational and Environmental Medicine
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• v.35
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• pp.48.1-48.13
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• 2023

Background: This study was conducted to identify the success rate for smoking cessation over time after participation in a therapeutic smoking cessation camp, and to identify how participant characteristics, including a supportive workplace environment for smoking cessation (SWESC), affect the success rate for smoking cessation. Methods: In all, 296 participants at smoking cessation camps in Ulsan between 2015 and 2020 were investigated. The success rates of smoking cessation after weeks 4, 6, 12, and 24 at camp were investigated. The participants were grouped as workers with an SWESC, and workers without an SWESC, and variables (age, education, household income, marital status, drinking, exercise, body mass index, morbidity, job, number of counseling sessions, cigarettes smoked per day and smoking initiation age) were investigated. Multiple logistic regression analysis was conducted at each time point. In addition, Cox regression analysis was performed to evaluate the variables affecting the success rate for smoking cessation over time. Results: The smoking cessation success rate of workers with an SWESC at week 24 (90.7%) was higher than that for workers without an SWESC (60.5%). Multiple logistic regression was performed to determine the relationship between each variable and the success rates for smoking cessation at week 6, 12, and 24. SWESC was confirmed as significant (p < 0.05) variables for increased success rate for smoking cessation at all 3 time points. After adjusting for all variables, the Cox proportional hazards survival analysis showed a hazard ratio of 6.17 for SWESC (p < 0.001,; 95% confidence interval: 3.08-12.38). Conclusions: At a professional treatment smoking cessation camp, participants with an SWESC showed a significantly higher success rate for smoking cessation. Supportive workplace environment for workers' health is expected to be an important factor for smoking cessation projects as well as other health promotion projects at workplace.

• Korean Journal of Radiology
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• v.21 no.6
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• pp.764-772
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• 2020

Objective: Laser ablation is a therapeutic modality used to reduce the volume of large benign thyroid nodules. Unsatisfactory reduction and regrowth are observed in some treated nodules. The aim of the study was to evaluate the long-term outcomes of laser treatment for solid nodules during a 5-year follow-up period, the regrowth rate, and the predictive risk factors of nodule regrowth. Materials and Methods: We retrospectively evaluated patients with benign, solid, cold thyroid nodules who underwent laser ablation and were followed-up for 5 years. According to the selection criteria, 104 patients were included (median baseline nodule volume, 12.5 mL [25.0-75.0%, 8-18 mL]; median energy delivered, 481.5 J/mL [25.0-75.0%, 370-620 J/mL]). Nodule volume, thyroid function test results, and ultrasound were evaluated at baseline and then annually after the procedure. Results: Of 104 patients, 31 patients (29.8%) had a 12-month volume reduction ratio (VRR) < 50.0% and 39 (37.5%) experienced nodule regrowth. Of these 39 patients, 17 (43.6%) underwent surgery and 14 (35.9%) underwent a second laser treatment. The rate of nodule regrowth was inversely related to the 12-month VRR, i.e., the lower the 12-month VRR, the higher the risk of regrowth (p < 0.001). The mean time for nodule regrowth was 33.5 ± 16.6 months. The 12-month VRR was directly related to time to regrowth, i.e., the lower the 12-month VRR, the shorter the time to regrowth (p < 0.001; R² = 0.3516). Non-spongiform composition increased the risk of regrowth with an odds ratio of 4.3 (95% confidence interval [CI] 1.8-10.2; p < 0.001); 12-month VRR < 50.0% increased the risk of regrowth with an odds ratio of 11.7 (95% CI 4.2-32.2; p < 0.001). Conclusion: The VRR of thyroid nodules subjected to similar amounts of laser energy varies widely and depends on the nodule composition; non-spongiform nodules are reduced to a lesser extent and regrow more frequently than spongiform nodules. A 12-month VRR < 50.0% is a predictive risk factor for regrowth and correlates with the time to regrowth.

• The Korean journal of internal medicine
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• v.39 no.2
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• pp.347-359
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• 2024

Background/Aims: Renal relapse has known to be a poor prognostic factor in patients with lupus nephritis (LN), but there were few studies that identified the risk factors of renal relapse in real world. We conducted this study based on 35-years of experience at a single center to find out predictors of renal relapse in Korean patients with LN after achieving complete response (CR). Methods: We retrospectively analyzed the clinical, laboratory, pathologic and therapeutic parameters in 296 patients of LN who reached CR. The cumulative risk and the independent risk factors for renal relapse were examined by Kaplan-Meier methods and Cox proportional hazards regression analyses, respectively. Results: The median follow-up period from CR was 123 months. Renal relapse had occurred in 157 patients. Renal relapse occurred in 38.2%, 57.6% and 67.9% of patients within 5-, 10-, and 20-year, respectively. The age at diagnosis of SLE and LN were significantly younger, and the proportions of severe proteinuria and serum hypoalbuminemia were higher in patients with renal relapse. Interestingly, the proportion of receiving cytotoxic maintenance treatment was higher in patients with renal relapse. In Cox proportional hazards regression analyses, only young-age onset of LN (by 10 years, HR = 0.779, p = 0.007) was identified to independent predictor of renal relapse. Conclusions: Young-age onset of LN was only independent predictor and the patients with severe proteinuria and serum hypoalbuminemia also tended to relapse more, despite of sufficient maintenance treatment. Studies on more effective maintenance treatment regimens and duration are needed to reduce renal relapse.

• Korean Circulation Journal
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• v.52 no.8
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• pp.606-620
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• 2022

Background and Objectives: Protein-losing enteropathy (PLE) is a devastating complication after the Fontan operation. This study aimed to investigate the clinical characteristics, treatment response, and outcomes of Fontan-associated PLE. Methods: We reviewed the medical records of 38 patients with Fontan-associated PLE from 1992 to 2018 in 2 institutions in Korea. Results: PLE occurred in 4.6% of the total 832 patients after the Fontan operation. After a mean period of 7.7 years after Fontan operation, PLE was diagnosed at a mean age of 11.6 years. The mean follow-up period was 8.9 years. The survival rates were 81.6% at 5 years and 76.5% at 10 years. In the multivariate analysis, New York Heart Association Functional classification III or IV (p=0.002), low aortic oxygen saturation (<90%) (p=0.003), and ventricular dysfunction (p=0.032) at the time of PLE diagnosis were found as predictors of mortality. PLE was resolved in 10 of the 38 patients after treatment. Among medical managements, an initial heparin response was associated with survival (p=0.043). Heparin treatment resulted in resolution in 4 patients. We found no evidence on pulmonary vasodilator therapy alone. PLE was also resolved after surgical Fontan fenestration (2/6), aortopulmonary collateral ligation (1/1), and transplantation (1/1). Conclusions: The survival rate of patients with Fontan-associated PLE has improved with the advancement of conservative care. Although there is no definitive method, some treatments led to the resolution of PLE in one-fourth of the patients. Further investigations are needed to develop the best prevention and therapeutic strategies for PLE.

• Journal of Life Science
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• v.34 no.8
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• pp.594-607
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• 2024

Plastic products have long been widely used in both industrial and household applications. However, tiny plastic particles derived from plastic products, such as microplastics (MPs) and nanoplastics (NPs), can infiltrate the human body through inhalation, ingestion, or skin contact. Once inside cells via endocytosis, MPs and NPs (MNPs) can trigger autophagy, but lysosomal dysfunction can block autophagic flux. Accumulating in the cytoplasm, these particles induce cellular stress, including oxidative stress from free radicals, mitochondrial dysfunction, and increased inflammatory response. Meanwhile, cellular senescence is a hallmark of aging and is defined as the stable termination of the cell cycle in response to cell damage and stress. In particular, the accumulation of oxidative stress, a key factor in inducing cellular senescence, induces the expression of major senescence markers. Senescent cells increase the secretion of senescence-associated secretory phenotype, including inflammatory cytokines and chemokines. Despite growing interest in how MNPs induce cellular senescence, there remains a gap regarding their onset and therapeutic targets. Therefore, this review focuses on identifying recent research trends on how MNPs induce cellular aging in key human cell types and proposes future research directions to overcome these challenges.

• Journal of Chest Surgery
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• v.40 no.4 s.273
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• pp.264-272
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• 2007

Background: Vascular endothelial growth factor (VEGF) plays an important role in angiogenesis, including stimulating the proliferation and migration of vascular smooth muscle cells (VSMCs). It has been known that diabetes is associated with accelerated cellular proliferation via VEGF, as compared to that under a normal glucose concentration. We investigated the effects of selective blockade of a VEGF receptor by using anti-Flt-1 peptide on the formation and hyperplasia of the neointima in balloon injured-carotid arteries of OLETF rats and also on the in vitro VSMCS' migration under high glucose conditions. Material and Method: The balloon-injury method was employed to induce neointima formation by VEGF. For f4 days beginning 2 days before the ballon injury, placebo or vascular endothelial growth factor receptor-1 (VEGFR-1) specific peptide (anti-Flt-1 peptide), was injected at a dose of 0.5mg/kg daily into the OLETF rats. At 14 days after balloon injury, the neointimal proliferation and vascular luminal stenosis were measured, and cellular proliferation was assessed by counting the proliferative cell nuclear antigen (PCNA) stained cells. To analyze the effect of VEGF and anti-Flt-1 peptide on the migration of VSMCs under a high glucose condition, transwell assay with a matrigel filter was performed. And finally, to determine the underlying mechanism of the effect of anti-Flt-1 peptide on the VEGF-induced VSMC migration in vitro, the expression of matrix metalloproteinase (MMP) was observed by performing reverse transcription-polymerase chain reaction (RT-PCR). Result: Both the neointimal area and luminal stenosis associated with neointimal proliferation were significantly decreased in the anti-Flt-1 peptide injected rats, ($0.15{\pm}0.04 mm^2$ and $ 36.03{\pm}3.78%$ compared to $0.24{\pm}0.03mm^2\;and\;61.85{\pm}5.11%$, respectively, in the placebo-injected rats (p<0.01, respectively). The ratio of PCNA(+) cells to the entire neointimal cells was also significantly decreased from $52.82{\pm}4.20%\;to\;38.11{\pm}6.89%$, by the injected anti-Flt-1 peptide (p<0.05). On the VSMC migration assay, anti-Flt-1 peptide significantly reduced the VEGF-induced VMSC migration by about 40% (p<0.01). Consistent with the effect of anti-Flt-1 peptide on VSMC migration, it also obviously attenuated the induction of the MMP-3 and MMP-9 mRNA expressions via VEGF in the VSMCS. Conclusion: Anti-Flt-1 peptide inhibits the formation and hyperplasia of the neointima in a balloon-injured carotid artery model of OLETF rats. Anti-Flt-1 peptide also inhibits the VSMCs' migration and the expressions of MMP-3 and MMP-9 mRNA induced by VEGF under a high glucose condition. Therefore, these results suggest that specific blockade of VEGFR-1 by anti-Flt-1 peptide may have therapeutic potential against the arterial stenosis of diabetes mellitus patients or that occurring under a high glucose condition.

• 한국균학회소식:학술대회논문집
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• 2015.05a
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• pp.59-59
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• 2015

Cryptococcus neoformans causes life-threatening meningoencephalitis in humans, but the treatment of cryptococcosis remains challenging. To develop novel therapeutic targets and approaches, signaling cascades controlling pathogenicity of C. neoformans have been extensively studied but the underlying biological regulatory circuits remain elusive, particularly due to the presence of an evolutionarily divergent set of transcription factors (TFs) in this basidiomycetous fungus. In this study, we constructed a high-quality of 322 signature-tagged gene deletion strains for 155 putative TF genes, which were previously predicted using the DNA-binding domain TF database (http://www.transcriptionfactor.org/). We tested in vivo and in vitro phenotypic traits under 32 distinct growth conditions using 322 TF gene deletion strains. At least one phenotypic trait was exhibited by 145 out of 155 TF mutants (93%) and approximately 85% of the TFs (132/155) have been functionally characterized for the first time in this study. Through high-coverage phenome analysis, we discovered myriad novel TFs that play critical roles in growth, differentiation, virulence-factor (melanin, capsule, and urease) formation, stress responses, antifungal drug resistance, and virulence. Large-scale virulence and infectivity assays in insect (Galleria mellonella) and mouse host models identified 34 novel TFs that are critical for pathogenicity. The genotypic and phenotypic data for each TF are available in the C. neoformans TF phenome database (http://tf.cryptococcus.org). In conclusion, our phenome-based functional analysis of the C. neoformans TF mutant library provides key insights into transcriptional networks of basidiomycetous fungi and ubiquitous human fungal pathogens.

• Journal of the Korean Society of Food Science and Nutrition
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• v.44 no.8
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• pp.1121-1127
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• 2015

This study investigated the effects of Myagropsis myagroides ethanol extract (MMEE) on 2,4-dinitrochlorobenzene (DNCB)-induced atopic dermatitis (AD)-like skin lesions in BALB/c mice. The effects of MMEE on DNCB-induced BALB/c mice were evaluated by examining skin symptom severity, levels of total immunoglobulin E (IgE), tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$), interleukin (IL)-4, and IL-10 in serum, and levels of IL-4, IL-5, IL-13, and $interferon-{\gamma}$ ($IFN-{\gamma}$) in splenocytes. MMEE significantly reduced the total clinical severity score, total IgE levels, as well as $TNF-{\alpha}$ and IL-4 production in an AD mouse model but increased IL-10 production. Production of IL-4, IL-5, and IL-13 in splenocytes was reduced by MMEE, whereas $IFN-{\gamma}$ production increased. These results suggest that MMEE can inhibit the development of AD-like skin lesions in BALB/c mice by modulating the immune response and may be an effective potential therapeutic agent for AD.

• Journal of Life Science
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• v.23 no.6
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• pp.812-824
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• 2013

Reserpine, an anti-hypertensive drug, is able to positively modulate several phenotypes associated with $A{\beta}$ toxicity in a Caenorhabditis elegans model of Alzheimer's disease (AD). We investigated into the therapeutic effects of reserpine on mammalian neurodegenerative disorders, and found that significant alteration of the key factors influencing AD was detected in Tg2576 mice after reserpine treatment for 30 days. The aggressive behavior of Tg2576 mice was significantly improved upon reserpine treatment, whereas their social contact was consistently maintained. Furthermore, the levels of $A{\beta}$-42 peptide in the hippocampus of the brain and blood serum were lower in the reserpine-treated group than in the vehicle-treated group. Among g-secretase components, the expression levels of PS-2, Pen-2, and APH-1 were slightly lower in reserpine-treated Tg2576 mice, although a significant change in nicastrin (NCT) expression was not detected. Furthermore, the serum level of nerve growth factor (NGF) increased in reserpine-treated Tg2576 mice compared with vehicle-treated mice. Among down-stream effectors of the NGF receptor TrkA signaling pathway, reserpine treatment induced elevation of TrkA phosphorylation and reduction of ERK phosphorylation. In addition, in the NGF receptor $p75^{NTR}$ signaling pathway, the expression levels of $p75^{NTR}$ and Bcl-2 were enhanced in reserpine-treated Tg2576 mice compared with vehicle-treated mice, whereas the expression level of RhoA declined. Overall, these results suggest that reserpine can help relieve AD pathogenesis in Tg2576 mice through downregulation of $A{\beta}$-42 deposition, alteration of ${\gamma}$-secretase components, and regulation of NGF metabolism.

• Microbiology and Biotechnology Letters
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• v.44 no.3
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• pp.268-277
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• 2016

This study aimed to investigate the anti-inflammatory effect of the ethanol extract from Chondrus ocellatus Holmes (COHEE) in RAW 264.7 cells and in a mouse ear edema model, by measuring the production of lipopolysaccharide-induced inflammatory response mediators. There were no cytotoxic effects on the proliferation of macrophages treated with COHEE compared with the control. COHEE inhibited the production of nitric oxide and pro-inflammatory cytokines [interleukin (IL)-6, tumor necrosis factor-α, and IL-1β]. The extract also reduced the expression of inducible nitric oxide synthase, cyclooxygenase-2, nuclear factor-κB p65, and phosphorylated mitogen-activated protein kinase in a dose-dependent manner. In the croton-oil-induced ear edema model, COHEE decreased the formation of mouse ear edema at the highest dose compared with the control, and histological analysis revealed that the epidermal/dermal tissue thickness and mast cell numbers were reduced. Therefore, these results suggest that COHEE may be a promising topical anti-inflammatory therapeutic material through its action of modulating NF-κB and the MAPK signaling pathway.