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The release of Chinese film director Feng Xiao Gang’s The Banquet in 2006 declares the first Chinese Hamlet film adaptation. Feng chooses to sinicize the play and interweaving cultural elements by framing the play into a Chinese martial art film and by applying Chinese Nuo mask and its variation in his filmic interpretation of the play. The frame of martial art film is heavily featured as the Chinese cultural touch deployed by the director in the transformation of a western play into a Chinese film, which proves to be an effective tool for displacing the western cultural elements with Chinese cultural ideology and principles. The use of the Nuo mask motif throughout the film is discussed with the following examples: 1. The director’s choice of using the Chinese Nuo mask in his adaptation of the play-within-the-play scene in the film, displacing the Mousetrap with its Nuo drama counterpart. 2. The director’s re-interpretation of Hamlet’s hesitation and madness, his representation of the Ghost and his symbolic approach to the building of characters by adopting a white paper mask. 3. The director’s transfer from the Ghost of Old Hamlet to copper carved mask symbolization. 4. The director’s building of characterization by using one’s own face as the mask. The framing of martial art film and the adoption of Nuo mask are the tools of sinicization in the process of the intercultural film adaptation of the western classic. The success of the film has explored the connections between the two cultures and challenged the transfer of Chinese culture into a western play.

In the post-COVID-19 era, Chinese holiday seekers have shown significant interest in outdoor leisure opportunities or rural tourism, with a notable increase in enotourism. Wine tasting and related experiences have extended beyond consumption to become more experiential and sophisticated. To better capture this deepening yet under-addressed experience, this study developed a multi-item scale to measure wine tourism experiences. The scale covers six dimensions, namely escapism, entertainment, esthetics, education, novelty and hedonism, which are based on Pine and Gilmore’s (1998) experience economy model. The scale measures a wide breadth of experiences that are associated with wine tourism in the new era. Hence, it provides revised and pertinent market intelligence for winery to better market their products.

Wine tourism is an increasingly prevalent form of tourism, but is still an emerging market in China. Wine tourism is highly experiential, yet only a few research works have focused on the antecedents and consequences of co-creation experience in the context of wine tourism. In this study, Chateau Changyu Rena Shaanxi, China, was selected as the site of research to explore the impacts of wine tourism experience on co-creation experience, perceived value, and consumer behavior. The Structure Equation Modeling (SEM) method has been used to analyze a sample of 536 respondents who have participated in wine tourism. The results show that most Chinese tourists participated in wine tourism for the first time and spent around 800 Renminbi for wine in average at the winery. In addition, this study is the first to confirm that autonomous of co-creation experience, entertainment, education, escapism, and novelty experience have positive effects on co-creation experience. Education experience, esthetic experience, escapism experience, and hedonism experience are positively correlated with perceived value. Co-creation experience and perceived value are positively correlated with word-of-mouth intention, revisit intention and purchase intention. The results of this study also provide implications for winery operators, guiding them to improve their business strategies, enrich wine tourism experience, encourage tourists to participate in co-creation activities, reward visitors for positive word-of-mouth promotion and offer cost-effective products.

No diálogo, nem sempre fácil, entre o mundo ocidental e a China, no século XVI, a tradução foi elemento essencial. Este artigo pretende ser um contributo para a história da tradução na China continental e em Macau, com destaque para o papel dos Jesuítas (Matteo Ricci, Michelle Ruggieri, Tomás Pereira, entre muitos outros) e, mais tarde, já no século XIX, o do Padre Joaquim Afonso Gonçalves. Eles foram determinantes para a afirmação da tradução em Macau e no interior da China, a qual é precursora do ensino do português em ambos os lugares, com a vitalidade que hoje tem.

The release of Chinese film director Feng Xiao Gang’s The Banquet in 2006 declares the first Chinese Hamlet film adaptation. Feng chooses to sinicize the play and interweaving cultural elements by framing the play into a Chinese martial art film and by applying Chinese Nuo mask and its variation in his filmic interpretation of the play. The frame of martial art film is heavily featured as the Chinese cultural touch deployed by the director in the transformation of a western play into a Chinese film, which proves to be an effective tool for displacing the western cultural elements with Chinese cultural ideology and principles. The use of the Nuo mask motif throughout the film is discussed with the following examples: 1. The director’s choice of using the Chinese Nuo mask in his adaptation of the play-within-the-play scene in the film, displacing the Mousetrap with its Nuo drama counterpart. 2. The director’s re-interpretation of Hamlet’s hesitation and madness, his representation of the Ghost and his symbolic approach to the building of characters by adopting a white paper mask. 3. The director’s transfer from the Ghost of Old Hamlet to copper carved mask symbolization. 4. The director’s building of characterization by using one’s own face as the mask. The framing of martial art film and the adoption of Nuo mask are the tools of sinicization in the process of the intercultural film adaptation of the western classic. The success of the film has explored the connections between the two cultures and challenged the transfer of Chinese culture into a western play.

Background: Amyloidosis is defined as a disorder characterized by the deposition of extracellular protein material of amyloid in tissues., Objectives: N-terminal pro-B-type natriuretic peptide (NT-proBNP) is used to predict the cardiac amyloidosis (CA), but its diagnostic effect on CA involvement remains unclear, especially in terms of specificity and sensitivity., Methods: A search for literature was conducted in the Pubmed, Embase, and Cochrane library databases, and QUADAS 2 was used for quality assessment. Midas command in Stata 12.0 was used to analyze the subject indicators. Cochran's Q and I2were to test for heterogeneity, and the significant heterogeneity was set at p < 0.05 and/or I2> 50%. Spearman correlation analysis was used to evaluate the threshold effect, and the publication bias was assessed using the asymmetry test. The statistical significance was set at p < 0.05., Results: As results, 10 sets of data from 7 studies were included for analysis, showing high methodological quality and minimal confounding bias. The sensitivity and specificity of NT-proBNP in the diagnosis of cardiac involvement for patients with amyloidosis were 0.93 and 0.84, respectively. ROC curves also suggested a high diagnostic validity of NT-proBNP with an AUC of 0.95. A Fagan's nomogram plot showed probabilities for NT-proBNP positive and negative in developing CA involvement were 90% and 8%, respectively. The Deek's funnel plot suggested no significant publication bias across included studies, and the results were stable and reliable., Conclusions: NT-proBNP plays the positive role in the early diagnosis of CA involvement with high sensitivity and specificity.

Introduction and Objectives: Thrombosis is involved in the onset and progression of ST-segment elevation myocardial infarction (STEMI). The aim of this study was to explore the expression level of serum- and glucocorticoid-inducible kinase 1 (SGK1) in intracoronary thrombus and the relationship between them., Methods: We identified 30 patients who received treatment in the Affiliated Hospital of Hangzhou Normal University between May 2018 to May 2020 and who underwent thrombus aspiration and percutaneous coronary intervention for ST-segment-elevation myocardial infarction. Additionally, we selected 30 patients with normal coronary angiography for the control group. We analyzed thrombus protein expression profiling by combining tandem mass tag labeling, high-performance liquid chromatography fractionation and mass spectrometry quantification approach., Results: The differentially regulated protein profiles revealed the alteration of serine-threonine/tyrosine-protein kinase, which was upregulated significantly in the experimental group. We selected SGK1 downstream factor for validation and found that the expression of SGK1 in the thrombus of STEMI was significantly increased. Immunohistochemistry (IHC) showed significantly increased expression of SGK1 in the thrombus of STEMI patients compared with the control group (17.21±2.36 vs. 4.14±1.17%, p<0.05). Similar findings were observed in the Western blot analysis (p<0.05). IHC showed that SGK1 expressed in a region similar to that of the platelets., Conclusion: This is the first quantitative proteomics study to assess thrombus in patients with STEMI. The expression of SGK1 in thrombus was significantly higher in patients with acute STEMI than in the control group. SGK1 might be involved in the platelet physiological process., (Copyright © 2022. Publicado por Elsevier España, S.L.U.)

Background: Cardiovascular disease is the major cause of death worldwide. Hypoxia-mediated apoptosis in cardiomyocytes is a major cause of cardiovascular disorders. Treatment with vascular endothelial growth factor (VEGF) protein has been tested but operational difficulties have limited its use. However, with the advancements of gene therapy, interest has risen in VEGF-based gene therapy in cardiovascular disorders. However, the precise mechanism by which VEGF replenishment rescues post-hypoxia damage in cardiomyocytes is not known., Objectives: To investigate the effect of post-hypoxia VEGF121 expression using neonatal rat cardiomyocytes., Methods: Cardiomyocytes isolated from neonatal rats were used to establish an in vitro model of hypoxia-induced cardiac injury. The effect of VEGF overexpression, alone or in combination with small-molecule inhibitors targeting calcium channel, calcium sensitive receptors (CaSR), and calpain on cell growth and proliferation on hypoxia-induced cardiomyocyte injury were determined using an MTT assay, TUNEL staining, Annexin V/PI staining, lactate dehydrogenase and caspase activity. For statistical analysis, a value of P<0.05 was considered to be significant., Results: The effect of VEGF121 was found to be mediated by CaSR and calpain but was not dependent on calcium channels., Conclusions: Our findings, even though using an in vitro setting, lay the foundation for future validation and pre-clinical testing of VEGF-based gene therapy in cardiovascular diseases.

Background: Atrial fibrillation is the most common persistent arrhythmia, and is the main factor that leads to thromboembolism., Objective: To investigate the value of left atrial diameter combined with CHA2DS2-VASc score in predicting left atrial/left atrial appendage thrombosis in non-valvular atrial fibrillation., Methods: This is a retrospective study. 238 patients with non-valvular atrial fibrillation were selected and divided into two groups: thrombosis and non-thrombosis. CHA2DS2-VASc score was determined. P<0.05 was considered statistically significant., Results: Multivariate logistic regression analysis revealed that the history of stroke/transient ischemic attack, vascular disease, CHA2DS2-VASc score, left atrial diameter (LAD), left ventricular end-diastolic dimension (LVEDD) and left ventricular ejection fraction (LVEF) were independent risk factors for left atrial/left atrial appendage thrombosis (p<0.05). Receiver operating characteristic curve analysis revealed that the area under the curve for the CHA2DS2-VASc score in predicting left atrial/left atrial appendage thrombosis was 0.593 when the CHA2DS2-VASc score was ≥3 points, and sensitivity and specificity were 86.5% and 32.6%, respectively, while the area under the curve for LAD in predicting left atrial/left atrial appendage thrombosis was 0.786 when LAD was ≥44.17 mm, and sensitivity and specificity were 89.6% and 60.9%, respectively. Among the different CHA2DS2-VASc groups, the incidence rate of left atrial/left atrial appendage thrombosis in patients with LAD ≥44.17 mm was higher than patients with LAD <44.17 mm (p<0.05)., Conclusion: CHA2DS2-VASc score and LAD are correlated with left atrial/left atrial appendage thrombosis in non-valvular atrial fibrillation. For patients with a CHA2DS2-VASc score of 0 or 1, when LAD is ≥44.17 mm, the risk for left atrial/left atrial appendage thrombosis remained high. (Arq Bras Cardiol. 2020; [online].ahead print, PP.0-0).

Background and Objectives: The mechanisms by which local anaesthetics cause neurotoxicity are very complicated. Apoptosis and autophagy are highly coordinated mechanisms that maintain cellular homeostasis against stress. Studies have shown that autophagy activation serves as a protective mechanism in vitro. However, whether it also plays the same role in vivo is unclear. The aim of this study was to explore the role of autophagy in local anaesthetic-induced neurotoxicity and to elucidate the mechanism of neurotoxicity in an intrathecally injected rat model., Methods: Eighteen healthy adult male Sprague-Dawley rats were randomly divided into three groups. Before receiving an intrathecal injection of 1% bupivacaine, each rat received an intraperitoneal injection of vehicle or rapamycin (1 mg.kg -1 ) once a day for 3 days. The pathological changes were examined by Haematoxylin and Eosin (HE) staining. Apoptosis was analysed by TdT-mediated dUTP Nick-End Labelling (TUNEL) staining. Caspase-3, Beclin1 and LC3 expression was examined by Immunohistochemical (IHC) staining. Beclin1 and LC3 expression and the LC3-II/LC3-I ratio were detected by western blot analysis., Results: After bupivacaine was injected intrathecally, pathological damage occurred in spinal cord neurons, and the levels of apoptosis and caspase-3 increased. Enhancement of autophagy with rapamycin markedly alleviated the pathological changes and decreased the levels of apoptosis and caspase-3 while increasing the expression of LC3 and Beclin1 and the ratio of LC3-II to LC3-I., Conclusions: Enhancement of autophagy decreases caspase-3-dependent apoptosis and improves neuronal survival in vivo. Activation of autophagy may be a potential therapeutic strategy for local anaesthetic-induced neurotoxicity., (Copyright © 2020. Publicado por Elsevier Editora Ltda.)

Introduction: Hepatic ischemia-reperfusion injury is a common pathophysiological process in liver surgery. Whether Propofol can reduce myocardial ischemia-reperfusion injury induced by hepatic ischemia-reperfusion injury in rats, together with related mechanisms, still needs further studies., Objective: To investigate if propofol would protect the myocardial cells from apoptosis with hepatic ischemia-reperfusion injury., Methods: Male Sprague-Dawley rats (n=18) were randomly allocated into three groups: Sham Group (Group S, n=6), Hepatic Ischemia-reperfusion Injury Group (Group IR, n=6) and Propofol Group (Group P, n=6). Group S was only subjected to laparotomy. Group IR was attained by ischemia for 30min and reperfusion for 4h. Group P was subjected identical insult as in Group IR with the administration of propofol started 10min before ischemia with 120mg.kg -1 , following by continuous infusion at 20mg.kg -1 .h -1 . Cell apoptosis was examined by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay. Endoplasmic reticulum Ca 2+ -ATPase2 (SERCA2) and cysteine-containing aspartic acid cleaved-caspase3 (cleaved-caspase3) were assayed by western blot and Altimeter polymerase chain reaction., Results: Apoptosis rate was increased, with mRNA and protein of SERCA2 down-regulated and cleaved-caspase3 up-regulated in Group IR compared with Group S (p<0.01). Apoptosis rate was decreased, with mRNA and protein of SERCA2 up-regulated and cleaved-caspase3 down-regulated in Group P compared with Group IR (p<0.01)., Conclusions: Propofol can reduce hepatic ischemia-reperfusion injury-induced myocardial cell apoptosis, meanwhile, can up-regulate mRNA and protein of SERCA2 in rats., (Copyright © 2018 Sociedade Brasileira de Anestesiologia. Publicado por Elsevier Editora Ltda. All rights reserved.)

Background: Coronary artery disease (CAD) and osteoporosis (OP) are common diseases in postmenopausal women. In both cross-sectional and longitudinal epidemiologic studies, low bone mass has been related to increased frequency of CAD. However, available data on the relationship between bone mineral density (BMD) and severity of coronary lesions is limited., Objective: To investigate association between the BMD and severity of coronary lesions assessed by Gensini score in postmenopausal women., Methods: This study included 122 postmenopausal women who were diagnosed with CAD. These patients were divided into two groups according to the severity of coronary lesions assessed by the Gensini score - patients with mild coronary lesions (Gensini score < 25) and patients with severe coronary lesions (Gensini score ≥ 25). Femoral neck mineral density was measured with dual energy X-ray absorptiometry (DXA)., Results: The study included postmenopausal women aged 64.31 ± 4.71 years, 85 of whom (69.7%) exhibited severe coronary lesions. Participants with severe coronary lesions had a significantly higher T score than did those with mild coronary lesions at the femoral neck (p < 0.05). The mean T-score was -0.84 ± 1.01 in mild coronary lesions group, -1.42 ± 1.39 in severe coronary lesions group (p < 0.05). Multivariable logistic regression analysis showed that osteopenia-osteoporosis at the Femoral neck (odds ratio 2.73; 95% confidence interval 1.06 to 6.13) was associated with an increased risk of developing severe coronary lesions. The multiple regression model showed that T-scores (b = -0.407, SE = 0.151, p=0.007) were the independent predictors of Gensini score., Conclusion: The relationship between severity of coronary lesions and BMD was significant in postmenopausal women. BMD, a low-cost technique involving minimal radiation exposure, widely used for osteoporosis screening, is a promising marker of severity of coronary lesions.

Background: Melatonin is a neuroendocrine hormone synthesized primarily by the pineal gland that is indicated to effectively prevent myocardial reperfusion injury. It is unclear whether melatonin protects cardiac function from reperfusion injury by modulating intracellular calcium homeostasis., Objective: Demonstrate that melatonin protect against myocardial reperfusion injury through modulating IP3R and SERCA2a to maintain calcium homeostasis via activation of ERK1 in cardiomyocytes., Methods: In vitro experiments were performed using H9C2 cells undergoing simulative hypoxia/reoxygenation (H/R) induction. Expression level of ERK1, IP3R and SERCA2a were assessed by Western Blots. Cardiomyocytes apoptosis was detected by TUNEL. Phalloidin-staining was used to assess alteration of actin filament organization of cardiomyocytes. Fura-2 /AM was used to measure intracellular Ca2+ concentration. Performing in vivo experiments, myocardial expression of IP3R and SERCA2a were detected by immunofluorescence staining using myocardial ischemia/ reperfusion (I/R) model in rats., Results: In vitro results showed that melatonin induces ERK1 activation in cardiomyocytes against H/R which was inhibited by PD98059 (ERK1 inhibitor). The results showed melatonin inhibit apoptosis of cardiomyocytes and improve actin filament organization in cardiomyocytes against H/R, because both could be reversed by PD98059. Melatonin was showed to reduce calcium overload, further to inhibit IP3R expression and promote SERCA2a expression via ERK1 pathway in cardiomyocytes against H/R. Melatonin induced lower IP3R and higher SERCA2a expression in myocardium that were reversed by PD98059., Conclusion: melatonin-induced cardioprotection against reperfusion injury is at least partly through modulation of IP3R and SERCA2a to maintain intracellular calcium homeostasis via activation of ERK1.

Background: Hyperlipidemia, which is characterized by an elevation of lipids in the bloodstream, is a major risk factor for cardiac disease., Objectives: The present study investigated the role of fibrosis in the progression of hyperlipidemia in the mice heart, and whether mast cell activation was associated with the fibrosis process., Methods: Hyperlipidemia was produced in C57BL / 6 mice by feeding them on a high-fat diet for 8 weeks.To assess tissue fibrosis, picrosirius red staining was performed. Hematoxylin & eosin (H&E) staining was performed to identify the histopathological changes in the hearts. Immunohistochemistry was also accomplished to determine the localization of transforming growth factor (TGF)-β and α-smooth muscle actin (α-SMA). Western blotting was performed to analyze the expression of chymase, tryptase, TGF-β, α-SMA and activity of Wnt/β-catenin pathway. At the end, serum total cholesterol (TC) and triglycerides (TG) levels were measured. All the values were expressed as means ± SD, the statistical significance level adopted was 5%., Results: Hyperlipidemia mice showed significantly increased collagen deposition in the hearts compared with normal mice. In addition, H&E staining showed significant cellular degeneration. Cardiac muscle was arranged in disorder with fracture in mice of the model group. Immunohistochemistry and western blot analysis revealed that expression levels of tryptase, chymase, β-catenin, TGF-β and α-SMA were significantly increased in the hyperlipidemia mice compared with the control group., Conclusions: The results indicated that mast cell activation might induce cardiac fibrosis by tryptase and chymase in hyperlipidemia, which had a close relationship with the increased activity of TGF-β/Wnt/β-catenin pathway.

Background: Activin receptor-like kinase 7 (ALK7) is a type I receptor for the TGF-β superfamily and has recently been demonstrated to play an important role in the maintenance of metabolic homeostasis., Objective: To investigate the association of the ALK7 gene polymorphism with metabolic syndrome (MetS) and cardiovascular remodeling in MetS patients., Methods: The single nucleotide polymorphism rs13010956 in the ALK7 gene was genotyped in 351 Chinese subjects undergoing carotid and cardiac ultrasonography. The associations of the ALK7 gene polymorphism with the MetS phenotype, MetS parameters, and cardiovascular ultrasonic features were analyzed., Results: The rs13010956 polymorphism in the ALK7 gene was found to be significantly associated with the MetS phenotype in females (p < 0.05) and was also significantly associated with blood pressure in the total (p < 0.05) and female populations (p < 0.01). Further analysis revealed that rs13010956 was associated with mean intima-media thickness of the carotid arteries in females (p < 0.05). After control for body mass index, blood pressure, fasting blood glucose, and triglycerides, rs13010956 was also found to be significantly associated with left ventricular mass index in the total (p < 0.05) and female populations (p < 0.05)., Conclusion: Our findings suggested that the ALK7 gene polymorphism rs13010956 was significantly associated with MetS risk in females and may be involved in cardiovascular remodeling in MetS patients.