• Journal of the Korean Society of Laryngology, Phoniatrics and Logopedics
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• v.33 no.3
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• pp.166-171
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• 2022

Background and Objectives Vocal fold (VF) scar is known to be the most common cause of dysphonia after laryngeal microsurgery (LMS). Steroids reduce postoperative scar formation by inhibiting inflammation and collagen deposition. However, the clinical evidence of whether steroids are helpful in reducing VF scar formation after LMS is still lacking. The purpose of this study is to determine whether intralesional VF steroid injection after LMS helps to reduce postoperative scar formation and voice quality. Materials and Method This study was conducted on 80 patients who underwent LMS for VF polyp, Reinke's edema, and leukoplakia. Among them, 40 patients who underwent VF steroid injection after LMS were set as the injection group, and patients who had similar sex, age, and lesion size and who underwent LMS alone were set as the control group. In each group, stroboscopy, multi-dimensional voice program, Aerophone II, and voice handicap index (VHI) were performed before and 1 month after surgery, and the results were statistically analyzed. Results There were no statistically significant differences in the distribution of sex, age, symptom duration, occupation and smoking status between each group. Both groups consisted of VF polyp (n=21), Reinke's edema (n=11), and leukoplakia (n=9). On stroboscopy, the lesion disappeared after surgery, and the amplitude and mucosal wave were symmetrical on both sides of the VFs in all patients. Acoustic parameters and VHI significantly improved after surgery in all patients. However, there was no significant difference between the injection and control group in most of the results. Conclusion There was no significant difference in the results of stroboscopy, acoustic, aerodynamic, and subjective evaluation before and after surgery in the injection group and the control group.

• The Journal of Internal Korean Medicine
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• v.44 no.3
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• pp.402-417
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• 2023

Objective: Liver fibrosis is a highly conserved wound-healing response and the final common pathway of chronic inflammatory injury. This study aimed to evaluate the potential anti-fibrotic effect of the combination of Rhei Radix et Rhizoma water extract (RW) and silymarin in a thioacetamide (TAA)-induced liver fibrosis model. Methods: The liver fibrosis mouse model was established through the intraperitoneal injection of TAA (1 week 100 mg/kg, 2-3 weeks 200 mg/kg, 4-8 weeks 400 mg/kg) three times per week for eight weeks. Animal experiments were conducted in five groups; Normal, Control (TAA-induced liver fibrosis mice), Sily (silymarin 50 mg/kg), RSL (RW 50 mg/kg+silymarin 50 mg/kg), and RSH (RW 100 mg/kg+silymarin 50 mg/kg). Biochemical analyses were measured in serum, including aspartate aminotransferase (AST), alanine aminotransferase (ALT), malondialdehyde (MDA), and ammonia levels. Liver inflammatory cytokines and fibrous biomarkers were measured by Western blot analysis, and liver histopathology was evaluated through tissue staining. Results: A significant decrease in the liver function markers AST and ALT and a reduction in ammonia and total bilirubin were observed in the group treated with RSL and RSH. Measurement of reactive oxygen species and MDA revealed a significant decrease in the RSL and RSH administration group compared to the TAA induction group. The expression of extracellular matrix-related proteins, such as transforming growth factor β1, α-smooth muscle actin, and collagen type I alpha 1, was likewise significantly decreased. All drug-administered groups had increased matrix metalloproteinase-9 but a decreasing tissue inhibitor of matrix metalloproteinase-1. RSL and RSH exerted a significant upregulation of NADPH oxidase 2, p22^phox, and p47^phox, which are oxidative stress-related factors. Furthermore, pro-inflammatory proteins such as cyclooxygenase 2 and interleukin-1β were markedly suppressed through the inhibition of nuclear factor kappa B activation. Conclusions: The administration of RW and silymarin suppressed the NADPH oxidase factor protein level and showed a tendency to reduce inflammation-related enzymes. These results suggest that the combined administration of RW and silymarin improves acute liver injury induced by TAA.

• The Korean Journal of Physiology and Pharmacology
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• v.27 no.4
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• pp.417-426
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• 2023

The TRPM4 gene encodes a Ca²⁺-activated monovalent cation channel called transient receptor potential melastatin 4 (TRPM4) that is expressed in various tissues. Dysregulation or abnormal expression of TRPM4 has been linked to a range of diseases. We introduced the hemagglutinin (HA) tag into the extracellular S6 loop of TRPM4, resulting in an HA-tagged version called TRPM4-HA. This TRPM4-HA was developed to investigate the purification, localization, and function of TRPM4 in different physiological and pathological conditions. TRPM4-HA was successfully expressed in the intact cell membrane and exhibited similar electrophysiological properties, such as the current-voltage relationship, rapid desensitization, and current size, compared to the wild-type TRPM4. The presence of the TRPM4 inhibitor 9-phenanthrol did not affect these properties. Furthermore, a wound-healing assay showed that TRPM4-HA induced cell proliferation and migration, similar to the native TRPM4. Co-expression of protein tyrosine phosphatase, non-receptor type 6 (PTPN6 or SHP1) with TRPM4-HA led to the translocation of TRPM4-HA to the cytosol. To investigate the interaction between PTPN6 and tyrosine residues of TRPM4 in enhancing channel activity, we generated four mutants in which tyrosine (Y) residues were substituted with phenylalanine (F) at the N-terminus of TRPM4. The YF mutants displayed properties and functions similar to TRPM4-HA, except for the Y256F mutant, which showed resistance to 9-phenanthrol, suggesting that Y256 may be involved in the binding site for 9-phenanthrol. Overall, the creation of HA-tagged TRPM4 provides researchers with a valuable tool to study the role of TRPM4 in different conditions and its potential interactions with other proteins, such as PTPN6.

• Journal of Life Science
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• v.34 no.5
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• pp.287-295
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• 2024

Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related mortality worldwide, necessitating novel therapeutic strategies. The chemotherapeutic agents used to treat HCC patients are toxic and have serious side effects. Therefore, we investigated the efficacy of anticancer drugs that reduce side effects by targeting tumor cells without causing cytotoxicity in healthy hepatocytes. Berberine, an isoquinoline alkaloid derived from plant compounds, has emerged as a potential candidate for cancer treatment due to its diverse pharmacological properties. The effect of berberine on HepG2 cell viability was determined using the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide assay. HepG2 cell proliferation was determined through a colony-forming assay. The effects of berberine on HepG2 cell migration were evaluated using a wound-healing assay. Berberine inhibited the proliferation of HepG2 cells, as well as colony formation and migration. Berberine treatment increased the expression of autophagy-related genes and proteins, including Beclin-1 and LC3-II, and elevated the activities and mRNA expression of Caspase-9 and Caspase-3. Additionally, in experiments utilizing the Cell-Derived Xenograft animal model, berberine treatment reduced tumor size and weight in a concentration-dependent manner. These results demonstrate the potential of berberine as a versatile anticancer agent with efficacy in both cellular and animal models of hepatocellular carcinoma. The findings herein shed light on berberine's efficacy against HCC, presenting opportunities for targeted and personalized therapeutic interventions.

• Biomolecules & Therapeutics
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• v.32 no.3
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• pp.368-378
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• 2024

Cordycepin, a valuable bioactive component isolated from Cordyceps militaris, has been reported to possess anti-cancer potential and the property to enhance the effects of chemotherapeutic agents in various types of cancers. However, the ability of cordycepin to chemosensitize cholangiocarcinoma (CCA) cells to gemcitabine has not yet been evaluated. The current study was performed to evaluate the above, and the mechanisms associated with it. The study analyzed the effects of cordycepin in combination with gemcitabine on the cancer stem-like properties of the CCA SNU478 cell line, including its anti-apoptotic, migratory, and antioxidant effects. In addition, the combination of cordycepin and gemcitabine was evaluated in the CCA xenograft model. The cordycepin treatment significantly decreased SNU478 cell viability and, in combination with gemcitabine, additively reduced cell viability. The cordycepin and gemcitabine co-treatment significantly increased the Annexin V+ population and downregulated B-cell lymphoma 2 (Bcl-2) expression, suggesting that the decreased cell viability in the cordycepin+gemcitabine group may result from an increase in apoptotic death. In addition, the cordycepin and gemcitabine co-treatment significantly reduced the migratory ability of SNU478 cells in the wound healing and trans-well migration assays. It was observed that the cordycepin and gemcitabine cotreatment reduced the CD44^highCD133^high population in SNU478 cells and the expression level of sex determining region Y-box 2 (Sox-2), indicating the downregulation of the cancer stem-like population. Cordycepin also enhanced oxidative damage mediated by gemcitabine in MitoSOX staining associated with the upregulated Kelch like ECH Associated Protein 1 (Keap1)/nuclear factor erythroid 2-related factor 2 (Nrf2) expression ratio. In the SNU478 xenograft model, co-administration of cordycepin and gemcitabine additively delayed tumor growth. These results indicate that cordycepin potentiates the chemotherapeutic property of gemcitabine against CCA, which results from the downregulation of its cancer-stem-like properties. Hence, the combination therapy of cordycepin and gemcitabine may be a promising therapeutic strategy in the treatment of CCA.

• Journal of Life Science
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• v.25 no.5
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• pp.523-532
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• 2015

A variety of previous pharmacological studies have suggested Liriope platyphylla (L. platyphylla) may exert beneficial biological effects on inflammation, diabetes, neurodegenerative disorder, obesity, constipation, and atopic dermatitis. In addition, hydrocolloid membranes (HCMs) have attracted attention in dermatological care, including in the treatment of scleroderma skin ulcers, cutaneous ulcers, permanent tympanic membrane perforations, pressure sores, and decubitus ulcers in the elderly. To investigate the therapeutic effects of HCM containing an aqueous extract of L. platyphylla (HCM-LP) on second-degree burn wounds, their physico-chemical properties were analyzed and the therapeutic effects were observed in SD rats after treatment with HCM-LP for 14 days. Significant declines in tensile strength (38.4%) and absorptiveness (46.3%), as well as an increase in surface roughness (38.1%) were detected in HCM-LP compared with that of HCM. In SD rats with burned skin, the wound diameter was shorter in the HCM-LP treated group than in the GZ group on post-surgical day 14, while the significant improvements in scar tissue reduction, epithelium regeneration, angiogenesis, and extracellular matrix deposition were observed in the HCM-LP-treated group during all experimental periods. Overall, these results suggest HCM-LP may accelerate the process of healing the burn injury skin of SD rats through the regulation of angiogenesis and connective tissue formation.

• Journal of Periodontal and Implant Science
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• v.35 no.4
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• pp.1019-1037
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• 2005

The major goals of periodontal therapy are the functional regeneration of periodontal supporting structures already destructed by periodontal disease as well as the reduction of signs and symptoms of progressive periodontal disease. There have been many efforts to develop materials and therapeutic methods to promote periodontal wound healing. There have been increasing interest on the chitosan made by chtin. Chitosan is a derivative of chitin made by deacetylation of side chains. Chitosan has been widely studied as bone substitution and membrane material in periodontology. Many experiments using chitosan in various animal models have proven its beneficial effects. Tetracycline has been considered for use in the treatment of chronic periodontal disease and gingivitis. The aim of this study is to evlauate the osteogenesis of tetracycline blended chitosan membranes on the calvarial critical size defect in Sprague Dawley rats. An 8mm surgical defect was produced with a trephine bur in the area of the midsagittal suture. The rats were divided into five groups: Untreated control group versus four experimental group. Four types of membranes were made and comparative study was been done. Two types of non-woven membranes were made by immersing non-woven chitosan into either the tetracycline solution or chitosan-tetracycline solution. Other two types of sponge membranes were fabricated by immersing chitosan sponge into the tetracycline solution, and subsequent freeze-drying. The animals were sacrificed at 2 and 8 weeks after surgical procedure. The specimens were examined by histologic analyses. The results are as follows: 1. Clinically the use of tetracycline blended chitosan membrane showed great healing capacity. 2. The new bone formations of all the experimental group, non-woven and sponge type membranes were greater than those of control group. But, there was no significant difference between the experimental groups. 3. Resorption of chitosan membranes were not shown in any groups at 2 weeks and 8 weeks. These results suggest that the use of tetracycline blended chitosan membrane on the calvarial defects in rats has significant effect on the regeneration of bone tissue in itself. And it implicate that tetracycline blended chitosan membrane might be useful for guided tissue regeneration.

• Journal of Plant Biotechnology
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• v.50
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• pp.1-10
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• 2023

Sweet potato (Ipomoea batatas L. Lam) is an economically important root crop and a valuable source of nutrients, processed foods, animal feeds, and pigment materials. However, during post-harvest storage, storage roots of sweet potatoes are susceptible to decay caused by various microorganisms and diseases. Post-harvest curing is the most effective means of healing wounds and preventing spoilage by microorganisms during storage. In this study, we aimed to identify proteins involved in the molecular mechanisms related to curing and study proteomic changes during the post-curing storage period. For this purpose, changes in protein spots were analyzed through 2D-electrophoresis after treatment at 33℃ (curing) and 15℃ (control) for three days, followed by a storage period of eight weeks. As a result, we observed 31 differentially expressed protein spots between curing and control groups, among which 15 were identified. Among the identified proteins, the expression level of 'alpha-amylase (spot 1)' increased only after the curing treatment, whereas the expression levels of 'probable aldo-keto reductase 2-like (spot 3)' and 'hypothetical protein CHGG_01724 (spot 4)' increased in both the curing and control groups. However, the expression level of 'sporamin A (spot 10)' decreased in both the curing and control treatments. In the control treatment, the expression level of 'enolase (spot 14)' increased, but the expression levels of 'chain A of actinidin-E-64 complex+ (spot 19)', 'ascorbate peroxidase (spot 22)', and several 'sporamin proteins (spot 20, 21, 23, 24, 27, 29, 30, and 31)' decreased. These results are expected to help identify proteins related to the curing process in sweet potato storage roots, understand the mechanisms related to disease resistance during post-harvest storage, and derive candidate genes to develop new varieties with improved low-temperature storage capabilities in the future.

• The korean journal of orthodontics
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• v.36 no.4
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• pp.242-250
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• 2006

Objective: Periodontal ligament fibroblasts have an ectomesenchymal origin and are thought to play a crucial role for not only homeostasis of periodontal tissues but also bone remodeling, wound healing and regeneration of tissues. Recently, it has been reported that UNC-50 is not expressed in gingival fibroblasts but in PDL fibroblasts. The purpose of this study was to examine the expression of UNC-50 and osteocalcin in the periodontium after application of intermittent force. Methods: Twelve rats had 40 grams of mesially-directed force applied at the upper molar for 1 hour/day. Four rats were sacrificed at 1, 3 and 5 days. Immunohistochemical localization of UNC-50 and osteocalcin antibody was carried out. The results showed apposition of new cellular cementum and a slight increase in periodontal space at the tension side. Results: Strong UNC-50 expression was observed in the differentiating cementoblasts close to PDL fibroblasts in the tension side whereas it was barely expressed at the compression side. Expression was strong at day 3, and decreased at day 5. Osteocalcin immunoreactivity expression was strong in differentiating cementoblasts at the tension side. Conclusion: It can be suggested that UNC-50 is related to the differentiation of cementoblasts, and may be responsible for the molecular event in PDL cells under mechanical stress.

• The korean journal of orthodontics
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• v.27 no.2
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• pp.349-357
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• 1997

Epidermal growth factor(EGF), a single chain polypeptide of 53 amino acids with a molecular weight of 6,045 Da, was first isolated from the male mouse submandibular glands. EGF stimulates cellular proliferation and differentiation in several tissues and accelerates the rate of wound healing. EGF is bound to the specific receptor(EGFR) on the cell membrane of its target cell. EGFR is a transmembrane glycoprotein with a molecular weight of 170,000 Da and is detectable on a large variety of cell types and tissues. The authors investigated the expression of EGFR in the normal and inflamed human gingival epithelium to study the role of EGFR in the inflammation of the gingival epithelium, and the expression of EGFR in the dental follicle by using in situ mRNA hybridization and immunohistochenistry. The results weree as follows : 1. The expression of EGFR mRNA in the normal gingival epithelium on in situ mRNA hybridization was mainly localized on the basal cell layer, and the spinous layer was weakly positive The granular and cornified layers were negative 2. The expression of EGFR protein in the normal gingival epithelium on inmunohistochemistry was localized on the cornified and granular layers, and the spinous layer was weakly positive. The basal cell layer was completely negative 3. The expression of EGFR mRNA in the inflamed gingival epithelium on in situ mRNA hybridization was evenly and homogeneously distributed in the whole layers of the gingival epithelium except the cornified layer. The staining intensity appeared to increase progressively from the basal cell layer to the cornified layer. 4. The expression of EGFR protein in the inflamed gingival epithelium on immunohistochemistry was evenly and homogeneously distributed in the whole layers of the gingival epithelium. The staining intensity appeared to increase progressively from the cornified layer to the basal cell layer. 5. Strong positive reaction was seen in the epithelial cell rests of Malassez, whereas only background staining was seen in other cells of the dental follicle. In conclusion, the up-regulation of EGFR in the inflamed gingival epithelium and the high amounts of EGFR in the epthelial cell rests of Malassez in the dental follicle can be regarded as responses to the possible damages to the oral environment to maintain the homeostatic conditions.