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In this work, stainless steel pickling sludge (SSPS) and Ni-bearing electroplating sludge (ES) were co-treated to prepare Ni matte and Fe–Cr–Si alloy. A two-stage sulfurization-smelting method was used for preparing the Ni matte. At the sulfurization stage, carbon, SSPS, and ES were mixed and reacted at 1000 °C. It was found that NiO in the SSPS and ES can be sulfurized to (Fe,Ni)0.955S by CaSO4. After that, the sulfurized sludge was smelted at 1450 °C, and the liquid Fe–Ni–S matte was separated from slag by gravity at this stage. The Ni grade (37.5 wt pct) of the matte prepared at a C/CaSO4 molar ratio of 4 was higher than most of the industrial mattes (13 to 35 wt pct). Meanwhile, the recovery efficiency of Ni was 98.1 pct. For recovering Cr, Fe–Cr–Si alloy was prepared by the silicothermic reduction of the smelting slag. The sulfur (0.008 wt pct) and carbon (0.01 wt pct) contents of the Fe–Cr–Si alloy produced were lower than the threshold values for commercial Fe–Cr–Si alloy (0.01 wt pct S, 0.02 wt pct C). Therefore, this alloy can be used for stainless steel making. [ABSTRACT FROM AUTHOR]

In the present work, a novel method of producing Ni–Fe–S matte from saprolite type laterite (SL) ores was proposed using CaS as the sulfurization agent at 1500 °C under Ar atmosphere. The prepared Ni–Fe–S matte could be used as the raw material for the preparation of metallic nickel. CaS was prepared by reducing CaSO4 with graphite under Ar atmosphere. It was found that as increasing CaS addition, the recovery extents of Ni increases, while the Ni grade of Ni–Fe–S matte decreases. When the CaS addition was 6 times of the stoichiometric quantity required for the sulfurization of NiO, the recovery extents of Ni, Ni grade and CaS utilization degree reach to 93.63 pct, 8.84 wt pct and 92.10 pct, respectively. Compared with the reported method of using S2 as the sulfurization agent, the use of CaS in the present work can reduce the SO2 emission and improve the recovery extent of Ni. Besides, the feasibility of using CaSO4 as the sulfurization agent was also investigated at 1500 °C. Unfortunately, the carbon, which was used to reduce the CaSO4, could also react with NiO and Fe2O3 to produce the Ni–Fe alloy at 1500 °C. Accordingly, CaS is a better sulfurization agent than CaSO4. [ABSTRACT FROM AUTHOR]

Phenolic compounds are widely present in domestic and industrial sewage and have serious environmental hazards. Electrochemical oxidation (EO) is one of the most promising methods for sewage degradation because of its high efficiency, environmental compatibility, and safety. In this work, we present an in-depth overview of the mechanism and factors affecting the degradation of phenolic compounds by EO. In particular, the effects of treatment of phenolic compounds with different anode materials are discussed in detail. The non-active anode shows higher degradation efficiency, less intermediate accumulation, and lower energy consumption than the active anode. EO combined with other treatment methods (biological, photo, and Fenton) presents advantages, such as low energy consumption and high degradation rate. Meanwhile, the remaining drawbacks of the EO process in the phenolic compound treatment system have been discussed. Furthermore, future research directions are put forward to improve the feasibility of the practical application of EO technology. [ABSTRACT FROM AUTHOR]

Stainless steel pickling sludge is the precipitate from the neutralization process of stainless steel pickling liquor. Until now, many methods about the harmless treatments of pickling sludge have been developed, and among them the most effective one is to produce Fe-Cr-Ni alloy by carbothermic reduction process. However, the carbon and sulfur (harmful elements for steel) contents of the produced Fe-Cr-Ni alloy are difficult to be controlled, especially for the high-CaSO4 sludge. The current paper proposed a new method to produce the low-carbon and low-sulfur Fe-Cr-Ni-Si alloy by using the high-CaSO4 stainless steel pickling sludge. Firstly, the sludge was pre-reduced by carbon at 1100 °C. Then, the pre-reduced sludge was mixed with silicon powder and reacted at 1550 °C for the deep reduction, separation, and desulfurization. By the current method, the Fe-Cr-Ni-Si alloy with a carbon content of 0.513 wt pct and a sulfur content of 0.003 wt pct was produced. Meanwhile, the Fe, Cr, and Ni contents in alloys were 59.600, 15.440, and 13.570 wt pct, with recovery rates of 97.99, 97.61, and 98.65 pct, respectively. Such an alloy can be used as the alloy additive for stainless steel production. [ABSTRACT FROM AUTHOR]

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In the present work, Zn–10Al–2Cu–0.05Ti (ZA10) alloy tubes with a diameter of 12.5 mm and wall thickness of 1.2 mm were fabricated by one-pass and double-pass Conform continuous extrusion. A stabilizing heat treatment [350 °C, 30 min (furnace cooling) + 120 °C, 12 h (air cooling)] was also applied to some of the double-pass tubes to improve the quality of their weld seams. The yield strength, ultimate tensile strength, elongation and expansion ratio of the one-pass continuous extrusion tube were 268.4 MPa, 294.3 MPa, 13.8% and 5.5%, respectively. Double-pass continuous extrusion improved these values to 278.4 MPa, 317.2 MPa, 15.4% and 11.4%, respectively. Double-pass tubes also had fewer aggregations of Al-α precipitates along the welding seam, which improved seam quality and caused cracks to appear in the matrix, away from the weld-affected zone, during expansion testing. Heat-treated double-pass tubes exhibited superior yield strength (283.9 MPa) and ultimate tensile strength (328.5 MPa) but lower elongation (10.2%) and expansion ratios (10.3%). Additionally, the heat-treated tubes exhibited markedly lower elongation at room temperature due to the remarkable blockage of dislocation motions by fine-scale lamellar (α + η) eutectoid structures and a lower size effect when stretched. [ABSTRACT FROM AUTHOR]

Software defect prediction is aimed to find potential defects based on historical data and software features. Software features can reflect the characteristics of software modules. However, some of these features may be more relevant to the class (defective or non-defective), but others may be redundant or irrelevant. To fully measure the correlation between different features and the class, we present a feature selection approach based on a similarity measure (SM) for software defect prediction. First, the feature weights are updated according to the similarity of samples in different classes. Second, a feature ranking list is generated by sorting the feature weights in descending order, and all feature subsets are selected from the feature ranking list in sequence. Finally, all feature subsets are evaluated on a k-nearest neighbor (KNN) model and measured by an area under curve (AUC) metric for classification performance. The experiments are conducted on 11 National Aeronautics and Space Administration (NASA) datasets, and the results show that our approach performs better than or is comparable to the compared feature selection approaches in terms of classification performance. [ABSTRACT FROM AUTHOR]

Edges are important cues for localizing object proposals. The recent progresses to this problem are mostly driven by defining effective objectness measures based on edge cues. In this paper, we develop a new representation named directional edges on which each edge pixel is assigned with a direction toward object center, through learning a direction prediction model with convolutional neural networks in a holistic manner. Based on directional edges, two new objectness measures are designed for ranking object proposals. Experiments show that the proposed method achieves 97 .1% object recall at an overlap threshold of 0 .5 and 81 .9% object recall at an overlap threshold of 0 .7 at 1 000 proposals on the PASCAL VOC 2007 test dataset, which is superior to the state-of-the-art methods. [ABSTRACT FROM AUTHOR]

On the global scale, hepatitis B virus (HBV) infection is the main cause of hepatocellular carcinoma (HCC) especially in regions of Asia where HBV infection is endemic. Epidemiological studies show that the incidence of inflammation-driven HCC in males is three times as high as in females. Recent studies suggest that sex hormones have a crucial role in the pathogenesis and development of HBV-induced HCC. We found that the estrogen/androgen signaling pathway is associated with decreased/increased transcription and replication of HBV genes and can promote the development of HBV infections by up/downregulating HBV RNA transcription and inflammatory cytokines levels, which in turn slow down the progression of HBV-induced HCC. Additionally, sex hormones can also affect HBV-related HCC by inducing epigenetic changes. The evidence that both morphology and function of the human liver are affected by sex hormones was found over 60 years ago. However, the underlying molecular mechanism largely remains to be elucidated. This review focuses mainly on the molecular mechanisms behind the sex difference in HCC associated with HBV and other factors. In addition, several potential treatment and therapeutic strategies for inflammation-driven HCC will be introduced in this review. [ABSTRACT FROM AUTHOR]

A couple with a proband child of GJB2 (encoding the gap junction protein connexin 26)-associated hearing impairment and a previous pregnancy miscarriage sought for a reproductive solution to bear a healthy child. Our study aimed to develop a customized preconception-to-neonate care trajectory to fulfill this clinical demand by integrating preimplantation genetic diagnosis (PGD), noninvasive prenatal testing (NIPT), and noninvasive prenatal diagnosis (NIPD) into the strategy. Auditory and genetic diagnosis of the proband child was carried out to identify the disease causative mutations. The couple then received in-vitro-fertilization treatment, and eight embryos were obtained for day 5 biopsy. PGD was performed by short-tandem-repeat linkage analysis and Sanger sequencing of GJB2 gene. Transfer of a GJB2c.235delC heterozygous embryo resulted in a singleton pregnancy. At the 13th week of gestation, genomic DNA (gDNA) from the trio family and cell-free DNA (cfDNA) from maternal plasma were obtained for assessment of fetal chromosomal aneuploidy and GJB2 mutations. NIPT and NIPD showed the absence of chromosomal aneuploidy and GJB2-associated disease in the fetus, which was later confirmed by invasive procedures and postnatal genetic/auditory diagnosis. This strategy successfully prevented the transmission of hearing impairment in the newborn, thus providing a valuable experience in reproductive management of similar cases and potentially other monogenic disorders. [ABSTRACT FROM AUTHOR]

Hepatocytes are critical for the maintenance of liver homeostasis, but its involvement in hepatic fibrogenesis remains elusive. Hepatocyte nuclear factor 1α (HNF1α) is a liver-enriched transcription factor that plays a key role in hepatocyte function. Our previous study revealed a significant inhibitory effect of HNF1α on hepatocellular carcinoma. In this study, we report that the expression of HNF1α is significantly repressed in both human and rat fibrotic liver. Knockdown of HNF1α in the liver significantly aggravates hepatic fibrogenesis in either dimethylnitrosamine (DMN) or bile duct ligation (BDL) model in rats. In contrast, forced expression of HNF1α markedly alleviates hepatic fibrosis. HNF1α regulates the transcriptional expression of SH2 domain-containing phosphatase-1 (SHP-1) via directly binding to SHP-1 promoter in hepatocytes. Inhibition of SHP-1 expression abrogates the anti-fibrotic effect of HNF1α in DMN-treated rats. Moreover, HNF1α repression in primary hepatocytes leads to the activation of NF-κB and JAK/STAT pathways and initiates an inflammatory feedback circuit consisting of HNF1α, SHP-1, STAT3, p65, miR-21 and miR-146a, which sustains the deregulation of HNF1α in hepatocytes. More interestingly, a coordinated crosstalk between hepatocytes and hepatic stellate cells (HSCs) participates in this positive feedback circuit and facilitates the progression of hepatocellular damage. Our findings demonstrate that impaired hepatocytes play an active role in hepatic fibrogenesis. Early intervention of HNF1α-regulated inflammatory feedback loop in hepatocytes may have beneficial effects in the treatment of chronic liver diseases. [ABSTRACT FROM AUTHOR]

Aim:To evaluate the effects of UDP-glucuronosyltransferases (UGTs) polymorphisms on the pharmacokinetics of the immunosuppressant mycophenolate mofetil (MMF) in Chinese renal transplant recipients.Methods:A total of 127 renal transplant patients receiving MMF were genotyped for polymorphisms in UGT1A9 −1818T>C, I399C>T, −118T9/10, −440C>T, −331T>C, UGT2B7 IVS1+985A>G, 211G>T, −900A>G, UGT1A8 518C>G and UGT1A7 622T>C. The plasma concentrations of the MMF active moiety mycophenolic acid (MPA) and main metabolite 7-O-MPA-glucuronide (MPAG) were analyzed using HPLC. Univariate and multivariate analyses were used to assess the effects of UGT-related gene polymorphisms on MPA pharmacokinetics.Results:The dose-adjusted MPA AUC0-12 h of the patients with the UGT2B7 IVS1+985AG genotype was 48% higher than that of the patients with the IVS1+985AA genotype, which could explain 11.2% of the inter-individual variation in MPA pharmacokinetics. The dose-adjusted MPAG AUC0-12 h of the patients with the UGT1A7 622CC and UGT1A9 −440CT/−331TC genotypes, respectively, was significantly higher than that of the patients with 622T homozygotes and −440C/−331T homozygotes. Furthermore, the genotypes UGT1A9 −1818T>C and UGT1A8 518C>G were associated with a low dose-adjusted MPAG AUC0-12 h.Conclusion:The UGT2B7 11+985A>G genotype is associated with the pharmacokinetics of MPA in Chinese renal transplant patients, which demonstrates the usefulness of this SNP for individualizing MMF dosing. [ABSTRACT FROM AUTHOR]

CKAP4, one kind of type II trans-membrane protein, plays an important role to maintain endoplasmic reticulum structure and inhibits the proliferation of bladder cancer cells by combining its ligand anti-proliferative factor (APF). However, the biological function of CKAP4 in the progression of liver cancer has not been clearly demonstrated. In the present study, we knocked down or overexpressed CKAP4 in hepatocellular carcinoma (HCC) cells and cell proliferation, invasion, and migration capacities were investigated by CCK-8 and transwell assays. In vivo tumor model in mice was used to evaluate the role of CKAP4 on growth and metastasis of HCC. The data documented that HCC cells with high CKAP4 levels were featured by low proliferation capability as well as low invasion potential. Interestingly, we found that CKAP4 suppressed the activation of epithelial growth factor receptor (EGFR) signaling, which may partly explain the role of CKAP4 in cell biological behavior of HCC. Further study revealed that CKAP4 could associate with EGFR at basal status and the complex was reduced upon EGF stimulation, leading to release EGFR into cytoplasm. Thus, we demonstrate the novel mechanism, for the first time, expression of CKAP4 regulates progression and metastasis of HCC and it may provide therapeutic values in this tumor. [ABSTRACT FROM AUTHOR]

Aim:Free fatty acid-induced lipotoxicity plays a crucial role in the progression of nonalcoholic fatty liver disease (NAFLD). In the present study we investigated the effects of a high-fat diet and free fatty acids on the autophagic process in hepatocytes in vivo and in vitro and the underlying mechanisms.Methods:LC3-II expression, a hallmark of autophagic flux, was detected in liver specimens from patients with non-alcoholic steatohepatitis (NASH) as well as in the livers of C57BL/6 mice fed a high-fat diet (HFD) up to 16 weeks. LC3-II expression was also analyzed in human SMMC-7721 and HepG2 hepatoma cells exposed to palmitic acid (PA), a saturated fatty acid. PA-induced apoptosis was detected by Annexin V staining and specific cleavage of PARP in the presence and absence of different agents.Results:LC3-II expression was markedly increased in human NASH and in liver tissues of HFD-fed mice. Treatment of SMMC-7721 cells with PA increased LC3-II expression in time- and dose-dependent manners, whereas the unsaturated fatty acid oleic acid had no effect. Inhibition of autophagy with 3MA sensitized SMMC-7721 cells to PA-induced apoptosis, whereas activation of autophagy by rapamycin attenuated PA-induced PARP cleavage. The autophagy-associated proteins Beclin1 and Atg5 were essential for PA-induced autophagy in SMMC-7721 cells. Moreover, pretreatment with SP600125, an inhibitor of JNK, effectively abrogated PA-mediated autophagy and apoptosis. Specific knockdown of JNK2, but not JNK1, in SMMC-7721 cells significantly suppressed PA-induced autophagy and enhanced its pro-apoptotic activity; whereas specific knockdown of JNK1 had the converse effect. Similar results were obtained when HepG2 cells were tested.Conclusion:JNK1 promotes PA-induced lipoapoptosis, whereas JNK2 activates pro-survival autophagy and inhibits PA lipotoxicity. Our results suggest that modulation of autophagy may have therapeutic benefits in the treatment of lipid-related metabolic diseases. [ABSTRACT FROM AUTHOR]

Background: The peritumoral environment has been implicated to be important in the process of metastasis and recurrence in hepatocellular carcinoma (HCC). Our aims were to assess the prognostic value of proline-rich tyrosine kinase 2 (Pyk2) in HCC and investigate related molecular mechanism. Methods: Expression of Pyk2 was tested by immunohistochemistry in tissue microarrays containing 141 paired HCC samples. Correlation between Pyk2 and vascular endothelial growth factor (VEGF) expression in clinical samples was analyzed by Spearman rank correlation. Matrigel invasion, anchorage-independent growth assay and immunoblotting were performed to study the effect of Pyk2 on the invasion and progression of HCC cells and phosphoinositide 3-kinase (PI3K)/AKT pathway activation. Results: Higher Pyk2 density in both tumor and peritumor was associated with lower overall survival ( P = 0.044; P = 0.041, respectively), serum AFP levels > 1,000 ng/ml ( P = 0.013; P = 0.032, respectively) and postoperative distant metastasis (both P < 0.001). However, only higher peritumoral Pyk2 density was related to lower disease-free survival ( P = 0.014) and vascular invasion ( P = 0.035). A significant correlation between Pyk2 and VEGF density in tumor or peritumoral liver tissue was observed ( r = 0. 3133, P = 0.0002; r = 0.5176, P < 0.0001, respectively). Immunoblotting showed that Pyk2 activated PI3K–AKT pathway to upregulate VEGF expression in HL-7702, SMMC-7721 and HepG2 cells. Conclusions: High Pyk2, especially peritumoral Pyk2 was associated with poor survival, disease recurrence, and metastasis in HCC. PI3K-AKT pathway was involved in Pyk2-mediated VEGF expression during HCC progression and invasion. [ABSTRACT FROM AUTHOR]

A quantum protocol for ( t, n)-threshold identity authentication based on Greenberger-Horne-Zeilinger states is presented. A trusted third party (TTP) can authenticate the users simultaneously when and only when t or more users among n apply for authentication. Compared with the previous multiparty simultaneous quantum identity authentication (MSQIA) protocols, the proposed scheme is more flexible and suitable for practical applications. [ABSTRACT FROM AUTHOR]

In a conventional quantum ( k, n) threshold scheme, a trusted party shares a quantum secret with n agents such that any k or more agents can cooperate to recover the original secret, while fewer than k agents obtain no information about the secret. Is the reconstructed quantum secret same with the original one? Or is the dishonest agent willing to provide a true share during the secret reconstruction? In this paper we reexamine the security of quantum ( k, n) threshold schemes and show how to construct a verifiable quantum ( k, n) threshold scheme by combining a qubit authentication process. The novelty of ours is that it can provide a mechanism for checking whether the reconstructed quantum secret is same with the original one. This mechanism can also attain the goal of checking whether the dishonest agent provides a false quantum share during the secret reconstruction such that the secret quantum state cannot be recovered correctly. [ABSTRACT FROM AUTHOR]

The association of viral mutations and haplotypic carriages with mutations in the preS region of hepatitis B virus (HBV) genotypes B and C with hepatocellular carcinoma (HCC) is of great significance for the prediction of this malignancy, but it remains obscure. We analyzed the preS sequences of HBV genotypes B and C from 1172 HBV-infected subjects including 231 patients with HCC. As compared with the HBV-infected subjects without HCC, C2875T, G2946C, A3054C, C3060A, T3066C, C3116T, A3120C, G3191A, A1C, C7A, C10A, A31C, C76T, G105C, and G147C in both genotypes were significantly associated with increased risks of HCC. C2875A, G2950A, G2951A, A3054T, C3060T, T3066A, T3069G, A3120T, and G3191C were significantly associated with increased risks of HCC in genotype C, whereas these mutations were inversely associated with HCC in genotype B. Multivariate regression analyses showed that C76A/T was a novel factor independently associated with an increased risk of HCC, as compared with those without HCC. The frequencies of haplotypes 2964A-3116T-preS2 start codon wild-type-7C, 2964C-3116T-7A-76C, and 2964A-3116T-7C-76A/T were significantly higher in the patients with HCC ( P<0.001), whereas a haplotypic carriage with a single mutation and another three wildtypes were inversely associated with HCC. Conclusively, the association of HBV mutations in the preS region with HCC depends on HBV genotype and haplotypic carriage with two or more mutations that are each associated with an increased risk of HCC independently. [ABSTRACT FROM AUTHOR]

To develop a standardized and well-rounded material available for hepatology research, the National Liver Tissue Bank (NLTB) Project began in 2008 in China to make well-characterized and optimally preserved liver tumor tissue and clinical database. From Dec 2008 to Jun 2010, over 3000 individuals have been enrolled as liver tumor donors to the NLTB, including 2317 cases of newly diagnosed hepatocellular carcinoma (HCC) and about 1000 cases of diagnosed benign or malignant liver tumors. The clinical database and sample store can be managed easily and correctly with the data management platform used. We believe that the high-quality samples with detailed information database will become the cornerstone of hepatology research especially in studies exploring the diagnosis and new treatments for HCC and other liver diseases. [ABSTRACT FROM AUTHOR]

β-catenin is a key molecule involved in both cell-cell adhesion and Wnt signaling pathway. In our study, we found that, in the development of hepatocellular carcinoma (HCC), β-catenin was correlated with hepatitis B virus (HBV) X gene encoded protein, which is essential for HBV infectivity and is a potential cofactor in viral carcinogenesis. The expression levels of wild-type β-catenin and E-cadherin were decreased in HepG2 cells expressing hepatitis B virus X protein (HBx), accompanied by destabilization of adherens junction. Reverse transcriptase PCR (RT-PCR), Northern and Western blot showed that reduction of wild-type β-catenin expression involved degradation of the protein. However, RNA interference (RNAi) and luciferase assay indicated that HBx enhanced β-catenin mediated signaling in HepG2 cells. In addition, immunohistochemical and Western blot analysis of β-catenin revealed that a decrease in the β-catenin protein level was found in 58.3% of HBV-related HCCs versus 19.2% of non-HBV-related tumors. Our data suggest that the expression of HBx contributed to the development of HCC, in part, by repressing the wild-type β-catenin expression and enforcing β-catenin-dependent signaling pathway, thus inducing cellular changes leading to acquisition of metastatic and/or proliferation properties. [ABSTRACT FROM AUTHOR]

Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome that elevates the risk of hepatocellular carcinoma (HCC). Although alteration of lipid metabolism has been increasingly recognized as a hallmark of cancer cells, the deregulated metabolic modulation of HCC cells in the NAFLD progression remains obscure. Here, we discovers an endoplasmic reticulum-residential protein, Nogo-B, as a highly expressed metabolic modulator in both murine and human NAFLD-associated HCCs, which accelerates high-fat, high-carbohydrate diet-induced metabolic dysfunction and tumorigenicity. Mechanistically, CD36-mediated oxLDL uptake triggers CEBPβ expression to directly upregulate Nogo-B, which interacts with ATG5 to promote lipophagy leading to lysophosphatidic acid-enhanced YAP oncogenic activity. This CD36-Nogo-B-YAP pathway consequently reprograms oxLDL metabolism and induces carcinogenetic signaling for NAFLD-associated HCCs. Targeting the Nogo-B pathway may represent a therapeutic strategy for HCC arising from the metabolic syndrome. Non alcoholic fatty liver disease (NAFLD) associates with an elevated risk of developing hepatocellular carcinoma (HCC). Here, the authors find that Nogo-B, an endoplasmic reticulum resident protein, is upregulated by lipid uptake and acts as an oncogene in NAFLD-associated HCC by promoting lipid droplet breakdown by lipophagy and triggering Hippo pathway dysregulation [ABSTRACT FROM AUTHOR]

Hepatocellular carcinoma (HCC) has become a leading cause of cancer-related death, making the elucidation of its underlying mechanisms an urgent priority. Inflammation is an adaptive response to infection and tissue injury under strict regulations. When the host regulatory machine runs out of control, nonresolving inflammation occurs. Nonresolving inflammation is a recognized hallmark of cancer that substantially contributes to the development and progression of HCC. The HCC-associated inflammation can be initiated and propagated by extrinsic pathways through activation of pattern-recognition receptors (PRRs) by pathogen-associated molecule patterns (PAMPs) derived from gut microflora or damage-associated molecule patterns (DAMPs) released from dying liver cells. The inflammation can also be orchestrated by the tumor itself through secreting factors that recruit inflammatory cells to the tumor favoring the buildup of a microenvironment. Accumulating datas from human and mouse models showed that inflammation promotes HCC development by promoting proliferative and survival signaling, inducing angiogenesis, evading immune surveillance, supporting cancer stem cells, activating invasion and metastasis as well as inducing genomic instability. Targeting inflammation may represent a promising avenue for the HCC treatment. Some inhibitors targeting inflammatory pathways have been developed and under different stages of clinical trials, and one (sorafenib) have been approved by FDA. However, as most of the data were obtained from animal models, and there is a big difference between human HCC and mouse HCC models, it is challenging on successful translation from bench to bedside. [ABSTRACT FROM AUTHOR]