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With declining birthrates, family travel has considerable potential in the cruise market. This study explores the motivation for joining family cruise travel, the needs of passengers, and the three stages of cruise travel experience (the expected, experience, and recall stages). This study adopts qualitative research and an in-depth survey method for investigation. Results reveal that “new experience,” “desire for cruise travel,” “convenience,” and “generating social topics/publicity” are the motivations to join family cruise travel. The results can serve as reference in the planning process of family cruise travel.

Background: Sesamin is a major bioactive compound in sesame seeds and has various biological properties, including anti-inflammatory and anticancer activities. Here, we explored whether sesamin activates p53, which is widely inhibited in cervical cancer cells, thereby inducing p53-mediated apoptosis. Methods: Human HeLa and SiHa cervical cancer cells and normal Hs68 dermal cells were used as cell models. Cell proliferation, cell cycle distribution, and apoptosis were evaluated by the CCK-8 assay and flow cytometry using PI/Annexin V staining, respectively. Protein expression and phosphorylation were determined using western blotting. The involvement of p53 in the apoptotic cascade was assessed by a specific inhibitor. Results: Sesamin (75 and 150 μM) clearly inhibited SiHa and HeLa cell proliferation in a dose-dependent fashion, but did not affect the proliferation of Hs68 cells. Meanwhile, sesamin increased the sub-G1 phase ratio and apoptosis, up to approximately 38.5% and 37.8%, respectively. Furthermore, sesamin induced p53 phosphorylation at serine-46 and serine-15 and upregulated the levels of PUMA, Bax, and PTEN, while inhibiting AKT phosphorylation at serine-473. Inhibition of p53 by pifithrin-α significantly reduced the levels of PUMA, Bax, and PTEN but restored AKT phosphorylation in SiHa cells exposed to sesamin. Pifithrin-α also reduced apoptosis and restored the proliferation of HeLa and SiHa cells exposed to sesamin. Conclusions: These findings indicate that sesamin inhibits cervical cancer cell proliferation, and its mechanism may be attributed to the induction of p53/PTEN-mediated apoptosis. This suggests that sesamin might be useful as an adjuvant in promoting anti-cervical cancer treatments.

Objective – The increasing growth of the Thai tourism market has resulted in international tourists flooding into Thailand and providing significant economic benefits for the country’s tourism development. The purpose of this research is to examine a comprehensive model for Thai tourism. This study aims to investigate how tourists’ trust can enhance their behaviour intentions in travelling to Thailand through perceived authenticity. Methodology/Technique – The research tests a model linking trust to authenticity, and behaviour intention to current Thai tourism. Using a convenience sampling method, a sample of 453 international Asian tourists who travelled to Thailand were surveyed. Findings – The findings show that different levels of trust directly influence tourists’ behavioural intentions, trust influences perceived authenticity, perceived authenticity further affects behaviour intention, and perceived authenticity mediates the relationship between tourists’ trust and their behavioural intention. Moreover, demographic factors moderate the effects of trust on tourists’ perceived authenticity. Novelty – The present research is expected to clarify the potential research topics in the field of Thai tourism development. Type of Paper: Empirical Keywords: Tourists’ Trust; Behaviour Intention; Perceived Authenticity; Thailand. Reference to this paper should be made as follows: Ya-Ping, A; Chang; Cheng-Y; Kuo. 2019. Effects of Tourists’ Trust on Behaviour Intention in the Thai Tourism Market: Mediating Effects of Perceived Authenticity, J. Mgt. Mkt. Review 4(3) 202 – 208 https://doi.org/10.35609/jmmr.2019.4.3(5) JEL Classification: M16, M30, M39.

Objective - General well-being (GWB) is important for students’ mental wellness. This paper explores the motivations of Chinese students who study in Thailand and applies the push and pull model to explain how motivations influence life satisfaction (LS) and GWB. Methodology/Technique – 398 convenience samples from Dhurakij Pundit University were analysed. Finding - The results show that ‘personal growth’ is the most important push factor for motivation, whereas ‘the convenience to go to other cities’ is the most important pull factor for motivation. Moreover, overseas study motivations positively influence LS and GWB. Novelty - The theoretical and practical implications and study limitations are also discussed herein. Type of Paper: Empirical. Keywords: Push and Pull Theory; Life Satisfaction; General Well-being; Chinese Student; Thailand. Reference to this paper should be made as follows: Yi, C; Kuo; Yih, J; Wong. 2019. Exploring Chinese Students’ Push and Pull Motivations in Influencing Life Satisfaction and General Well-being in Thailand, Global J. Bus. Soc. Sci. Review 7 (3): 178 – 184. https://doi.org/10.35609/gjbssr.2019.7.3(2) JEL Classification: M10, M14, M19.

Background Autologous chimeric antigen receptor (CAR) T cell therapy is a promising therapeutic strategy for treating hematologic malignancies. A spectrum of serious complications caused by CAR-T cells has caught great attention. We developed a novel CAR against CD19 namely UWC19, consisting anti-CD19 single-chain variable fragment (scFv) hinged with 4-1BB and CD3z signaling domains. In this study, preclinical assessments of UWC19 were conducted to evaluate the safety and efficacy in vitro and in vivo. Methods To evaluate the binding activity of UWC19 cells to CD19, we measured the saturation degree of CAR with human CD19 molecules using flow cytometry in vitro. The antitumor efficacy of UWC19 cells was determined by in vitro cytotoxicity assay against CD19 positive cells and in vivo using a xenograft mouse model. Cross tissue reactivity of UWC19 cells was examined by co-culturing with cell lines from difference human tissues. Tumorigenicity was determined by subcutaneously injecting UWC19 in immunodeficient mice. Persistence was analyzed using quantitative PCR. Results We showed that UWC19 CAR T cells exerted highly specific binding affinity and cytotoxicity against CD19+ cells in vitro. In vivo, UWC19 CAR T cells are able to fully control disease progression in a Raji-xenografted immunodeficient mouse model. UWC19 exerted no obvious effects on the mean body mass and graft versus host disease were observed in surviving mice. We showed that UWC19 cells specifically recognized and eliminated CD19 positive cells, whereas CD19 negative cells were much less affected. No tumorigenicity of UWC19 in immunodeficient mice was observed. Conclusions UWC19 treatment effectively eliminated CD19 positive tumor cells with favorable toxicity profile. The findings suggest encouraging clinical prospects for its use in patients with CD19 positive B cell malignancies. Our study presented an alternative evaluation strategy for CAR-T cell products.

// Chun-Hsiang Lin 1, * , Hui-Han Lin 1, 2, * , Cheng-Yi Kuo 3 , Shao-Hsuan Kao 1, 4 1 Institute of Biochemistry, Microbiology and Immunology, Chung Shan Medical University, Taichung, Taiwan 2 Surgical Department Cardiovascular Division, China Medical University Hospital, Taichung, Taiwan 3 Department and Graduate Institute of Biology and Anatomy, National Defense Medical Center, Taipei, Taiwan 4 Clinical Laboratory, Chung Shan Medical University Hospital, Taichung, Taiwan * These authors contributed equally to this work Correspondence to: Shao-Hsuan Kao, email: kaosh@csmu.edu.tw Keywords: Der p 2, non-small cell lung cancer, integrin, urokinase-type plasminogen activator, urokinase-type plasminogen activator receptor Received: August 12, 2016 Accepted: December 27, 2016 Published: January 05, 2017 ABSTRACT House dust mite (HDM) allergens are one of the major causes leading to respiratory hypersensitiveness and airway remodeling. Here we hypothesized that a major HDM allergen Der p 2 could increase cell motility and invasiveness of non-small cell lung cancer (NSCLC) cells. Our results showed that low dose (1 and 3 μg/mL) recombinant Der p 2 protein (DP2) enhanced the migration and invasiveness of human NSCLC cell A549, H1299 and CL1-5, but nonsignificantly altered their growth. Further investigation revealed that integrin αV level was increased and its downstream signaling including focal adhesion kinase (FAK) and paxillin were activated in A549 cells exposed to DP2. In parallel, DP2 also activated the FAK-associated signaling effectors such as Src, phosphatidyl inositol 3-kinase (PI3K), AKT, p38 mitogen-activated protein kinase (P38), extracellular signal-regulated kinase 1/2 (ERK1/2) and c-Jun N-terminal kinase (JNK). Our findings also revealed that DP2 increased expression level of urokinase type plasminogen-activated kinase (uPA) and uPA receptor (uPAR), and subsequently enhanced the binding of uPAR to integrin αV. Moreover, the involvement of toll-like receptor 2/4 (TLR2/4)-triggered ERK1/2 activation in the increased expression of uPA and uPAR was also demonstrated. Collectively, these findings indicate that DP2 can enhance cell motility and invasiveness of NSCLC cells, attributing to TLR2/4-ERK1/2 activation, increased uPA and uPAR expression, enhanced binding of uPAR to integrin αV, and the consequent FAK signaling cascades. Thus, we suggest that DP2 may exacerbate NSCLC via promoting metastatic ability of carcinoma cell.

This study clarified the controversial travel constraints in the tourism literature and test the moderating role of cross-cultural adaptation (CCA) on the relationship between travel constraints and travel intention. In this study, 897 questionnaires were collected from Chinese students studying in Thailand. Structural equation modeling was adopted to test the proposed model, and the moderating effect of CCA was examined via multigroup analysis. Results demonstrated that interpersonal constraints positively influenced students’ travel intentions, whereas intrapersonal and structural constraints negatively affected such intentions. A significant moderating effect of CCA was also observed in the relationship between “interpersonal constraints and travel intentions” and “structural constraints and travel intentions”. Theoretical and practical implications for academics and practitioners in tourism and education management are provided.

Background: Adenine is a purine with a role in cellular respiration and protein synthesis. It is considered for its pharmacological potential. We investigated whether anti-inflammatory effect of adenine benefits on the proliferation and maturation of osteoblastic cells. Methods: Human osteoblast-like cells (MG-63) were cultured with adenine under control conditions or pre-treated with 10ng/mL of tumor necrosis factor-&alpha, (TNF-&alpha, ) followed by adenine treatment. Cell viability was examined using dimethylthiazol diphenyltetrazolium bromide (MTT) assay. Expression of cytokines and osteogenic markers were analyzed using quantitative PCR (qPCR) and ELISA. Enzyme activity of alkaline phosphatase (ALP) and collagen content were measured. Results: TNF-&alpha, exposure led to a decreased viability of osteoblastic cells. Treatment with adenine suppressed TNF-&alpha, induced elevation in IL-6 expression and nitrite oxide production in MG-63 cells. Adenine induced the osteoblast differentiation with increased transcript levels of collage and increased ALP enzyme activity. Conclusions: Adenine exerts anti-inflammatory activity in an inflammatory cell model. Adenine benefits osteoblast differentiation in normal and inflammatory experimental settings. Adenine has a potential for the use to treat inflammatory bone condition such as osteoporosis.

Adenosine 5'-monophosphate-activated protein kinase (AMPK) is a key regulator of cellular energy homeostasis and involved in modulating several important cellular mechanism including inflammation. Here we demonstrated that a novel AMPK activator, ENERGI-F704, dose-dependently activated AMPK in human umbilical vein endothelial cells (HUVECs). The pharmacological AMPK inhibitor, compound C, abolished the phosphorylation of threonine 172 residue on AMPK induced by ENERGI-F704. Importantly, ENERGI-F704 treatment did not affect HUVECs viability at the tested concentration. It was also observed that ENERGI-F704 significantly reduced the expression of inflammation cytokine, IL-6, in the high glucose cultured HUVECs during the long culture period. Furthermore, ENERGI-F704 suppressed the high glucose induced monocytotic adhesion to HUVECs. Collectively, our data demonstrated that ENERGI-F704 is of use in the application of attenuating the high glucose induced chronic inflammation in endothelial cells. 

Keywords: Adenine; Aminoimidazole carboxamide ribonucleotide; AMP-activated protein kinase; Dermal papilla; Senescence

Glucagon-like peptide-1 (GLP-1) and its analogues are reported to exert wide-ranging cardiovascular actions in preclinical and clinical studies. We thus investigated whether the GLP-1 receptor agonist, exendin-4, has inhibitory effects on LPS-stimulated inflammatory response in cardiomyoblasts.H9c2 cardiomyoblasts were exposed to LPS and treated with exendin-4. Expressions of proinflammatory mediators were assessed using quantitative real-time PCR. Nuclear localization of NF-κB was examined using immunoblotting. mRNA expression of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) production were evaluated by q PCR and NO assay. Furthermore, anti-apoptotic effect of exendin-4 in LPS-stimulated H9c2 cells was determined using qPCR and immunoblot.Exposure to LPS increased mRNA expressions of TNF-α, COX-2 and MMP-9 in H9c2 cells. It also caused increases in iNOS mRNA expression and NF-κB nuclear translocation. Exendin-4 dose-dependently downregulated mRNA levels of TNF-α, COX-2 and MMP-9 in LPS-stimulated H9c2 cells. It also reduced NF-κB nuclear translocation. Treatment with exendin-4 showed no effect on LPS-induced apoptosis in H9c2 cells.Exendin-4 exerts an effect on cardiomyoblast exposed to LPS by inhibiting mRNA expression of inflammatory mediators and suppressing NF-κB activation. These effects are consistent with some of the observed anti-inflammatory properties of exendin-4, as well as its beneficial actions on the cardiovascular system.

Non-proteolytic group 2 allergen, Der p 2 (DP2) is known as a major allergen derived from house dust mite Dermatophagoides pteronyssinus.Paracellular epithelial barrier, being composed of a number of tight junction (TJ) molecules, plays pivotal roles in resistance of pathogen invading. However, whether DP2 affects epithelial TJ molecules is unclear. Therefore, we aimed to investigate the effects of DP2 on epithelial TJ molecules, and the mechanism by which expression of junction molecules is regulated by DP2. Cell cycle and mRNA expression of TJ proteins of lung alveolar cell A549 were analyzed by RT-PCR and flow cytometry. Level of claudin-2, subcellular distribution of b-catenin and kinase activation was determined using immunoblot. Our findings revealed that DP2 had no significant influence on cell cycle distribution but affected mRNA expression of TJ molecules including claudin-2, occludin, and ZO-1 in A549 cells. Our results showed that DP2 significantly elevated level of claudin-2 and increased expression and nuclear translocation of b-catenin. Moreover, DP2 enhanced the phosphorylation of glycogen synthase kinase-3b (GSK-3b) and its potential upstream regulator Akt. The DP2-induced claudin-2 expression was also suppressed by GSK-3b inhibitor (lithium chloride) and phosphatidyl inositol 3-phosphate kinase (PI3K) inhibitor (wortamannin). Taken together, these findings showed that DP2 increased claudin-2 expression and its cell surface distribution in A549 cells, which may attribute to phosphorylation of GSK-3b and Akt and the consequent increase and nuclear translocation of b-catenin. It is suggested that presence of DP2 may alter epithelial junction by regulating expression of TJ molecules.

Ocimum gratissimum(OG) is widely used as a traditional herb for its antibacterial activity in Taiwan. Recently, antitumor effect of OG on breast cancer cell is also reported; however, the effects of OG on human pulmonary adenocarcinoma cell A549 remain unclear. Therefore, we aimed to investigate whether aqueous OG extract (OGE) affects viability of A549 cells and the signals induced by OGE in A549 cells. Cell viability assays revealed that OGE significantly and dose-dependently decreased the viability of A549 cell but not that of BEAS-2B cell. Morphological examination and DAPI staining indicated that OGE induced cell shrinkage and DNA condensation for A549 cells. Further investigation showed that OGE enhanced activation of caspase-3, caspase-9 and caspase-8 and increased protein level of Apaf-1 and Bak, but diminished the level of Bcl-2. Additionally, OGE inhibited the phosphorylation of extracellular signal-regulated kinase (ERK) yet enhanced the phosphorylation of c-Jun N-terminal kinase (JNK) and p38 MAP kinase (p38). In conclusion, our findings indicate that OGE suppressed the cell viability of A549 cells, which may result from the activation of apoptotic signaling and the inhibition of anti-apoptotic signaling, suggesting that OGE might be beneficial to lung carcinoma treatment.

Adenosine 5′-monophosphate-activated protein kinase (AMPK) is a key regulator of cellular energy homeostasis via modulating metabolism of glucose, lipid, and protein. In addition to energy modulation, AMPK has been demonstrated to associate with several important cellular events including inflammation. The results showed that ENERGI-F704 identified from bamboo shoot extract was nontoxic in concentrations up to 80 μM and dose-dependently induced phosphorylation of AMPK (Thr-172) in microglia BV2 cells. Our findings also showed that the treatment of BV2 with ENERGI-F704 ameliorated the LPS-induced elevation of IL-6 and TNF-αproduction. In addition, ENERGI-F704 reduced increased production of nitric oxide (NO) and prostaglandin E2 (PGE2) via downregulating the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2), respectively. Moreover, ENERGI-F704 decreased activated nuclear translocation and protein level of NF-κB. Inhibition of AMPK with compound C restored decreased NF-κB translocation by ENERGI-F704. In conclusion, ENERGI-F704 exerts inhibitory activity on LPS-induced inflammation through manipulating AMPK signaling and exhibits a potential therapeutic agent for neuroinflammatory disease.

Treatment of P(2-py)3 with Mo(CO)6 or M(CO)3(CH3CN)3 (M Cr, W) in CH3CN affords compounds of the type, P(2-py)3M(CO)3 (1a ,M Cr; 1b ,M Mo; 1c ,M W). Complex P(2-py)3Mo(CO)3·CH2Cl2 was structurally characterized, and its ORTEP drawing shows an almost perfect octahedral arrangement around the Mo center, and the P(2-py)3 ligand occupying the facial position of the octahedron through the coordination of three pyridyl nitrogen atoms. Substitution of CO ligands can take place when treating compounds 1b and 1c with one or two equiv. of NOBF4 in CH3NO2 solvent to afford [P(2-py)3M(CO)3 n(NO)n](BF4)n (2a ,M Mo, n1; 2b ,M W, n1; 3a ,M Mo, n 2; 3b ,M W, n 2). These singly and doubly charged cationic species have been characterized by 1 H-, 13 C-, 31 P-, 19 F-NMR and IR spectroscopy, as well as elemental analysis. The CO lability of 3a and 3b generated the 16-electron species, [P(2-py)3M(NO)2] 2 , which binds to most Lewis basic donor ligands to give complexes of the type [P(2-py)3M(L)(NO)2](BF4)2 (L nitriles, aldehydes). A single crystal of [P(2py)3M(CH3CH2CN)(NO)2](BF4)2·CH3NO2 was also isolated and structurally characterized. The crystallographic analysis indicated an octahedral arrangement about the Mo metal center. The 1 H-NMR downfield shift of the metal-coordinated crotonaldehyde in compounds 4c and 5c is used as a qualitative measurement of relative Lewis acidity, and the acid strength of [P(2-py)3M(NO)2] 2 is comparable to that of TiCl4 when M Mo and to BF3 and AlCl3 when M W. The Diels‐Alder reactions between cyclohexadienes and methyl vinyl ketone were catalyzed by 0.3 mol% of [P(2-py)3W(CO)(NO)2](BF4)2 (3b )t o afford an average 94% conversion and 83% isolated yield. © 1999 Elsevier Science S.A. All rights reserved.

The complex [P(2-py) 3 W(CO)(NO) 2 ](BF 4 ) 2 ( 1 ) is an excellent catalyst precursor for Diels-Alder reactions of 1,3-diene and α,β-unsaturated ketones and/or aldehydes with a catalyst loading as low as 0.3 mol%.

One of the long-sought `holy grails' of polymer characterization has been the simultaneous determination of polymer composition as a function of molecular weight distribution. The recent commercialization of a solvent evaporative interface between a Gel Permeation Chromatograph (GPC) and a Fourier Transform Infrared (FTIR) Spectrometer has provided one useful solution to the problem of determining polymer composition as a function of molecular weight for a range of polymers. This study will focus on the use of a solvent evaporative interface in conjunction with a GPC-viscometer chromatograph and a FTIR spectrometer in order to provide functional group information as a function of molecular weight. The solvent evaporative interface will be described and its use with a GPC-viscometer/FTIR system will be discussed in terms of operational variable and data analysis considerations. Application of the GPC-viscometer/solvent evaporative interface/FTIR system to a variety of polymer and coatings systems as a tool for product problem solving and elucidation will be presented. In addition, examples of the use of the solvent evaporative interface to elucidate compositional heterogeneity of copolymers will be illustrated. The potential use of the solvent evaporative interface in GPC/LC cross fractionation studies for very fine elucidation of polymer compositional heterogeneity will be discussed.

Cell migration plays a pivotal role in airway repair and remodeling involved in respiratory diseases such as asthma. Interleukin-6 (IL-6) and fascin-1 are involved in cell migration upon stimulation; however, the roles of IL-6 and fascin-1 in migration of airway epithelial cell remain sketchy. The present study was aimed to investigate influence of IL-6 on cell motility with emphasis on the association with fascin-1. Wound healing assay and transmigration assay were performed to examine effect of IL-6 on migration and invasiveness of human bronchial epithelial cell BEAS-2B. Level of mRNA expression was determined by RT-PCR and quantitative real-time RT-PCR (Q-PCR). Involvement of kinase and transcription factor signaling in IL-6-induced cell migration was investigated using immunoblot and specific inhibitors. IL-6 significantly augmented cell migration and invasiveness in parallel with elevated fascin-1 expression. Further investigation showed that IL-6 dose-dependently upregulated fascin-1 expression in both mRNA and protein levels. We showed that IL-6 activated Akt and inhibited glycogen synthase kinase-3β (GSK-3β), highly associating with fascin-1 mRNA expression. Additionally, IL-6-induced migration was significantly diminished by phosphatidyl inositol 3-phosphate kinase (PI3K) inhibitor (wortamannin) and β-catenin inhibitor FH535. Moreover, LiCl and SB216763, inhibitors of GSK-3β augmented cell migration as well as fascin-1 mRNA expression. Conclusively, these findings reveal that IL-6-induced migration of BEAS-2B cell may be attributed to activation of Akt, inhibition of GSK-3β, and the associated increase of β-catenin and fascin-1 expression, indicating an important role of Akt/GSK-3β signaling and β-catenin/fascin-1 in IL-6 associated airway remodeling.

This study is to investigate anti-inflammatory and anti-cachectic effect of Qing-Shu-Yi-Qi-Tang (QSYQT) in RAW 264.7 cells and Lewis lung cancer cells bearing mice. We examined the effect of QSYQT on LPS-induced inflammatory activity in a murine macrophage cell line, Raw 264.7. We evaluated cachectic parameters, such as weight loss, food intake and tumor size in tumor-bearing and non-tumor-bearing mice treated with QSYQT decoction or a normal diet. Cytokine production in cell culture and in cachectic mice was quantified by ELISA. NF-kB expression was measured using real-time polymerase chain reaction (PCR). QSYQT significantly reduced the IL-1β, IL-6 and TNF-α production in LPS-stimulated RAW 264.7 cells. Treatment of QSYQT prevented weight loss in tumor-bearing mice without affecting food intake or tumor growth. Furthermore, the level of proinflammatory cytokines, IL-1β, IL-6 and TNF-α in sera were significantly reduced in tumor-bearing mice treated with QSYQT. NF-kB expression in spleen of LLC-derived mice was decreased in the presence of QSYQT. Our results revealed that QSYQT exerts an anti-cachectic effect on LLC-induced cachectic mice. The effect is conclusively associated with modulation of IL-6 production through NF-kB. Key words: Chinese traditional medicine, cachexia, anti-inflammation, IL-6, NF-kB, palliative medicine.

Cystamine, a disulphide metabolite, has been demonstrated to ameliorate various lupus-associated tissue damages by animal models. However, effects of cystamine on apoptosis of cardiac tissue, a main cardiac damage attributing to lupus, are less obvious. Therefore, we aimed to investigate whether or not cystamine possesses anti-apoptotic effects with emphasis on LV tissue of lupus-prone mice NZB/W-F1. Cystamine treatment was performed by daily intraperitoneal administration. Morphology and apoptotic status of ventricular tissues in the treated mice were assessed by microscopy and TUNEL assay, respectively. Levels of apoptotic biomarkers were determined using immunoblot. Our results revealed that cystamine significantly attenuated the apoptosis of LV tissues in NZB/W-F1 mice, whereas the morphology of the tissues was slightly altered. In addition, cystamine reduced level of Fas and inhibited activation of caspase-8. Cystamine also increased level of Bcl-2 and phosphorylation of Bad, and decreased level of Bad and truncated Bid (tBid). Moreover, level of cytosolic cytochrome c and Apaf-1, and activation of caspase-9 and caspase-3 were suppressed in response to cystamine treatment. In Balb/c mice, as normal control mice, changes in cell morphology and levels of the tested apoptotic components were found insignificant in the LV tissues. These findings indicate that cystamine treatment attenuates apoptosis of LV tissues of NZB/W-F1 mice through suppressing both intrinsic and extrinsic apoptotic pathways. Therefore, cystamine is considered beneficial to alleviating lupus-associated cardiac damages.

The AMP-activated protein kinase (AMPK) signaling system plays a key role in cellular stress by repressing the inflammatory responses induced by the nuclear factor-kappa B (NF-κB) system. Previous studies suggest that the anti-inflammatory role of AMPK involves activation by adenine, but the mechanism that allows adenine to produce these effects has not yet been elucidated. In human umbilical vein endothelial cells (HUVECs), adenine was observed to induce the phosphorylation of AMPK in both a time- and dose-dependent manner as well as its downstream target acetyl Co-A carboxylase (ACC). Adenine also attenuated NF-κB targeting of gene expression in a dose-dependent manner and decreased monocyte adhesion to HUVECs following tumor necrosis factor (TNF-α) treatment. The short hairpin RNA (shRNA) against AMPK α1 in HUVECs attenuated the adenine-induced inhibition of NF-κB activation in response to TNF-α, thereby suggesting that the anti-inflammatory role of adenine is mediated by AMPK. Following the knockdown of adenosyl phosphoribosyl transferase (APRT) in HUVECs, adenine supplementation failed to induce the phosphorylation of AMPK and ACC. Similarly, the expression of a shRNA against APRT nullified the anti-inflammatory effects of adenine in HUVECs. These results suggested that the role of adenine as an AMPK activator is related to catabolism by APRT, which increases the cellular AMP levels to activate AMPK.

Providing VCR-like functions in distributed environments is not trivial, especially for multi-stream multimedia presentations, which may contain continuous media, e.g., audio and video, and static media, e.g., text and image. In this paper we: point out the main problems in interactive multimedia communications; propose some concepts to solve the problems; identify the control architecture for processing user interactions; and propose the synchronization control scheme accordingly.