Purpose: As the visual expression cue that can easily reveal and imprint the brand image to consumers becomes more important, franchise coffee shops are making various efforts to establish design elements and brand identity. Therefore, the purpose of this study is to examine the structural model between design elements, brand identity, brand association, brand personality, and brand image of franchise coffee shops from various angles, and to suggest a plan for using visual elements makes a brand image on the franchise in the future. Research design, data, and methodology: This study tests the structural relationship between design elements, brand identity, brand association, brand personality, and brand image of franchise coffee shops. design elements are divided into three attributes (interior design, product design). And brand identity is divided into two attributes (brand name, brand symbol/logo). In order to achieve the purposes of this research, research model and hypotheses were developed based on previous researches. All constructs were measured with multiple items developed and tested in the previous studies. The data were collected from 380 customers who visited franchise coffee shops and were analyzed through SPSS 26.0 and SmartPLS 3.0 statistical package program. Result: As a result of this study, first, it is confirmed that product design has a positive effect on brand association toward coffee shops. Second, interior design and product design have a positive effect on brand personality. Third, all brand identity have a significant positive impact on brand association and brand personality. Finally, brand association and brand personality of coffee specialty shops have a positive effect on brand image. Conclusions: The following implications of this study are as follows. This study is confirmed that there is an effect of design elements attributes and brand identity attributes on brand association and brand personality. And, the brand image was found to be influenced by brand association and brand personality. This suggests that it can be used to establish visible marketing strategies for franchise coffee shops. Therefore, it is necessary to further improve efforts to raise the level of the brand image through visual factors such as unusual interior design, product packages.
Objectives : A transition course of 'Introduction to Clinical Korean Medicine' was developed to meet the demands for better preparation for clinical application of Korean Medicine within the curriculum. A Korean Medical Classics curriculum reflecting such demands was newly designed. Methods : Based on the 'Introduction to Clinical Medicine(ICM)' course of the Medical School curriculum that follows the medical education guideline, the 'Introduction to Clinical Korean Medicine(ICKM)' course was designed and developed. The role of Korean Medical Classics was suggested in the process. Results : In the following course, Korean Medical diagnosis, diagnostics, patient intake methods reflecting the Korean Medical diagnostic system, clinical skills, basic skills, treatment planning, patient education, etc. are included. Faculty members of the basic sectors of the Korean Medical school will participate in this curriculum, of which a head will be appointed to overlook the curriculum. In the case of Korean Medical Classics, previous learning outcomes need to be reorganized based on clinical expression while clinical case studies need to be added to course material. A more active approach utilizing new pedagogic strategies and teaching methods should be taken. Conclusions : The Korean Medical Classics curriculum could effectively take on the introductory role to clinical Korean Medicine, successfully strengthening the connection between the basic and clinical Korean Medicine to improve learners' satisfaction.
Current strategies of strain improvement processes are mainly focused on enhancing the synthetic pathways of the products. However, excessive metabolic flux often creates metabolic imbalances, which lead to growth retardation and ultimately limit the yield of the product. To solve this problem, we applied a dynamic regulation strategy to produce $\text\tiny{L}$-phenylalanine ($\text\tiny{L}$-Phe) in Escherichia coli. First, we constructed a series of Phe-induced promoters that exhibited different strengths through modification of the promoter region of tyrP. Then, two engineered promoters were separately introduced into a Phe-producing strain xllp1 to dynamically control the expression level of one pathway enzyme AroK. Batch fermentation results of the strain xllp3 showed that the titer of Phe reached 61.3 g/l at 48 h, representing a titer of 1.36-fold of the strain xllp1 (45.0 g/l). Moreover, the $\text\tiny{L}$-Phe yields on glucose of xllp3 (0.22 g/g) were also greatly improved, with an increase of 1.22-fold in comparison with the xllp1 (0.18 g/g). In summary, we successfully improved the titer of Phe by using dynamic regulation of one key enzyme and this strategy can be applied for improving the performance of strains producing other aromatic amino acids and derived compounds.
in the conclusion, appealing ways of expression regarding a wider and more variated range are to be tested and it is stressed the necessity of this to be shown to the general public through an ongoing constructive research on the originality of contents arising from the diversity of music genres And, concerning dance music, it is also pointed out the necessity of in-depth research on the rhythms that take into account the universal emotions of the general public to create diverse music that harmonizes with the dance and can be enjoyed by all. In the world of music, just a simplest attempt can bring about many changes. Depending on the identity of those who lead it, that change's appearance or shape may also be different. Moreover, changes arisen from testing simplified rhythms will let experts to create new music. K-Pop is to test, more than anything, diverse strategies and new changes to be selected by such a wide public. However, such changes ought not to degenerate into mere imitations and can neither become obsolete. The reason lies in the fact that the current efforts for the sake of diversification and creativity of K-Pop genre might well remain as the traditional elements of the K-pop of the future.
Phagocytosis is a fundamental process in which phagocytes capture and ingest foreign particles including pathogenic bacteria. Several oral pathogens have anti-phagocytic strategies, which allow them to escape from and survive in phagocytes. Impaired bacteria phagocytosis increases inflammation and contributes to inflammatory diseases. The purpose of this study is to investigate the influences of various agents on oral pathogenic phagocytosis. To determine phagocytosis, Streptococcus mutans, Fusobacterium nucleatum, Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis were stained with 5-(and-6)-carboxyfluorescein diacetate succinimidyl ester (CFSE), and was measured using flowcytometery and confocal microscopy. The influencing factors on phagocytosis were evaluated through the pretreatment of ROS inhibitor (N-acetyl-L-cysteine (NAC)), lysozyme, potassium chloride (KCI) and adenosine triphosphate (ATP) in THP-1 cells. Expression of pro-inflammatory cytokines was determined by enzyme-linked immunosorbent assay (ELISA). The phagocytosis of various bacteria increased in a MOI-dependent manner. Among the tested bacteria, phagocytosis of P. gingivalis showed the highest fluorescent intensity at same infection time. Among the tested inhibitors, the NAC treatment significantly inhibited phagocytosis in all tested bacteria. In addition, NAC treatment indicated a similar pattern under the confocal microscopy. Moreover, NAC treatment significantly increased the bacteria-induced secretion of $IL-1{\beta}$ among the tested inhibitors. Taken together, we conclude that the phagocytosis occurs differently depending on each bacterium. Down-regulation by ROS production inhibited phagocytosis and lead increased of oral pathogens-associated inflammation.
Pietzner, Klaus;Nasser, Sara;Alavi, Sara;Darb-Esfahani, Silvia;Passler, Mona;Muallem, Mustafa Zelal;Sehouli, Jalid
Journal of Gynecologic Oncology
/
v.29
no.6
/
pp.93.1-93.11
/
2018
The introduction of checkpoint inhibitors revolutionized immuno-oncology. The efficacy of traditional immunotherapeutics, like vaccines and immunostimulants was very limited due to persistent immune-escape strategies of cancer cells. Checkpoint inhibitors target these escape mechanisms and re-direct the immune system to anti-tumor toxicity. Phenomenal results have been reported in entities like melanoma, where no other therapy was able to demonstrate survival benefit, before the introduction of immunotherapeutics. The first experience in ovarian cancer (OC) was reported for nivolumab, a fully human anti-programmed cell death protein 1 (PD1) antibody, in 2015. While the data are extraordinary for a mono-immunotherapeutic agent and very promising, they do not match up to the revolutionary results in entities like melanoma. The key to exceptional treatment response in OC, could be the identification of the most immunogenic patients. We hypothyse that BRCA mutation could be a predictor of improved response in OC. The underlying DNA-repair-deficiancy should result in increased immunogenicity because of higher mutational load and more neoantigen presentation. This hypothesis was not tested to date and should be subject to future trials. The present article gives an overview of the immunologic background of checkpoint inhibition (CI). It presents current data on nivolumab and other checkpoint-inhibitors in solid tumors and OC specifically and depicts important topics in the management of this novel substance group, such as side effect control, diagnostic PD-1/programmed cell death-ligand 1 (PD-L1) expression assessment and management of pseudoprogression.
Choi, Eunju;Kim, Eunji;Kim, Ji Hye;Yoon, Keejung;Kim, Sunggyu;Lee, Jongsung;Cho, Jae Youl
Journal of Ginseng Research
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v.43
no.4
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pp.692-698
/
2019
Background: Breast cancer is a severe disease and the second leading cause of cancer death in women worldwide. To surmount this, various diagnosis and treatment options for breast cancer have been developed. One of the most effective strategies for cancer treatment is to induce apoptosis using naturally occurring compounds. Compound K (CK) is a ginseng saponin metabolite generated by human intestinal bacteria. CK has been studied for its cardioprotective, antiinflammatory, and liver-protective effects; however, the role of CK in breast cancer is not fully understood. Methods: To investigate the anticancer effects of CK in SKBR3 and MDA-MB-231 cells, cell viability assays and flow cytometry analysis were used. In addition, the direct targets of CK anticancer activity were identified using immunoblotting analysis and overexpression experiments. Invasion, migration, and clonogenic assays were carried out to determine the effects of CK on cancer metastasis. Results: CK-induced cell apoptosis in SKBR3 cells as determined through 3-(4-5-dimethylthiazol-2-yl)-2-5-diphenyltetrazolium bromide assays, propidium iodide (PI) and annexin V staining, and morphological changes. CK increased the cleaved forms of caspase-7, caspase-8, and caspase-9, whereas the expression of Bcl-2 was reduced by CK. In assays probing the cell survival pathway, CK activated only AKT1 and not AKT2. Moreover, CK inhibited breast cancer cell invasion, migration, and colony formation. Through regulation of AKT1 activity, CK exerts anticancer effects by inducing apoptosis. Conclusion: Our results suggest that CK could be used as a therapeutic compound for breast cancer.
To adapt to environmental changes and to maintain cellular homeostasis, microorganisms adjust the intracellular concentrations of biochemical compounds, including metal ions; these are essential for the catalytic function of many enzymes in cells, but excessive amounts of essential metals and heavy metals cause cellular damage. Metal-responsive transcriptional regulators play pivotal roles in metal uptake, pumping out, sequestration, and oxidation or reduction to a less toxic status via regulating the expression of the detoxification-related genes. The sensory and regulatory functions of the metalloregulators have made them as attractive biological parts for synthetic biology, and the exceptional sensitivity and selectivity of metalloregulators toward metal ions have been used in heavy metal biosensors to cope with prevalent heavy metal contamination. Due to their importance, substantial efforts have been made to characterize heavy metal-responsive transcriptional regulators and to develop heavy metal-sensing biosensors. In this review, we summarize the biochemical data for the two major metalloregulator families, SmtB/ArsR and MerR, to describe their metal-binding sites, specific chelating chemistry, and conformational changes. Based on our understanding of the regulatory mechanisms, previously developed metal biosensors are examined to point out their limitations, such as high background noise and a lack of well-characterized biological parts. We discuss several strategies to improve the functionality of the metal biosensors, such as reducing the background noise and amplifying the output signal. From the perspective of making heavy metal biosensors, we suggest that the characterization of novel metalloregulators and the fabrication of exquisitely designed genetic circuits will be required.
Lee, Tae-Jin;Kang, Hee-Kyoung;Berry, Jeffrey C.;Joo, Hong-Gu;Park, Changwon;Miller, Mark J.;Choi, Kyunghee
Biomolecules & Therapeutics
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v.29
no.5
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pp.545-550
/
2021
Chemotherapy-induced alopecia and hair loss can be stressful in patients with cancer. The hair grows back, but sometimes the hair tends to stay thin. Therefore, understanding mechanisms regulating hair regeneration may improve the management of chemotherapy-induced alopecia. Previous studies have revealed that chemotherapeutic agents induce a hair follicle vascular injury. As hair growth is associated with micro-vessel regeneration, we postulated that the stimulation of angiogenesis might enhance hair regeneration. In particular, mice treated with 5-fluorouracil (5-FU) showed delayed anagen initiation and reduced capillary density when compared with untreated controls, suggesting that the retardation of anagen initiation by 5-FU treatment may be attributed to the loss of perifollicular micro-vessels. We investigated whether the ETS transcription factor ETV2 (aka ER71), critical for vascular development and regeneration, can promote angiogenesis and hair regrowth in a 5-FU-induced alopecia mouse model. Tie2-Cre; Etv2 conditional knockout (CKO) mice, which lack Etv2 in endothelial cells, presented similar hair regrowth rates as the control mice after depilation. Following 5-FU treatment, Tie2-Cre; Etv2 CKO mice revealed a significant reduction in capillary density, anagen induction, and hair restoration when compared with controls. Mice receiving lentiviral Etv2 injection after 5-FU treatment showed significantly improved anagen induction and hair regrowth. Two-photon laser scanning microscopy revealed that enforced Etv2 expression restored normal vessel morphology after 5-FU mediated vessel injury. Our data suggest that vessel regeneration strategies may improve hair regrowth after chemotherapeutic treatment.
Aziz, Nur;Kim, Eunji;Yang, Yanyan;Kim, Han Gyung;Yu, Tao;Cho, Jae Youl
BMB Reports
/
v.55
no.8
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pp.389-394
/
2022
In particular, the phenomenon of c-Jun degradation within the inflammatory response has not yet been fully analyzed. In order to verify this, we investigated LPS-stimulated murine macrophages pre-treated with sodium orthovanadate (SO) in order to uncover the regulatory mechanisms of the MAPKs which regulate c-Jun degradation within the inflammatory response. Through our study, we found that SO suppressed the production of prostaglandin E2 (PGE2) and the expression of COX-2 in LPS-stimulated RAW264.7 cells. Additionally, SO decreased total c-Jun levels, without altering the amount of mRNA, although the phospho-levels of p38, ERK, and JNK were strongly enhanced. Through the usage of selective MAPK inhibitors, and knockdown and overexpression strategies, p38 was revealed to be a major MAPK which regulates c-Jun degradation. Further analysis indicates that the phosphorylation of p38 is a determinant for c-Jun degradation, and is sufficient to induce ubiquitination-dependent c-Jun degradation, recovered through MG132 treatment. Therefore, our results suggest that the hyperphosphorylation of p38 by SO contributes to c-Jun degradation, which is linked to the suppression of PGE2 secretion in inflammatory responses; and thus, finding drugs to increase p38 activity could be a novel strategy for the development of anti-inflammatory drugs.
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