This study was conducted by empirically analyzing the relation between effects of positive emotional response of female customers, who have at some point consumed food at Korean restaurants in Busan, and behavioral intention according to their food service consumption propensity. In order to achieve the objective of the study, the questionnaire survey was performed from March $10^{th}$ to $25^{th}$, and frequency analysis, confirmatory factor analysis, reliability analysis, correlation analysis, and SEM (structure equation model) were conducted by using SPSS 18.0 and AMOS for 248 questionnaires. As a result of an exploratory factor analysis, five factors were confirmed. In a confirmatory factor analysis, the average variance extracted (AVE) and composite reliability (CR) were confirmed as .508 to .665 and .905 to .946 respectively, which proved the convergent validity. In a hypothesis test, Hypothesis 1 was determined that the food service consumption propensity positively effects on emotional response. The results were as follows: the taste driven (${\beta}$=.325, t=3.907, p<.001), the health driven (${\beta}$=.190, t=2.688, p<.001), and the atmosphere driven (${\beta}$=.188, t=2.515, p<.001). Therefore, Hypothesis 1 was selected. Hypothesis 1 has determined that positive emotional response beneficially affects behavioral intention. As a result of an analysis, the standardized path coefficient was (${\beta}$=.496, t=6.388, p<.001), so Hypothesis 1 was selected. This result suggests that the taste driven factor has the biggest influence on emotional response in the food service consumption propensity for female customers, and food service business operators should strive to make a good restaurant atmosphere for customers to get positive emotional response (pleasure, comfort, satisfaction, and joy).
Abnormal activation of nuclear factor kappa B ($NF-{\kappa}B$) probably plays an important role in the pathogenesis of Duchenne's muscular dystrophy (DMD). In this report, we evaluated the efficacy of curcumin, a potent $NF-{\kappa}B$ inhibitor, in mdx mice, a mouse model of DMD. We found that it improved sarcolemmic integrity and enhanced muscle strength after intraperitoneal (i.p.) injection. Histological analysis revealed that the structural defects of myofibrils were reduced, and biochemical analysis showed that creatine kinase (CK) activity was decreased. We also found that levels of tumor necrosis factor alpha ($TNF-\alpha$), interleukin-1 beta ($IL-1\beta$) and inducible nitric oxide synthase (iNOS) in the mdx mice were decreased by curcumin administration. EMSA analysis showed that $NF-{\kappa}B$ activity was also inhibited. We thus conclude that curcumin is effective in the therapy of muscular dystrophy in mdx mice, and that the mechanism may involve inhibition of $NF-{\kappa}B$ activity. Since curcumin is a non-toxic compound derived from plants, we propose that it may be useful for DMD therapy.
Purpose: This study aimed to develop and test a structural model for chemotherapy-related cognitive impairment of breast cancer patients based on a literature review and Hess and Insel's chemotherapy-related cognitive change model. Methods: The Participants consisted of 250 patients who were ${\geq}19$ years of age. The assessment tools included the Menopause Rating Scale, Symptom Experience Scale, Hospital Anxiety and Depression Scale, Everyday Cognition, and Functional Assessment of Cancer Therapy-Breast Cancer. Data were analyzed using the SPSS 21.0 and AMOS 21.0 programs. Results: The modified model was a good fit for the data. The model fit indices were ${\chi}^2=423.18$ (p<.001), ${\chi}^2/df=3.38$, CFI=.91, NFI=.91, TLI=.89, SRMR=.05, RMSEA=.09, and AIC=515.18. Chemotherapy-related cognitive impairment was directly influenced by menopausal symptoms (${\beta}=.38$, p=.002), depression and anxiety (${\beta}=.25$, p=.002), and symptom experiences (${\beta}=.19$, p=.012). These predictors explained 47.7% of the variance in chemotherapy-related cognitive impairment. Depression and anxiety mediated the relations among menopausal symptoms, symptom experiences, and with chemotherapy related cognitive impairment. Depression and anxiety (${\beta}=-.51$, p=.001), symptom experiences (${\beta}=-.27$, p=.001), menopausal symptoms (${\beta}=-.22$, p=.008), and chemotherapy-related cognitive impairment (${\beta}=-.15$, p=.024) had direct effects on the quality of life and these variables explained 91.3%. Conclusion: These results suggest that chemotherapy-related toxicity is highly associated with cognitive decline and quality of life in women with breast cancer. Depression and anxiety increased vulnerability to cognitive impairment after chemotherapy. Nursing intervention is needed to relieve chemotherapy-related toxicity and psychological factor as well as cognitive decline for quality of life in patients undergoing chemotherapy.
This study examined how empowerment of restaurant cooks influences job satisfaction, organizational commitment, and customer orientation, targeting 260 restaurant cooks in the Busan area. SPSS 18.0 was employed to perform frequency, factor, reliability, and multiple (simple) regression analyses. Empowerment was analyzed using 3 factors (self-authority, meaning and competence) while job satisfaction, organizational commitment, and customer orientation were analyzed using 1 factor each. Results of a correlation analysis of the hypothesized model revealed positive correlations among the variables. Multiple (simple) regression analyses of the hypothesized model found that the sub empowerment factors will have a positive influence on job satisfaction with self-authority (${\beta}$=.372, p<.001), meaning (${\beta}$=.451, p<.001), competence (${\beta}$=.240, p<.001). It was also found that the sub empowerment factors will have a positive influence on organizational commitment with self-authority (${\beta}$=.433, p<.001), meaning (${\beta}$=.473, p<.001), competence (${\beta}$=.302, p<.001). Lastly, the hypotheses that job satisfaction will have a positive influence on organizational commitment (${\beta}$=.775, p<.001), that job satisfaction will have a positive influence on customer orientation (${\beta}$=.467, p<.001), and that organizational commitment will have a positive influence on customer orientation (${\beta}$=.567, p<.001) were adopted.
Potentially lethal damage repair (PLDR) in HFL-I was investigated by delayed plating experiments. The surviving fraction data were fitted to the linear Quadratic equation ($LogSn=-n{\gamma}({\alpha}d+{\beta}d^2$) where ${\gamma}=1$ for immediate plating). And a repair factor ${\gamma}$ was developed to compare survival for immediate and delayed plating. When we only took into account the repair factor of PLDR ${\gamma}$ which was derived from the delay assay, the cell survival response th fractionated carbon ion irradiation was not fully matched. This gap suggested that consideration of another repair process is necessary. So this suggests that the various repair process plays an important role in the fractionated irradiations.
Though many genetic and epigenetic alterations have been identified in hamster oral carcinogenesis model, there is no information about the possible role of transforming growth factor related with oral cancer. The purpose of this paper was to find the expression patterns of transforming growth factor alpha and beta during the stages of complete oral carcinogenesis model in hamster. 0.5% 9, 10-dimethyl-1, 2-benzanthracene(DMBA) in mineral oil was topically applied to the buccal pouch of 75 hamster three times a week during the experimental periods. The experimental animals were subdivided into two groups of control and experiment. Only the mineral oil was applied to the control group. 0.5% DMBA in mineral oil was applied to the experimental groups of 6, 8, 10, 12, 14, 16, 18 and 20 weeks. The expression of the $TGF-{\alpha}$ and $TGF-{\beta}$ protein were evaluated by the distribution and intensity of positive cells during the carcinogenesis using the immunohistochemical study. The following results were obtained ; 1. The buccal pouch epithelium of hamster was histologically changed to the dysplasia at 6, 8, 10 weeks, carcinoma in situ at 12 weeks, and squamous cell carcinoma at 14 weeks. 2. The expression of the $TGF-{\alpha}$ was restricted to the parabasal and basal layers of the normal and dysplastic mucosa, but those positive cells were extended to the spinous layers of the epithelium in the carcinoma. 3. The degree of $TGF-{\alpha}$ expression was markedly decreased in the carcinoma at 16, 18, 20. The strong positive staining in the center of cancer islands and weak positive staining in periphery of tumor were seen at the stage of squamous cell carcinoma. 4. The positive index of the $TGF-{\alpha}$ had a tendency to increase with DMBA- applied time. There was a statistically significant difference between 12, 18, 20 experimental group and control group (p<0.05). 5. The expression of the $TGF-{\beta}$ was shown at the cytoplasm of all control and experimental groups, and the parabasal and basal layers of the normal and dyslastic mucosa, but it was shown at the basal layers of the epithelium in the carcinoma. 6. $TGF-{\beta}$ was expressed diffusely at 16, 18, 20 experimental group. The strong positive staining in the center of cancer islands and positive staining in periphery of tumor were seen at the stage of squamous cell carcinoma. From the above findings, the expression of $TGF-{\alpha}$ and ${\beta}$ in oral carcinogenesis model seems to have two formal stages, the first being an overexpression step as reaction to uncontrolled growth and the second being one in which external protein accumulate in the surrounding stroma and intracytoplasm. Overexpression of $TGF-{\alpha}$ and ${\beta}$ may have important cooperative roles for the promotion of cancer and factor of prognosis.
Purpose : Transforming growth factor (TGF)-${\beta}1$ reportedly increases neuronal survival by inhibiting the induction of inducible nitric oxide synthase (NOS) in astrocytes and protecting neurons after excitotoxic injury. However, the neuroprotective mechanism of $TGF-{\beta}1$ on hypoxic-ischemic (HI) brain injury in neonatal rats is not clear. The aim of this study was to determine whether $TGF-{\beta}1$ has neuroprotective effects via a NO-mediated mechanism and N-methyl-D-aspartate (NMDA) receptor modulation on perinatal HI brain injury. Methods : Cortical cells were cultured using 19-day-pregnant Sprague-Dawley (SD) rats treated with $TGF-{\beta}1$ (1, 5, or 10 ng/mL) and incubated in a 1% O2 incubator for hypoxia. Seven-day-old SD rat pups were subjected to left carotid occlusion followed by 2 h of hypoxic exposure (7.5% $O_2$). $TGF-{\beta}1$ (0.5 ng/kg) was administered intracerebrally to the rats 30 min before HI brain injury. The expressions of NOS and NMDA receptors were measured. Results : In the in vitro model, the expressions of endothelial NOS (eNOS) and neuronal NOS (nNOS) increased in the hypoxic group and decreased in the 1 ng/mL $TGF-{\beta}1-treated$ group. In the in vivo model, the expression of inducible NOS (iNOS) decreased in the hypoxia group and increased in the $TGF-{\beta}1$-treated group. The expressions of eNOS and nNOS were reversed compared with the expression of iNOS. The expressions of all NMDA receptor subunits decreased in hypoxia group and increased in the $TGF-{\beta}1$-treated group except NR2C. Conclusion : The administration of $TGF-{\beta}1$ could significantly protect against perinatal HI brain injury via some parts of the NO-mediated or excitotoxic mechanism.
Journal of the Korea Academia-Industrial cooperation Society
/
v.20
no.3
/
pp.447-454
/
2019
The purpose of this study aims to be used as base data of a policy which forms university students' appropriate behavior for the prevention of infection by analyzing some university students' prevention awareness of new type of infection. A self-administered questionnaire survey about students' seriousness, sensitivity, self-efficacy, and prevention behavior intent of new infection, was conducted in an university located in Gyeonbuk from April. 30th to May. 11th, 2018. Analyzing factors which affect the prevention behavior intent of infection with controlled general factor and health behavior, the prevention behavior intent was increased by ${\beta}=.125$ as seriousness increases and ${\beta}=.709$ as self-efficacy increases in Model 2, final model. However, sensitivity has no significant effect on the prevention behavior intent. Originally sensitivity has to be a significant factor regarding to the prevention behavior intent of new infection. But the result that sensitivity has no influence at all, shows that the students are insensitive to new diseases as they don't fear or sense danger of new infection. Therefore, a disease control policy which helps to increase sensitivity has to be established.
Journal of the Korean Society of Propulsion Engineers
/
v.4
no.4
/
pp.9-17
/
2000
The crystal growth and dissolution rates were calculated by solving a model equation, which involved the dissolution of the metastable phase($\beta$-HNIW) and growth of the stable phase($\varepsilon$-HNIW), together with the mass balance equation. The model has been successfully used to simulate available kinetic data for the $\beta$$\longrightarrow$$\varepsilon$ polymorphic transformation via a solution phase. From the effectiveness factor based on the two-step model, it was found that the surface integration contribution to the process was comparatively small, and a diffusion dependency decreased with an increase of the mass fraction of chloroform in the mixed solvents of ethyl acetate and chloroform. Appling these kinetics in process simulation allowed for the prediction of the product size of $\varepsilon$-HNIW.
Many studies have focused on the tumor suppressive role of $TGF-{\beta}$ signaling during the early stages of tumorigenesis by activating the target genes involved in cytostasis and apoptosis. We investigated the effects of $TGF-{\beta}$ inhibition on early tumorigenesis in the liver, by employing diverse inhibitory methods. Strikingly, $TGF-{\beta}$ inhibition consistently suppressed hepatic tumorigenesis that was induced either by activated RAS plus p53 downregulation or by the co-activation of RAS and TAZ signaling; this demonstrates the requirements for canonical $TGF-{\beta}$ signaling in tumorigenesis. Moreover, we found that Snail is the target gene of the $TGF-{\beta}$ signaling pathway that promotes hepatic carcinogenesis. The knockdown of Snail suppressed the early tumorigenesis in the liver, as did the $TGF-{\beta}$ inhibition, while the ectopic expression of Snail restored tumorigenesis that was suppressed by the $TGF-{\beta}$ inhibition. Our findings establish the oncogenic $TGF-{\beta}$-Smad-Snail signaling axis during the early tumorigenesis in the liver.
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