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Podocytes are unique, highly specialized, terminally differentiated cells, which are restricted in a post-mitotic state with limited ability to repair or regenerate. Re-entering the mitotic phase causes podocyte mitotic catastrophe, thereby leading to podocyte death and glomerular injury. Myeloid-derived growth factor (MYDGF) is a novel secreted protein and plays an important role in the regulation of cardiovascular function. However, whether MYDGF is expressed in kidney parenchymal cells and whether it has biological functions in the kidney remain unknown. Here, we found that MYDGF was expressed in kidney parenchymal cells and was significantly reduced in podocytes from mice with models of focal segmental glomerulosclerosis and diabetic kidney disease. Podocyte-specific deletion of Mydgf in mice exacerbated podocyte injury and proteinuria in both disease models. Functionally, MYDGF protected podocytes against mitotic catastrophe by reducing accumulation of podocytes in the S phase, a portion of the cell cycle in which DNA is replicated. Mechanistically, MYDGF regulates the expression of the transcription factor RUNX2 which mediates some MYDGF effects. Importantly, a significant reduction of MYDGF was found in glomeruli from patients with glomerular disease due to focal segmental glomerulosclerosis and diabetic kidney disease and the level of MYDGF was correlated with glomerular filtration rate, serum creatinine and podocyte loss. Thus, our studies indicate that MYDGF may be an attractive therapeutic target for glomerular disease.

Renal tubulointerstitial fibrosis is the hallmark of chronic kidney disease (CKD) and the best predictor of renal survival. However, current treatments for CKD remain extremely limited. Therefore, novel therapeutic targets are urgently needed to either stop or reverse CKD progression. The present study was designed to explore the potential role of GPR87, a member of the G protein-coupled receptors (GPCRs) family, in the pathogenesis of tubulointerstitial fibrosis. It was found that GPR87 was significantly induced in the kidney, especially in tubular areas, from different mouse models of renal fibrosis, including unilateral ureteral obstruction (UUO) nephropathy, aristolochic acid nephropathy, and diabetic nephropathy, respectively. Tubule-specific GPR87 deletion dramatically ameliorated tubulointerstitial fibrosis in UUO mice. Mechanistically, GPR87 accelerated glycolysis and mitochondrial injury by YAP-hexokinase-2 signaling, thereby promoting renal fibrosis. Importantly, the upregulation of GPR87 was also found in the kidney from patients with various CKD, indicating that the induction of GPR87 may be a common feature of human kidney diseases. Collectively, our studies for the first time demonstrate that GPR87 plays a pivotal role in renal fibrosis at least in part by accelerating glycolysis and mitochondrial injury, suggesting that targeting GPR87 may represent a novel therapeutic strategy for patients with CKD.

BACKGROUND Hepatocellular carcinoma (HCC) is one of the most common cancers in the world. HCC recurrence and metastasis (most of which are pulmonary metastases ) are the main causes of death in patients. This study aimed to construct a model to analyze and evaluate the relationship between HHC and scientific publications in lung metastatic tumors. OBJECTIVE Hepatocellular carcinoma (HCC) is one of the most common cancers in the world. HCC recurrence and metastasis (most of which are pulmonary metastases ) are the main causes of death in patients. This study aimed to construct a model to analyze and evaluate the relationship between HHC and scientific publications in lung metastatic tumors. METHODS Collect original research articles related to hepatocellular carcinoma and pulmonary metastases published in the Web of Science Core Collection database before January 5, 2023. Understand the development status of the field of hepatocellular carcinoma and pulmonary metastases through co-authored scientific knowledge maps of countries/regions, institutions and authors, and analyze the subject through co-occurrence keyword maps, co-cited author maps, and distribution of highly cited papers Research hotspots in the field, analyze the research frontiers of the subject field through the co-occurrence keyword frequency and emergence analysis map, and explore the global development trend of the subject field through the co-cited reference map. RESULTS A total of 971 articles related to HCC and lung metastasis were included. Both the number of articles published and the frequency of citations have increased significantly over the past five years. The countries/regions, institutions, scholars and journals with the largest number of published articles are China, Fudan Univ, Tang ZY (Zhongshan Hosp, Key Lab Carcinogenesis & Canc Invas, Liver Canc Inst, Fudan Univ) and Hepatology. The countries/regions, institutions, scholars and journals with the most influential published articles are USA, Fudan Univ, Fan J (Zhongshan Hosp, Key Lab Carcinogenesis & Canc Invas, Liver Canc Inst, Fudan Univ) and Am J Clin Pathol. Mol Cancer is the most Effective Journal. The top five co-occurrence keywords are hepatocellular carcinoma, expression, cancer, cell and invasion. The current research frontiers are promote，hepatocellular carcinoma (HCC) and suppresse. CONCLUSIONS Chinese scholars and research institutions have absolute academic leadership in the field of HCC and lung metastatic tumor research. The results of this quantitative study can provide a reference for government departments to formulate/modify health policies or measures. At the same time, this research can also help relevant scholars accurately identify research hotspots and frontiers in the research of HCC and lung metastatic tumors, and play an important guiding role in subsequent research.

In this study, barium zirconate powder was prepared by a solid-state reaction using different barium and zirconium sources. Thermal analysis and phase identification demonstrated that barium zirconate could be synthesized from barium hydroxide at a lower temperature than from barium carbonate. Copper oxide was used as a dopant to improve the sintering performance of the barium zirconate; sintered samples with 2 mol% copper oxide exhibited relatively superior comprehensive performance. The mechanical properties and thermal stability of barium zirconate were characterized; the internal composition structure of the samples prepared with basic zirconium carbonate was uneven, resulting in somewhat reduced performance. The samples maintained a high elastic modulus and strength before and after thermal shock. It was observed under an electron microscope that a liquid phase was generated inside the samples after thermal shock, and numerous barium zirconate whiskers were formed. The whiskers ensured that the sample could withstand greater thermal stress, thus exhibiting excellent thermal shock stability. This work demonstrates the promising potential of barium zirconate in the field of high-temperature materials.

Purpose Neoadjuvant concurrent chemoradiation therapy (nCRT) plus surgery has been a standard treatment for locoregionally advanced esophageal cancer and carcinoma of the gastroesophageal junction (EC/GEJ), but the optimal preoperative radiation dose is still unclear. We performed this systematic review to explore the treatment efficacy and toxicity of different radiation dose levels and find an optimal dose‐fractionation strategy in EC/GEJ patients receiving nCRT. Methods and Materials Embase and Ovid Medline were searched for articles involving cases of operable squamous and adenocarcinoma of the esophagus and GEJ in which patients received nCRT up to a dose of 50.4 Gy in 28 fractions that were published until July 2019, when the search was performed. Physical dose distributions were converted to biologically equivalent doses (BEDs), which were described in units of gray (alpha/beta). Pooled rates of overall survival (OS), progression-free survival (PFS), failure patterns, and toxicities were compared between lower-dose radiation therapy (LDRT; BED ≤48.85 Gy10) and higher-dose radiation therapy (HDRT; BED >48.85 Gy10) for patients treated with nCRT. Results A total of 110 studies with 7577 EC/GEJ patients receiving nCRT were included in this pooled analysis. Both the PFS and OS rates of patients receiving LDRT were significantly higher than those of patients receiving HDRT. Patients receiving LDRT had improved safety regarding treatment-related adverse events and lower distant failure rates than patients receiving HDRT. Utilization of modern radiation therapy (RT) techniques, including 3-dimensional conformal RT and intensity modulated RT, was associated with improved oncologic outcomes compared with 2-dimensional methods. Subgroup analysis showed that EC/GEJ patients receiving conventionally fractionated radiation to a dose of 40.0 to 41.4 Gy in 20-23 fractions showed improved OS compared with those receiving radiation above this dose. Conclusions Based on the limited data, nCRT using BED ≤48.85 Gy10 was suitable for locoregionally advanced, resectable EC/GEJ. A total dose of 40.0 to 41.4 Gy in 20 to 23 fractions using modern RT techniques might provide the optimal therapeutic ratio.

Laser communication is essential part of maritime-terrestrial-air intelligent communication/sensor network. Among them, different modulation formats would play a unique role in specific applications. Based on Rytov theory, we discussed system performance of the maritime laser communication with repeated coding technology in several modulation schemes. The closed-form expression of average bit error rate (BER) from weak to moderate atmospheric turbulence described by log-normal distribution is given. Differential phase shift keying (DPSK) modulation, as a potential solution for future maritime laser communication, has attracted a lot of attention. We analyzed the effects of atmospheric turbulence parameters (visibility, refractive index structure coefficient, non-Kolmogorov spectral power-law exponent, turbulence inner scale) and DPSK system parameters (receiver aperture diameter, repeat time) on average BER in detail. Compared with the aperture-averaging effects, the system BER can be well suppressed through increasing repeat time. This work is anticipated to provide a theoretical reference for maritime laser communication systems.

Background: Podocytes (highly specialized and terminally differentiated epithelial cells) are integral components of the glomerular filtration barrier that are vulnerable to a variety of injuries and, as a result, they undergo a series of changes ranging from hypertrophy to detachment and apoptosis. Podocyte injury is a major determinant in proteinuric kidney disease and identification of potential therapeutic targets for preventing podocyte injury has clinical importance. Although numerous studies have achieved dramatic advances in the understanding of podocyte biology and its relevance to renal injury, few effective and specific therapies are available. Summary: Epigenetic modifications have been proven to play important roles in the pathogenesis of kidney diseases. Among them, histone deacetylase (HDAC)-mediated epigenetic acetylation in the kidney has attracted much attention, which may play multiple roles in both kidney development and the pathogenesis of kidney disease. Recent studies have demonstrated that HDAC protect against podocyte injury by regulation of inflammation, apoptosis, autophagy, mitochondrial function, and insulin resistance. In this review, we summarize recent advances in the understanding of the functions and regulatory mechanisms of HDAC in podocytes and associated proteinuric kidney diseases. In addition, we provide evidence of the potential therapeutic effects of HDAC inhibitors for proteinuric kidney disease. Key Messages: Pharmacological targeting of HDAC-mediated epigenetic processes may open new therapeutic avenues for chronic kidney disease.

This study was aimed to investigate the combined effects of metformin hydrochloride and insulin during gestational diabetes mellitus. A total 136 patients were randomly divided into study and control group. The control group was treated with insulin only while the study group was additionally treated with metformin hydrochloride. Maternal-infant outcomes and the levels of fasting blood glucose (FBG), 2h postprandial blood glucose (2hPG), glycosylated hemoglobin (HbA1c), total cholesterol (TC), total bilirubin (TBil), uric acid (UA) and microalbunminuria (mAlb) before and after treatment were compared. In post-treatment, the levels of FBG, 2h PG and HbA1c were decreased significantly (p0.05) in both groups compared with pre-treatment. The levels of TC, TBil, UA and mAlb in both groups were significantly improved compared with pre-treatment. Levels of TC, UA and mAlb in the study group were significantly lower while TBil level was higher than control group. Compared to the control group, the incidence of gestational hypertension and premature delivery were significantly lower in the study group. There was no significant difference in the incidence of neonatal respiratory distress. The combination of metformin hydrochloride and insulin has significant effect in the treatment of gestational diabetes mellitus.

Aiming at the 1vs1 confrontation problem in a complex environment where obstacles are randomly distributed, the DDPG (deep deterministic policy gradient) algorithm is used to design the maneuver decision-making method of UAVs. Traditional methods generally assume that all obstacles are known globally. In this paper, a UAV airborne lidar detection model is designed, which can effectively solve the problem of obstacle avoidance when facing a large number of unknown obstacles. On the basis of the designed model, the idea of transfer learning is used to transfer the strategy trained by one UAV in a simple task to a new similar task, and the strategy will be used to train the strategy of the other UAV. This method can improve the intelligence of the UAVs in both sides alternately and progressively. The simulation results show that the transfer learning method can speed up the training process and improve the training effect.

Intermediate volatility organic compounds (IVOCs) in outdoor air have been reported in recent years with focus on characterizing IVOCs and their contributions to the formation of secondary organic aerosol (SOA). Little has been studied on the different behaviors of IVOCs in particulate matter (PM) dominated winter pollution weather and ozone (O3) dominated summer pollution weather. In this study, we collected and analyzed outdoor airborne IVOCs in an urban location in Shanghai during PM dominated pollution events in winter (ten samples) and O3 dominated pollution events in summer (22 samples). IVOCs were categorized into n-alkanes, polycyclic aromatic hydrocarbons (PAHs) and unspeciated complex mixture (UCM) that includes unspeciated branched alkanes (b-alkanes) and other unidentified IVOCs. In winter samples total IVOCs concentrations were up to 114 μg/m3 and UCM IVOCs accounted for 91% ± 3%, while in summer samples total IVOCs concentrations were only up to 17.2 μg/m3 and UCM accounted for 69% ± 14%. The average concentration of primary IVOCs which are directly from emission sources, was 35.1 ± 16.1 μg/m3 and 4.0 ± 2.2 μg/m3 in winter and summer, respectively. IVOCs were found to have statistically significant positive correlations with PM (PM2.5, PM10) but not with O3 in both winter and summer samples. Statistically significantly inverse relationships between O3 and C12 C14 n-alkanes and between O3 and two to three rings PAHs in summer samples were observed, indicating that these relatively more volatile IVOCs might be actively involved in atmospheric photochemical reactions in the atmosphere in summer. Our study revealed different behaviors of IVOCs in winter and summer pollution events in Shanghai; however, more research is needed to better understand the contribution of IVOCs to SOA, and the underlying photochemical reactions of IVOCs during O3 dominated air pollution events.

Label-free biosensing based on the nanoporous anodic alumina (NAA) membrane emerged as a versatile biosensing platform in the recent decade. In the present work, we developed a new immunosensing strategy based on the nanochannels of NAA and the ion pair interaction mediated by electrochemistry of C60. The NAA served as the matrix for the immobilization of the capture antibodies. The incubation of target antigens resulted in the formation of the immunocomplexes and thus an increase of the steric hindrance of the nanochannels. Therefore, the concentration of the redox probe transported through the nanochannels decreases, which can be detected at the working electrode modified with C60. Herein, we initially found that the cathodic peak ascribed to the reduction of C60 to C60– was obviously enhanced by the presence of the redox probe K3[Fe(CN)6] and which was contributed to the formation of a ternary ion association complex among C60, tetraoctylammonium bromide, and K3[Fe(CN)6]. Therefore, the transportation ...

Long noncoding RNAs (lncRNAs) are increasingly recognized as indispensable components of the regulatory network in the progression of various cancers, including nonsmall cell lung cancer (NSCLC). The lncRNA prostate cancer associated transcript 1 (PCAT1) has been involved in tumorigenesis of multiple malignant solid tumors, but it is largely unknown that what is the role of lncRNA-PCAT1 and how it functions in the progression of lung cancer. Herein, we observed that lncRNA PCAT1 expression was upregulated in both human NSCLC tissues and cell lines, which was determined by qualitative polymerase chain reaction analysis. Then, gain-and loss-of-function manipulations were performed in A549 cells by transfection with a specific short interfering RNA against PCAT1 or a pcDNA-PCAT1 expression vector. The results showed that PCAT1 not only promoted NSCLC cell proliferation and invasion but also inhibited cell apoptosis. Bioinformatics and expression correlation analyses revealed that there was a potential interaction between PCAT1 and the dyskerin pseudouridine synthase 1 (DKC1) protein, an RNA-binding protein. Then, RNA pull-down assays with biotinylated probes and transcripts both confirmed that PCAT1 directly bounds with DKC1 that could also promote NSCLC cell proliferation and invasion and inhibit cell apoptosis. Moreover, the effects of PCAT1 and DKC1 on NSCLC functions are synergistic. Furthermore, PCAT1 and DKC1 activated the vascular endothelial growth factor (VEGF)/protein kinase B (AKT)/Bcl-2/caspase9 pathway in NSCLC cells, and inhibition of epidermal growth factor receptor, AKT, or Bcl-2 could eliminate the effect of PCAT1/DKC1 co-overexpression on NSCLC cell behaviors. In conclusion, lncRNA PCAT1 interacts with DKC1 to regulate proliferation, invasion, and apoptosis in NSCLC cells via the VEGF/AKT/Bcl-2/caspase9 pathway.

Casticin, a flavonoid isolated from Vitex species, has been found to have anti-tumor property in multiple human cancers. The present study aimed to investigate the effect of casticin on the proliferation and apoptosis of esophageal cancer (EC) cells, and further illustrate the underlying mechanisms. In in vitro studies, human EC cell lines TE-1 and ECA-109 were treated with various concentrations of casticin (low-, middle-, and high-dose groups). The results showed that casticin dose-dependently inhibited the proliferation and clonogenicity of EC cells and induced cell cycle arrest in sub-G1 and G2 phases. Furthermore, casticin markedly enhanced EC cell apoptosis as detected by flow cytometry and Hoechst 33342 staining. The level of anti-apoptotic Bcl-2 protein was decreased, while the levels of pro-apoptotic Bax, cleaved-caspase-3, cleaved-caspase-9, and cleaved-PARP were conversely increased in casticin-treated TE-1 and ECA-109 cells. Moreover, casticin decreased the mitochondrial membrane potential and increased the release of mitochondrial cytochrome C into cytoplasm. In addition, the JNK signaling pathway was involved in casticin-medicated anti-proliferation and pro-apoptosis. Cells pretreated with SP600125, a JNK pathway inhibitor, partially abolished the effect of casticin. Finally, the anti-tumor property of casticin was confirmed in in vivo xenograft models. Overall, we provided both in vitro and in vivo evidences that casticin inhibited the proliferation and induced apoptosis of EC cells, and the anti-tumor action of casticin was mediated, in part, by the mitochondrial-dependent apoptosis and the activation of JNK signaling pathway.

We propose a novel orbital angular momentum (OAM) space division multiplexing system based on Lommel–Gaussian (LMG) beam, which utilizes different transverse wavenumbers under the same topological charge. Using the random phase screen method and diffraction theory, the evolution of light field and mode crosstalk are effectively analyzed during transmission. Owing to the non-diffracting feature, LMG beams are more robust than traditional Laguerre–Gaussian (LG) beams through spatial spectrum analysis under the same intensity. More importantly, the results show that the shape of demultiplexed spot is related to the symmetry of original OAM-carrying beam and LMG beams with smaller scaling factor are better for detection. This work is anticipated to open up new perspectives for future high-capacity communication missions.

Labeling with redox reporter is often required in developing electrochemical bioassay for most proteins or nucleic acid biomarkers. Herein, a label-free ratiometric immunosensing platform is firstly developed by integrating the antibody-conjugated nanochannels with a smart modified electrode. The electrode modifier is the composite of C60, tetraoctylammonium bromide (TOA+) and Prussian blue (PB). Cyclic voltammograms of the ultimate C60-TOA+/PB modified electrode exhibited two pairs of peaks at 0.15 V and −0.13 V, ascribing to the redox of PB and C60, respectively. With the addition of K3[Fe(CN)6] in the electrolyte solution, the peaks of PB decreased due to the adsorption of [Fe(CN)6]3− while the peaks of C60 increased because of the formation of the ternary complex (TC) C60-TOA+-[Fe(CN)6]3−. As a result, the peak current ratio IPB/ITC decreased gradually with the increment of the concentration of [Fe(CN)6]3−. For the nanochannels-based immunosensing platform, the steric hindrance of the bioconjugated nanochannels varied with the loading amount of the target CA125, and thus [Fe(CN)6]3− passing through the channels was quantitatively affected. And the higher CA125 level was, the less [Fe(CN)6]3− concentration was. And thus, the ratio IPB/ITC monitored at the C60-TOA+/PB modified electrode increased with the increase of the concentration of CA125. The ratiometric immunoassay featured a linear calibration range from 1.0 U mL−1 to 100 U mL−1 with a low detection limit of 0.86 U mL−1. In addition, the ratiometric immunosensing platform demonstrated good specificity and stability as well as acceptable accuracy in overcoming the effect of electrode passivation which was an inherent problem of electroanalysis.

p38 mitogen-activated protein kinase (MAPK) signaling has been implicated in the cancer development and progression. However, the precise mechanism of this association remains unknown. The aim of the present study was to evaluate the association between p38 and cancer progression, including investigations into the effects on cell proliferation, resistance to thalidomide, indoleamine 2,3-dioxygenase (IDO) expression and prognosis in patients with esophageal cancer. The present retrospective study included patients with stage I-III esophageal cancer. A total of 228 patients with esophageal cancer were recruited to analyze the expression of phosphorylated (p)-p38 and IDO in tumor, and normal tissues through immunohistochemistry. Depression status was measured using the Zung Self-Rating Depression Scale. P38 cDNA was transfected into esophageal cancer cells to assess tumor cell viability, sensitivity to thalidomide treatment and IDO gene expression. Western blotting and flow cytometry was used to analyze protein expression alterations, and apoptosis in esophageal cancer cells. P-p38 protein was expressed in 68.9% of cancer tissues, and was significantly associated with depressive symptoms, tumor recurrence and poor survival of patients. In vitro experiments revealed that the expression of p-p38 induced esophageal cancer Eca-109 and TE-1 cell viability, and resistance to thalidomide treatment, as well as in the expression of IDO without the application of lipopolysaccharides. Further follow-up of patients revealed that depression was also an independent factor for early recurrence and overall survival rate. Altered p38 MAPK expression was associated with poor outcome in patients with esophageal cancer. p38 may be a potential biomarker for the prediction of depressive symptoms and prognosis in patients with esophageal cancer.

DEAD (Asp-Glu-Ala-Asp) box protein 5 (DDX5), a prototypical member of the DEAD/H-box protein family, has been involved in several human malignancies. However, the expression and biological role of DDX5 in esophageal cancer (EC) remain largely unknown. In this study, we examined the role of DDX5 in regulating EC cell proliferation and tumorigenesis and explored its possible molecular mechanism. We found that DDX5 was overexpressed in human EC cell lines. In addition, knockdown of DDX5 significantly inhibited the proliferation of EC cells in vitro and the growth of EC xenografts in vivo. Knockdown of DDX5 also suppressed the migration/invasion and epithelial-to-mesenchymal transition (EMT) phenotype in EC cells. Furthermore, we observed that knockdown of DDX5 inhibited the expression of β-catenin, c-Myc, and cyclin D1 in EC cells. In conclusion, our findings provide the first evidence that siRNA-DDX5 inhibited the proliferation and invasion of EC cells through suppressing the Wnt/β-catenin signaling pathway. Therefore, DDX5 may be a novel potential therapeutic target for the prevention and treatment of EC.

Label-free biosensing based on the nanoporous anodic alumina (NAA) membrane emerged as a versatile biosensing platform in the recent decade. In the present work, we developed a new immunosensing strategy based on the nanochannels of NAA and the ion pair interaction mediated by electrochemistry of C

The ribosomal protein (RP)‐p53 pathway has been shown to play a key role in apoptosis and senescence of cancer cells. miR-1908 is a newly found miRNA that was reported to have prognostic potential in melanoma. However, its role and mechanism in the progression of non-small cell lung cancer (NSCLC) are largely unknown. In this study, we found that expression of miR-1908 was significantly downregulated in human NSCLC cell lines, including SK-MES-1, A549, and NCI-H460. Then the role of miR-1908 in NSCLC cell proliferation was explored. The miR-1908 mimic was transfected into NSCLC cell lines, and their proliferation was detected. MTT and Cell Titer-Blue H analyses showed that the cell proliferation was notably reduced by the miR-1908 mimic transfection. Moreover, we found the RP‐p53 pathway was activated by miR-1908 mimic. Moreover, the miR-1908 inhibitor transfection had a completely opposite effect on the NSCLC cell proliferation than that of miR-1908 mimic. To explore the underlying mechanism of that, TargetScan bioinformatics server and 3′-UTR luciferase reporter assay were applied to identify the targets of miR-1908. Our results showed that AKT1 substrate 1 (AKT1S1), a newly proven suppressor of the RP‐p53 pathway, was a target of miR-1908, suggesting a probable mechanism for miR-191 suppressing NSCLC cell proliferation. Our findings provide a novel molecular target for the regulation of NSCLC cell proliferation.

The incidence of non-small cell lung cancer (NSCLC) has significantly increased in China, while the prognosis of affected patients is poor. The pathogenesis of NSCLC is thought to be regulated by microRNAs (miRs). The present study used a miR array in order to determine the expression of miR-361-5p, which was significantly lower in NSCLC tissues compared with that in adjacent tissues, indicating a crucial role of miR-361-5p during the progression of NSCLC. Furthermore, the effects of transfection-induced upregulation of miR-361-5p on the NSCLC cell line H23 were assessed. Overexpression of miR-361-5p inhibited the proliferation and colony formation ability of H23 cells. In addition, apoptosis of H23 cells was induced by upregulation of miR-361-5p. Furthermore, signal transducer and activator of transcription 6 (STAT6) was confirmed as a direct target of miR-361-5p by a dual-luciferase reporter assay. Moreover, inhibition of STAT6 by small interfering RNA or miR-361-5p also decreased the expression of B-cell lymphoma extra large (Bcl-xL). In vivo, miR-361-5p significantly reduced tumor growth in a nude mouse xenograft model, and suppressed STAT6 and Bcl-xL expression. In conclusion, the present study indicated that miR-361-5p may represent a novel molecular tool for therapeutic and diagnostic strategies in NSCLC.

Lung cancer is the leading cause of cancer-related mortality worldwide. The majority of lung cancers are sporadic, and familial cases are extremely rare. Previous studies have mainly focused on sporadic lung cancer and identified a large quantity of driver genes. However, familial lung cancers are rarer and studied less. The present study recruited a Chinese family in which multiple members had developed lung squamous carcinoma. To find the causative mutations, whole exome sequencing was conducted using a peripheral blood sample of one lung squamous carcinoma patient, and certain variants were validated in more samples. Whole exome sequencing analysis obtained ~2.0 Gb of data (an average of 60x depth for each targeted base), and further validation experiments identified two functional variants in two cancer-related genes (c.1218delA:p.E406fs in PDE4DIP and C1342A:p.L448I in CLTCL1). This study therefore provides useful sources for the further study of hereditary lung cancer.

Objective: To evaluate the diagnostic value of endoscopic ultrasonography (EUS) in preoperative staging of esophageal carcinoma (EC).Material and methods: A total of 86 surgical patients with EC who were confirmed by endoscopy and biopsy underwent preoperative TN staging with EUS examination. The EUS findings were compared with surgical pathologic results.Results: The accuracy of EUS in T and N staging of EC was 82.6% and 84.9%, respectively. While determining whether EC invades the muscularis propria or outer membrane, EUS had the favorable sensitivity, specificity, positive predictive value and negative predictive value. The short-axis diameter of lymph nodes of 5mm had high sensitivity and negative predictive value to determine malignance with low specificity and positive predictive value. The short-axis diameter of 10mm presented the satisfactory sensitivity, specificity, positive predictive value and negative predictive value.Conclusion: EUS can accurately determine the TN staging of EC and p...

MicroRNAs (miRNAs) play critical roles in the development and progression of various cancers, including non-small-cell lung cancer (NSCLC). Studies have suggested that miR-330-5p is involved in the progression of several cancers. However, the role of miR-330-5p in NSCLC remains unclear. We investigated the effect on and mechanism of miR-330-5p in the progression of NSCLC. We found that miR-330-5p was significantly downregulated in NSCLC tissues and cell lines as detected by real-time quantitative polymerase chain reaction (RT-qPCR). The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), bromodeoxyuridine (BrdU), colony formation and cell cycle assays showed that overexpression of miR-330-5p markedly inhibited cell growth. Annexin V-FITC/PI and caspase-3 activity assays showed that overexpression of miR-330-5p significantly promoted cell apoptosis of NSCLC cells. Bioinformatics analysis and dual-luciferase reporter assays confirmed NIN/RPN12 binding protein 1 (NOB1) as a target gene of miR-330-5p. RT-qPCR and Western blot analysis showed that overexpression of miR-330-5p inhibited the expression of NOB1 as well as cyclin D1 and cyclin-dependent kinase 4 in NSCLC cells. Moreover, overexpression of NOB1 markedly reversed the miR‑330-5p-mediated inhibitory effect on NSCLC cell growth. Correlation analysis showed that miR‑330-5p expression was inversely correlated with NOB1 mRNA expression in NSCLC tissues. Taken together, our results indicate that miR-330-5p inhibits NSCLC cell growth through downregulation of NOB1 expression. Our study suggests that miR-330-5p may serve as a potential therapeutic target for the treatment of NSCLC.

Compared with the Intrusion Detection (ID) based on pattern matching, the model-checking-based methods can find the complex attacks. But their rates of missing report are still high. To solve this problem, we firstly use the Interval Temporal Logic with Past Construct (ITLPC) formulae to describe some signatures for network attacks. And then, we can use some automata to establish models of audit logs. On the basis of it, automata, i.e., attack models, and ITLPC formulae, i.e., signatures, constitute the two inputs of the ITLPC model checking algorithm. Therefore, a new model-checking-based ID algorithm is obtained by calling the ITLPC algorithm. Compared with the existing methods, the new method is more powerful, as shown in the experimental simulations.

A digital CMOS output interface circuit is proposed, which lowers down the peak and lengthen the duration of the pulse of current supplied by the power supply to reduce the SSN (simultaneously-switching noise) effects. The simulation shows that the maximal SSN voltage of the proposed circuit is 331.5mV compared to 662.4mV of the traditional one.

Compared with the intrusion detection based on pattern matching, the method which is based on model checking can detect the complex attacks. But all of the existing algorithms are only used to detect some specific types of attacks. To solve this problem, we firstly use the Linear Temporal Logic with Past Construct (LTLPC) formulae to set up formal sub-models for the five kinds of attackers, the four kinds of attack processes and the eight kinds of attack effects. According to their universal relationship and the semantic relation of variety of LTLPC operators, we obtain the above sub-models together, thus, the universal models described by LTLPC formulae for universal attacks are formed. On this base, we implement an intrusion detection method based on LTLPC for detecting all types of attacks. Compared with the existing methods, the detecting ability of the new method is more comprehensive.

In this paper, we present an efficient approach based on Smoothed Particle Hydrodynamics (SPH) to simulate nearly incompressible fluids. The proposed method is an extension of the traditional SPH method designed for compressible fluids. We first introduce a new scheme for pressure evaluation to satisfy the incompressibility constraints. Then novel calculation methods for pressure force and viscosity force are discussed. Finally, the results demonstrate that our method is more capable of realistically simulating fluids with near-incompressibility than previous method.

In this paper, we find that factors which affect energy consumption are steel ratio coefficient and process energy consumption by analyzing energy consumption of every process in integrated steel works. On this basis we point out the main reason for the high energy consumption of iron and steel industry in China is that integrated steel works examine the production process without system energy saving ideas. Therefore we propose the countermeasures of energy saving in iron and steel industry in China in aspects of energy management and control center, iron-making system, steel-making system, steel rolling system, as well as secondary energy recovery, which is aimed at providing a way for energy saving and emissions reduction of iron and steel industry in China.

Background miR-126 is a key regulator of oncogenic processes. It is functionally linked to cellular proliferation, survival and migration. Vascular endothelial growth factor A (VEGF-A), which is regarded as a tumorgenesis activator, could directly target miR-126 in several tumors. However, the mechanism in esophageal cancer remains unclear. Methods and results In this study, the expression of miR-126 and VEGF-A were assessed in esophageal cancer tissues and esophageal cancer cell lines. We found that miR-126 has significantly lower expression in esophageal cancer tissues and esophageal cancer cell lines than in healthy tissues, while the expression of VEGF-A is high. Luciferase reporter assays were performed to investigate the relationship between VEGF-A and miR-126. We confirmed that VEGF-A is a target for miR-126. Furthermore, the proliferation of esophageal cancer cells with miR-126 overexpression and miR-126 knockdown was monitored using the MTT assay. The results showed that miR-126 could inhibit esophageal cancer cell proliferation in vitro. The effect of miR-126 was also detected in BALB/c nude mice with transplanted esophageal cancer cells. In vivo study showed that tumor growth was significantly suppressed by miR-126 overexpression. Conclusions We believe that restoring miR-126 levels may be a promising therapeutic approach in cases of esophageal cancer.

In order to improve the accuracy of people counting in video surveillance, the method for people counting based on the moving feature of the mass is proposed. We obtain the orientation and energy density of mass through the optical flow algorithm, and get the information about the size of mass to design the feature of mass. The people counting model is obtained by training a support vector machine (SVM) classifier with the moving feature and shape feature of mass. The experimental results confirm that our approach improves the accuracy of people counting.

The upgrade project of the Beijing Electron Positron Collider (BEPCII) and its injector linac is working well. The linac upgrade aims at a higher injection rate of 50 mA/min into the storage ring, which requires an injected beam with low emittance, low energy spread and high beam orbit and energy stabilities. This goal is finally reached recently by upgrading the linac components and by dealing with rich and practical beam physics, which are described in this study.