The same

finding was reported by Rosenberg et al[15] for implants with hydroxyapatite surface enhanced by patients’ conditions (periodontally compromised). This may be due to ease of microbial adhesion to rough compared to the machined surface. Teughels et al[24] conducted a systematic review of the literature on the effect of material characteristics and/or surface topography of the implant in the development of the biofilm (plaque), concluding that implant surfaces with a higher Ixazomib nmr degree of roughness (R = 0.2 μm) facilitate biofilm formation. In a retrospective evaluation of predisposing conditions for the occurrence of retrograde peri-implant pathology in Brånemark system implants, Quirynen et al[12] observed a higher incidence of retrograde peri-implant pathology in TiUnite (rough) (Nobel Biocare) implants. The components of an implant-prosthetic rehabilitation (abutment, abutment screw, and crown/prosthesis)

may relate to the occurrence of peri-implant pathology, to the extent that they are part of the equation when the disease occurs by occlusal overload.[25] Regarding the abutments, there is no evidence that the different surface topography influences the accumulation of plaque either in the animal model[26] or in a human model as evidenced by Van Assche et al[27] through Roscovitine mw a randomized clinical trial comparing the accumulation of plaque on different surfaces. Regarding the type of prosthetic reconstruction, a higher incidence of implant failures and prosthetic complications have been observed in partially edentulous patients rehabilitated with a fixed partial prosthesis supported by two implants compared to a prosthesis supported by three or more implants.[28-30] This may occur due to a biomechanically unfavorable situation with respect to the number of implants supporting the structure.[31] The type of restorative material used in the prosthesis ranges from acrylic, metal-acrylic, metal-ceramic, and to ceramic. The academic hypothesis of using acrylic as a means

of reducing the concentration of occlusal stress on the bone/implant interface[32] 上海皓元医药股份有限公司 acting as a shock absorbing agent has been postulated; this assumption is supported by finite element analysis studies and mathematical models.[33, 34] However, there were no significant differences in marginal bone loss between implants restored with ceramic or acrylic in clinical studies.[35] The presence of cantilevers in a fixed prosthesis has been considered a risk factor due to the considerable increase of occlusal load on the implants, especially the most distal implant.[32] These results have been supported by in vitro studies,[36-38] suggesting a maximum limit of a 15-mm-long cantilever in the mandible.[38] A recent meta-analysis from retrospective cohort studies concluded that there were no differences in bone loss in implants supporting a cantilever because of this factor per se.

S. lycopersicum showed increased POD

activity in the presence of TYLCV. The activity of the enzyme was higher in mature than in juvenile leaves. In general, both infected and healthy leaves exhibited greater POD activity during whitefly infestation. In Quizartinib datasheet the infested juvenile leaves, POD activity was much lower in the healthy leaves and increased gradually with period of exposure to B. tabaci B infestation. In contrast, the activity of the enzyme remained low in infested mature leaves in both the presence and absence of the virus even with increased exposure time. Determination of the distribution of an insect pest is critical for sampling and management. Leaf age is presumed to be associated with the within-host distribution of the geminivirus vector MK2206 B. tabaci. Juvenile leaves will usually attract more insects due to increased nutritional value and weaker defences. Our results highlight the importance of leaf age/position on the whitefly – host plant – geminivirus interactions and have important implications for sampling and control strategies. “
“The movement protein (NSm) gene of Groundnut bud necrosis virus (GBNV) isolates from pea, mungbean, cowpea, French bean, tomato and potato collected from different locations of India were

compared to study their diversity. The NSm gene sequences of all the GBNV isolates were highly conserved and had only 0–3% diversity in amino acids and 0–10% in nucleotides. Comparison of amino acid sequence of NSm gene of 25 GBNV isolates revealed the presence of many conserved regions. Both ‘D-motif’ and ‘G-residue’, the conserved regions of ‘30K superfamily’ of virus movement protein, were present in all the isolates. Clustering of the GBNV isolates does not appear to be based on their place of origin and host plant species. “
“Plants medchemexpress of alfalfa (Medicago sativa) exhibiting general stunting, proliferation

and phyllody associated with leaf yellowing and reddening were observed in three localities of Central Serbia. Phytoplasma strains belonging to 16SrIII-B and 16SrXII-A groups were detected and identified by RFLP and sequence analysis of 16S rDNA. Stolbur phytoplasma tuf gene RFLP analysis showed the presence of the TufAY-b-type phytoplasma subgroup in 80% of symptomatic samples. This is the first report of 16SrIII-B and 16SrXII-A phytoplasma groups affecting alfalfa in Serbia. “
“Phytoplasmas were detected in Sophora japonica cv. golden and Robinia pseudoacacia with diseased branches of witches’-broom collected in Haidian district, Beijing, China. Phytoplasma cells were observed in phloem sieve elements of symptomatic S. japonica cv. golden by transmission electron microscopy. The presence of phytoplasmas was further confirmed by sequence determination of partial gene sequences of 16S rDNA, rp (ribosomal protein) and secY.

S. lycopersicum showed increased POD

activity in the presence of TYLCV. The activity of the enzyme was higher in mature than in juvenile leaves. In general, both infected and healthy leaves exhibited greater POD activity during whitefly infestation. In CHIR99021 the infested juvenile leaves, POD activity was much lower in the healthy leaves and increased gradually with period of exposure to B. tabaci B infestation. In contrast, the activity of the enzyme remained low in infested mature leaves in both the presence and absence of the virus even with increased exposure time. Determination of the distribution of an insect pest is critical for sampling and management. Leaf age is presumed to be associated with the within-host distribution of the geminivirus vector Selleck C646 B. tabaci. Juvenile leaves will usually attract more insects due to increased nutritional value and weaker defences. Our results highlight the importance of leaf age/position on the whitefly – host plant – geminivirus interactions and have important implications for sampling and control strategies. “
“The movement protein (NSm) gene of Groundnut bud necrosis virus (GBNV) isolates from pea, mungbean, cowpea, French bean, tomato and potato collected from different locations of India were

compared to study their diversity. The NSm gene sequences of all the GBNV isolates were highly conserved and had only 0–3% diversity in amino acids and 0–10% in nucleotides. Comparison of amino acid sequence of NSm gene of 25 GBNV isolates revealed the presence of many conserved regions. Both ‘D-motif’ and ‘G-residue’, the conserved regions of ‘30K superfamily’ of virus movement protein, were present in all the isolates. Clustering of the GBNV isolates does not appear to be based on their place of origin and host plant species. “
“Plants 上海皓元 of alfalfa (Medicago sativa) exhibiting general stunting, proliferation

and phyllody associated with leaf yellowing and reddening were observed in three localities of Central Serbia. Phytoplasma strains belonging to 16SrIII-B and 16SrXII-A groups were detected and identified by RFLP and sequence analysis of 16S rDNA. Stolbur phytoplasma tuf gene RFLP analysis showed the presence of the TufAY-b-type phytoplasma subgroup in 80% of symptomatic samples. This is the first report of 16SrIII-B and 16SrXII-A phytoplasma groups affecting alfalfa in Serbia. “
“Phytoplasmas were detected in Sophora japonica cv. golden and Robinia pseudoacacia with diseased branches of witches’-broom collected in Haidian district, Beijing, China. Phytoplasma cells were observed in phloem sieve elements of symptomatic S. japonica cv. golden by transmission electron microscopy. The presence of phytoplasmas was further confirmed by sequence determination of partial gene sequences of 16S rDNA, rp (ribosomal protein) and secY.

Our new challenge is to

understand the mechanisms underlying more common, but less well-defined, mucocutaneous bleeding (MCB) disorders. Present diagnostic testing for platelet function disorders and von Willebrand’s Disease often fails to identify the cause of bleeding in individuals with inherited MCB. The buy BGB324 diligent study of patients with inherited platelet disorders has taught us much about the haemostatic function of platelets. Glanzmann thrombasthenia (GT) and Bernard–Soulier syndrome (BSS) were identified by astute clinicians early in the last century, and the development of the platelet aggregometer in the early 1960s facilitated the identification of additional disorders affecting platelet function, including abnormalities of agonist receptors, storage granules and calcium flux [1,2]. Subsequently, molecular technology and informative animal models have defined the basis for many of the classic inherited platelet disorders, and have enhanced our understanding of platelet function. However, the prevalence of primary platelet disorders is unknown. We have assumed that many patients with mild mucocutaneous bleeding (MCB) have platelet function abnormalities, but have not successfully Selleckchem DAPT identified specific molecular defects, or definitive diagnostic testing. This review will discuss some of the known molecular and

structural defects in inherited platelet disorders, with particular emphasis on the clinical and laboratory presentation of GT, and on the present limitations of laboratory diagnosis for MCB. Platelets play a central role in the haemostatic process at sites of vascular injury. They function as circulating monitors of the integrity of the blood vessel wall; the dynamics of blood flow dictate that platelets are found primarily along the vessel wall, well positioned for rapid response to endothelial damage. Fundamental to their

‘first responder’ role is their ability 上海皓元 to be captured by exposed collagen fibrils and von Willebrand factor (VWF) in the subendothelial matrix, resulting in transformation from inactive to activated cells that adhere tightly to the injury site and to each other. Activated platelets undergo rapid cytoskeletal rearrangement, which allow them to spread on the sub-endothelial matrix, maximizing surface contact at the damaged site. The adherent platelets provide a base upon which additional platelets can accumulate to form the primary platelet plug [3]. Activated platelets release soluble mediators such as ADP and thromboxane (Tx) A2 that recruit additional platelets, which bind to the layer of adherent platelets. This is facilitated by a conformational change in the αIIbβ3 integrin leading to the expression of an adhesive protein-binding domain.

Although promising, there was a large variability in methods used for dynamic testing and, therefore, it remains unclear which dynamic testing methods are most appropriate for patients with cognitive impairments. More research is warranted to further evaluate and refine dynamic testing methodology and to further elucidate its predictive validity concerning rehabilitation outcomes relative to other cognitive and functional status indices. “
“Children with attention-deficit hyperactivity disorder (ADHD) and traumatic brain injury

(TBI) show deficient response inhibition. ADHD itself is a common consequence of TBI, known as secondary ADHD (S-ADHD). Similarity in inhibitory control in children with TBI, S-ADHD, and ADHD would implicate impaired frontal-striatal systems; however, it is first necessary to delineate similarities

and differences in inhibitory control in these conditions. We compared performance of children with ADHD and Roscovitine supplier those with TBI without pre-injury ADHD on a stop signal, response inhibition task. Participants were 274 children aged 6–14 years. There were 92 children with ADHD, 103 children with TBI, and 79 typically developing children who served as controls. Among the TBI participants, injury severity ranged from mild to severe. Children with ADHD and TBI showed deficient inhibition. The deficit in children with ADHD was as great AUY-922 manufacturer as or greater than that in children with TBI, regardless of degree of TBI severity or the MCE presence of S-ADHD. The finding indicates that TBI results in deficient inhibition regardless of the development

of S-ADHD. “
“Visual spatial memory was assessed using the Visual Spatial Learning Test (VSLT) in individuals with mild to moderate Huntington’s disease (HD), pre-manifest gene carriers for HD, and demographically similar controls. The VSLT has been demonstrated to be a valid, normed measure of non-verbal memory involving minimal motoric responses. The VSLT assesses immediate and delayed memory for designs, positions of the designs, and design/position associations. The HD group was significantly impaired (p < .05) relative to both the control and Pre-HD groups on immediate and delayed memory for the designs, positions, and design/position associations. Although there were no differences between the Pre-HD and control groups on immediate or delayed memory for designs or positions, the Pre-HD group was significantly impaired (p < .05) relative to the control group on immediate and delayed memory for design/position associations. The results offer novel insight into a relatively unexamined memory deficit that may occur in gene carriers for HD prior to phenoconversion. The data indicate that the VSLT may be a useful measure of visuospatial memory during the premanifest and manifest stages of HD. "
“Executive dysfunction can be present from the early stages of Parkinson’s disease (PD).

Mild inflammatory cell infiltration was defined by a small number of inflammatory cells that were scattered throughout the HPF. In severe inflammation, many diffuse inflammatory cells were observed. Samples were considered to have moderate inflammation when they showed between mild and severe inflammation. Although find more obliterative phlebitis is a characteristic histological feature of IgG4-SC, it was not assessed in the present study because it usually occurs in relatively large veins that were not sampled by the endoscopic biopsies. IgG4 immunostaining was carried out with an autostainer (HX System

Benchmark, Ventana Medical Systems, Tucson, AZ, USA) following the manufacturer’s instructions. The primary antibody was an anti-IgG4 mouse monoclonal antibody (ZYMED Laboratory, San Francisco, CA, USA). Before incubating with the primary antibodies, the sections were pretreated with proteinase. IgG4-positive plasma cells were counted in the most inflamed HPF (10× eyepiece and 40× lens) in both the Vater’s ampulla and bile duct biopsies. The degrees of inflammatory cell infiltration (mild/moderate/severe),

plasma cells, eosinophils, and the numbers of IgG4-positive plasma cells on ampullary and bile duct biopsies were compared RG7420 molecular weight between the three groups using Tukey’s test. The numbers of IgG4-positive plasma cells in the ampullary and bile duct biopsies, and the clinical characteristics (swelling of Vater’s ampulla or the pancreatic head) of patients with IgG4-SC were also analyzed using χ2-test and Fisher’s test. A value of P < 0.05 was considered statistically significant. All of the analyses were carried out using spss II for Windows, Version 8.0.1. J (SPSS, Chicago, IL, USA). The results of the histological examination of the ampullary biopsies are summarized in Table 1. There were no significant differences

in the degrees of inflammatory cell infiltration, plasma cell infiltration (> 20 cells/HPF) and eosinophil infiltration (> 20 cells/HPF) among three disease groups. Three IgG4-SC cases had severe inflammatory cell infiltration (Fig. 1c), although they were not associated with the irregular fibrosis that is typically observed in surgical AIP or IgG4-SC specimens. The bile 上海皓元 duct biopsies showed inflammatory cell infiltration, fibrosis and stromal edema to varying degrees in each case of IgG4-SC. Of the 29 IgG4-SC patients, 10 (34%) had plasma cell infiltrations greater than 20 cells/HPF, although this increase was not significantly greater than that observed in samples from PSC and pancreatobiliary carcinoma patients (Table 1). Interestingly, five of these cases (17% of all IgG4-SC patients, four with AIP and one with cholangitis only) showed lymphoplasmacytic infiltration intermixed with irregular fibrosis, which was corresponding to lymphoplasmacytic sclerosing pancreatitis and cholangitis (a pathological term of AIP/IgG4-SC) (Figs 1f,2a).

Mild inflammatory cell infiltration was defined by a small number of inflammatory cells that were scattered throughout the HPF. In severe inflammation, many diffuse inflammatory cells were observed. Samples were considered to have moderate inflammation when they showed between mild and severe inflammation. Although AZD1208 obliterative phlebitis is a characteristic histological feature of IgG4-SC, it was not assessed in the present study because it usually occurs in relatively large veins that were not sampled by the endoscopic biopsies. IgG4 immunostaining was carried out with an autostainer (HX System

Benchmark, Ventana Medical Systems, Tucson, AZ, USA) following the manufacturer’s instructions. The primary antibody was an anti-IgG4 mouse monoclonal antibody (ZYMED Laboratory, San Francisco, CA, USA). Before incubating with the primary antibodies, the sections were pretreated with proteinase. IgG4-positive plasma cells were counted in the most inflamed HPF (10× eyepiece and 40× lens) in both the Vater’s ampulla and bile duct biopsies. The degrees of inflammatory cell infiltration (mild/moderate/severe),

plasma cells, eosinophils, and the numbers of IgG4-positive plasma cells on ampullary and bile duct biopsies were compared AUY-922 between the three groups using Tukey’s test. The numbers of IgG4-positive plasma cells in the ampullary and bile duct biopsies, and the clinical characteristics (swelling of Vater’s ampulla or the pancreatic head) of patients with IgG4-SC were also analyzed using χ2-test and Fisher’s test. A value of P < 0.05 was considered statistically significant. All of the analyses were carried out using spss II for Windows, Version 8.0.1. J (SPSS, Chicago, IL, USA). The results of the histological examination of the ampullary biopsies are summarized in Table 1. There were no significant differences

in the degrees of inflammatory cell infiltration, plasma cell infiltration (> 20 cells/HPF) and eosinophil infiltration (> 20 cells/HPF) among three disease groups. Three IgG4-SC cases had severe inflammatory cell infiltration (Fig. 1c), although they were not associated with the irregular fibrosis that is typically observed in surgical AIP or IgG4-SC specimens. The bile 上海皓元 duct biopsies showed inflammatory cell infiltration, fibrosis and stromal edema to varying degrees in each case of IgG4-SC. Of the 29 IgG4-SC patients, 10 (34%) had plasma cell infiltrations greater than 20 cells/HPF, although this increase was not significantly greater than that observed in samples from PSC and pancreatobiliary carcinoma patients (Table 1). Interestingly, five of these cases (17% of all IgG4-SC patients, four with AIP and one with cholangitis only) showed lymphoplasmacytic infiltration intermixed with irregular fibrosis, which was corresponding to lymphoplasmacytic sclerosing pancreatitis and cholangitis (a pathological term of AIP/IgG4-SC) (Figs 1f,2a).

The model is based on an shRNA sequence targeting Lrh-1 (NR5A2) cloned behind a doxycycline-responsive promoter. The construct is targeted at the Rosa26 locus along with the enhanced tet-repressor (Fig. 1A). The resulting C57BL/6J mice were bred to be heterozygous for the knockdown cassette and WT littermates lacking the targeting construct were used as controls. Lrh-1 gene knockdown was induced by doxycycline administration by way of the food for 5 weeks. As shown in Fig.

1B, http://www.selleckchem.com/products/PLX-4032.html hepatic Lrh-1 mRNA levels were reduced by ≈90%-95%, whereas the reduction of Lrh-1 expression in small intestine was ≈60%-70% in male and female mice (Fig. 1B). The expression of Shp, a well-established Lrh-1 target gene,22, 23 was robustly reduced in liver (Fig. 1B). In contrast, levels of steroidogenic factor-1, the closest paralog of LRH-1, in the ovaries were unaltered upon expression of the shRNA (data not shown), indicating that knockdown is specific for Lrh-1. There were no overt abnormalities noticed in either group. Plasma aspartate aminotransferase and alanine aminotransferase activities were unchanged (Fig. 1C), implying that knockdown of hepatic Lrh-1 has no detrimental effect on hepatocyte

cell integrity. As our Maraviroc model is fundamentally different from two previously reported ones,30, 31 we first analyzed a number of general metabolic parameters. As shown in Supporting Table 1, plasma cholesterol and triglyceride levels were unaltered and plasma lipoprotein profiles were found to be unchanged between wildtype and knockdown animals (data not shown). Two previous reports showed that bile salt composition rather than synthesis rate was altered in liver-specific

Lrh-1 knockout mice.30, 31 Consistent with this, hepatic Cyp7a1 mRNA levels remained unaltered or were even slightly induced, whereas those of Cyp8b1 were reduced. We also found that knockdown of LRH-1 resulted in a significant reduction of Cyp8b1 mRNA levels (Fig. 2A). Surprisingly, hepatic MCE Cyp7a1 mRNA levels were increased upon LRH-1 knockdown (Fig. 2A). Several genes implicated in hepatic bile salt transport (e.g., Ntcp, Abcb11/Bsep, and Abcb4/Mdr2) were all mildly reduced upon LRH-1 knockdown (Fig. 2A), in agreement with previous findings.31 We next tested whether the physicochemical properties of the neutral sterol fraction as well as the bile salt pool were affected upon LRH-1 knockdown. LRH-1 knockdown did not significantly alter amounts or relative abundances of each of the major neutral sterols in feces (Supporting Fig. 1A-C). In agreement with induced Cyp7a1 levels, the total amount of fecal bile salts secreted per day, reflecting hepatic synthesis, was slightly increased (males +57%, females +59%) (Fig. 2B). The primary bile salts cholate (CA) and chenodeoxycholate (CDCA) are the direct products of de novo bile salt synthesis. Modifications of these bile salts in liver and intestine give rise to differentially structured primary and secondary bile salts, respectively.

The presence of esophageal and gastric varices was noted and classified according to the Japanese Research Society of Portal Hypertension

(7). During the procedure, 2 gastric biopsy specimens were taken from each patient. One biopsy specimen was taken from the antrum and one from the fundus for histopathological examination. Biopsy specimens were analyzed by the same histopathologist click here during the study period. The gastritis was classified as either chronic active or nonactive. Nonactive gastritis was defined by the presence of mononuclear cell infiltration and active gastritis by the presence of neutrophils and/or erosions. H Pylori infection was reported on the histology. Children with Portal hypertension were subsequently

studied. The underlying liver disease, the duration of evolution of the disease, the medical treatment, the presence of systemic or gastrointestinal symptoms, and the indications for upper Fulvestrant manufacturer gastrointestinal endoscopy were recorded for those patients. The patients were divided into 2 groups. Group 1 included 190 patients with Portal hypertension without liver cirrhosis (i.e. Portal Cavernoma,Peri Portal fibrosis due to Schistomaisis and congenital hepatic fibrosis). Group 2 included 60 patients with liver disease progressing toward cirrhosis (infectious hepatitis, Idiopathic cirrhosis, Progressive Familiar Intra hepatic Cholestasis (PFIC), Wilson disease, or other metabolic liver diseases.) The x2 test was used to compare qualitative variables, and the Fisher exact test for comparison between small groups. P < 0.05 was considered significant. The study was approved by Al Nileen University Ethical committee. Results: Among 2000 patients enrolled during the study period, 250 (12.5%) received a diagnosis of Portal hypertension and were therefore included in the study. The median age of the patients at the time of endoscopy was 5 years 9 months (range, 5 months–15 years). The median time between the diagnosis of liver disease and endoscopy was 2 years 3 months (range, 2 months–8 years). Table

1 summarizes the clinical MCE公司 characteristics of the patients. Portal Hypertensive Gastropathy was found in 150 of 250 patients (60%). Moderate PHG was found in 104 of 250 patients and severe PHG in 41 patients (31 of whom had liver cirrhosis). Esophageal varices were found in 135 of 250 patients (54%) (Grade I, n = 52; grade II, n = 62; and grade III, n = 21). The hemorrhagic aspect of the esophageal mucosa was observed in 21 patients. No patient had gastric varices (8). Gastritis was found in 145 of 250 (58%) patients (antrum, n = 70; fundus, n = 75). No glandular atrophy or intestinal metaplasia was seen in the patients in the study. In the group 2 patients (n = 60), PHG was found in 35 patients with Liver Cirrhosis associated with chronic gastritis (active, n = 25; nonactive, n = 20). Esophageal varices were found in 15 patients.

Compared with LPS alone, the ethanol induction group produced significantly more TNF-α, nuclear NF-κB p65 and less cytoplasm IκB-α under LPS stimuli. CMZ abolished the effects of ethanol on LPS-stimulated NF-κB translocation

and TNF-α generation in Kupffer cells. In cultured Kupffer cell, using CMZ as inhibitor, ethanol-induced CYP2E1 overexpression was proved to contribute to the sensitization of Kupffer cells to LPS stimuli, with amplification of ROS production and activation of NF-κB, resulting in increased TNF-α production. “
“Human hepatocellular carcinoma (HCC) is an inflammation-induced cancer, which is the third-leading cause of cancer mortality worldwide. We investigated see more www.selleckchem.com/products/i-bet-762.html the role of the chemokine receptors, CCR5 and CCR1, in regulating inflammation and tumorigenesis in an inflammation-induced HCC model in mice. Multidrug resistance 2 gene (Mdr2)-knockout (Mdr2-KO) mice spontaneously develop chronic cholestatic hepatitis and fibrosis that is eventually followed by HCC. We generated two new strains from the Mdr2-KO mouse, the Mdr2:CCR5 and the Mdr2:CCR1 double

knockouts (DKOs), and set out to compare inflammation and tumorigenesis among these strains. We found that in Mdr2-KO mice lacking the chemokine receptor, CCR5 (Mdr2:CCR5 DKO mice), but not CCR1 (Mdr2:CCR1 DKO), macrophage recruitment and trafficking to the liver was 上海皓元 significantly reduced. Furthermore, in the absence of CCR5, reduced inflammation was also associated with reduced periductal accumulation of CD24+ oval cells and abrogation of fibrosis. DKO mice for Mdr2 and CCR5 exhibited a significant

decrease in tumor incidence and size. Conclusions: Our results indicate that CCR5 has a critical role in both the development and progression of liver cancer. Therefore, we propose that a CCR5 antagonist can serve for HCC cancer prevention and treatment. (Hepatology 2013;53:1021–1030) In 1863, Virchow hypothesized that cancer originated at sites of chronic inflammation. Indeed, a growing body of evidence indicates that many malignancies are initiated by infections and chronic inflammation, accounting for over 20% of malignancy cases worldwide. However, the molecular and cellular mechanisms revealing how chronic inflammation leads to tumorigenesis remain largely unknown.[1-3] Human hepatocellular carcinoma (HCC), a primary malignancy of the liver and the third-leading cause of cancer mortality worldwide,[4, 5] is an example of inflammation-induced cancer. In humans, chronic viral hepatitis, metabolic liver diseases, and alcohol abuse cause chronic inflammation; this, in turn, can induce fibrosis, cirrhosis, and cancer.[6, 7] Chemokines and chemokine receptors function in the initiation and maintenance of inflammation and fibrosis[1] and might play a crucial role in the chronic inflammation that leads to tumorigenesis.