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We aimed to explore the correlation between blood lipids (high density lipoprotein cholesterol [HDL-C] and apolipoprotein A1 [ApoA1]) and epidermal growth factor receptor (EGFR) T790M mutation, as well as its predictive role in clinical efficacy and progression-free survial (PFS) in advanced non-small cell lung cancer (NSCLC) patients treated with EGFR tyrosine kinase inhibitors (EGFR-TKI).We retrospectively collected information of 153 patients with advanced NSCLC harboring exon EGFR mutation and receiving EGFR-TKI.The best cutoff value for HDL-C and ApoA1 was determined to be 1.15 and 1.14 mmol/l. The overall response rate (ORR) was 67.7% in the high HDL-C group and 46.6% in the low HDL-C group, respectively. The ORR of the high ApoA1 group showed a significant increase than that of the low ApoA1 group (68.1% vs. 38.5%). The mean ApoA1 level of the EGFR T790M mutation-positive group was significantly higher than that of the EGFR T790M mutation-negative group (1.13 g/l vs. 1.01 g/l). Patients with high ApoA1 levels were related to the EGFR T790M mutation (r = 0.324). (3) The median progression-free survival (PFS) of the high HDL-C group and low HDL-C group were 13.00 months and 10.20 months. The median PFS of the high ApoA1 group and the low ApoA1 group were 12.10 and 10.00 months, respectively. Multivariate Cox stepwise regression model analysis demonstrated ECOG PS, pathological type and HDL-C were confirmed as critical and independent predictors of PFS.Patients with EGFR T790M mutations often show higher ApoA1 levels. Peripheral serum HDL-C and ApoA1 before treatment can be used as potential significant factors for predicting clinical efficacy and PFS in advanced NSCLC patients treated with EGFR-TKI.

Previously, we identified differentially expressed proteins, including ADFP, between lung adenocarcinoma (LAC) tissue and paired normal bronchioloalveolar epithelium. In this study, we investigated the role of ADFP in LAC. ADFP levels in the serum of patients with lung cancer and benign diseases were measured by enzyme‐linked immunosorbent assays (ELISA). shRNA was used to knock‐down or overexpress ADFP in A549 and NCI‐H1299 cells. The biological function of ADFP and its underlying mechanisms was evaluated in vivo and in vitro. ADFP was highly expressed in the serum of lung cancer patients, especially those with LAC. ADFP promoted cell proliferation and up‐regulated the p‐Akt/Akt ratio in A549 and NCI‐H1299 cells in vitro. Furthermore, in nude mice, ADFP promoted tumour formation with high levels of p‐Akt/Akt, Ki67 and proliferating cell nuclear antigen (PCNA). Similar to the effect of ADFP knock‐down, MK‐2206 (a phosphorylation inhibitor of Akt) reduced A549 and NCI‐H1299 cell proliferation. In ADFP‐overexpressing A549 and NCI‐H1299 cells, proliferation was suppressed by MK‐2206 and returned to the control level. ADFP did not regulate invasion, migration or adhesion in LAC cells. Together, these results suggest that ADFP promotes LAC cell proliferation in vitro and in vivo by increasing Akt phosphorylation level.

This study aimed to investigate the role of DEAD-box helicase 47 (DDX47) in lung adenocarcinoma (LUAD). Our results demonstrated that DDX47 was highly expressed in LUAD tissues, and its high expression predicted a poor prognosis. Bioinformatics analysis indicated that DDX47 involved RNA processing and cell division. Furthermore, knockdown of DDX47 reduced cell proliferation and migration in vitro. In sum, our data confirmed the cancer-promoting effect of DDX47.

Lung adenocarcinoma (LUAD) is a major subtype of non-small cell lung cancer. Despite significant progress in its diagnosis and treatment, the mortality and morbidity rate of LUAD remains high worldwide. The aim of the present study was to perform a systematic investigation of the tumor microenvironment (TME) and identify TME-related genes of prognostic value in patients with LUAD. Firstly, the immune scores and stromal scores of patients with LUAD from The Cancer Genome Atlas were calculated using the Estimation of STromal and Immune cells in MAlignant Tumors using Expression data algorithm, and a total of 281 prognostic TME-related genes were identified. Subsequently, functional analysis and protein-protein interaction network analysis revealed that these genes were mainly related to immune response, inflammatory response and chemotaxis. Finally, two independent LUAD cohorts from the Gene Expression Omnibus database were used to validate these genes, and 4 genes (GTPase IMAP family member 1, T-cell surface glycoprotein CD1b, integrin alpha-L and leukocyte surface antigen CD53) were identified, and downregulation of these genes was indicated to be associated with poor overall survival rate in patients with LUAD. In conclusion, a comprehensive analysis of TME was performed and 4 prognostic TME-related genes in patients with LUAD were identified.

Aims: This study aimed to explore the validation and the diagnostic value of multiple right ventricle (RV) volumes and functional parameters parameters derived from a novel artificial intelligence (AI)-based three-dimensional echocardiography (3DE) algorithm compared to cardiac magnetic resonance (CMR). Methods and Results: 51 patients with a broad spectrum of clinical diagnoses were finally included in this study. AI-based RV 3DE was performed in a single-beat HeartModel mode within 24 hours after CMR. Whether in the entire population or the patients with moderate and poor image quality, RV volumes and right ventricular ejection fraction (RVEF) measured by AI-based 3DE showed a statistically significant correlation with the corresponding CMR analysis (P

Background: Previous studies suggested that myocardial work (MW) may identify abnormalities in the left ventricular (LV) function and establish a more sensitive index for LV dysfunction at the early stage. This study aimed to explore the value of global and regional MW parameters in predicting high-risk stable coronary artery disease (SCAD) patients with normal wall motion and preserved LV function.Patients and Methods: A total of 131 patients, who were clinically diagnosed as SCAD with normal wall motion and LV function, were finally included in this study. Global MW parameters, including global work index (GWI), global constructive work (GCW), global waste work (GWW), and global work efficiency (GWE) were measured with non-invasive LV pressure-strain loops constructed from speckle-tracking echocardiography. Regional myocardial work index (RWI) and work efficiency (RWE) were also calculated according to the perfusion territory of each major coronary artery. All patients underwent coronary angiography and were divided into the high-risk SCAD group, the non-high-risk SCAD group, and the No SCAD group according to the range and degrees of coronary arteries stenosis.Results: The global longitudinal strain (GLS), GWI and GCW were statistically different (P < 0.001) among the three groups. In the high-risk SCAD group, GLS, GWI, and GCW were significantly lower than the other two groups (P < 0.05). Receiver operating characteristic analysis demonstrated GWI and GCW could predict high-risk SCAD at a cutoff value of 1,808 mm Hg% (sensitivity, 52.6%; specificity, 87.8%; predictive positive value, 76.3%; predictive negative value, 69.9%) and 2,308 mm Hg% (sensitivity, 80.7%; specificity, 64.9%; predictive positive value, 63.3%; predictive negative value, 80.0%), respectively. Multivariate analyses showed that carotid plaque, decreased GWI, and GCW was independently related to high-risk SCAD. The cutoff values of RWILAD, RWILCX, and RWIRCA were 2,156, 1,929, and 1,983 mm Hg% in predicting high-risk SCAD, respectively (P < 0.001). When we combined RWI in two or three perfusion regions, the diagnostic performance of SCAD was improved (P < 0.001).Conclusions: Both global and regional MW parameters have great potential in non-invasively predicting high-risk SCAD patients with normal wall motion and preserved LV function, contributing to the early identification of high-risk patients who may benefit from revascularization therapy.

Background: Coronavirus disease 2019 can result in myocardial injury in the acute phase. However, information on the late cardiac consequences of coronavirus disease 2019 (COVID-19) is limited.Methods: We conducted a prospective observational cohort study to investigate the late cardiac consequences of COVID-19. Standard echocardiography and myocardial strain assessment were performed, and cardiac blood biomarkers were tested in 86 COVID-19 survivors 327 days (IQR 318–337 days) after recovery. Comparisons were made with 28 age-matched and sex-matched healthy controls and 30 risk factor-matched patients.Results: There were no significant differences in all echocardiographic structural and functional parameters, including left ventricular (LV) global longitudinal strain, right ventricular (RV) longitudinal strain, LV end-diastolic volume, RV dimension, and the ratio of peak early velocity in mitral inflow to peak early diastolic velocity in the septal mitral annulus (E/e') among COVID-19 survivors, healthy controls and risk factor-matched controls. Even 26 patients with myocardial injury at admission did not have any echocardiographic structural and functional abnormalities. There were no significant differences among the three groups with respect to serum concentrations of N-terminal pro-B-type natriuretic peptide (NT-proBNP) and high-sensitivity cardiac troponin I (cTnI).Conclusion: This study showed that COVID-19 survivors, including those with myocardial injury at admission and those with severe and critical types of illness, do not have any echocardiographic evidence of cardiac structural and functional abnormalities 327 days after diagnosis.

Background Desmoglein-2 (DSG2), a desmosomal adhesion molecule, is found to be closely related to tumorigenesis in recent years. However, the clinical value of DSG2 in lung adenocarcinoma remains unclear. Methods Real-time reverse transcription-quantitative polymerase chain reaction (qRT-PCR) was utilized to detect the expression of DSG2 in 40 paired lung adenocarcinoma tissues and corresponding non-cancerous tissues. Data from The Cancer Genome Atlas (TCGA) and Oncomine datasets were also downloaded and analyzed. The correlation between DSG2 and clinicopathological features was investigated. The expression of DSG2 protein by immunohistochemical was also detected from tissue microarray and the Human Protein Atlas database. Integrated meta-analysis combining the three sources (qRT-PCR data, TCGA data and Oncomine datasets) was performed to evaluate the clinical value of DSG2. Univariate and multivariate Cox regression analyses were used to explore the prognostic value of DSG2. Then, co-expressed genes were calculated by Pearson correlation analysis. Gene Ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were used to investigate the underlying molecular mechanism. The expression level in lung adenocarcinoma and prognostic significance of the top ten co-expressed genes were searched from Gene Expression Profiling Interactive Analysis (GEPIA) online database. Results DSG2 was highly expressed in lung adenocarcinoma tissues based on qRT-PCR, TCGA and Oncomine datasets. The protein expression of DSG2 was also higher in lung adenocarcinoma. According to qRT-PCR and TCGA, high DSG2 expression was positively associated with tumor size (p = 0.027, p = 0.001), lymph node metastasis (p = 0.014, p < 0.001) and TNM stage (p = 0.023, p p = 0.001) and poor progression-free survival (HR = 1.475; 95% CI [1.102–1.974], p Conclusions The expression of DSG2 is related to the tumor size, lymph node metastasis and TNM stage. Also, DSG2 predicts poor prognosis in lung adenocarcinoma.

Platelet-endothelial interactions have been linked to increased inflammatory activation and a prothrombotic state in atherosclerosis. The interaction between von Willebrand factor (vWF)-A1 domain and platelet glycoprotein (GP) Ib/IX plays a significant role in mediating the adhesion of platelets to the injured endothelium. In the present study, contrast-enhanced ultrasound (CEU) molecular imaging with microbubbles bearing the vWF-A1 domain was performed to non-invasively monitor activated platelets on the vascular endothelium in the procession of atherosclerosis. A targeted CEU contrast agent was prepared by attaching the vWF-A1 domain to the shell of microbubbles (MbA1). Rat isotype control antibody was used to produce control (Mbctrl) microbubbles. The binding of MbA1 and Mbctrl to activated platelets was assessed in in vitro flow chamber experiments. Apolipoprotein E (ApoE-/-) deficient mice were studied as a model of atherosclerosis. At 8, 16 and 32 weeks of age, CEU molecular imaging of the proximal aorta with MbA1 and Mbctrl was performed and the imaging signals from microbubbles were quantified. Atherosclerotic lesion severity and platelets on the endothelial surface were assessed by histology and immunohistochemistry. In in vitro flow chamber studies, attachment of MbA1 to activated platelets on culture dishes was significantly greater than that of Mbctrl across a range of shear stresses (P

BACKGROUND Small cell lung cancer (SCLC) is highly aggressive and is associated with a dismal prognosis. However, there are no clinically recognized biomarkers for early diagnosis. In this study, we used quantitative proteomics to build differential mitochondrial protein profiles that may be used for early diagnosis and investigated the pathogenesis of lung cancer. METHODS We cultured SCLC cells (NCI-H446) and normal human bronchial epithelial cells (16-HBE); mitochondria were extracted and purified using differential and Percoll density gradient centrifugation. Subsequently, we used Western blot analysis to validate mitochondrial purity and labeled proteins/peptides from NCI-H446 and 16-HBE cells using relative and absolute quantification of ectopic tags. We then analyzed mixed samples and identified proteins using two-dimensional liquid chromatography-tandem mass spectrometry. Additionally, we performed subsequent bioinformatic proteome analyses using the programs ExPASy, GOA, and STRING. Finally, the relationship between ornithine aminotransferase expression and clinicopathological features in lung cancer patients was evaluated using immunohistochemistry. RESULTS One hundred and fifty-three mitochondrial proteins were differentially expressed between 16-HBE and NCI-H446 cells. The expression of 30 proteins between 16-HBE and NCI-H446 cells increased more than 1.3-fold. The upregulation of ornithine aminotransferase was associated with pathological grade and clinical tumor node metastasis stage. CONCLUSION Our experiment represented a promising method for building differential mitochondrial protein profiles between NCI-H446 and 16-HBE cells. Such analysis may also help to identify novel biomarkers of lung cancer.

OBJECTIVES Multiple types of mediastinal masses, especially masses in the anterior mediastinum, may be encountered in routine echocardiographic examinations for symptomatic or asymptomatic patients. The aim of this study was to evaluate the diagnostic value of transthoracic echocardiography combined with contrast-enhanced ultrasonography in determining the location, composition, and vascularization of mediastinal masses. METHODS A retrospective analysis was conducted on 48 consecutive patients who first had a diagnosis of mediastinal masses by echocardiography. The location of the mass, tissue components, and relationships with the heart and great vessels were analyzed on the basis of multiple transthoracic echocardiographic views. Further contrast-enhanced ultrasonography was performed to determine the vascularization of masses in 25 patients. The clinical, computed tomographic, and histopathologic findings were all recorded and analyzed. RESULTS The localization, ultrasonographic characteristics of the mass, degree of vascularization, and relationships with the heart and great vessels assessed on echocardiography allowed a correct diagnosis in most of the cases. CONCLUSIONS Transthoracic echocardiography is a useful method for diagnosing mediastinal. Further contrast-enhanced ultrasonography could provide more details on the degree of vascularization, which could facilitate accurate diagnosis and differentiation diagnosis.

An increasing number of studies have indicated that the abnormal expression of certain long non-coding RNAs (lncRNAs) is linked to the overall survival (OS) of patients with lung adenocarcinoma (LUAD). The aim of the present study was to establish an lncRNA signature to predict the survival of patients with LUAD. The gene expression profiles and associated clinical information of patients with LUAD were downloaded from The Cancer Genome Atlas database. The cohort was randomly sub-divided into training and verification cohorts. Univariate Cox regression analysis was performed on differentially expressed lncRNAs in the training cohort to select candidate lncRNAs closely associated with survival. Next, a risk score (RS) model consisting of 5 lncRNAs was established by multivariate Cox regression analysis on candidate lncRNAs. Using the median RS obtained from the training cohort as a cut-off point, patients were classified into high- and low-risk groups. Kaplan-Meier survival analysis revealed a significant difference in OS between high- and low-risk groups. The survival prediction ability of the 5-lncRNA signature was further tested in the verification and total cohorts. The results proved that the 5-lncRNA signature had good reliability and stability in survival prediction for patients with LUAD. The univariate Cox regression analysis for the 5-lncRNA signature in each cohort indicated that the 5-lncRNA signature was closely associated with survival. Multivariate Cox regression analysis and stratification analysis proved that the prognostic signature was an independent predictor of survival for patients with LUAD. In addition, functional enrichment analysis indicated that the 5 prognostic lncRNAs may be involved in the tumorigenesis of LUAD through cancer-associated pathways and biological processes. Taken together, the present study provided a 5-lncRNA signature that may serve as an independent survival predictor for patients with LUAD.

miR-367 is one of the most abundant miRNAs in human embryonic stem cells (hESCs) and is mainly involved in maintaining the pluripotency of stem cells. However, its role in cancer development remains poorly understood. In the present study, we explored the function and mechanism of the endogenous miR-367 in non-small cell lung cancer (NSCLC). In the present study, we demonstrated that the level of miR-367 in NSCLC was significantly higher than that in adjacent normal tissues, and its upregulation was positively correlated with tumor size, tumor differentiation and tumor-node-metastasis (TNM) stage. miR-367 was an indicator of a poorer prognosis in NSCLC patients. Furthermore, overexpression of miR-367 significantly inhibited apoptosis and enhanced proliferation by promoting cell cycle transition from G1 to S phase. In contrast, knockdown of miR-367 markedly reversed the cellular events observed with miR-367 overexpression. Moreover, we identified that F-box and WD repeat domain-containing 7 (FBXW7) is a novel target of miR-367. It reverses the oncogenic effects of miR-367 by downregulating its substrates, c-Myc and c-Jun, in NSCLC cells. Finally, studies in vivo revealed that knockdown of miR-367 inhibited the growth of xenografts in the nude mice by increasing the expression of FBXW7. In summary, our findings indicate that miR-367 exerts tumor-promoting effect by negatively regulating FBXW7 in NSCLC, and it could become a potential therapeutic target for NSCLC intervention.

Long non-coding RNAs (lncRNAs) have been involved in occurrence and progression of multiple cancers. In the present study, we investigated the role of lncRNA Gm15290 in the proliferation and invasion of non-small cell lung cancer (NSCLC) cells. First, we found that lncRNA Gm15290 was markedly up-regulated in tumor tissues from NSCLC patients and NSCLC cell lines, compared with adjacent normal tissues and normal lung cell line HBE respectively. Then, different concentrations of pcDNA-Gm15290 expression vector and Gm15290 siRNA were respectively transfected into A549 NSCLC cells. Our results showed that overexpression of Gm15290 significantly increased the proliferation and invasion of A549 cells and suppressed cell apoptosis. Knockdown of Gm15290 suppressed A549 cell proliferation and invasion and promoted cell apoptosis. Subsequently, we explored the underlying mechanism through which Gm15290 promoted cell proliferation and invasion. The output of RNA hybrid bioinformatic tool revealed that Gm15290 potentially interacted with tumor suppressor miR-615-5p which displayed an opposite expression pattern in the cell lines and a strong negative correlation with the levels of Gm15290 in NSCLC patients (r2 = 0.9677, P

Long non-coding RNAs (lncRNAs) have been involved in occurrence and progression of multiple cancers. In the present study, we investigated the role of lncRNA Gm15290 in the proliferation and invasion of non-small cell lung cancer (NSCLC) cells. First, we found that lncRNA Gm15290 was markedly up-regulated in tumor tissues from NSCLC patients and NSCLC cell lines, compared with adjacent normal tissues and normal lung cell line HBE respectively. Then, different concentrations of pcDNA-Gm15290 expression vector and Gm15290 siRNA were respectively transfected into A549 NSCLC cells. Our results showed that overexpression of Gm15290 significantly increased the proliferation and invasion of A549 cells and suppressed cell apoptosis. Knockdown of Gm15290 suppressed A549 cell proliferation and invasion and promoted cell apoptosis. Subsequently, we explored the underlying mechanism through which Gm15290 promoted cell proliferation and invasion. The output of RNA hybrid bioinformatic tool revealed that Gm15290 potentially interacted with tumor suppressor miR-615-5p which displayed an opposite expression pattern in the cell lines and a strong negative correlation with the levels of Gm15290 in NSCLC patients (r2 = 0.9677, P

Lung cancer is one of the most common types of malignancy worldwide. The prognosis of lung cancer is poor, due to the onset of metastases. The aim of the present study was to examine lung cancer metastasis-associated genes. To identify novel metastasis-associated targets, our previous study detected the differentially expressed mRNAs and long non-coding RNAs between the large-cell lung cancer high-metastatic 95D cell line and the low-metastatic 95C cell line by microarray assay. In the present study, these differentially expressed genes (DEGs) were analyzed via bioinformatics methods, including Gene Ontology functional analysis and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis. A protein-protein interaction network was subsequently constructed using the Search Tool for the Retrieval of Interacting Genes/Proteins online database and Cytoscape software, and 17 hub genes were screened out on the basis of connectivity degree. These hub genes were further validated in lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) using the online Gene Expression Profiling Interactive Analysis database. A total of seven hub genes were identified to be significantly differentially expressed in LUAD and LUSC. The prognostic information was detected using Kaplan-Meier plotter. As a result, five genes were revealed to be closely associated with the overall survival time of patients with lung cancer, including phosphoinositide-3-kinase regulatory subunit 1, FYN, thrombospondin 1, nonerythrocytic α-spectrin 1 and secreted phosphoprotein 1. In addition, lung cancer and adjacent lung tissue samples were used to validate these hub genes by reverse transcription-quantitative polymerase chain reaction. In conclusion, the results of the present study may provide novel metastasis-associated therapeutic strategies or potential biomarkers in non-small cell lung cancer.

Multiple types of mediastinal masses, especially masses in the anterior mediastinum, may be encountered in routine echocardiographic examinations for symptomatic or asymptomatic patients. The aim of this study was to evaluate the diagnostic value of transthoracic echocardiography combined with contrast-enhanced ultrasonography in determining the location, composition, and vascularization of mediastinal masses.A retrospective analysis was conducted on 48 consecutive patients who first had a diagnosis of mediastinal masses by echocardiography. The location of the mass, tissue components, and relationships with the heart and great vessels were analyzed on the basis of multiple transthoracic echocardiographic views. Further contrast-enhanced ultrasonography was performed to determine the vascularization of masses in 25 patients. The clinical, computed tomographic, and histopathologic findings were all recorded and analyzed.The localization, ultrasonographic characteristics of the mass, degree of vascularization, and relationships with the heart and great vessels assessed on echocardiography allowed a correct diagnosis in most of the cases.Transthoracic echocardiography is a useful method for diagnosing mediastinal. Further contrast-enhanced ultrasonography could provide more details on the degree of vascularization, which could facilitate accurate diagnosis and differentiation diagnosis.

Long non-coding RNAs (lncRNAs) have been involved in occurrence and progression of multiple cancers. In this study, weinvestigated the role of lncRNA Gm15290 in the proliferation and invasion of non-small cell lung cancer (NSCLC) cells. First, we found that lncRNA Gm15290 was markedly upregulated in tumor tissues from NSCLC patients and NSCLC cell lines, compared with adjacent normal tissues and normal lung cell line HBE respectively. Then, different concentrations of pcDNA-Gm15290 expression vector and Gm15290 siRNA were respectively transfected into A549 NSCLC cells. Our results showed that overexpression of Gm15290 significantly increased the proliferation and invasion of A549 cells, and suppressed cell apoptosis. Knockdown of Gm15290 suppressed A549 cell proliferation and invasion, and promoted cell apoptosis. Subsequently, we explored the underlying mechanism through which Gm15290 promoted cell proliferation and invasion. The output of RNAhybrid bioinformatic tool revealed that Gm15290 potentially interacted with tumor suppressor miR-615-5p which displayed an opposite expression pattern in the cell lines and a strong negative correlation with the levels of Gm15290 in NSCLC patients (r2 = 0.9677, P < 0.0001). The results of RNA pull-down assays confirmed that Gm15290 directly bound with miR-615-5p. Gm15290 negatively regulated the expression of miR-615-5p and increased the protein levels of miR-615-5p target genes, including IGF2, AKT2 and SHMT2. Moreover, miR-615-5p mimic could antagonize the promoting effect of Gm15290 on cell proliferation and invasion.

Background Growing evidence indicates that the cross-linked N-telopeptide of type I collagen (NTx) is likely to be involved in the development of bone metastasis among lung cancer patients. We perform a meta-analysis to disclose the correlation between bone metastasis and NTx and also to evaluate its value in diagnosis of bone metastasis (BM) in lung cancer. Method Electronic databases were searched and calculated the weighted mean difference (WMD) with 95% confidence interval (CI) to assess the expression difference of NTx between BM+ and BM- lung cancer patients. Moreover, we conducted a sensitivity and specificity test and drew a summary receiver operating characteristic curve (SROC) to assess the diagnostic value of NTx in discerning bone metastasis. Results A total of eleven studies with 1108 individuals were included in this analysis. The results showed an increased NTx was correlated with the incidence of lung cancer (P < 0.001). The overall sensitivity and specificity of serum NTx (sNTx) for discerning bone metastasis was 0.74 (95% CI = 0.67 to 0.79) and 0.85 (95% CI = 0.80 to 0.89), respectively. As for urine NTx (uNTx) the pooled sensitivity and specificity was 0.77(95% CI = 0.67 to 0.86) and 0.81(95% CI = 0.76 to 0.86). The area under the SROC curve was 0.8889(SE = 0.0255) and 0.8655(SE = 0.0254) for sNTx and uNTx respectively. Conclusions The elevation of NTx in lung cancer was positively related with the development and progression of bone metastasis. A higher specificity over sensitivity of NTx suggested that it is a more accurate biomarker to distinguish patients without bone metastasis. Regarding SROC curve, sNTx may be a better choice.

The high-resolution nonlinear simultaneous inversion of petrophysical parameters is based on Bayesian statistics and combines petrophysics with geostatistical a priori information. We used the fast Fourier transform-moving average (FFT-MA) and gradual deformation method (GDM) to obtain a reasonable variogram by using structural analysis and geostatistical a priori information of petrophysical parameters. Subsequently, we constructed the likelihood function according to the statistical petrophysical model. Finally, we used the Metropolis algorithm to sample the posteriori probability density and complete the inversion of the petrophysical parameters. We used the proposed method to process data from an oil field in China and found good match between inversion and real data with high-resolution. In addition, the direct inversion of petrophysical parameters avoids the error accumulation and decreases the uncertainty, and increases the computational efficiency.

In recently years, fast growing wireless communication systems have encouraged the need for dual-band, multiband and UWB antennas. These systems include Bluetooth which operates at the band 2.4 GHz and WiLAN which operates at 3.5 GHz. Using several radiating patches and reactive load to obtain dual-band or multiband usually increase the difficulty and cost of production. The resulting broadband microstrip antenna also has much a increased antenna size. The microstrip antenna which combination of gap-coupled and multilayer stacked has been proposed to make the antenna work in multiband and broadband. A gap-coupled microstrip antenna by using additional patches directly coupled to its radiating edges can enhancement the bandwidth and the size of antenna can not be increased. The patch referenced the gap-coupled of H type. By embedding slits can change the current flow of the patch and obtained new resonant point. Each layer of multilayer stacked has the same size and structure. Between of the two patches there is no media because this design can reduce weight. The multilayer stacked can obtain multi-frequency operation, and the structure of microstrip antenna is similar to the conventional microstrip antenna, it is very convenience. The proposed microstrip antenna was performed by using the simulator software Ansoft HFSS. The result shows that the microstrip antenna can work at 860MHz and 2.62 GHz and the microstrip antenna has wide bandwidth, good return loss, radiation pattern and current distribution.

RNA helicase DHX9 is a member of human RNA enzymes. Previous studies have reported that DHX9 is highly expressed in various types of malignant tumor. However, its role in the progression of lung cancer remains to be fully clarified. The present study aims to investigate the oncogenic role of DHX9 in serum, tissues and lung cancer cell lines in vitro. We used RNA interference to downregulate DHX9 expression in A549 cells using a small interfering RNA lentiviral vector. Subsequently, enoxacin was used to inhibit cell proliferation, and this effect was detected using MTT. The results showed that DHX9 was overexpressed in the serum and tissues of lung cancer, especially in small cell lung cancer. Though enoxacin suppressed the proliferation of NSCLC cells, the inhibition effect was diminished when DHX9 was knocked down. In conclusion, the present study provided evidence suggesting that DHX9 was overexpressed in lung cancer and may contribute to the growth of lung cancer, and enoxacin may inhibit the proliferation based on DHX9. Thus DHX9 may be used as a diagnostic marker and a potential therapeutic target for the treatment of NSCLC.

A ring-expansion protocol that consisted of the 1,2-addition of various enolate nucleophiles to 6-trimethylsiloxy-2-cyclohexene-1-one (1) and the NaIO(4)-promoted oxidative ring opening of the resulting diols 2, followed by an intramolecular Knoevenagel condensation, furnished versatile dihydrotropones 6. Maintaining Z-configuration in the oxidative ring-opening products 3 is crucial for the success of the ring-expansion strategy. Dihydrotropones 6 are ripe for further elaborations such as oxidation to tropones 8 and Diels-Alder reaction with the Danishefsky's diene 10 to afford polycyclic compounds 12.

Summary Fluid bulk modulus can directly represent fluid characteristics. It is a sensitive indicator for reservoir fluid identification. In this abstract, a direct stochastic seismic inversion method is used with Gassmann equation and critical porosity model to estimate fluid bulk modulus. It can effectively integrate the high-frequency information of well-logging data and have a higher resolution. And the method is formulated in a Bayesian framework. Firstly, we can get the priori information of fluid bulk modulus through sequential Gaussian simulation (SGS) with a new implementation method, which can improve computation speed. Then we apply Metropolis sampling algorithm in order to obtain an exhaustive description of the posteriori probability density. Of which SGS is the most commonly used geostatistical simulation algorithm and it can combine the simulation and Kriging (well-logging data conditioning) steps elegantly. According to the numerical calculations, we can conclude that SGS with the new implementation way can improve the computational efficiency and the final inversion results match real data well.

Summary Simultaneous inversion of petrophysical parameters based on Metropolis sampling algorithm is formulated in the Bayesian framework, combining statistical petrophysics with the geostatistical priori information. Firstly, we can get the geostatistical priori information through Fast Fourier Transform- Moving Average (FFT-MA) and Gradual Deformation Method (GDM). Then according to the statistical petrophysical model, we can get the relation of elastic parameters and petrophysical parameters. Based on the petrophysical relation, we can construct the likelihood function. Finally, we apply Metropolis sampling algorithm in order to obtain an exhaustive description of the posteriori probability density. Compared to deterministic inversion, the inversion method we proposed can integrate high-frequency information of well-logging data and have a higher resolution. According to the numerical calculations, we can conclude that the final inversion results match the model well and have a higher resolution. In addition, the direct inversion of petrophysical parameters avoids the accumulation of error and reduces the transmission of uncertainty. And it can increase the computation efficiency.

Summary This abstract presents stochastic inversion of petrophysical properties based on mixed priori information. It is formulated in a Bayesian framework, combining fractal and low-frequency priori information with the statistical petrophysical model. Firstly, we can get the priori information of petrophysical properties through fractal Gaussian model and Kriging algorithm. Then according to the statistical petrophysical model, we can get the relation of elastic parameters and petrophysical properties. Based on the petrophysical relation, we can construct the likelihood function. Finally we apply SA-PSO optimization algorithm in order to obtain an exhaustive description of the posteriori probability density. Compared with deterministic inversion, the method we proposed can integrate high-frequency information of well-logging data and have a higher resolution. And priori information contains low-frequency components, so the inversion results are broadband. According to the numerical calculations, we can conclude that the inversion results match the model well and have a higher resolution. In addition, we apply the direct inversion method, which avoids the accumulation of error and reduces the transmission of uncertainty.

A ring-expansion protocol that consisted of the 1,2-addition of various enolate nucleophiles to 6-trimethylsiloxy-2-cyclohexene-1-one (1) and the NaIO4-promoted oxidative ring opening of the result...