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In the previous studies, circular RNA (circRNA) has been shown to be closely related to the occurrence and development of various cancers. However, the role and mechanism of circ-ATIC in the progression of esophageal squamous cell carcinoma (ESCC) is not yet clear. Quantitative real-time PCR was used to detect the expression levels of circ-ATIC, microRNA (miR)-326 and inhibitor of DNA binding 1 (ID1) in tissues (n = 50) and cells. Cell counting kit 8 assay, colony formation assay, flow cytometry, wound-healing assay and transwell assay were performed to measure the proliferation, apoptosis, migration, and invasion of cells. In addition, the oxidative stress of cells was evaluated by detecting the productions of superoxide dismutase and malondialdehyde. Animal studies were implied to explore the role of circ-ATIC in ESCC tumor growth. The relationship between circ-ATIC and miR-326 or ID1 was determined by dual-luciferase reporter assay and RNA immunoprecipitation assay. Additionally, the protein expression of ID1 was examined by western blot assay. Circ-ATIC was found to be upregulated in ESCC tissues and cells. Silenced circ-ATIC suppressed the proliferation, migration, invasion, promoted the apoptosis and oxidative stress of ESCC cells. The tumor growth of ESCC also was inhibited by circ-ATIC knockdown. Furthermore, we found that circ-ATIC could sponge miR-326, and miR-326 could target ID1. The rescue experiments revealed that miR-326 inhibitor could reverse the negative regulation of circ-ATIC silencing on ESCC progression, and ID1 overexpression also inverted the inhibitory effect of miR-326 on ESCC progression. In addition, we confirmed that the expression of ID1 was positively regulated by circ-ATIC. Our study showed that circ-ATIC facilitated the progression of ESCC by regulating the miR-326/ID1 axis, indicating that circ-ATIC might be a target for ESCC treatment.

Background: Multiple rib fractures can lead to flail chest with up to 35% mortality rate due to severe pulmonary complications. Current treatments of flail chest remain controversial. Studies have shown that surgical treatments can improve outcomes and reduce mortality, comparing to non-operative treatments. Current surgical fixation methods focus on stabilization of ribs on the outward facing side, and they require division of intercostal muscles. Damages to surrounding nerves and vessels may lead to chronic pain. This study tests a novel interior fixation method that minimizes neurovascular injuries. Methods: Twelve healthy canines were divided in two surgical operation groups for exterior and interior fixation using titanium metal plates. Osteotomy with oblique fractures was prepared under general anesthesia. Exterior fixation was performed in open surgery. Interior fixation was minimally invasive using custom made tools including a flexible shaft extension screwdriver, solid plate stand, guiding wire loop and metal plates with threaded holes. Results: Respiratory and cardiovascular functions (RR, PO2, PCO2, SpO2, and HR) together with body temperature were measured before anesthesia and within 48 hours after surgery. The difference in measurements was not statistically significant between the two groups before surgery with P values greater than 0.05. However, the interior group canines had better RR and PO2 values starting from the 24th hour, and better PCO2, SpO2, and HR values starting from the 48th hour. It took longer operation time to complete the minimally invasive interior fixation surgery (P value less than 0.001), but the total blood loss was less than the exterior fixation group (P value less than 0.001). Results also showed that interior group canines suffered less pain, and they had quicker recovery in gastrointestinal and physical mobility. Conclusions: The investigative interior fixation method was safe and effective in rib stabilization on a canine rib fracture model, comparing to the exterior fixation method. The interior fixation was minimally invasive, with less damages to tissues and nerves surrounding the ribs, leading to better postoperative outcomes.

Aim: Demonstrate the function of dysregulated miR-365a-5p–PELI3 signaling axis in the generation of gefitinib resistance during treatment for non-small-cell lung cancer (NSCLC). Patients & methods: All the NSCLC patients who participated in this research were recruited from the Second Hospital of Hebei Medical University. PC9 cells and PC9GR cells were cultured for in vitro experiments. Results: Patients who were primary resistant to EGFR-tyrosine kinase inhibitor had lower miR-365a-5p levels. MiR-365a-5p directly targeted PELI3 mRNA. MiR-365a-5p overexpression enhanced the function of gefitinib in inhibiting cell viability. Tumor growth was suppressed through miR-365a-5p in nude mice. Conclusion: Dysregulated miR-365a-5p–PELI3 signaling axis triggered the generation of gefitinib resistance in NSCLC.

In this study, we set out to characterize the expression status of long non-coding RNA (lncRNA) Myocardial Infarction Associated Transcript (MIAT) in non-small cell lung cancer (NSCLC) and elucidate its mechanistic contribution to this disease. Relative expression levels of MIAT, Pellino E3 Ubiquitin Protein Ligase Family Member 3 (PELI3), and microRNA (miR)-128-3p were analyzed by real-time polymerase chain reaction. PELI3 protein level was determined by immunoblotting. Cell viability and proliferation were evaluated by the MTT assay and colony formation assay, respectively. Cell invasion and migration were assessed by wound-healing closure and transwell assays, respectively. The regulatory actions of miR-128-3p on both MIAT and PELI3 were interrogated by luciferase reporter assay. We demonstrated the aberrant upregulation of MIAT in NSCLC and its association with tumor progression. We further uncovered the negative correlation among MIAT, PELI3, and miR-128-3p. MIAT deficiency significantly compromised cell viability, proliferation, invasion, and migration, while increased miR-128-3p and decreased PELI3 expressions. Application of miR-128-3p inhibitor significantly stimulated luciferase activities driven by both MIAT and PELI3 promoter and phenotypically promoted cell viability, proliferation, migration, and invasion. Our study highlighted the mechanistic contribution of the MIAT/miR-128-3p/PELI3 signaling cascade in NSCLC.

Non-small cell lung cancer (NSCLC) is the leading cause of cancer mortality worldwide. Tyrosine kinase inhibitors (TKIs) are currently the most effective chemotherapy for NSCLC. However, most cancer patients develop TKI resistance at tumor relapse stage. We firstly measured the expression change of miR-519d-3p in TKI resistance NSCLC cells. We then ectopically expressed miR-519-3p in TKI resistant cells to study its functional impact on cell proliferation, migration, invasion and cell sensitivity to gefitinib. The downstream target of miR-519-3p was identified by bioinformatics and validated in luciferase reporter assay and western blotting analysis. We also studied the reversing effect of the candidate target in NSCLC cells expressing miR-519d-3p. Lastly, we compared the miR-519d-3p level in NSCLC patients with good or poor response to gefitinib. miR-519d-3p level was downregulated in TKI resistant NSCLC cells. The restoration of miR-519d-3p in these NSCLC cells inhibited cell proliferation, invasion and migration; enhanced cell sensitivity to gefitinib. EPAS1 was identified and validated as downstream target of miR-519d-3p. Co-expressing EPAS1 antagonized the inhibitory effect of miR-519d-3p on NSCLC cells. MiR-519d-3p was downregulated in NSCLC patients with poor response to gefitinib. Targeting miR-519d-3p/EPAS1 axis may provide alternative treatment for TKI-resistant NSCLC.

Non-small-cell lung cancer (NSCLC) is a major cause of cancer-related death globally. Endothelial PAS domain-containing protein 1 (EPAS1) is a homolog of the hypoxia-inducible factor 1α and has been reported to confer tyrosine kinase inhibitor (TKI) resistance in NSCLC, but its role in peritoneal carcinomatosis of NSCLC is unknown. PC14HM, a high metastatic potential subline of NSCLC cell line PC14, was derived. Stable shRNA knockdown of EPAS1 was then established in PC14HM cells and subjected to assessment regarding the effects on proliferation and viability, xenograft tumor growth, metastatic potential, mesothelial–mesenchymal transition (MMT)-related characteristics and peritoneal carcinomatosis in a mouse model. EPAS1 expression was elevated in PC14HM cells. Knockdown of EPAS1 inhibited the proliferation and viability of PC14HM cells in vitro and suppressed tumorigenesis in vivo. In addition, the metastatic features and in vitro productions of MMT-inducing factors in PC14HM cells was also associated with EPAS1. More importantly, knockdown of EPAS1 drastically suppressed peritoneal carcinomatosis of PC14HM cells in vivo. EPAS1 promotes peritoneal carcinomatosis of NSCLC through enhancement of MMT and could therefore serve as a prognostic marker or a therapeutic target in treating NSCLC, particularly in patients with peritoneal carcinomatosis.

The satellite-borne Moderate Resolution Imaging Spectroradiometer (MODIS) aerosol optical depth (AOD) is widely used to estimate ground-level fine ambient particulate matter (PM2.5) concentrations to evaluate their health effects. The associated estimation accuracy is often reduced by AOD missing values and by insufficiently accounting for the spatio-temporal PM2.5 variations. In this study, we aim to estimate ground-level PM2.5 concentrations at a fine resolution with improved accuracy by fusing fine-scale satellite and ground observations in the populated and polluted Beijing-Tianjin-Hebei (BTH) area of China in 2014. We employed a Bayesian-based statistical downscaler to model the spatio-temporal linear AOD-PM2.5 relationships. We used a 3km MODIS AOD product, which was resampled to a 4km resolution in a Lambert conic conformal projection, to assist comparison and fusion with predictions by atmospheric chemistry models. A two-step method was used to fill the missing AOD values to obtain a full AOD dataset with complete spatial coverage. The downscaler has a good performance in the fitting procedure (R2=0.75) and in the cross validation procedure (R2=0.58 by random method and R2=0.47 by city-specific method). The number of missing AOD values was serious and related to elevated PM2.5 concentrations. The gap-filled AOD values corresponded well with our understanding of PM2.5 pollution conditions in BTH. The prediction accuracy of PM2.5 concentrations were improved in terms of their annual and seasonal mean. As a result of its fine spatio-temporal resolution and complete spatial coverage, the daily PM2.5 estimation dataset could provide extensive and insightful benefits to related studies in the BTH area. This may include understanding the formation processes of regional PM2.5 pollution episodes, evaluating daily human exposure, and establishing pollution controlling measures.

Empirical regression models for next-day forecasting of PM 2.5 and O 3 air pollution concentrations have been developed and evaluated for three large Chinese cities, Beijing, Nanjing and Guangzhou. The forecast models are empirical nonlinear regression models designed for use in an automated data retrieval and forecasting platform. The PM 2.5 model includes an upwind air quality variable, PM24, to account for regional transport of PM 2.5 , and a persistence variable (previous day PM 2.5 concentration). The models were evaluated in the hindcast mode with a two-year air quality and meteorological data set using a leave-one-month-out cross validation method, and in the forecast mode with a one-year air quality and forecasted weather dataset that included forecasted air trajectories. The PM 2.5 models performed well in the hindcast mode, with coefficient of determination (R 2 ) values of 0.54, 0.65 and 0.64, and normalized mean error (NME) values of 0.40, 0.26 and 0.23 respectively, for the three cities. The O 3 models also performed well in the hindcast mode, with R 2 values of 0.75, 0.55 and 0.73, and NME values of 0.29, 0.26 and 0.24 in the three cities. The O 3 models performed better in summertime than in winter in Beijing and Guangzhou, and captured the O 3 variations well all the year round in Nanjing. The overall forecast performance of the PM 2.5 and O 3 models during the test year varied from fair to good, depending on location. The forecasts were somewhat degraded compared with hindcasts from the same year, depending on the accuracy of the forecasted meteorological input data. For the O 3 models, the model forecast accuracy was strongly dependent on the maximum temperature forecasts. For the critical forecasts, involving air quality standard exceedences, the PM 2.5 model forecasts were fair to good, and the O 3 model forecasts were poor to fair.

In recent years, the quality of urban atmospheric environment in China has caused widespread concern in the whole society. Improving air quality has become a major content of air pollution prevention and control in China. To do a good job in atmospheric prevention and control, we must investigate and analyze the sources of major atmospheric pollutants and their pollution characteristics firstly. With the acceleration of urbanization, the air pollution situation in Jinan city has become an environmental problem that people are particularly worried about. Based on the monitoring data of Jinan atmospheric environment, this paper analyzed the monthly average concentration values of PM2.5, PM10, NO2 and SO2 in Jinan City from 2015 to 2017. Meanwhile, the main reasons for the air pollution in Jinan City were clarified in detail. Finally, air pollution control strategies were proposed corresponding the aspects of pollution sources, topography and meteorological conditions, rational planning, environmental supervision capabilities, environmental awareness, and practical treatment technologies in Jinan City. These measures can provide a theoretical basis for relevant leading departments to build a beautiful city.

The accuracy in estimated fine particulate matter concentrations (PM2.5), obtained by fusing of station-based measurements and satellite-based aerosol optical depth (AOD), is often reduced without accounting for the spatial and temporal variations in PM2.5 and missing AOD observations. In this study, a city-specific linear regression model was first developed to fill in missing AOD data. A novel interpolation-based variable, PM2.5 spatial interpolator (PMSI2.5), was also introduced to account for the spatial dependence in PM2.5 across grid cells. A Bayesian hierarchical model was then developed to estimate spatiotemporal relationships between AOD and PM2.5. These methods were evaluated through a city-specific 10-fold cross-validation procedure in a case study in North China in 2014. The cross validation R(2) was 0.61 when PMSI2.5 was included and 0.48 when PMSI2.5 was excluded. The gap-filled AOD values also effectively improved predicted PM2.5 concentrations with an R(2) = 0.78. Daily ground-level PM2.5 concentration fields at a 12 km resolution were predicted with complete spatial and temporal coverage. This study also indicates that model prediction performance should be assessed by accounting for monitor clustering due to the potential misinterpretation of model accuracy in spatial prediction when validation monitors are randomly selected.

Particulate matter with an aerodynamic diameter of 2.5 μm or less (PM2.5) is the main air pollutant in Beijing. To have a comprehensive understanding of concentrations, compositions and sources of PM2.5 in Beijing, recent studies reporting ground-based observations and source apportionment results dated from 2000 to 2012 in this typical large city of China are reviewed. Statistical methods were also used to better enable data comparison. During the last decade, annual average concentrations of PM2.5 have decreased and seasonal mean concentrations declined through autumn and winter. Generally, winter is the most polluted season and summer is the least polluted one. Seasonal variance of PM2.5 levels decreased. For diurnal variance, PM2.5 generally increases at night and decreases during the day. On average, organic matters, sulfate, nitrate and ammonium are the major compositions of PM2.5 in Beijing. Fractions of organic matters increased from 2000 to 2004, and decreased afterwards. Fractions of sulfate, nitrate and ammonium decreased in winter and remained largely unchanged in summer. Concentrations of organic carbon and elemental carbon were always higher in winter than in summer and they barely changed during the last decade. Concentrations of sulfate, nitrate and ammonium exhibited significant increasing trend in summer but in reverse in winter. On average they were higher in winter than in summer before 2005, and took a reverse after 2005. Receptor model results show that vehicle, dust, industry, biomass burning, coal combustion and secondary products were major sources and they all increased except coal combustions and secondary products. The growth was decided both changing social and economic activities in Beijing, and most likely growing emissions in neighboring Hebei province. Explicit descriptions of the spatial variations of PM2.5 concentration, better methods to estimate secondary products and ensemble source apportionments models to reduce uncertainties would remain being open questions for future studies.

Background: Long noncoding RNAs (lncRNAs) are a new class of cancer regulators. Here, we aimed to investigate the diagnostic and therapeutic values of an lncRNA, differentiation antagonizing noncoding RNA (DANCR), in lung cancer. Methods: Real-time polymerase chain reaction was used to compare DANCR levels in normal and cancerous lung tissues as well as lung cancer cells. Lentiviral transduction was used to induce DANCR overexpression or silencing in vitro, followed by monitoring cell proliferation, colony formation, and changes in microRNA-216a (miR-216a) expression. DANCR-specific small hairpin RNA transduction was used to establish cells with stable DANCR knockdown, and silenced cells were used to initiate lung tumor xenografts, followed by monitoring tumor growth. Results: DANCR upregulation was seen in lung cancer, particularly in high-grade lung cancer tissues and aggressive cancer cells. Ectopic DANCR expression induced lung cancer cell proliferation and colony formation, whereas DANCR silencing induced opposing effects. The miR-216a level in cancer cells was negatively correlated with DANCR expression. The DANCR knockdown reduced the growth of tumor xenografts in vivo. Conclusion: DANCR upregulation is a potential indicator of aggressive lung cancer. Silencing of DANCR has great potential as a potent therapeutic strategy in lung cancer.

Particulate matter with an aerodynamic diameter of 2.5 micrometers or less (PM2.5) is a primary pollutant in most cities in China. PM2.5 poses a significant human health risk, especially in the most densely populated urban areas. We used observations of PM2.5 and backward air mass trajectories modeled by HYSPLIT-4. We characterize how air movement patterns influence pollution levels in four large cities of China. Then we developed a method to evaluate regional and local sources and contributions of PM2.5. For Beijing and Shanghai, PM2.5 concentrations are sensitive to air moving direction, indicating significant influence of air movement on PM2.5 pollution. In Beijing, PM2.5 concentrations were higher when the air masses were from the south and the east. In Shanghai, pollution was greater with northerly air mass flows. Regional contributions of PM2.5 in Beijing during 2013 were 46, 62, 52, and 39% in spring, summer, autumn and winter, respectively. In Shanghai, regional contributions over four seasons were 36, 39, 45, and 35%. In Guangzhou and Chengdu, PM2.5 concentrations were more sensitive to speed rather than direction of air mass movements, indicating weaker pollution pathways. In Guangzhou, regional contributions were smaller over the four seasons: 15, 28, 16, and 22% while in Chengdu, they are 21, 52, 28, and 14%. These results are comparable to previous results obtained using complex atmospheric chemical transport models.

Determining water flux as well as emission and uptake rates of various greenhouse gases, including ${\bf CO}_{\bf 2}$ , ${\bf CH}_{\bf 4}$ , and ${\bf N}_{\bf 2}{\bf O}$ , is one of the key research issues when performing agricultural and ecological research in relation to global change. There are four important and desired functions for the community to effectively collaborate with each other when performing studies in this area: metadata description, data interchange speciation, relational database, and online analysis. Since these four are still not fully available among the flux data networks, the design goal of FluxDataONE is to demonstrate an integrated solution for the management, visualization, and analysis of flux data when fulfilling large-scale collaborative agricultural and ecological studies. The major components of FluxDataONE are metadata description standard dedicated for flux data, flux data interchange specification, a relational database-based flux data storage solution, a versatile way to integrate analysis function modules, and finally an integrated research environment for flux data discovery, visualization, and analysis. This paper introduces the system design, the recent progress, and a research use case. FluxDataONE is promising in improving the research efficiency, enabling large-scale collaborative research, and accelerating the scientific insights for the agricultural and ecology communities.

Oesophageal cancer (OC) is one of the most fatal malignancies in the world, and chemoresistance restricts the therapeutic outcome of OC. Long noncoding RNA (lncRNA) was reported to play roles in multiple cancer types. Yet, the function of lncRNA in chemoresistance of OC has not been reported. A lncRNA gene, PCAT-1, showed higher expression in OC tissues, especially higher in secondary OC compared with normal mucosa tissues. Overexpression of PCAT-1 increased the proliferation rate and growth of OC cells. Inhibition of PCAT-1 decreased proliferation and growth of OC cells, and increased cisplatin chemosensitivity. In a mouse OC xenograft model, PCAT-1 inhibition repressed OC growth in vivo. Therefore, PCAT-1 may potentially serve as a therapeutic target for treating OC. PCAT-1 promotes development of OC and represses the chemoresistance of OC to cisplatin, and silencing of PCAT-1 may be a therapeutic strategy for treating OC.

Long-term air quality observations are seldom analyzed from a dynamic view. This study analyzed fine particulate matter (PM2.5) pollution processes using long-term PM2.5 observations in three Chinese cities. Pollution processes were defined as linearly growing PM2.5 concentrations following the criteria of coefficient of determination R2 > 0.8 and duration time T ≥ 18 hrs. The linear slopes quantitatively measured pollution levels by PM2.5 concentrations rising rates (PMRR, μg/(m3·hr)). The 741, 210 and 193 pollution processes were filtered out, respectively, in Beijing (BJ), Shanghai (SH), and Guangzhou (GZ). Then the relationships between PMRR and wind speed, wind direction, 24-hr backward points, gaseous pollutants (CO, NO2 and SO2) concentrations, and regional PM2.5 levels were studied. Inverse relationships existed between PMRR and wind speed. The wind directions and 24-hr backward points converged in specific directions indicating long-range transport. Gaseous pollutants concentrations increased at variable rates in the three cities with growing PMRR values. PM2.5 levels at the upwind regions of BJ and SH increased at high PMRRs. Regional transport dominated the PM2.5 pollution processes of SH. In BJ, both local contributions and regional transport increased during high-PMRR pollution processes. In GZ, PM2.5 pollution processes were mainly caused by local emissions.

Long-term air quality observations are seldom analyzed from a dynamic view. This study analyzed fine particulate matter (PM2.5) pollution processes using long-term PM2.5 observations in three Chinese cities. Pollution processes were defined as linearly growing PM2.5 concentrations following the criteria of coefficient of determination R2 > 0.8 and duration time T ≥ 18 hrs. The linear slopes quantitatively measured pollution levels by PM2.5 concentrations rising rates (PMRR, μg/(m3·hr)). The 741, 210 and 193 pollution processes were filtered out, respectively, in Beijing (BJ), Shanghai (SH), and Guangzhou (GZ). Then the relationships between PMRR and wind speed, wind direction, 24-hr backward points, gaseous pollutants (CO, NO2 and SO2) concentrations, and regional PM2.5 levels were studied. Inverse relationships existed between PMRR and wind speed. The wind directions and 24-hr backward points converged in specific directions indicating long-range transport. Gaseous pollutants concentrations increased at variable rates in the three cities with growing PMRR values. PM2.5 levels at the upwind regions of BJ and SH increased at high PMRRs. Regional transport dominated the PM2.5 pollution processes of SH. In BJ, both local contributions and regional transport increased during high-PMRR pollution processes. In GZ, PM2.5 pollution processes were mainly caused by local emissions.

Lung cancer is one of the most malignant cancers with a high metastatic potential. The purpose of this study was to study the role and the underlying mechanism of miR-214 in lung cancer progression. The expression of miR-214 in normal lung and lung cancer tissue was analyzed by quantitative real-time PCR analysis. Furthermore, H1299 cells were infected with miR-214 lentivirus, and the effect of infection on cell viability and migration was analyzed. Carboxypeptidase-D (CPD), as a potential target of miR-214, was characterized in either normal lung or lung cancer tissues. The interaction of CPD expression with the tumor suppressing effect of miR-214 was characterized. We demonstrated that low miR-214 expression is a hallmark of lung cancer, especially high-grade and metastatic cancer. In vitro studies in H1299 cells confirmed that low miR-214 expression is associated with enhanced proliferation and migratory abilities. Similarly, CPD overexpression coincides with high-grade lung cancer and the CPD overexpression could reverse the inhibitory effects of miR-214. miR-214 is a tumor suppressor in lung cancer. miR-214 inhibits lung cancer progression by targeting CPD. The miR-214-CPD axis may be a therapeutic axis for lung cancer patients.

The satellite-borne Moderate Resolution Imaging Spectroradiometer (MODIS) aerosol optical depth (AOD) is widely used to estimate ground-level fine ambient particulate matter (PM

Estimating exposures to PM2.5 within urban areas requires surface PM2.5 concentrations at high temporal and spatial resolutions. We developed a mixed effects model to derive daily estimations of surface PM2.5 levels in Beijing, using the 3 km resolution satellite aerosol optical depth (AOD) calibrated daily by the newly available high-density surface measurements. The mixed effects model accounts for daily variations of AOD-PM2.5 relationships and shows good performance in model predictions (R(2) of 0.81-0.83) and cross-validations (R(2) of 0.75-0.79). Satellite derived population-weighted mean PM2.5 for Beijing was 51.2 μg/m(3) over the study period (Mar 2013 to Apr 2014), 46% higher than China's annual-mean PM2.5 standard of 35 μg/m(3). We estimated that more than 19.2 million people (98% of Beijing's population) are exposed to harmful level of long-term PM2.5 pollution. During 25% of the days with model data, the population-weighted mean PM2.5 exceeded China's daily PM2.5 standard of 75 μg/m(3). Predicted high-resolution daily PM2.5 maps are useful to identify pollution "hot spots" and estimate short- and long-term exposure. We further demonstrated that a good calibration of the satellite data requires a relatively large number of ground-level PM2.5 monitoring sites and more are still needed in Beijing.

Lung cancer, especially non-small cell lung cancer (NSCLC), is the major cause of cancer death worldwide. Mutations in epidermal growth factor receptor (EGFR) and hepatocyte growth factor receptor (c-Met), both of which are receptor tyrosine kinases, have been identified in a considerable percentage of NSCLC patients. EGFR and c-Met share the same downstream pathways and cooperate not only in promoting metastasis but also in conferring resistance to tyrosine kinase inhibitor (TKI) therapies in NSCLC. MicroRNAs (miRNAs) are a family of small non-coding RNAs, usually 21-25 nucleotides long, and are critical in regulating gene expression. Abnormal miRNA expression has been implicated in the initiation and progression in many forms of cancers, including lung cancer. In this study, we found that miR-200a is downregulated in NSCLC cells, where it directly targets the 3′-UTR of both EGFR and c-Met mRNA. Overexpression of miR-200a in NSCLC cells significantly downregulates both EGFR and c-Met levels and severely inhibits cell migration and invasion. Moreover, in NSCLC cell lines that are resistant to gefitinib, a drug often used in TKI therapies to treat NSCLC, miR-200a expression is able to render the cells much more sensitive to the drug treatment.

Eddy covariance flux data measures carbon dioxide and water vapor fluxes within the atmosphere boundary layer. Large volume of flux data has been accumulated, shared and exchanged within the ecological research communities. However, a standardized way of describing the characteristics of the flux data, and the data processing procedures is still missing. This problem prevents the flux data from being well utilized beyond the ecological communities, being easily understood by the researchers from other fields, and being integrated with the research data accumulated in other domains. This research presents a metadata architecture for eddy covariance flux data based on ISO 19115: Geographic information - Metadata standard. The content and structure of the proposed metadata are illustrated in UML (unified modelling language). A XML schema implementation of the metadata standard is also presented. Finally, an application case study of utilizing this metadata proposal for the US-China Carbon Consortium group is introduced and discussed.