The purpose of this study is to empirically examine the causal relationship of CSR activities, customer trust and CCID, customer behavior intention(B.I) in the relationship between CSR activities and customer behavior intention(B.I) in the insurance industry, thereby enable top management of insurance company to take it in their consideration that CSR activity help link to customer behavioral intention by customer trust in them and CCID. To achieve the purpose of the study, the hypothesis was established based on preceding research and theoretical background regarding CSR, trust, CCID, behavioral intention(B.I). And this study conducted AMOS statistical analysis based on effective 526 survey data collected from insurance customers across country through online research company. The result of this empirical study is as follows. First, insurance company's CSR activity has a positive impact on customer's trust and CCID, but it did not have a direct significant effect on the customer's behavioral intention(B.I). Second, both customer's trust and CCID have a positive and significant effect on customer's behavioral intention. Third, we have also found that both Trust and CCID played a mediating role between CSR activity and B,I. Fourth, it was found that authenticity did not moderate the enfluence relationship between CSR activity and Trust, CCID. The result of this study shows that insurance company's active CSR activity increase customer trust, thereby create a sense of unity between the customer and the company, In addition, it shows that when CSR activities are mediated by customer trust and CCID, it could lead to customer behavioral intention(B.I) such as repurchasing and positive word-of-mouth activities. to others. The result of this study will contribute to the future research on CSR literature and the marketing strategy of insurance companies.
Seo, Geun-Young;Park, Hyo-Jin;Jang, Sung-Geun;Park, Young-Hyun
Journal of the Korean Society of Food Science and Nutrition
/
v.35
no.8
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pp.979-984
/
2006
Although iron is essential for many physiological processes, excess iron can lead to tissue damage by promoting the generation of reactive oxygen species (ROS). There is increasing evidence that ROS might play an important role in the pathogenesis of cardiovascular disease. However, the effects of iron excess on platelet function and the thrombotic response to vascular injury are not well understood. We examined the effects of iron excess-induced oxidative stress and the antioxidants on platelet aggregation. Oxidative stress was accessed by either free iron $(Fe^{+2})$ or hydrogen peroxide $(H_2O_2)$, as well as their combination on washed rabbit platelets (WPs) in vitro. When WPs were stimulated with either $Fe^{+2}$ alone or a subthreshold concentration of collagen, which gave an aggregatory curve with a little effect, and a dose dependent increase in platelet aggregation was observed by increasing concentrations of $Fe^{+2}$ with $H_2O_2$. This aggregation was associated with the iron-catalyzed formation of hydroxyl radicals from $H_2O_2$, and were inhibited by NAD/NADP (proton acceptor), catalase $(H_2O_2\;scavenger)$, tiron (iron chelator), mannitol (hydroxyl radical scavenger), and indomethacin (cyclooxygenase inhibitor), but not by NADH/NADPH (proton donor), superoxide mutase, and aspirin. However, NADH/NADPH, an essential cofactor for the antioxidant capacity by the supply of reducing potentials, showed the effect of an enhanced radical formation, suggesting a role for NADH/NADPH-dependent oxidase. These results suggest that iron $(Fe^{+2})$ can directly interact with washed rabbit platelets and this aggregation be mediated by OH formation as in the Fenton reaction, inhibited by radical scavengers.
Background : Since the exact pathogenesis of sepsis-induced ARDS has not been elucidated, the mechanisms of enhanced neutrophilic respiratory burst were probed in endotoxin primed neutrophils associated with the roles of phospholipase A2(PLA2), platelet activating factor(PAF) and apoptosis. Methods : In isolated fresh human neutrophils, effects of the inhibition of PLA2 and PAF on the apoptosis were examined by the method of Annexin-FITC/dual PIflow cytometry. The roles of PLA2 and PAF on the neutrophilic respiratory burst were also examined by measuring oxidant generation in cytochrome-c reduction assay. Activities of the PLA2 and lysoPAF acetyltransferase (lysoPAF AT) of the neutrophils were determined to understand the effect of endotoxin on these enzymatic activities which may be related to the neutrophilic respiratory burst and apoptosis. In addition, the role roles of PLA2 and PAF in neutrophilic adhesion to bovine endothelial cells were examined in vitro by neutrophil adhesion assay. To investigate the effect of oxidants on pulmonary surfactant, cytochemical ultrastructural microscopy was performed. To inhibit PLA2 and PAF, non-specific PLA2 inhibitor mepacrine (100 nM) and WEB 2086 (100 nM) or ketotifen fumarate (10 ${\mu}g$/ml) were used respectively in all in vitro experimental sets. WEB 2086 is PAF receptor antagonist, and ketotifen fumarate is a lyso PAF AT inhibitor. Results: The mapacrine treatment, provided and the endotoxin (ETX) treatment, resulted in increased apoptosis of neutrophils (p<0.001) while treatments of WEB 2086 and ketotifen did not. The inhibition of PLA2 and PAF decreased (p<0.001) production of oxidants from PMA-stimulated neutrophils. While endotoxin increased the PLA2 activity of neutrophils (p<0.01), mepacrine supressed (p<0.001) the activity, provided after treatment of ETX. The lyso PAF actyltransferase activity (lyso PAF AT) increased (p<0.01) after treatment of ETX. In contrast, mepacrine, WEB 2086 and ketotifen showed a tendency of decreasing the activity after treatment of ETX. The treatment of ETX incresed (p<0.001) neutrophil adhesion to endothelial cells, which was reversed by inhibition of PLA2 and PAF (p<0.01). The binding of oxidants to pu1monary surfactant was identified histologically. Conclusions : The enhanced neutrophilic respiratory burst by ETX plays a pivotal role in the pathogenesis of ARDS in terms of oxidayive oxidative stress. Increased production of oxidants from neutrophils is mediated by the activations of PLA2 and lyso PAF AT.
H2AX, a crucial component of chromatin, is implicated in DNA repair, cell cycle check point and tumor suppression. The aim of this study was to identify direct binding partners of H2AX to regulate cellular responses to above mechanisms. Literature reviews and bioinformatical tools were attempted intensively to find binding partners of H2AX, which resulted in identifying two potential proteins, breast cancer-1 (BRCA1) and BRCA1-associated RING domain 1 (BARD1). Although it has been reported in vivo that BRCA1 co-localizes with H2AX at the site of DNA damage, their biochemical mechanism for H2AX were however only known that the complex monoubiquitinates histone monomers, including unphosphorylated H2AX in vitro. Therefore, it is important to know whether the complex directly interacts with H2AX, and also which regions of these are specifically mediated for the interaction. Using in vitro GST pull-down assay, we present here that BRCA1 and BARD1 directly bind to H2AX. Moreover, through combinational approaches of domain analysis, fragment clonings and in vitro binding assay, we revealed molecular details of the BRCA1-H2AX and BARD1-H2AX complex. These data provide the potential evidence that each of the BRCA1 nuclear localization signal (NLS) and BARD1 BRCA1 C-terminal (BRCT) repeat domain is the novel mediator of H2AX recognition.
Cathepsin K (cat K) is the major cysteine protease expressed in osteoclasts and was thought to play a key role in matrix degradation during bone resorption. It was shown that the intracellular maturation of cat K was prevented by the cAMP antagonist, Rp-cAMP, and the protein kinase A (PKA) inhibitors of KT5720 and H89. In contrast, forskolin, a adenylate cyclase agonist, rather induced Cat K processing and maturation in osteoclasts. Furthermore, to determine whether cat K processing and maturation signaling involves protein kinase C (PKC), mouse total bone cells were treated with calphostin C, a specific inhibitor of PKC, however, no effect was observed, indicating that calphostin C did not affect to osteoclast-mediated cat K processing and maturation. Thus, it is indicated that the cAMP-PKA signaling pathway regulates cat K maturation in osteoclasts. Since secreted proenzymes have the potential to reenter the cell via M6P receptor, to prevent this possibility, it was tested cAMP antagonist Rp-cAMP and the PKA inhibitors KT5720 and H89 in the absence or presence of M6P. Inhibition of cat K processing by Rp-cAMP, KT5720, or H89 was observed in a dose-dependent manner. Furthermore, the addition of M6P resulted in enhanced potency of Rp-cAMP, KT5720 and H89. These dose-dependently inhibited in vitro bone resorption with a potency similar to that observed for inhibition of cat K processing.
Asia-Pacific Journal of Business Venturing and Entrepreneurship
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v.12
no.4
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pp.159-174
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2017
The purpose of this study was to examine whether the entrepreneurship education through team learning positively influences the effectiveness of team learning and the satisfaction of entrepreneurship curriculum. To do this, we analyzed the questionnaire data of 149 students who took the entrepreneurship course that was conducted by the team learning method focused on problem solving task among the entrepreneurship courses opened in the venture autonomous major. First, we examined the effect of team learning effectiveness and entrepreneurial education satisfaction on the effectiveness of the team learning by individual's intention for startup, diversity of team members, and supporting activities of assistants as independent variables. For this, hierarchical regression analysis was conducted to examine whether independent variables influenced the effectiveness of team learning, and whether the effectiveness of team learning mediates between these independent variables and entrepreneurial education satisfaction. The results of this study support the hypothesis that supporting activities of assistants will influence team learning effectiveness. However, the hypothesis that individual's intention for startup or team diversity influences team learning effectiveness was rejected. On the other hand, the results of the regression analysis show that individual's intention for startup has a significant effect on the satisfaction of entrepreneurship education. In addition, the effectiveness of team learning was found to be influential on the educational satisfaction, and it was verified that the effectiveness of team learning was mediating between the supporting activities of assistants and the satisfaction of entrepreneurship education. Especially, as a result of the hierarchical regression analysis, it was found that the significance of the supporting activities of assistants decreased remarkably. This suggests that the mediating path that affects the satisfaction of entrepreneurship education is very meaningful through the effectiveness of the team learning although the supporting activities of assistants are partially mediated. As a result of this study, it was found that the supporting activities of assistants are important in the team learning entrepreneurship education and it is also confirmed that the individual's intention for startup is also important. Especially, supporting activities of assistants were found to be an important factor affecting the satisfaction of entrepreneurship education through the effectiveness of team learning. Therefore, I think that it is essential to designing a practical education course that meets individual's intention for startup in the entrepreneurship education of university students and networking with the participation of internal and external experts or entrepreneurs. In addition, I think that it is necessary to think more thoughtfulness about the composition of team members in the team learning, and to provide more meticulous support to the effectiveness of the team learning.
The pathogenic effort of high glucose, possibly in concert with fatty acids, is mediated to vascular complications of diabetes via increased production of reactive oxygen species(ROS), reactive nitrogen species(RNS), and subsequent oxidative stress. This study was carried out to investigate the suppressive effect of buchu(Allium tuberosum) on oxidative stress in streptozotocin(STZ)-induced diabetes in Sprague Dawley male rats. The effect of buchu supplementation (10%) on lipid peroxidation, and antioxidative defense system in blood and liver was compared among normal rats fed basal diet(normal) and diabetic rats fed basal diet(DM-control) or 10% buchu-supplemented diet(DM-buchu). Diabetes was experimentally induced by the femoral muscle injection of 50 mg STZ per kg of body weight. Animals were sacrificed after 4 wks of experimental diets feeding. The induction of diabetes by STZ elevated the level of lipid peroxidation represented by thiobarbituric acid-reactive substances(TBARS) and conjugated dienes in plasma, LDL, liver, and erythrocytes. 10% buchu-supplemented diet significantly reduced the levels of conjugated dienes in erythrocytes(p<0.05) and lowered TBARS in liver and LDL to the levels of control. Induction of diabetes by STZ elevated Mn-superoxide dismutase(Mn-SOD) activity and lowered activities of glutathionine reductase(GSH-red) and glutathionine peroxidase(GSH-px). Catalase activity was not affected by the induction of diabetes by STZ. However, buchu supplementation to diabetic rats significantly elevated catalase activity(p<0.05) and slightly elevated GSH-px and GSH-red activities in liver. GSH levels of blood and liver were lowered or not changed by induction of diabetes by STZ, respectively, while buchu supplementation to diabetic rats significantly elevated hepatic GSH level (p<0.05). In conclusion, it can be concluded that buchu might be a food source to attenuate oxidative stress in diabetic patients by inhibiting lipid peroxidation, by increasing hepatic GSH level, and by inducing anti-oxidative enzyme systems.
This study was conducted to investigate the effect of Makgeolli (MG) and Makgeolli GiGemi (MGG) on blood flow, serum lipid improvement in vivo, and inhibition of angiotensin converting enzyme (ACE) in vitro. The activities of serum AST and ALT were increased by ovariectomy. Serum AST levels were decreased to $77.71{\pm}13.97$ and $74.57{\pm}14.90\;unit/ml$ in the OVX-MG50 and OVX-MGG50 groups compared to the OVX-control group ($91.14{\pm}12.02\;unit/ml$). Serum ALT levels were decreased to $34.00{\pm}8.41$ and $30.43{\pm}3.60\;unit/ml$ in OVX-MG50 and OVX-MGG50 groups compared to the OVX-control group ($37.14{\pm}5.40\;unit/ml$). Serum total cholesterol and triglyceride contents decreased in the sham group compared with OVX-control group by ovariectomy. Six weeks feeding of MG and MGG resulted in a decrease to $116.14{\pm}36.02$ and $109.14{\pm}11.55\;mg/dl$ compared to the OVX-control group ($120.43{\pm}8.36\;mg/dl$) in serum total cholesterol, and triglyceride levels were decreased to $52.43{\pm}12.41$ and $47.29{\pm}12.08\;mg/dl$ in the OVX-MG50 and OVX-MGG50 groups compared to the OVX-control group ($58.57{\pm}5.47\;mg/dl$). The level of HDL-cholesterol in the OVX-control group was significantly reduced to $51.29{\pm}20.49\;mg/dl$ compared to the sham group ($72.29{\pm}10.29\;mg/dl$), but it was increased to $70.71{\pm}19.53$ and $62.00{\pm}20.20\;mg/dl$ with MG and MGG supplementation. Furthermore, the effect of the MG group was higher than the MGG group. Microscopic observation showed that whole blood passed smoothly through the micro channels in the MG and MGG supplemented groups. The platelet aggregation ability of the groups treated with MG and MGG was less than that of the OVX-control group. In vitro assay, the angiotensin converting enzyme (ACE) activity was significantly inhibited by MG and MGG (82.6% and 68.9% inhibition at 0.4 g/ml). These results suggest that the beneficial effects of MG and MGG may be used to improve on the lipid metabolic syndrome of menopausal women. In addition, MG and MGG might improve blood homeostasis mediated activities via antiplatelets and MG and MGG may be used as antihypertensive functional foods and nutraceuticals.
Kim, Seung-Hun;Nam, Gae-Won;Kang, Byung-Young;Lee, Hae-Kwang;Moon, Seong-Joon;Chang, Ih-Seop
Journal of the Society of Cosmetic Scientists of Korea
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v.31
no.1
s.49
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pp.97-102
/
2005
One of the key molecules involved in skin moisture is hyaluronan (hyaluronic acid, HA) with its associated water of hydration. The predominant component of the ECM (extracellular matrix) of skin is HA. It Is the primordial and the simplest of the GAGs (glycosaminoglycans), a water-sorbed macromolecule In extracellular matrix, Included between the vital cells of epidermis. In the skin, HA was previously thought to derive extlusively from dermis. But, recent studies revealed that HA could be synthesized in epidermis. Flavonoids are polyphenolic compounds that is found mainly in foods of plant origin. Kaempferol was known to increase glutathione synthesis in human keratinocyte. And quercetin blocked PPAR-meidated keratinocyte differentiation as lipoxygenase inhibitors. In this study, we sought to evaluate the effect of flavonid, kaempferol and quercetin on production HA in keratinocyte. We examined the changes of three human hyaluronan synthase genes (HASI, HAS2, HAS3) expression by semi-quantitative RT-PCR when kaempferol or quercetin was added to cultured human keratinocytes. We found that these flavonoids slightly upregulated HAS2, HAS3 mRNA after 24 h. And we investigated the effect on HA production by ELISA. When we evaluated the level of HA in culture medium after 24 h incubation. We found enhanced accumulation of HA in the culture medium. Although the effects of above flavonoids are less than retinoic acid, the data indicate that kaempferol, quercetin can dose-dependently increase the level of HA in epidermis cell line. It suggested that flavonoid, kaempferol, and quercetin increased production of HA in skin and it helped to elevate skin moisture and improve facial wrinkle.
Kim, Min Yeung;Ji, Seon Yeong;Hwangbo, Hyun;Lee, Hyesook;Kim, Tae Hee;Yoon, Seonhye;Kim, Hyun Jin;Kim, Sung Yeon;Kim, Tae Jung;Kim, Min Ji;Jung, Ha Eun;Choi, Yung Hyun
Journal of Life Science
/
v.31
no.10
/
pp.885-897
/
2021
Schisandrae Fructus (SF) and Corni Fructus (CF) have been used for a long time for the prevention and treatment of various diseases. Although reports have highlighted the possibility of inhibiting the onset and progression of benign prostatic hyperplasia (BPH), studies on related mechanisms are still lacking. In this study, we investigated the potential of SF and CF in improving BPH by using a dihydrotestosterone (DHT)-induced in vitro BPH model using LNCaP prostate carcinoma cells. According to our results, water and ethanol extracts of SF and CF significantly inhibited the proliferation of LNCaP cells by DHT treatment and markedly downregulated the expression of DHT-induced BPH biomarkers and growth factors. They also regulated the expression of apoptosis regulatory factors and significantly reduced DHT-mediated oxidative stress. In addition, the protective effect on major factors involved in the pathogenesis of BPH was more effective in the ethanol extract treatment group than in the water extract group. Furthermore, the improvement effect on BPH was higher in the 1:1 combined treatment group than in the ethanol extract alone treatment group of SF and CF, and 60% ethanol extracts showed a better effect than 40% ethanol extracts. Therefore, our findings demonstrate that SF and CF can protect against BPH by preventing the hyperproliferation of prostate cells through the inhibition of the androgen signaling pathway, which was correlated with their antioxidant activities. Therefore, SF and CF extracts may be useful in the clinical treatment of BPH, and the combination of these two extracts can be synergistic.
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