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Background Hepatocellular carcinoma (HCC) is one of the most common malignant cancers with a high incidence and high mortality in East Asia. Identifying biomarkers and clarifying the regulatory mechanisms of HCC are of great importance. Herein, we report the role and mechanism of activating transcription factor 3 (ATF3), a member of the ATF/cAMP-responsive element-binding protein family of transcription factors in HCC. Methods ATF3 overexpression vector and shRNAs were transfected into HCC cancer cells to upregulate or downregulate ATF3 expression. In vitro and in vivo assays were performed to investigate the functional role of ATF3 in hepatocellular carcinoma. RNA-Seq was performed to screen the differentially expressed genes downstream of ATF3. The dual-luciferase reporter assay, chromatin immunoprecipitation (Ch-IP) analysis and functional rescue experiments were used to confirm the target gene regulated by ATF3. Tissue microarrays (TMAs) comprising 236 human primary HCC tissues were obtained and immunohistochemical staining were carried out to analyze the clinical significance of ATF3. Results The results indicate that ATF3 significantly inhibited the proliferation and mobility of HCC cells both in vitro and in vivo. Cysteine-rich angiogenic inducer 61 (CYR61) is a key target for transcriptional regulation by ATF3. Both ATF3 and CYR61 were consistently downregulated in human HCC tissues, and their expression levels were significantly and positively correlated with each other. Conclusions Our findings indicate that ATF3 functions as a tumor suppressor in HCC through targeting and regulating CYR61. Electronic supplementary material The online version of this article (10.1186/s13046-018-0919-8) contains supplementary material, which is available to authorized users.

This paper proposes a constant on time variable frequency controlled resonant switched-capacitor (RSC) converter for driving high power light-emitting diodes (LEDs). The on time of a transistor is set constant which is less than the time constant τ of capacitor charge loop, as a result, the RSC converter has a wide operation range. In contrast to the conventional constant current DC drivers (the output current regulation is achieved by using the digital control circuit), the simple analog circuit is adopted to acquire the regulation issue. The output current value of the RSC converter could be kept constant by varying the switching frequency. On the other hand, the output current could be rearranged by setting the related reference value. In the RSC converter presented in this paper, a small value inductor is injected into the charge loop of RSC converter to improve the switching behavior of the converter. A 10W RSC converter was built to verify the modeling method and the proposed control method. The experiments and simulation were conducted to demonstrate the feasibility of the proposed control method. The experimental and simulated results show that, with the proposed control method, the RSC converter provides fast dynamical response speed with good regulation. What's more, the RSC converter presents robust performance. This control method is a general control method and it could be expanded to other topologies of RSC converters.

Previous studies have shown that the oxidation of Fe(II) by molecular oxygen can lead to the co-oxidation of As(III) at neutral pH. However, the mechanism of As(III) oxidation in the presence of Fe(II) with respect to the interaction between As(III) and Fe(II) is still unclear. In this work, we examined the oxidation of As(III) in the presence of Fe(II) in air-saturated water, which is affected by pH, co-existing phosphate, and scavengers (tert-butanol, superoxide dismutase, catalase and dimethylsulfoxide). Results confirm that the formation of the Fe(II)–As(III) complex (formation constant, KFe(II)–As(III) = 103.86 M–1) plays an extremely important role in the initial stage of As(III) oxidation at pH 7.25. The oxidation of Fe(II)–As(III) promotes the production of H2O2 and colloidal ferric hydroxide. H2O2 reacts with the Fe(II)–As(III) complex through oxidizing Fe(II) to Fe(IV), which then causes the partial oxidation (ca. 50%) of As(III). The other part of As(III) oxidation by H2O2 occurs, in the form of Fe(III)–As(III) complex, through direct electron transfer from As(III) to H2O2 but not through Fe(IV). This work provides new mechanistic insight into arsenic and iron redox chemistry in the environment and furthers our understanding of Fenton reactions at neutral pH.

Hepatocellular carcinoma (HCC) is the most common form of liver cancer and is typically diagnosed at advanced stages. Identification and characterisation of genes within amplified and deleted chromosomal loci can provide new insights into the pathogenesis of cancer and lead to new approaches for diagnosis and therapy. In our previous study, we found a recurrent region of copy number amplification at 19p13.2 in hepatocellular carcinoma (HCC). In the present study, we performed integrated copy number analysis and expression profiling at this locus and a putative cancer gene, SMARCA4/BRG1, was uncovered in this region. BRG1 is a part of the large ATP-dependent chromatin remodelling complex SWI/SNF. The function of BRG1 in various cancers is unclear, including its role in HCC tumorigenesis. Here, we found that BRG1 is upregulated in HCC and that its level significantly correlates with cancer progression in HCC patients. Importantly, we also found that nuclear expression of BRG1 predicts early recurrence for HCC patients. Furthermore, we demonstrated that BRG1 promotes HCC cell proliferation in vitro and in vivo. BRG1 was observed not only to facilitate S-phase entry but also to attenuate cell apoptosis. Finally, we discovered that one of the mechanisms by which BRG1 promotes cell proliferation is the upregulation of SMAD6. These findings highlight the important role of BRG1 in the regulation of HCC proliferation and provide valuable information for cancer prognosis and treatment.

Table S1. Sequences of primers, probes and shRNA used for experiments in this study. Table S2. The antibodies for the Western blotting. Table S3. RNA-seq of differentially expressed genes in ATF3 overexpression SK-Hep1 cells. Table S4. RNA-seq of differentially expressed genes in ATF3 knockdown SMMC-7721 cells. Table S5. The antibodies for the IHC. Figure S1. The differential expression of ATF3 in HCC cell lines. Figure S2. ATF3 inhibited HCC cell proliferation in vitro by MTT assay. Figure S3. ATF3 suppressed HCC mobility in vitro. Figure S4. CYR61 suppressed HCC mobility in vitro. Figure S5. qRT-PCR analysis of the mRNA levels to confirm the differential expression of other genes identified from the ATF3 RNA-Seq results as targets of ATF3 in HCC cell lines with ATF3 overexpression or knockdown. (DOCX 3516 kb)

As one of the most toxic heavy metals, the oxidation of inorganic arsenic has drawn great attention among environmental scientists. However, little has been reported on the solar photochemical behavior of arsenic species on top-soil. In the present work, the influencing factors (pH, relative humidity (RH), humic acid (HA), trisodium citrate, and additional iron ions) and the contributions of reactive oxygen species (ROS, mainly HO and HO2/O2(-)) to photooxidation of As(III) to As(V) on kaolinite surfaces under UV irradiation (λ=365nm) were investigated. Results showed that lower pH facilitated photooxidation, and the photooxidation efficiency increased with the increase of RH and trisodium citrate. Promotion or inhibition of As(III) photooxidation by HA was observed at low or high dosages, respectively. Additional iron ions greatly promoted the photooxidation, but excessive amounts of Fe(2+) competed with As(III) for oxidation by ROS. Experiments on scavengers indicated that the HO radical was the predominant oxidant in this system. Experiments on actual soil surfaces proved the occurrence of As(III) photooxidation in real topsoil. This work demonstrates that the photooxidation process of As(III) on the soil surface should be taken into account when studying the fate of arsenic in natural soil newly polluted with acidic wastewater containing As(III).

Transformation of inorganic arsenic species has drawn great concern in recent decades because of worldwide and speciation-dependent pollution and the hazards that they pose to the environment and to human health. As(III) photooxidation in aquatic systems has received much attention, but little is known about photochemical transformation of arsenic species on top soil. As(III) photooxidation on natural montmorillonite under UV-A radiation was investigated by using a moisture- and temperature-controlled photochemical chamber with two black-light lamps. Initial As(III) concentration, pH, layer thickness, humic acid (HA) concentration, the presence of additional iron ions, and the contribution of reactive oxygen species (ROS) were examined. The results show that pH values of the clay layers greatly influenced As(III) photooxidation on montmorillonite. As(III) photooxidation followed the Langmuir–Hinshelwood model. HA and additional iron ions greatly promoted photooxidation, but excess Fe(II) competed with As(III) for oxidation by ROS. Scavenging experiments revealed that natural montmorillonite induced the conversion of As(III) to As(V) by generating ROS (mainly HO• and HO2 •/O2 •−) and that HO• radical was the predominant oxidant in this system. Our work demonstrates that photooxidation on the surface of natural clay minerals in top soil can be important to As(III) transformation. This allows understanding and predicting the speciation and behavior of arsenic on the soil surface.

In our previous studies, we reported that CD133(+) cancer stem cells (CSCs) were chemoresistant in hepatocellular carcinoma (HCC) and that isocorydine treatment decreased the percentage of CD133(+) CSCs. Here, we found that a derivative of isocorydine (d-ICD) inhibited HCC cell growth, particularly among the CD133(+) subpopulation, and rendered HCC cells more sensitive to sorafenib treatment. d-ICD inhibited IGF2BP3 expression in a time-dependent manner, and IGF2BP3 expression negatively correlated with d-ICD-induced growth suppression. IGF2BP3 overexpression enriched the CD133(+) CSC subpopulation in HCC, enhanced tumor sphere formation and suppressed the cytotoxic effects of sorafenib and doxorubicin. The expression of drug resistance-related genes, including ABCB1 and ABCG2, and the CSC marker CD133 expression was increased after IGF2BP3 overexpression. The significance of these observations was underscored by our findings that high IGF2BP3 expression predicted poor survival in a cohort of 236 patients with HCC and positively correlated with ABCG2 and CD133 expression in vivo. These results suggested that the d-ICD may inhibit HCC cells growth by IGF2BP3 decrease and that IGF2BP3 may serve as a therapeutic target for HCC.

The Hausdorff dimensions of some refined irregular sets associated with β-expansions are determined for any β > 1. More precisely, Hausdorff dimensions of the sets $$\left\{ {x \in \left[ {0,1} \right):\mathop {\lim }\limits_{n \to \infty } \tfrac{{S_n (x,\beta )}} {n} = \alpha _1 ,\mathop {\lim \sup }\limits_{n \to \infty } \tfrac{{S_n (x,\beta )}} {n} = \alpha _2 } \right\}, \alpha _1 ,\alpha _2 \geqslant 0$$ are obtained completely, where S n (x, β) = Σ = 1 e k (x, β) denotes the sum of the first n digits of the β-expansion of x. As an application, we present another concise proof of that the set of points x ∈ [0, 1) satisfying $$\mathop {\lim }\limits_{n \to \infty } \tfrac{{S_n (x,\beta )}} {n}$$ does not exist is of full Hausdorff dimension.

Nanostructured iron oxides with superparamagnetism were synthesized from colloidal particles of hydrous iron oxide. The synthesis procedure involved preparation of acetone-nanoparticle composite and calcination of the composite in air or nitrogen. The effects of calcination temperature and atmosphere on the properties of the products were investigated. Powder X-ray diffraction, 57Fe Mossbauer spectra, transmission electron microscopy, nitrogen sorption, thermal analysis and vibrating-sample magnetometry were applied to characterize the materials. The products calcined in flowing air are composed of nanoparticles, while those calcined in flowing nitrogen contain nanosheets. The former has larger specific surface areas, whereas the latter has stronger saturation magnetization in external magnetic field. Increasing calcination temperature reduced the specific surface area of the product, whereas enhanced its saturation magnetization. Furthermore, the iron oxides with superparamagnetism showed good affinity to arsenite, and therefore they could be potential adsorbents for arsenic remediation in water.

Background and Aim Angiopoietin-like protein 2 (ANGPTL2) plays various roles in metabolism, vascular biology, inflammation, and tumor metastasis, but little is known about its function in human hepatocellular carcinoma (HCC) metastasis. This study aimed to further explore the function of ANGPTL2 on migration and invasion of liver cancer cells. Methods Quantitative real-time polymerase chain reaction, Western blotting, immunohistochemistry, transwell migration, and invasion assays were performed to clarify the function of ANGPTL2 in the regulation of cell migration and invasion in human HCC. Results In HCC patients, ANGPTL2 expression was higher in HCC tissues compared with matched noncancerous liver tissues. And the ANGPTL2 levels of HCC tissues positively correlated with intrahepatic metastasis in HCC patients. Overexpression of ANGPTL2 significantly increased migration and invasion of HCC cells in vitro, and promoted intrahepatic and distal pulmonary metastasis in vivo, while knockdown of endogenous ANGPTL2 resulted in a reduced migration and invasion in vitro. Colony formation assay and 3-(4,5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay showed ANGPTL2 did not affect cell proliferation in vitro, whereas overexpression of ANGPTL2 promoted tumor formation in xenograft animal model. Conclusions Our findings show that ANGPTL2 drives human HCC metastasis and provides a potential therapeutic target for HCC treatment.

Background: The cross-section of thoracolumbar vertebral body is kidney-shaped with depressed posterior boundary. The anterior wall of the vertebral canal is separated from the posterior wall of the vertebral body on the lateral X-ray image. This study was designed to determine the sagittal distance between the anterior border of the vertebral canal and the posterior border of the vertebral body (DBCV) and to analyze the potential role of DBCV in the estimation of cement leakage during percutaneous vertebroplasty (PVP) or percutaneous kyphoplasty (PKP). Methods: We retrospectively recruited 233 patients who had osteoporotic vertebral compression fractures and were treated with PVP or PKP. Computed tomography images of T11–L2 normal vertebrae were measured to obtain DBCV. The distance from cement to the posterior wall of the vertebral body (DCPW) of thoracolumbar vertebrae was measured from C-arm images. The selected vertebrae were divided into two groups according to DCPW, with the fracture levels, fracture grades and leakage rates of the two groups compared. A relative operating characteristic (ROC) curve was applied to determine whether the DCPW difference can be used to estimate the degree of cement leakage. The data were processed by statistical software SPSS version 21.0 using independent sample t-test and Chi-square tests. Results: The maximum DBCV was 6.40 mm and the average DBCV was 3.74 ± 0.95 mm. DBCV appeared to be longer in males than in females, but the difference was not statistically significant. The average DCPW of type-B leakage vertebrae (2.59 ± 1.20 mm) was shorter than that of other vertebrae (7.83 ± 2.38 mm, P < 0.001). The leakage rate of group DCPW ≤6.40 mm was lower than that of group DCPW >6.40 mm for type-C and type-S, but much higher for type-B. ROC curve revealed that DCPW only has a predictive value for type-B leakage (area under the curve: 0.98, 95% confidence interval: 0.95–0.99, P < 0.001), and when the cut-off value was 4.05 mm, the diagnostic sensitivity and the specificity were 94.87% and 93.02%, respectively. Conclusions: Depression of the thoracolumbar posterior vertebral body may be informative for the estimation of cement location on C-arm images. To reduce type-B leakage, DCPW should be made longer than DBCV on C-arm images for safety during PVP or PKP.

Objective.To explore the antiprostate cancer effects of Celastrol on prostate cancer cells’ proliferation, apoptosis, and cell cycle distribution, as well as the correlation to the regulation of hERG.Methods.DU145 cells were treated with various concentrations of Celastrol (0.25–16.0 μmol/L) for 0–72 hours. MTT assay was used to evaluate the inhibition effect of Celastrol on the growth of DU145 cells. Cell apoptosis was detected through both Annexin-V FITC/PI double-labeled cytometry and Hoechst 33258. Cell cycle regulation was examined by a propidium iodide method. Western blot and RT-PCR technologies were applied to assess the expression level of hERG in DU145 cells.Results.Celastrol presented striking growth inhibition and apoptosis induction potency on DU145 cellsin vitroin a time- and dose-dependent manner. The IC50value of Celastrol for 24 hours was 2.349 ± 0.213 μmol/L. Moreover, Celastrol induced DU145 cell apoptosis in a cell cycle-dependent manner, which means Celastrol could arrest DU145 cells in G0/G1phase; accordingly, cells in S phase decreased gradually and no obvious changes were found in G2/M phase cells. Through transmission electron microscope, apoptotic bodies containing nuclear fragments were found in Celastrol-treated DU145 cells. Overexpression of hERG channel was found in DU145 cells, while Celastrol could downregulate it at both protein and mRNA level in a dose-dependent manner (P<0.01).Conclusions.Celastrol exhibits its antiprostate cancer effects partially through the downregulation of the expression level of hERG channel in DU145 cells, suggesting that Celastrol may be a potential agent against prostate cancer with a mechanism of blocking the hERG channel.

Guanine nucleotide binding protein, alpha inhibiting activity polypeptide 3 (GNAI3) is involved in many biological processes. However, its biological function in hepatocellular carcinoma (HCC) remains unclear. An immunohistochemical staining analysis revealed that GNAI3 protein was down-regulated in HCC compared to non-cancerous liver. Furthermore, transwell assays indicated that GNAI3 inhibits HCC cell migration and invasion. Using software predictions and experimental screening, we found that miR-222 could directly bind to GNAI3 mRNA and decrease GNAI3 protein expression in HCC cells. Moreover, miR-222 was up-regulated in HCC and negatively correlated with GNAI3 protein expression. These results indicated that down-regulation of GNAI3 might be caused by up-regulation of miR-222 in HCC. In conclusion, GNAI3 was down-regulated by miR-222 in HCC, and this deregulation promoted migration and invasion of HCC. These findings extended our insight into the complex molecular mechanisms underlying the invasion and metastasis of HCC and may provide new therapeutic targets.

// Yan Li 1,* , Dan Xu 1,* , Chunyang Bao 1,* , Yuannv Zhang 1 , Di Chen 1 , Fangyu Zhao 1 , Jie Ding 2 , Linhui Liang 2 , Qifeng Wang 2 , Li Liu 2 , Jinjun Li 1 , Ming Yao 1 , Shenglin Huang 2 and Xianghuo He 1,2 1 State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China 2 Fudan University Shanghai Cancer Center and Institutes of Biomedical Sciences, Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China * These authors contributed equally to this work Correspondence: Xianghuo He, email: // Shenglin Huang, email: // Keywords : MicroRNA-135b; RECK; EVI5; HSF1; Hepatocellular Carcinoma Received : September 24, 2014 Accepted : December 10, 2014 Published : December 11, 2014 Abstract MicroRNAs (miRNAs) often localize to chromosomal fragile sites and are associated with cancer. In this study, we screened for the aberrant and functional miRNAs in the regions of copy number alterations (CNAs) in hepatocellular carcinoma (HCC), and found that miR-135b was frequently amplified and upregulated in HCC tissues. The expression level of miR-135b was inversely correlated with the occurrence of tumor capsules. In addition, miR-135b promoted HCC cell migration and invasion in vitro and metastasis in vivo . The reversion-inducing-cysteine-rich protein with kazal motifs (RECK) and ecotropic viral integration site 5 (EVI5) were identified as the direct and functional targets of miR-135b in HCC. Furthermore, we observed that heat shock transcription factor 1 (HSF1) directly activated miR-135b expression, consequently enhancing HCC cell motility and invasiveness. The newly identified HSF1/miR-135b/RECK&EVI5 axis provides novel insight into the mechanisms of HCC metastasis, which may facilitate the development of new therapeutics against HCC.

Nanostructured iron oxides have been widely used in catalysis, adsorption, sensor, biomedicine, and so on. In this study, iron oxide nanoparticles containing nanosized cavities were prepared by hydrothermal treatment of a colloidal dispersion of iron hydroxide. The as-prepared sample and the one calcined in air at 450 °C were composed of well-dispersed rhombohedral-like α-Fe 2 O 3 nanoparticles; calcining in nitrogen resulted in a composite of α-Fe 2 O 3 and γ-Fe 2 O 3 having superparamagnetic property. Moreover, the iron oxide nanoparticles calcined in air or nitrogen have 7–15 nm- and 5–12 nm-diameter cavities, respectively. These peculiar structures might be conducive for some applications such as adsorption involving large molecules.

Unlike mammals, in palmipedes de novo lipogenesis from diet takes place mostly in the liver. The French Landes Goose is famous for its high capacity and susceptibility to fatty liver production. While miRNAs play a critical role in the posttranscriptional regulation of gene expression, miRNAs that are involved in the regulation of goose hepatic steatosis have yet to be elucidated. Using high-throughput sequencing, we analyzed miRNAs expression profile of Landes goose liver after overfeeding for 21 days. Aan-miR-122-5p was the most frequently sequenced known miRNA, but it was unchanged after overfeeding. Compared with normal liver, we identified that 16 conserved miRNAs were up-regulated while the other 9 conserved miRNAs were down-regulated in fatty livers. Many of their predicted target genes played key roles in metabolic pathways leading to the development of hepatic steatosis in the goose by KEGG pathways analysis. ACSL1 and ELOVL6 were critical genes in hepatic lipid metabolism and had opposite expression patterns with aan-miR-203a and aan-miR-125b-5p, respectively. And we validated that aan-miR-203a and aan-miR-125b-5p might involve in the regulation of hepatic lipid metabolism by targeting ACSL1 and ELOVL6, respectively. These results add to our current understanding of the regulation network in goose lipid metabolism.

We show that the set defined by digit restrictions contains arbitrarily long arithmetic progressions if and only if its Assouad dimension is one. Moreover, we show that for any $0\le s\le 1$, there exists some set on $\mathbb{R}$ with Hausdorff dimension $s$ whose Fourier dimension is zero and it contains arbitrarily long arithmetic progressions., 12 pages, 1 figures. We consider more general model and gave a new proof for Proposition 3.1

Hepatocellular carcinoma (HCC) is the leading cause of cancer-related mortality in China, and the molecular mechanism of uncontrolled HCC progression remains to be explored. NK3 homeobox 1 (NKX3.1), an androgen-regulated prostate-specific transcription factor, suppresses tumors in prostate cancer, but its role in HCC is unknown, especially in hepatocellular carcinoma. In the present study, the differential expression analyses in HCC tissues and matched adjacent noncancerous liver tissues revealed that NKX3.1 is frequently down-regulated in human primary HCC tissues compared with matched adjacent noncancerous liver tissues. We also noted that NKX3.1 significantly inhibits proliferation and mobility of HCC cells both in vitro and in vivo. Furthermore, NKX3.1 overexpression resulted in cell cycle arrest at the G1/S phase via direct binding to the promoter of forkhead box O1 (FOXO1) and up-regulation of expression. Of note, FOXO1 silencing in NKX3.1-overexpressing cells reversed the inhibitory effects of NKX3.1 on HCC cell proliferation and invasion. Consistently, both FOXO1 and NKX3.1 were down-regulated in human HCC tissues, and their expression was significantly and positively correlated with each other. These results suggest that NKX3.1 functions as a tumor suppressor in HCC cells through directly up-regulating FOXO1 expression.

Long noncoding RNAs (lncRNAs) have been associated with hepatocellular carcinoma (HCC), but the underlying molecular mechanisms of their specific association with hepatocarcinogenesis have not been fully explored. Methods: miR503HG was identified by microarray and validated by real-time PCR. Survival analysis was evaluated using the Kaplan-Meier method and assessed using the log-rank test. In vitro and in vivo assays were preformed to explore the biological effects of miR503HG in HCC cells. The interaction of miR503HG with HNRNPA2B1 was identified by RNA pull-down and RNA immunoprecipitation. Expression of HNRNPA2B1 was examined by western blotting, immunofluorescence and immunohistochemical analyses, while HNRNPA2B1 ubiquitination was detected by immunoprecipitation. Results: We have identified 713 differentially expressed lncRNAs in 12 pairs of HCC tissues compared with corresponding noncancerous liver tissues. One of these lncRNAs, miR503HG, the host gene of miR503, is markedly decreased in HCC. Expression level of miR503HG is significantly associated with the time to recurrence and overall survival and is an independent risk factor for recurrence and survival. Enhanced expression of miR503HG could noticeably inhibit HCC invasion and metastasis in vitro and in vivo. Further investigation suggested that miR503HG could specifically interact with the heterogeneous nuclear ribonucleoprotein A2/B1 (HNRNPA2B1). miR503HG promoted HNRNPA2B1 degradation via the ubiquitin-proteasome pathway, which reduced the stability of p52 and p65 mRNA, and simultaneously suppressed the NF-κB signaling pathway in HCC cells. In addition, miR503HG can function synergistically with miR503 to inhibit HCC migration. Conclusion: Our findings support a role for miR503HG in tumor recurrence risk and survival prediction in HCC patients. We demonstrate a novel mechanism by which miR503HG inhibits the NF-κB signaling pathway and exerts its metastatic tumor suppression function through modulating the ubiquitination status of HNRNPA2B1.

Primary non-Hodgkin's lymphoma of the vertebra is rare in the spine of the elderly. The clinical presentation and radiological features are unspecific, which make it more difficult for diagnosis. We report a case of a 79-year-old woman complaining of serious backache without any injury. The magnetic resonance imaging (MRI) showed invasion of the fifth thoracic vertebra with the posterior vertebral body wall defect. There was a high suspicion that the patient had a metastatic tumor of the vertebra. A percutaneous vertebroplasty was performed under fluoroscopic guidance, which was used to treat the osteoporotic vertebral compression fracture, vertebral metastases, verte-bral hemangioma, and multiple myeloma. The pain was rapidly and conspicuously relieved after the procedure. The visual analog scale (VAS) score decreased from 8 preoperatively to 2 postoperatively. The imaging examination postoperatively revealed a small amount cement leaking into the spinal canal, but there were no symptoms and no complications in our patient. During vertebroplasty, a biopsy was done by biopsy needle before injection of the cement (polymethyl methacrylate). The histopathological examination revealed a diffuse large B-cell lymphoma. No new evidence of any other lesion was found during a 6-month follow-up period. The patient was diagnosed with primary bone lymphoma finally. Due to the previous condition of the patient, R-miniCHOP chemotherapy was applied following the surgery in the department of hematology. Until the 9 months follow-up, the clinical result was still satisfactory.Vertebroplasty, polymethyl methacrylate, biopsy, spine, lymphoma, large B-cell, diffuse.

MDIG is known to be overexpressed in many types of human cancers and has demonstrated predictive power in the prognosis of cancer, although the functions and mechanisms of MDIG in liver cancer, especially in hepatocellular carcinoma (HCC), are still unknown. In this study, we report that MDIG and MYC were negatively regulated by IKZF1. MDIG overexpression substantially promoted HCC cell proliferation, cell migration and spreading, whereas knockdown of MDIG would reverse above-mentioned effect. MDIG effects on tumour cell growth were further demonstrated in a tumour xenograft model. Moreover, MDIG had effects on the level of p21(CIP1/WAF1) via H3K9me3 expression in HCC. MDIG was also found to be closely related to the sorafenib resistance of HCC cells in vitro. Clinically, we found that MDIG was frequently overexpressed in human HCCs (69.7%; n=155) and was significantly associated with histological grade and hepatitis B virus infection. Our findings indicate that MDIG plays an important role in HCC progression via MDIG/H3K9me3/p21(CIP1/WAF1) signalling and serves as a potential therapeutic target.

In this meta-analysis, evidence of an association between type 2 diabetes mellitus (T2DM) and low-energy fractures has been evaluated including 12 observational studies. The results suggested that T2DM patients had an enhanced risk of low-energy fractures. Type 1 diabetes mellitus (T1DM) patients have been shown to be at enhanced risk of fracture injury, but less is known about low-energy fractures among patients with T2DM. We performed a meta-analysis of 12 observational studies identified in Medline and EMBASE that included 938,742 participants, including 30,827 low-energy fracture cases. The incidence rate ratios (IRRs) of low-energy fractures were determined using a random-effects model. The IRRs of low-energy fracture for men and women were 1.37 (95% confidence interval [CI], 0.94–2.00; p = 0.096) and 1.22 (95% CI, 1.09–1.35; p = 0.000), respectively, and the overall IRR was 1.23 (95% CI, 1.12–1.35; p = 0.000). The IRRs for hip and vertebral fractures were 1.08 (95% CI, 1.02–1.15; p = 0.007) and 1.21 (95% CI, 0.98–1.48; p = 0.073), respectively. The IRRs of low-energy fracture in case-control, prospective, retrospective, and cross-sectional studies were 1.18 (95% CI, 0.81–1.72; p = 0.380), 1.17 (95% CI, 1.05–1.32, p = 0.006), 1.15 (95% CI, 1.02–1.29; p = 0.020), and 1.60 (95% CI, 1.21–2.12; p = 0.001), respectively. The IRRs of low-energy fracture for less than 5 years, 5 to 10 years, and more than 10 years were 1.30 (95%, CI 1.13–1.50; p = 0.000), 1.05 (95% CI, 1.03–1.08; p = 0.000), and 1.19 (95% CI, 1.00–1.41; p = 0.049), respectively. Patients with T2DM had a greater risk of low-energy fracture especially of the hip, compared with that in non-diabetic subjects. However, since according to our funnel plot a publication bias may be present and due to study heterogeneity as well as the limited number of publications, the finding needs to be interpreted with caution.

// Lin Zhang 1,* , Hong Li 1,* , Chao Ge 1 , Meng Li 1 , Fang-yu Zhao 1 , He-lei Hou 1 , Miao-xin Zhu 1 , Hua Tian 1 , Li-xing Zhang 1 , Tao-yang Chen 2 , Guo-ping Jiang 3 , Hai-yang Xie 3 , Ying Cui 4 , Ming Yao 1 and Jin-jun Li 1 1 State Key Laboratory of Oncogenes and Related Genes, Shanghai Cancer Institute, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China 2 Qi Dong Liver Cancer Institute, Qi Dong, China 3 Department of General Surgery, the First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China 4 Cancer Institute of Guangxi, Nanning, China * These authors contributed equally to this work Correspondence: Jin-jun Li, email: // Keywords : Ikaros; CD133; hepatocellular carcinoma; cancer stem cells Received : August 01, 2014 Accepted : September 24, 2014 Published : September 25, 2014 Abstract CD133 is a cellular surface glycoprotein that has been reported as a marker for the enrichment of cancer stem cells (CSCs). However, the regulatory mechanism of CD133 remains unknown. CSCs have been proposed to contribute to radioresistance and multi-drug resistance. The elucidation of key regulators of CD133 and CSCs is critical for the development of CSC-targeted therapy. In this study, we showed that Ikarosinhibited the expression of CD133 via direct binding to the CD133 P1 promoter and repressed the tumorigenic and self-renewal capacity of CD133 + cancer stem-like cells in hepatocellular carcinoma (HCC). We found that Ikaros interacted with CtBP as a transcription repressor complex, which inhibited CD133 expression in HCC. We also demonstrated that Ikaros expression was up-regulated by ETS1 which activity was regulated by MAPKs pathway. Furthermore, decreased expression of Ikaroswas significantly associated with poor survival in HCC patients. Overall, our study identifies that Ikaros plays a role as a transcription repressor in HCC and is a new reactivated therapeutic target for the treatment of HCC. Meanwhile, our findings provide evidence that Ikaros could be an attractive inhibitor of the target gene CD133, which reactivates anticancer mechanisms in targeted CSC therapy.

Mesoporous iron oxide-silica composite with a high silica content was synthesized by hydrothermal method, and another composite material with a high iron content was obtained by etching part of silica in alkaline solution. Gold catalysts were loaded onto both composites by a deposition-precipitation method, and used for CO oxidation. The samples were characterized by Brumauer-Emmet-Teller (BET), X-ray diffraction (XRD), X-ray photoelectron spectra (XPS), transmission electron microscope (TEM) and scanning electron microscope (SEM) techniques. Both composites had high specific surface areas and were amorphous. The Au nanoparticles dispersed on the surface of the composites existed in metallic state. Composite with high silica content was not suitable for Au loading, and its supported gold catalyst showed poor performance in catalytic reaction. In contrast, composite with high iron content allowed efficient Au loading, and CO could be oxidized completely at low temperature on its supported gold catalyst. The effects of deposition-precipitation pH values on Au loading and activity of the catalyst were investigated, and the results indicated that Au loading was the highest and the catalyst was the most active for CO oxidation when the synthesis pH was adjusted to 8.

Rising temperatures are severely affecting the mortality, laying performance, and meat quality of duck. Our aim was to investigate the effect of acute heat stress on the expression of heat shock proteins (HSPs: HSP90, 70, 60, 40, and 10) and inflammatory factors (nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2)) and antioxidant enzyme activity (superoxide dismutase (SOD), malondialdehybe (MDA), catalase (CAT), total antioxidant capacity (T-AOC)) in livers of ducks and to compare the thermal tolerance of Pekin and Muscovy ducks exposed to acute heat stress. Ducks were exposed to heat at 39 ± 0.5 °C for 1 h and then returned to 20 °C for 1 h followed by a 3-h recovery period. The liver and other tissues were collected from each individual for analysis. The mRNA levels of HSPs (70, 60, and 40) increased in both species, except for HSP10, which was upregulated in Muscovy ducks and had no difference in Pekin ducks after heat stress. Simultaneously, the mRNA level of HSP90 decreased in the stress group in both species. Morphological analysis indicated that heat stress induced tissue injury in both species, and the liver of Pekin ducks was severely damaged. The activities of several antioxidant enzymes increased in Muscovy duck liver, but decreased in Pekin duck. The mRNA levels of inflammatory factors were increased after heat stress in both duck species. These results suggested that heat stress could influence HSPs, inflammatory factors expression, and the activities of antioxidant enzymes. Moreover, the differential response to heat stress indicated that the Muscovy duck has a better thermal tolerance than does the Pekin duck.

Manganese oxides with various morphologies and crystal structures for catalytic oxidation of air pollutants were synthesized by reacting fresh manganese hydroxide and acetic acid (HAc) at an HAc/Mn molar ratio of 1, 2 or 3. The characterizations and activity tests indicates that the HAc/Mn ratio has significant influence on the properties and the catalytic activities of the produced manganese oxides. Manganese oxide produced at an HAc/Mn ratio of 2 is composed of nanorods having relatively uniform diameters, and it possesses the most reducible manganese oxide species and the highest content of surface adsorbed oxygen species, which could contribute to its best activity in the catalytic deep oxidation of toluene. Manganese oxide produced at an HAc/Mn ratio of 3 possesses the largest specific surface area and is the most efficient in the catalytic oxidation of carbon monoxide. Palladium was impregnated onto manganese oxide at a loading of 0.3 wt% to investigate their combined effects on catalytic destruction of the pollutants. The incorporation of palladium causes decreased activity in catalytic oxidation of toluene, which might be associated with the reduction in the amount of active surface oxygen species on the catalyst. In contrast, palladium actually promotes the catalytic oxidation of carbon monoxide probably due to the additional adsorption of carbon monoxide on noble metal.

For one-dimensional simple symmetric random walks, we prove that the irregular set associated with the rate of returns to the origin is residual.

To identify cancer-related proteins, we used isobaric tags in a relative and absolute quantitation (iTRAQ) proteomic approach and SWATH™ quantification approach to analyze the secretome of an isogenic pair of highly metastatic and low metastatic non-small-cell lung cancer (NSCLC) cell lines. In addition, we compared two groups of pooled serum samples (12 early-stage and 12 late-stage patients) to mine data for candidates screened by iTRAQ-labeled proteomic analysis. A total of 110 proteins and 71 proteins were observed to be significantly differentially expressed in the cell line secretome and NSCLC sera, respectively. Among these proteins, CD109 was found to be highly expressed in both the highly metastatic cell line secretome and the group of late-stage patients. A sandwich ELISA assay also demonstrated an elevation of serum CD109 levels in individual NSCLC patients (n = 30) compared with healthy subjects (n = 19). Furthermore, CD109 displayed higher expression in lung cancer tissues compared with their matched noncancerous lung tissues (n = 72). In addition, the knockdown of CD109 influenced several NSCLC cell bio-functions, for instance, depressing cell growth, affecting cell cycle phases. These phenomena suggest that CD109 plays a critical role in NSCLC progression. Biological significance We simultaneously applied two quantitative proteomic approaches—iTRAQ-labeling and SWATH™—to analyze the secretome of metastatic cell lines, in order to explore the cancer-associated proteins in conditioned media. In this study, our results indicate that CD109 plays a critical role in non-small-cell lung cancer (NSCLC) progression, and is overexpressed in advanced NSCLC.

A series of CuCeO x binary oxide catalysts with high specific surface area and mesoporous structure were synthesized by a facile self-precipitation approach. Toluene and propanal were adopted as the probe pollutants to evaluate their catalytic performance. The techniques such as XRD, N 2 adsorption/desorption, FE-SEM, TEM, H 2 -TPR, XPS, Raman, DRUV–vis, and XANES, were employed for catalyst characterization. It is shown that plenty of Cu 2+ ions in mesoporous CuCeO x oxides are incorporated into CeO 2 lattice in the form of Cu x Ce 1− x O 2− δ solid solution, which produces large amounts of oxygen vacancies in the interface of CuO x and CeO 2 oxides. Meanwhile, the Cu 2+ -O 2− -Ce 4+ connection in the solid solution can act as a bridge for oxygen transfer between Cu and Ce, and enhance the reducibility of both components. The activity of mesoporous CuCeO x catalysts exhibits a volcano-type behavior with the increase of the Cu content, and the sample with Cu/Ce atomic ratio of 3/7 exhibits the highest catalytic efficiency. At GHSV of 36,000 h −1 , the temperatures for 90% toluene and propanal conversion over Cu 0.3 Ce 0.7 O x sample are 212 and 192 °C, respectively, which are much lower than the catalysts synthesized via the incipient impregnation and thermal combustion methods. The co-combustion result demonstrates that propanal oxidation can be remarkably suppressed by the introduction of toluene due to the stronger surface affinity of toluene molecules. It can be concluded that both the higher surface oxygen adspeices concentration and better low-temperature reducibility were responsible for the superior activity of mesoporous CuCeO x catalysts.

Ribonucleotide reductase (RR)M2B is an enzyme belonging to the ribonucleotide reductase enzyme family, which is essential for DNA synthesis and repair. RRM2B plays an important role in tumor progression and metastasis; however, little is known about the expression and underlying molecular mechanisms of RRM2B in hepatocellular carcinoma (HCC). In the present study, we report that down-regulation of RRM2B in HCC is negatively associated with intrahepatic metastasis, regardless of p53 status. Moreover, the ectopic overexpression of RRM2B decreased HCC cell migration and invasion in vitro, whereas silencing RRM2B expression resulted in increased migration and invasion in vitro and intrahepatic and lung metastasis in vivo. Additionally, knockdown of RRM2B by short hairpin RNA (shRNA) in HCC cells was associated with epithelial-mesenchymal transition (EMT), including the down-regulation of E-cadherin, and the concomitant up-regulation of N-cadherin and slug. A further experiment showed that RRM2B inhibited cell migration and spreading through regulation of the early growth response protein 1 (Egr-1) / phosphatase and tensin homolog (PTEN) / Akt1 pathway. Consistently, we also detected a significant correlation between RRM2B and E-cadherin protein expression in HCC tissues. Furthermore, Egr-1 also directly bound to the RRM2B promoter and repressed RRM2B transcription, thereby establishing a negative regulatory feedback loop. Conclusion: These findings indicate that RRM2B suppresses cell migration and spreading by way of modulation of the Egr-1/PTEN/Akt1 pathway. (Hepatology 2014;59:1459-1470)

MicroRNAs (miRNAs) are endogenous small noncoding RNAs plays a critical role in posttranscriptional regulation of gene expression. Broodiness is observed in most avian species and influences egg production. Several genes are known to play an important role in regulating the progress of reproduction. The goose is one of the most important waterfowls. However, the involvement of miRNAs in the broodiness behavior of Ansercygnoides (Swan Goose) is unknown. High-throughput sequencing and bioinformatics analysis were used to identify the miRNAs involved in egg-laying and brooding behavior of geese in our study. The results showed 38 up-regulated and 14 down-regulated known miRNAs/miRNA*s with reads >1,000 in at least one group and a fold change of >2.0, compared with those of the egg-laying group (P < 0.001). We also identified 114 and 94 novel miRNAs in the broody and egg-laying groups, respectively. Of these, 4 novel miRNAs were differentially expressed between the two groups. The study showed the expression of small RNAs in goose reproduction and identified known and novel miRNAs regulated in broodiness. The results reveal that these differentially expressed miRNAs may be involved in broodiness of A.cygnoides.

We have previously identified 1 241 regions of somatic copy number alterations (CNAs) in hepatocellular carcinoma (HCC). In the present study, we found that a novel recurrent focal amplicon, 1q24.1-24.2, targets the MPZL1 gene in HCC. Notably, there is a positive correlation between the expression levels of MPZL1 and intrahepatic metastasis of the HCC specimens. MPZL1 can significantly enhance the migratory and metastatic potential of the HCC cells. Moreover, we found that one of the mechanisms by which MPZL1 promotes HCC cell migration is by inducing the phosphorylation and activation of the pro-metastatic protein, cortactin. Additionally, we found that Src kinase mediates the phosphorylation and activation of cortactin induced by MPZL1 overexpression. Taken together, these findings suggest that MPZL1 is a novel pro-metastatic gene targeted by a recurrent region of copy number amplification at 1q24.1-24.2 in HCC.

Hepatocellular carcinoma is highly chemoresistant, and ATP-binding cassette subfamily G member 2 (ABCG2) is thought to play a critical role in this drug resistance. The present study aims to develop effective therapeutic strategies to decrease ABCG2 expression level and to surmount drug resistance in hepatocellular carcinoma chemotherapy. First, we verified a positive correlation between the ABCG2 protein level and the drug resistance of hepatocellular carcinoma cell lines. ABCG2 was preferentially expressed in highly chemoresistant hepatocellular carcinoma cancer stem cells (CSC) enriched with CD133. In addition, ABCG2 was N-linked glycosylated in hepatocellular carcinoma cells, and this modification was involved in sustaining its protein stability. The N-linked glycosylation (NLG) inhibitor tunicamycin dramatically reduced ABCG2 expression, altered its subcellular localization, and reversed its drug efflux effect in multiple hepatocellular carcinoma cell lines. Furthermore, tunicamycin reduced the expression levels of several CSC markers and suppressed the tumorigenicity of CD133+ CSCs. Tunicamycin combined with cisplatin (CDDP) inhibited proliferating cell nuclear antigen (PCNA) expression and increased the cleavage of PARP; this effect was partially rescued by the overexpression of ABCG2 or Akt-myr. The combination therapy more effectively suppressed tumor growth in xenograft mice than did single-agent therapy with either drug. Finally, the CDDP treatment combined with UDP-GlcNAc-dolichol-phosphate N-acetylglucosamine-1 phosphate transferase (DPAGT1) knockdown recapitulated the effect observed when CDDP was used in combination with tunicamycin. In summary, our results suggest that tunicamycin may reverse the drug resistance and improve the efficacy of combination treatments for hepatocellular carcinomas by targeting the DPAGT1/Akt/ABCG2 pathway. Mol Cancer Ther; 12(12); 2874–84. ©2013 AACR.

The decolorization of Orange II in goethite/UV system was investigated. It was discovered that the optimum condition is: pH=3, [α-FeOOH]=0.5 g/L, [Orange II]=10 mg/L. Furthermore, the absorption of Orange II on goethite, and the effect of pH values, goethite dosage and carboxylate on the decolorization were investigated. The decolorization efficiency was 90% after 6h irradiation when the concentration of pyruvic acid was 1.0mmol/L, α-FeOOH concentration was 0.3 g/L, and Orange II concentration was 10 mg/L at pH 3.0. Besides, total organic carbon (TOC) and chemical oxygen demand (COD) were determined, and a possible reaction mechanism was prompted as well.

Photooxidation of arsenite(As(III)) in a suspension of natural montmorillonite under the irradiation of metal halide lamp ( λ ≥ 313 nm)has been investigated. The results showed that the natural montmorillonite induced the photooxidation of As(III) by generating hydroxyl radicals (HO ) and hydroperoxyl/superoxide radicals (HO 2 /O 2 − ). HO which was responsible for the As(III) photooxidation. Approximately 38% of HO was generated by the photolysis of ferric ions, and the formation of the remaining 62% was strongly dependent on the HO 2 /O 2 − . The presence of free ironions (Fe 2+ and Fe 3+ ), made significant contributions to the photogeneration of these reactive oxygen species (ROS). The photooxidation of As(III) in natural montmorillonite suspensions was greatly influenced by the pH values. The photooxidation of As(III) by natural montmorillonite followed the Langmuir–Hinshelwood equation. In addition, the photooxidation of As(III) could be enhanced by the addition of humic acid. This work demonstrates that photooxidation may be an important environmental process for the oxidation of As(III) and may be a way to remove As(III) from acidic surface water containing iron-bearing clay minerals.

Let μ be a self-similar measure supported on a self-similar set K with the open set condition. For x ∈ K , let A ( D ( x ) ) be the set of accumulation points of D r ( x ) = log μ ( B ( x , r ) ) log r as r ↘ 0 . In this paper, we show that for any closed non-singleton subinterval I ⊂ R , the set of points x for which the set A ( D ( x ) ) equals I is either empty or residual.

Let $f$ be a continuous map on a compact metric space. In this paper, under the hypothesis that $f$ satisfies the specification property, we prove that the set consisting of those points for which the Birkhoff ergodic average does not exist is either residual or empty.

Nuclear factor kappa B (NF-κB) is an important factor linking inflammation and tumorigenesis. In this study we experimentally demonstrated through a high-throughput luciferase reporter screen that NF-κB signaling can be directly targeted by nearly 29 microRNAs (miRNAs). Many of these miRNAs can directly target NF-κB signaling nodes by binding to their 3′ untranslated region (UTR). miR-195, a member of the miR-15 family, is frequently down-regulated in gastrointestinal cancers, especially in hepatocellular carcinoma (HCC). The expression level of miR-195 is inversely correlated with HCC tumor size. We further show that miR-195 suppresses cancer cell proliferation and migration in vitro and reduces tumorigenicity and metastasis in vivo. Additionally, miR-195 may exert its tumor suppressive function by decreasing the expression of multiple NF-κB downstream effectors by way of the direct targeting of IKKα and TAB3. Conclusion: Multiple miRNAs are involved in the NF-κB signaling pathway and miR-195 plays important inhibitory roles in cancer progression and may be a potential therapeutic target. (Hepatology 2013;58:654–666)

Manganese oxide catalyst was prepared by a novel dispersion–precipitation method, which involved synthesis of stable aqueous dispersion of manganese oxide nanoparticles and the subsequent precipitation by dilution-induced destabilization. The characterizations indicated that the thus prepared catalyst was composed of nanorod particles with a Hausmannite structure of Mn 3 O 4 , and had a high reducibility. In comparison to the catalysts prepared by alkaline-salt reaction or calcination of manganese acetate, this catalyst prepared by the new method showed much better performance in the catalytic complete oxidation of airborne carbon monoxide and toluene, which is possibly attributed to the smaller particle sizes and higher oxygen mobility.

Let $f$ be a continuous transformation of a compact metric space $(X,d)$ and $\varphi$ any continuous function on $X$. In this paper, under the hypothesis that $f$ satisfies the specification property, we determine the topological entropy of the following sets: $$K_{I}=\Big\{x\in X: A\big(\frac{1}{n}\sum_{i=0}^{n-1}\varphi(f^{i}(x))\big)=I\Big\},$$ where $I$ is a closed subinterval of $\mathbb{R}$ and $A(a_{n})$ denotes the set of accumulation points of the sequence $\{a_{n}\}_{n}$. Our result generalizes the classical result of Takens and Verbitskiy ( Ergod. Th. Dynam. Sys., 23 (2003), 317-348 ). As an application, we present another concise proof of the fact that the irregular set has full topological entropy if $f$ satisfies the specification property.

We prove that the Assouad dimensions of a class of Moran sets coincide with their upper box dimensions and packing dimensions.

Forkhead box P1 (FOXP1) belongs to a family of winged-helix transcription factors that are involved in the processes of cellular proliferation, differentiation, metabolism, and longevity. FOXP1 can affect cell proliferation and migratory ability in hepatocellular carcinoma (HCC) in vitro. However, little is known about the mechanism of FOXP1 in the proliferation of HCC cells. This study aimed to further explore the function of FOXP1 on the proliferation of HCC cells as well as the relevant mechanism involved. Western blot analysis, tumor xenograft models, and flow cytometry analysis were performed to elucidate the function of FOXP1 in the regulation of cell proliferation in human HCC. We observed that silencing FOXP1 significantly suppressed the growth ability of HCC cells both in vitro and in vivo. In addition, knockdown of FOXP1 induced G1/S phase arrest, and the expression of total and phosphorylated Rb (active type) as well as the levels of E2F1 were markedly decreased at 24 h; however, other proteins, including cyclin-dependent kinase (CDK) 4 and 6 and cyclin D1 did not show noticeable changes. In conclusion, downregulation of FOXP1 inhibits cell proliferation in hepatocellular carcinoma by inducing G1/S phase cell cycle arrest, and the decrease in phosphorylated Rb is the main contributor to this G1/S phase arrest.

Percutaneous vertebroplasty (PVP) has been shown to release spinal pain and stabilize the vertebral body. PVP is suggested as an alternative treatment in spinal metastasis. Although cervical metastases is less prevalent than thoracic and lumbar spine, PVP procedure in cervical vertebrae remains technical challenging. We retrospectively analyzed the data from patients (n=9) who underwent PVP using anterolateral approach to treat severe neck pain and restricted cervical mobility from metastatic disease. Patients were rated using modified Tokuhashi score and Tomita score before the procedure. Visual analog scale (VAS), neck disability index (NDI), analgesic use, and imaging (X-ray or CT) were evaluated before PVP and 3 days, 3 months, and 6 months after PVP. All patients were in late stage of cancer evaluated using modified Tokuhashi and Tomita score. The cement leakage rate was 63.6% (14 of the 22 vertebrae) with no severe complications. VAS, NDI, and analgesic use were significantly decreased 3 days after the procedure and remained at low level until 6 months of follow-up. Our result suggested PVP effectively released the pain from patients with cervical metastasis. The results warrant further clinical investigation.

Background Snail is a typical transcription factor that could induce epithelial-mesenchymal transition (EMT) and cancer progression. There are some related reports about the clinical significance of snail protein expression in gastric cancer. However, the published results were not completely consistent. This study was aimed to investigate snail expression and clinical significance in gastric cancer. Results A systematic review of PubMed, CNKI, Weipu, and Wanfang database before March 2015 was conducted. We established an inclusion criterion according to subjects, method of detection, and results evaluation of snail protein. Meta-analysis was conducted using RevMan4.2 software. And merged odds ratio (OR) and 95 % CI (95 % confidence interval) were calculated. Also, forest plots and funnel plot were used to assess the potential of publication bias. A total of 10 studies were recruited. The meta-analysis was conducted to evaluate the positive rate of snail protein expression. OR and 95 % CI for different groups were listed below: (1) gastric cancer and para-carcinoma tissue [OR = 6.15, 95 % CI (4.70, 8.05)]; (2) gastric cancer and normal gastric tissue [OR = 17.00, 95 % CI (10.08, 28.67)]; (3) non-lymph node metastasis and lymph node metastasis [OR = 0.40, 95 % CI (0.18, 0.93)]; (4) poor differentiated cancer, highly differentiated cancer, and moderate cancer [OR = 3.34, 95 % CI (2.22, 5.03)]; (5) clinical stage TI + TII and stage TIII + TIV [OR = 0.38, 95 % CI (0.23, 0.60)]; (6) superficial muscularis and deep muscularis [OR = 0.18, 95 % CI (0.11, 0.31)]. Conclusions Our results indicated that the increase of snail protein expression may play an important role in the carcinogenesis, progression, and metastasis of gastric cancer. And this result might provide instruction for the diagnosis, therapy, and prognosis of gastric cancer.