Myeloid-derived suppressor cells alleviate adverse ventricular remodeling after acute myocardial infarction.

The fundamental pathophysiological mechanism in the progression of chronic heart failure following acute myocardial infarction (AMI) is ventricular remodeling, in which innate and adaptive immunity both play critical roles. Myeloid-derived suppressor cells (MDSCs) have been demonstrated to function in a range of pathological conditions, such as infections, inflammation, autoimmune diseases, and tumors. However, it is unclear how MDSCs contribute to cardiac remodeling following AMI. This study aimed to identify the function and underlying mechanism of MDSCs in controlling cardiac remodeling following AMI. Following AMI in mice, MDSCs frequencies changed dynamically, considerably increased on day 7 in blood, spleens, lymph nodes and hearts, and decreased afterwards. Consistently, mice with AMI displayed enhanced cardiac function on day 14 post-AMI, reduced infract size and higher survival rates on day 28 post-AMI following the adoptive transfer of MDSCs. Furthermore, MDSCs inhibited the inflammatory response by decreasing pro-inflammatory cytokine (TNF-α, IL-17, Cxcl-1, and Cxcl-2) expression, up-regulating anti-inflammatory cytokine (TGF-ß1, IL-10, IL-4, and IL-13) expression, reducing CD3+ T cell infiltration in the infarcted heart and enhancing M2 macrophage polarization. Mechanistically, MDSCs improved the release of anti-inflammatory factors (TGF-ß1 and IL-10) and decreased the injury of LPS-induced cardiomyocytes in vitro in a manner dependent on cell-cell contact. Importantly, blockade of IL-10 partially abolished the cardioprotective role of MDSCs. This study found that MDSCs contributed to the restoration of cardiac function and alleviation of adverse cardiac remodeling after AMI possibly by inhibiting inflammation.

Protective effects of methyl protodioscin against lipid disorders and liver injury in hyperlipidemic gerbils.

Methyl protodioscin (MPD) is the main component of total diosgenin, which was reported to reduce cholesterol and triglyceride levels potentially. This study aimed to investigate the beneficial effects of MPD against lipid disorder in hyperlipidemic gerbils induced by a high-fat diet (HFD). Hyperlipidemia was induced in gerbils by feeding them with HFD for six weeks, and a daily oral dose of MPD solution (25 and 50 mg/kg/day) was administered. This study investigated blood lipid levels and hepatic lipid accumulation in hyperlipidemic gerbils. The potential mechanism of MPD was explored by detecting the expression level of genes, including SREBPs, ACC, FASN, HMGCR, PCSK9, and LDL-R. The results showed that MPD treatment decreased the body weight, the relative weight of the liver, blood lipid, and hepatic lipid levels of gerbils fed with HFD. The administration of MPD alleviates liver steatosis and injury in gerbils fed with an HFD. MPD treatment reduced the expression of HMGCR, increased the expression of LDL-R, and decreased the expression of PCSK9 for cholesterol reduction. Additionally, MPD treatment reduced the expression of hepatic ACC and FASN for triglycerides reduction. The underlying mechanisms for these effects are attributed to MPD-induced inhibition of protein expression of LXR, SREBP1, and SREBP2. This study demonstrates that MPD protects gerbils against lipid disorders and liver injury by suppressing hepatic SREBPs expression.

Long non-coding RNA BC002811 Promotes Gastric Cancer Metastasis by Regulating SOX2 Binding to the PTEN Promoter.

There is increasing evidence that long non-coding RNAs (lncRNAs) are involved in the pathogenesis and progression of gastric cancer (GC), however, the underlying mechanisms remain poorly understood. In this study, we identified lncRNA BC002811 as a critical regulator of GC development and progression. BC002811 was upregulated in GC tissues and cell lines, and that high expression of BC002811 was indicative of a reduction in overall survival of GC patients. Our research reveals that BC002811 promoted GC cell proliferation, migration, invasion, and inhibition of apoptosis in vitro, as well as accelerated tumor growth and metastasis in vivo. We also found that BC002811 upregulated MMP2 and MMP9 and promoted GC cell metastasis partially through downregulating PTEN expression. BC002811 may act as a molecular decoy for the transcription factor SOX2, thereby inhibiting the transcription of PTEN by blocking SOX2 binding to the PTEN promoter. Our study advances the understanding of the role of BC002811 in the pathogenesis of GC and provides new molecular targets for therapeutic intervention against GC metastasis.

Stratified analysis of multiple management of gastric cancer: A population-based study of incidence, mortality and DALY.

The aim was to illuminate the difference in incidence, mortality, and disability-adjusted life-years (DALYs) of gastric cancer (GC) between the United States of America (US) and China. The multiple management was analyzed with stratification to explore an effective survival improvement strategy. The Global Burden of Disease Study data was analyzed to assess GC morbidity, mortality and DALYs from 1990 to 2019 in the US and China. The age-period-cohort model was established to generate estimation of metrics. Verification was completed and stratified analysis of the multiple management was performed by accessing data of Surveillance, Epidemiology, and End Results database in 1992 to 2019. Continuous downtrends in GC incidence, mortality and DALYs from 1990 to 2019 and persistent uptrends in 1-, 3-year survival from 1992 to 2019 were observed in the US population. In the Chinese population, the overall trends of incidence, mortality and DALYs decreased with a fluctuating manner. The lower overall survival rates were observed in elderly, unmarried patients, distant disease and poor grade, as well as patients lacking of medical treatment (P < .05). In stratified analyses, single local therapy decreased and the other modalities increased over time across different stages. Moreover, combined treatment and single systemic therapy decreased, but single local and conservative therapy increased with age. The study quantified the incidence, GC-specific mortality and DALYs in the US and China and estimated stage profiles, 1- and 3-year survival in the US. The heavy burden on later-onset GC (>70) and potential increase on early-onset GC (<40) needed to be addressed. Combined modalities and single chemotherapy were becoming more widely used over time, however, their uses decreased with age because of poor physical fitness. Our findings provide new insights into management tailoring appropriately to specific subgroups contributes to the increasing survival rate.

Dihydromyricetin promotes apoptosis, suppresses proliferation and tumor necrosis factor-α-mediated nuclear factor kappa-B activation in nasopharyngeal carcinoma CNE-2 cell.

OBJECTIVE: To investigate the efficacy of dihydromyricetin (DMY) on nasopharyngeal carcinoma (NPC) cell proliferation, apoptosis and to reveal the underlying mechanism in vitro experiments. METHODS: The CNE-2 cell line was treated with different concentrations of DMY and the effects of DMY on cell viability and proliferation were evaluated using cell counting kit-8 (CCK-8) assay and plate colony formation assay. Cellular apoptosis was detected by flow cytometry following Annexin V fluorescein isothiocyanate/propidine iodide staining. Nuclei morphology was observed under a fluorescence microscope following Hoechst 333258 staining. The expression of phosphorylated inhibitor of nuclear factor kappa-B kinase subunit beta (p-IKKß), phosphorylated inhibitor of nuclear factor kappa-B kinase subunit alpha (p-IKKα), inhibitor of nuclear factor kappa-B alpha (IκB-α), nuclear factor kappa-B (NF-κB)/p65 was examined by Western blot analysis and the nuclear translocation of NF-κB/p65 was observed using a confocal laser scanning microscopy. RESULTS: DMY inhibited the proliferative capability and colony formation of NPC CNE-2 cells. Meanwhile, DMY induced apoptosis of CNE-2 cells in a dose and time-dependent manner via upregulating B-cell lymphoma-2 associated X, but downregulating B-cell lymphoma-2 and pro-caspase-3. Importantly, we found that DMY suppressed tumor necrosis factor alpha (TNF-α)-mediated NF-κB activation via inhibiting p-IKKß, p-IKKα and blocking NF-κB subunit p65. CONCLUSION: Our experiments demonstrated that DMY had significant antiproliferative and apoptosisinducing effects on CNE-2 cells. Additionally, DMY promoted inactivation of p-IKKß, p-IKKα, and blocked the nuclear translocation of NF-κB subunit p65. These results suggest that DMY may be an important therapeutic approach for NPC.

Integrated analysis of microRNA and transcription factors in the bone marrow of patients with acute monocytic leukemia.

Acutemonocytic leukemia (AMoL) is a distinct subtype of acute myeloid leukemia (AML) with poor prognosis. However, the molecular mechanisms and key regulators involved in the global regulation of gene expression levels in AMoL are poorly understood. In order to elucidate the role of microRNAs (miRNAs/miRs) and transcription factors (TFs) in AMoL pathogenesis at the network level, miRNA and TF expression level profiles were systematically analyzed by miRNA sequencing and TF array, respectively; this identified 285 differentially expressed miRNAs and 139 differentially expressed TFs in AMoL samples compared with controls. By combining expression level profile data and bioinformatics tools available for predicting TF and miRNA targets, a comprehensive AMoL-specific miRNA-TF-mediated regulatory network was constructed. A total of 26 miRNAs and 23 TFs were identified as hub nodes in the network. Among these hubs, miR-29b-3p, MYC, TP53 and NFKB1 were determined to be potential AMoL regulators, and were subsequently extracted to construct sub-networks. A hypothetical pathway model was also proposed for miR-29b-3p to reveal the potential co-regulatory mechanisms of miR-29b-3p, MYC, TP53 and NFKB1 in AMoL. The present study provided an effective approach to discover critical regulators via a comprehensive regulatory network in AMoL, in addition to enhancing understanding of the pathogenesis of this disease at the molecular level.

Dolichosin A, a coumestan isolated from Glycine tabacina, inhibits IL-1ß-induced inflammation in SW982 human synovial cells and suppresses RANKL-induced osteoclastogenesis: From network pharmacology to experimental pharmacology.

ETHNOPHARMACOLOGICAL RELEVANCE: Glycine tabacina (Labill.) Benth has been used as a traditional Chinese herbal medicine for the treatment of rheumatoid arthritis (RA) and joint infection. It is also one of the sources of the renowned native herbal medicine 'I-Tiao-Gung' in Taiwan. AIM OF THE STUDY: This study aimed to investigate anti-arthritic effects and underlying mechanisms of dolichosin A (DoA), a coumestan compound isolated from G. tabacina, by the integration of network pharmacology and experimental pharmacology. MATERIALS AND METHODS: Putative therapeutic targets and potential pharmacological mechanisms of DoA for RA treatment were predicted by network pharmacology approach. The regulated network of DoA acting on RA was constructed using Cytoscape 3.7.1. Anti-arthritic effects of DoA and predicted mechanisms were further validated using IL-1ß-induced SW982 human synovial cell model and RANKL-induced osteoclastogenesis model. RESULTS: A regulatory network of DoA-targets-pathways-RA was successfully constructed using network pharmacology approach. In this network, 65 candidate targets of DoA related to its therapeutic effect on RA were identified and the functional enrichment analysis revealed that these candidate targets were significantly involved in 12 central signaling pathways such as PI3K/AKT pathway, MAPK pathway and osteoclast differentiation. Furthermore, we found that DoA could significantly inhibit IL-1ß-induced inflammation in SW982 human synovial cells, as evidenced by the decreased levels of pro-inflammatory mediators (TNF-α, IL-6 and COX-2) and MMP-3. DoA also suppressed RANKL-induced osteoclastogenesis in vitro, as evidenced by decreased number of TRAP-positive multinucleated osteoclasts and reduced TRAP activity. Further experimental mechanism evidence confirmed the predicted results of network pharmacology that the blockade of PI3K/AKT and MAPK pathways activation was closely associated with these regulated processes of DoA. CONCLUSIONS: Our results demonstrated that DoA exhibited strong anti-arthritic activity through suppressing PI3K/AKT and MAPK pathways activation in activated synovial cells and osteoclasts, suggesting its potential as a hopeful candidate for the development of novel agents for the prevention and treatment of RA.

Evaluation of an innovative mobile health programme for the self-management of chronic obstructive pulmonary disease (MH-COPD): protocol of a randomised controlled trial.

INTRODUCTION: Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death globally. In outpatient care, the self-management of COPD is essential, but patient adherence to this remains suboptimal. The objective of this study is to examine whether an innovative mobile health (mHealth)-enabled care programme (MH-COPD) will improve the patient self-management and relevant health outcomes. METHODS AND ANALYSIS: A prospective open randomised controlled trial has been designed. In the trial, patients with COPD will be recruited from The Prince Charles Hospital, Brisbane, Australia. They will then be randomised to participate in either the MH-COPD intervention group (n=50 patients), or usual care control group (UC-COPD) (n=50 patients) for 6 months. The MH-COPD programme has been designed to integrate an mHealth system within a clinical COPD care service. In the programme, participants will use a mHealth application at home to review educational videos, monitor COPD symptoms, use an electronic action plan, modify the risk factors of cigarette smoking and regular physical activity, and learn to use inhalers optimally. All participants will be assessed at baseline, 3 months and 6 months. The primary outcomes will be COPD symptoms and quality of life. The secondary outcomes will be patient adherence, physical activity, smoking cessation, use of COPD medicines, frequency of COPD exacerbations and hospital readmissions, and user experience of the mobile app. ETHICS AND DISSEMINATION: The clinical trial has been approved by The Prince Charles Hospital Human Research Ethics Committee (HREC/16/QPCH/252). The recruitment and follow-up of the trial will be from January 2019 to December 2020. The study outcomes will be disseminated according to the Consolidated Standards of Reporting Trials statement through a journal publication, approximately 6 months after finishing data collection. TRIAL REGISTRATION NUMBER: ACTRN12618001091291.

Adenylyl cyclase 1 as a major isoform to generate cAMP signaling for apoA-1-mediated cholesterol efflux pathway.

HDL apoA-1-mediated cholesterol efflux pathway requires multiple cellular proteins and signal transduction processes, including adenylyl cyclase (AC)/cAMP signaling. Due to the existence of multiple transmembrane AC isoforms, it was not known how many AC isoforms are expressed and which ones are essential for cholesterol efflux in macrophage foam cells. These questions were investigated in THP-1 macrophages in this study. Quantitative RT-PCR detected mRNAs for all nine transmembrane AC isoforms, but only the mRNA and protein of the AC1 isoform were consistently upregulated by cholesterol loading and apoA-1. AC1 shRNA interference decreased AC1 mRNA and protein levels, resulting in reduction of apoA-1-mediated cAMP production and cholesterol efflux, while the intracellular cholesterol levels remained high. Confocal microscopy showed that apoA-1 promoted translocation of cholesterol and formation of cholesterol-apoA-1 complexes (protrusions) on the cholesterol-loaded macrophage surface. AC1 shRNA-interfered macrophages showed no translocation of cholesterol to the cell surface. AC1 shRNA interference also disrupted cellular localization of the intracellular cholesterol indicator protein adipophillin, and the expression as well as surface translocation of ABCA1. Together, our results show that AC1 is a major isoform for apoA-1-activated cAMP signaling to promote cholesterol transport and exocytosis to the surface of THP-1 macrophage foam cells.

[Application of vascular repair and reconstruction in surgical treatment of superior vena cava syndrome caused by thoracic tumor].

Objective: To summarize the clinical experience of vascular repair and reconstruction for treating superior vena cava syndrome (SVCS) caused by thoracic tumor. Methods: Between October 2008 and June 2016, 26 patients with thoracic tumor and SVCS were admitted. There were 18 males and 8 females, aged from 27 to 70 years (mean, 45.9 years). Tumor was typed as B1-B3 thymoma in 13 cases, thymic carcinoma in 6 cases, large B-cell lymphoma in 3 cases, T lymphocytic lymphoma in 1 case, malignant teratoma in 1 case, right lung squamous cell carcinoma in 1 case, and carcinoid in 1 case. The tumor diameter ranged from 8 to 15 cm with an average of 10 cm. The patients had different degrees of neck, face, and upper extremity edema, jugular vein distention, and chest wall collateral venous filling. The superior vena cava pressure was 2.45-5.39 kPa. After excision of tumor and invading superior vena cava, 7 patients underwent superior vena cava reconstruction and 19 patients underwent artificial vascular replacement. Results: There was no perioperative death, and the symptoms of superior vena cava obstruction were eliminated. Postoperative pulmonary infection, respiratory muscle weakness, and right chylothorax occurred in 4 cases, 1 case, and 1 case respectively. Twenty-four patients were followed up 2-92 months (mean, 37 months), and 2 patients failed to be followed up. At 1, 3, and 5 years, the survival rate was 83.3% (20/24), 41.7% (10/24), and 25% (6/24), respectively. In 6 patients with 5-year survival, there were 1 case of type B1 thymoma, 3 cases of type B3 thymoma, and 2 cases of large B-cell lymphoma. Conclusion: For preoperative evaluation of SVCS caused by resectable thoracic tumors, vascular repair and recons-truction technique can be used to quickly and effectively relieve the clinical symptoms and improve the quality of life.

Galangin Induces Autophagy via Deacetylation of LC3 by SIRT1 in HepG2 Cells.

Galangin suppresses proliferation and induces apoptosis and autophagy in hepatocellular carcinoma (HCC) cells, but the precise mechanism is not clear. In this study, we demonstrated that galangin induced autophagy, enhanced the binding of SIRT1-LC3 and reduced the acetylation of endogenous LC3 in HepG2 cells. But this autophagy was inhibited by inactivation of SIRT1 meanwhile, galangin failed to reduce the acetylation of endogenous LC3 after SIRT1 was knocked-down. Collectively, these findings demonstrate a new mechanism by which galangin induces autophagy via the deacetylation of endogenous LC3 by SIRT1.

ß-COP as a Component of Transport Vesicles for HDL Apolipoprotein-Mediated Cholesterol Exocytosis.

OBJECTIVE: HDL and its apolipoproteins protect against atherosclerotic disease partly by removing excess cholesterol from macrophage foam cells. But the underlying mechanisms of cholesterol clearance are still not well defined. We investigated roles of vesicle trafficking of coatomer ß-COP in delivering cholesterol to the cell surface during apoA-1 and apoE-mediated lipid efflux from fibroblasts and THP-1 macrophages. METHODS: shRNA knockout, confocal and electron microscopy and biochemical analysis were used to investigate the roles of ß-COP in apolipoprotein-mediated cholesterol efflux in fibroblasts and THP-1 macrophages. RESULTS: We showed that ß-COP knockdown by lentiviral shRNA resulted in reduced apoA-1-mediated cholesterol efflux, while increased cholesterol accumulation and formation of larger vesicles were observed in THP-1 macrophages by laser scanning confocal microscopy. Immunogold electron microscopy showed that ß-COP appeared on the membrane protrusion complexes and colocalized with apoA-1 or apoE during cholesterol efflux. This was associated with releasing heterogeneous sizes of small particles into the culture media of THP-1 macrophage. Western blotting also showed that apoA-1 promotes ß-COP translocation to the cell membrane and secretion into culture media, in which a total of 17 proteins were identified by proteomics. Moreover, ß-COP exclusively associated with human plasma HDL fractions. CONCLUSION: ApoA-1 and apoE promoted transport vesicles consisting of ß-COP and other candidate proteins to exocytose cholesterol, forming the protrusion complexes on cell surface, which were then released from the cell membrane as small particles to media.

Methyl protodioscin increases ABCA1 expression and cholesterol efflux while inhibiting gene expressions for synthesis of cholesterol and triglycerides by suppressing SREBP transcription and microRNA 33a/b levels.

Sterol regulatory element-binding proteins (SREBPs) regulate homeostasis of LDL, HDL and triglycerides. This study was aimed to determine if inhibition of SREBPs by methyl protodioscin (MPD) regulates downstream gene and protein expressions of lipid metabolisms. In THP-1 macrophages, MPD increases levels of ABCA1 mRNA and protein in dose- and time-dependent manners, and apoA-1-mediated cholesterol efflux. The underlying mechanisms for the effects is that MPD inhibits the transcription of SREBP1c and SREBP2, and decreases levels of microRNA 33a/b hosted in the introns of SREBPs, which leads to reciprocally increase ABCA1 levels. In HepG2 cells, MPD shows the same effects as these observed in THP-1 macrophages. MPD also decreases the gene expressions of HMGCR, FAS and ACC for cholesterol and fatty acid synthesis. MPD further promotes LDL receptor through reducing the PCSK9 level. Collectively, the study demonstrates that MPD potentially increase HDL cholesterol while reducing LDL cholesterol and triglycerides.

Galangin suppresses HepG2 cell proliferation by activating the TGF-ß receptor/Smad pathway.

Galangin can suppress hepatocellular carcinoma (HCC) cell proliferation. In this study, we demonstrated that galangin induced autophagy by activating the transforming growth factor (TGF)-ß receptor/Smad pathway and increased TGF-ß receptor I (RI), TGF-ßRII, Smad1, Smad2, Smad3 and Smad4 levels but decreased Smad6 and Smad7 levels. Autophagy induced by galangin appears to depend on the TGF-ß receptor/Smad signalling pathway because the down-regulation of Smad4 by siRNA or inhibition of TGF-ß receptor activation by LY2109761 blocked galangin-induced autophagy. The down-regulation of Beclin1, autophagy-related gene (ATG) 16L, ATG12 and ATG3 restored HepG2 cell proliferation and prevented galangin-induced apoptosis. Our findings indicate a novel mechanism for galangin-induced autophagy via activation of the TGF-ß receptor/Smad pathway. The induction of autophagy thus reflects the anti-proliferation effect of galangin on HCC cells.

Effectiveness of a web- and mobile phone-based intervention to promote physical activity and healthy eating in middle-aged males: randomized controlled trial of the ManUp study.

BACKGROUND: The high number of adult males engaging in low levels of physical activity and poor dietary practices, and the health risks posed by these behaviors, necessitate broad-reaching intervention strategies. Information technology (IT)-based (Web and mobile phone) interventions can be accessed by large numbers of people, yet there are few reported IT-based interventions targeting males' physical activity and dietary practices. OBJECTIVE: This study examines the effectiveness of a 9-month IT-based intervention (ManUp) to improve the physical activity, dietary behaviors, and health literacy in middle-aged males compared to a print-based intervention. METHODS: Participants, recruited offline (eg, newspaper ads), were randomized into either an IT-based or print-based intervention arm on a 2:1 basis in favor of the fully automated IT-based arm. Participants were adult males aged 35-54 years living in 2 regional cities in Queensland, Australia, who could access the Internet, owned a mobile phone, and were able to increase their activity level. The intervention, ManUp, was based on social cognitive and self-regulation theories and specifically designed to target males. Educational materials were provided and self-monitoring of physical activity and nutrition behaviors was promoted. Intervention content was the same in both intervention arms; only the delivery mode differed. Content could be accessed throughout the 9-month study period. Participants' physical activity, dietary behaviors, and health literacy were measured using online surveys at baseline, 3 months, and 9 months. RESULTS: A total of 301 participants completed baseline assessments, 205 in the IT-based arm and 96 in the print-based arm. A total of 124 participants completed all 3 assessments. There were no significant between-group differences in physical activity and dietary behaviors (P≥.05). Participants reported an increased number of minutes and sessions of physical activity at 3 months (exp(ß)=1.45, 95% CI 1.09-1.95; exp(ß)=1.61, 95% CI 1.17-2.22) and 9 months (exp(ß)=1.55, 95% CI 1.14-2.10; exp(ß)=1.51, 95% CI 1.15-2.00). Overall dietary behaviors improved at 3 months (exp(ß)=1.07, 95% CI 1.03-1.11) and 9 months (exp(ß)=1.10, 95% CI 1.05-1.13). The proportion of participants in both groups eating higher-fiber bread and low-fat milk increased at 3 months (exp(ß)=2.25, 95% CI 1.29-3.92; exp(ß)=1.65, 95% CI 1.07-2.55). Participants in the IT-based arm were less likely to report that 30 minutes of physical activity per day improves health (exp(ß)=0.48, 95% CI 0.26-0.90) and more likely to report that vigorous intensity physical activity 3 times per week is essential (exp(ß)=1.70, 95% CI 1.02-2.82). The average number of log-ins to the IT platform at 3 and 9 months was 6.99 (SE 0.86) and 9.22 (SE 1.47), respectively. The average number of self-monitoring entries at 3 and 9 months was 16.69 (SE 2.38) and 22.51 (SE 3.79), respectively. CONCLUSIONS: The ManUp intervention was effective in improving physical activity and dietary behaviors in middle-aged males with no significant differences between IT- and print-based delivery modes. TRIAL REGISTRATION: Australian New Zealand Clinical Trials Registry: ACTRN12611000081910; https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?ACTRN=12611000081910 (Archived by WebCite at http://www.webcitation.org/6QHIWad63).

Berberine hydrochloride impact on physiological processes and modulation of twist levels in nasopharyngeal carcinoma CNE-1 cells.

OBJECTIVE: The main purpose of this work was to investigate the effect of berberine hydrochloride (BH) on the proliferation, apoptosis, migration, and invasion of CNE-1 nasopharyngeal carcinoma cells. Our results shed light on the functional components of traditional Chinese herbs for potential use in modern medicine. METHODS: The CNE-1 cell line was treated with different concentrations of BH and effects on cell viability and proliferation were evaluated using the Cell Counting Kit-8 (CCK-8) assay. Anti-migratory and anti-invasive actions of BH were investigated using wound healing assays and the Millicell Hanging cell culture insert system, respectively. Expression of the epithelial-mesenchymal transition (EMT)-related gene twist (Twist) was analyzed by real-time PCR and Western blotting. Apoptosis was estimated with an annexin-V fluorescein (FITC) apoptosis detection kit, as well as with reference to levels of activated caspase-3 of CNE-1 cells before and after treatment with BH utilizing fluorescence spectroscopy. RESULTS: BH was capable of reducing proliferation and viability of CNE-1 cells in a dose- and time-dependent manner, also demonstrating anti-migratory and anti-invasive capacities which correlated with reduction in expression of Twist. Finally, BH was able to induce significant amounts of apoptosis in CNE-1 cells, as demonstrated by an increase in the activity of caspase-3 and in annexin-V staining following treatment. CONCLUSION: BH extracted from rhizoma coptidis demonstrated an ability to block proliferation, induce apoptosis, and impair the migration and invasion of the CNE-1 cell line Considering these properties, our results suggest that BH could be an important compound for consideration in the treatment of nasopharyngeal carcinoma.

Pumping through porous hydrophobic/oleophilic materials: an alternative technology for oil spill remediation.

Recently, porous hydrophobic/oleophilic materials (PHOMs) have been shown to be the most promising candidates for cleaning up oil spills; however, due to their limited absorption capacity, a large quantity of PHOMs would be consumed in oil spill remediation, causing serious economic problems. In addition, the complicated and time-consuming process of oil recovery from these sorbents is also an obstacle to their practical application. To solve the above problems, we apply external pumping on PHOMs to realize the continuous collection of oil spills in situ from the water surface with high speed and efficiency. Based on this novel design, oil/water separation and oil collection can be simultaneously achieved in the remediation of oil spills, and the oil sorption capacity is no longer limited to the volume and weight of the sorption material. This novel external pumping technique may bring PHOMs a step closer to practical application in oil spill remediation.

Examining participant engagement in an information technology-based physical activity and nutrition intervention for men: the manup randomized controlled trial.

BACKGROUND: Males experience a shorter life expectancy and higher rates of chronic diseases compared to their female counterparts. To improve health outcomes among males, interventions specifically developed for males that target their health behaviors are needed. Information technology (IT)-based interventions may be a promising intervention approach in this population group, however, little is known about how to maximize engagement and retention in Web-based programs. OBJECTIVE: The current study sought to explore attributes hypothesized to influence user engagement among a subsample of participants from the ManUp study, a randomized controlled trial testing the efficacy of an interactive Web-based intervention for promoting physical activity and nutrition among middle-aged males. METHODS: Semistructured interviews were conducted and audiotaped with 20 of the ManUp participants. Interview questions were based on a conceptual model of engagement and centered on why participants took part in the study, what they liked and did not like about the intervention they received, and how they think the intervention could be improved. Interview recordings were transcribed and coded into themes. RESULTS: There were five themes that were identified in the study. These themes were: (1) users' motives, (2) users' desired outcomes, (3) users' positive experiences, (4) users' negative emotions, and (5) attributes desired by user. CONCLUSIONS: There is little research in the field that has explored user experiences in human-computer interactions and how such experiences may relate to engagement, especially among males. Although not conclusive, the current study provides some insight into what personal attributes of middle-aged males (such as their key motives and goals for participating) and attributes of the intervention materials (such as usability, control, and interactivity) may impact on user engagement in this group. These findings will be helpful for informing the design and implementation of future health behavior interventions for males. TRIAL REGISTRATION: Australian New Zealand Clinical Trials Registry: ACTRN12611000081910; https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?ACTRN=12611000081910 (Archived by WebCite at http://www.webcitation.org/6M4lBlvCA).

Effectiveness of a website and mobile phone based physical activity and nutrition intervention for middle-aged males: trial protocol and baseline findings of the ManUp Study.

BACKGROUND: Compared to females, males experience higher rates of chronic disease and mortality, yet few health promotion initiatives are specifically aimed at men. Therefore, the aim of the ManUp Study is to examine the effectiveness of an IT-based intervention to increase the physical activity and nutrition behaviour and literacy in middle-aged males (aged 35-54 years). METHOD/DESIGN: The study design was a two-arm randomised controlled trial, having an IT-based (applying website and mobile phones) and a print-based intervention arm, to deliver intervention materials and to promote self-monitoring of physical activity and nutrition behaviours. Participants (n = 317) were randomised on a 2:1 ratio in favour of the IT-based intervention arm. Both intervention arms completed assessments at baseline, 3, and 9 months. All participants completed self-report assessments of physical activity, sitting time, nutrition behaviours, physical activity and nutrition literacy, perceived health status and socio-demographic characteristics. A randomly selected sub-sample in the IT-based (n = 61) and print-based (n = 30) intervention arms completed objective measures of height, weight, waist circumference, and physical activity as measured by accelerometer (Actigraph GT3X). The average age of participants in the IT-based and print-based intervention arm was 44.2 and 43.8 years respectively. The majority of participants were employed in professional occupations (IT-based 57.6%, Print-based 54.2%) and were overweight or obese (IT-based 90.8%, Print-based 87.3%). At baseline a lower proportion of participants in the IT-based (70.2%) group agreed that 30 minutes of physical activity each day is enough to improve health compared to the print-based (82.3%) group (p = .026). The IT-based group consumed a significantly lower number of serves of red meat in the previous week, compared to the print-based group (p = .017). No other significant between-group differences were observed at baseline. DISCUSSION: The ManUp Study will examine the effectiveness of an IT-based approach to improve physical activity and nutrition behaviour and literacy. Study outcomes will provide much needed information on the efficacy of this approach in middle aged males, which is important due to the large proportions of males at risk, and the potential reach of IT-based interventions. TRIAL REGISTRATION: ACTRN12611000081910.

[Study on the effect and its mechanisms of genistein on the cell cycle of highly metastatic ovarian carcinoma HO-8910PM cells].

OBJECTIVE: To study the effect and its possible mechanism of genistein on the cell cycle of human highly metastatic ovarian carcinoma HO-8910PM cells. METHODS: Trypan blue stain assay was used to examine the effect of genistein on proliferation of HO-8910PM cells after 24 hours treatment. The cell cycle was assessed by flowcytometry (FCM). The expression level of NF-kappaB (p65) and the level of VEGF were assessed by Western blot analysis. RESULTS: Genistein could inhibit the proliferation of HO-8910PM cell and block the cell cycle at G1 phase. The expession level of NF-kappaB (P65) protein decreased obviously in HO-8910PM cells treated with 25 approximately 100 micromol/L genistein for 24 hours, and the effect appeared in the experssion of VEGF. CONCLUSION: The effect on cell cycle of genistein is involved in the decreasing expression of NF kappaB (p65) and the level of VEGF.