37 Sixty-one children presenting with intestinal symptoms were en

37 Sixty-one children presenting with intestinal symptoms were enrolled prospectively, with fecal S100A12 and calprotectin measured.

Thirty one of these children were shown to have IBD on subsequent tests. In these children, both fecal S100A12 (median: 55.2 mg/kg) and calprotectin (median: 1265 mg/kg) were elevated compared to those children without IBD (n = 30, S100A12 median: 1.1 mg/kg, P < 0.0001; calprotectin median: 30.5 mg/kg, P < 0.0001). Upon further analysis, using a cut-off of 10 mg/kg, S100A12 gave a sensitivity and specificity of 97%, respectively, for the detection of IBD. However, a 50 mg/kg cut-off for calprotectin yielded a sensitivity of 100% and specificity of 67%, lower than the specificities reported by other studies.50 Both fecal markers were superior compared to the sensitivities and specificities of any standard inflammatory test in this population.37 Several

studies have also demonstrated selleck products a role for S100A12 in the adult setting. Foell et al.35 demonstrated correlations between serum S100A12 and disease activity, and showed that serum levels fell after intervention with infliximab. Subsequent studies have also shown elevated serum S100A12 in IBD, however, with only modest sensitivities and specificities in distinguishing IBD and non-IBD patients.21,51 Following earlier work examining serum levels of S100A12 in the context of IBD, Kaiser et al.49 illustrated that fecal S100A12 levels could distinguish IBD from IBS, check details with 86% sensitivity and 96% specificity, and to also differentiate IBD from normal

controls, with 86% sensitivity and 100% specificity. Their study also find more demonstrated that S100A12 was superior to calprotectin or other biomarkers in correlation, with an inflammatory score incorporating endoscopic and histological findings.49 The role of S100A12 as a marker of future relapse has not yet been considered in pediatric or adult settings. Prospective studies are required to elucidate this potential role. Lactoferrin is an iron-binding glycoprotein identified in the secretions overlying most mucosal surfaces that interact directly with external pathogens, including saliva, tears, vaginal secretions, feces, synovial fluid, and mammalian breast milk.52–54 Lactoferrin is a major component of the secondary granules of polymorphonuclear neutrophils and is shown to be a primary factor in the acute inflammatory response.54,55 In the intestinal lumen, fecal lactoferrin levels quickly increase with the influx of neutrophils during inflammation.12 Lactoferrin has antibacterial activity and is resistant to proteolysis in the feces;56 it is unaffected by multiple freeze/thaw cycles54 and might remain stable in stool for as long as 5 days, compared to 7 days for calprotectin.24,57 Following storage at room temperature for 48 h, fecal concentrations of lactoferrin were 90% of initial levels, contrasting with fecal concentrations of calprotectin being 82%.

The history revealed no other

The history revealed no other Buparlisib mouse remarkable features. The examination revealed a palpable spleen. The investigations were normal as per previous case except for ESR >100 mmHg and CRP >200 mg/L. Ultrasound abdomen revealed splenomegaly with irregular hypoechoic regions and CECT of the abdomen confirmed multiple splenic abcesses. Blood cultures

grew Burkholderia pseudomallei. Blood picture was suggestive of bacterial sepsis and fever responded to IV meropenem. Conclusion: In patients with PUO and splenic abscesses in endemic areas, melioidosis should be entertained as a possible differential diagnosis. Key Word(s): 1. PUO Presenting Author: RAVINDRA L SATARASINGHE Additional Authors: SACHITH C WIJESIRIWARDENA, CHAMPIKA GAMAKARANAGE, NARMATHEY THAMBIRAJAH Corresponding Author: RAVINDRA L SATHARASINGHE Affiliations: Sri Jayawardenepura General Hospital, Sri Jayawardenepura General Hospital, Sri Jayawardenepura General Hospital Objective: To report a rare cause for haemoperitoneum. There are many causes resulting in a haemoperitoneum such as blunt or penentrating trauma

to the abdomen, tumour-associated haemorrhage or in blood dyscrasias. Splenic infarctions as a cause of frank hemoperitoneum has not been documented before, to the best of our knowledge. Methods: Case notes of a 54 year old adult Sri Lankan male, Selinexor who had been diagnosed to have chronic alcoholic cirrhosis, portal hypertension and bronchial check details asthma, admitted with an acute abdomen and a hypotensive

state were retrospectively analysed. Examination had revealed presence of free fluid with mild tenderness and guarding of the abdomen. His previous abdominal scan revealed no ascites. Results: The investigations revealed the following: On the FBC, Hb was 11.5 g/dl, while other indices and cell lines were normal. CRP was 23 mg/L and the other biochemical and hematological investigations were unremarkable. Ultrasound abdomen showed free fluid. Peritoneal tap was blood stained with a Hb of 11.5 g/dl. Cells were obscured by blood. Clotting screen was normal. The first contrast CT scan abdomen was inconclusive and showed old findings of liver disease and the second paracentesis was dry. Second contrast CT abdomen done the following day revealed a peripheral splenic infarction. The patient had an uneventful recovery. Conclusion: Peripheral splenic infarction should be entertained as a cause for frank hemoperitoneum. Key Word(s): 1. Hemoperitoneum; 2.

4%) patients who remained alive (x2 = 59, P < 002) In addition

4%) patients who remained alive (x2 = 5.9, P < 0.02). In addition, the mortality figure increases markedly in patients with fibrosis stage ≥ 2; 32 of 47 (68.1%) patients who died had fibrosis stage ≥2 as compared to 20 of 71 (28.2%) patients who remained alive (x2 = 18.3, P < 0.001). Further, when all patients with fibrosis stage 1-4 were called

NASH in the study by Soderberg et al.,4 the overall mortality was markedly higher in the NASH group as compared to the non NASH group as illustrated in Fig. 2B in the paper. Similarly, when liver biopsies showing only steatosis or steatosis with nonspecific inflammation were called Procaspase activation non NASH, and all other biopsies including those with fibrosis stage 1-4 were called NASH in a recent study,3 the liver-related mortality in the NASH group was significantly higher than in the non NASH group. Based on all this,

it seems the presence and severity of fibrosis dictates both overall and liver-related mortality in patients with NAFLD. Fibrosis stage is in fact the histological feature with the highest inter-rater agreement with reported values of 0.5 (moderate)12 and 0.84 (excellent),11 and the highest intra-rater agreement with reported values of 0.69 (good)13 and 0.85 (excellent).11 What still remains unknown, however, is what long-term prognostic information, if any, can be obtained from grading the severity of inflammation and hepatocyte ballooning. The study by Soderberg LDK378 et 上海皓元医药股份有限公司 al.4 suggests that requiring those histological features for NASH classification (i.e., using the NASH-CRN scoring system) the long-term mortality of those with

definitive NASH is not significantly different from those with non NASH. Unfortunately, the study by Soderberg et al.4 along with the two other studies2, 3 that included liver biopsy did not analyze the prognostic relevance of inflammation and hepatocyte ballooning adjusted by presence and severity of fibrosis. Only a large appropriately powered study of several hundreds of patients who underwent liver biopsy and have follow-up data for several years or decades will answer those questions. In the meantime, when the practicing hepatologist is counseling patients in regards to long-term prognosis, it seems important to pay more attention to presence and severity of fibrosis on liver biopsy regardless of the pathologist’ labeling of NASH or non NASH. “
“Aims:  Metformin is a biguanide that has been widely used to treat type 2 diabetes. Several studies have shown that metformin is also effective in treating cancer, including hepatocellular carcinoma (HCC). The objective of this study was to evaluate the antitumor effects of metformin in HCC, and to investigate the potential molecular target(s) of metformin-mediated antitumor activity. Methods:  The antiproliferative effects of metformin were assessed in human HCC cell lines and normal human liver cells at various concentrations.

that vascular findings in AIP improve in most patients who receiv

that vascular findings in AIP improve in most patients who receive corticosteroid treatment is interesting and points towards reversibility of such changes, at least in a subset of patients. These promising results should now be confirmed by future studies. “
“To examine the effect of nucleoside analog (NA) therapy on clinical outcome in patients with hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) who underwent curative therapy. A total of 131 patients with HBV-related HCC who underwent curative therapy were analyzed. They were divided into an NA group who received NA therapy (n = 99, GS-1101 price group A) and a control group (n = 32, group B). Group A was further

classified into two groups of patients who either received NA therapy before HCC therapy (n = 34, group Aa) or who received NA therapy with initial HCC CHIR-99021 supplier therapy (n = 65, group Ab). Overall survival (OS) and recurrence-free survival (RFS) were compared in the three groups. The 1- and 3-year cumulative OS rates were both in group Aa, 100% and 88.0%

in group Ab, and 100% and 75.7% in group B (overall significance, P = 0.002), respectively. The corresponding RFS rates were 93.1% and 36.0% in group Aa, 78.3% and 45.7% in group Ab, and 78.0% and 38.0% in group B (overall significance, P = 0.734), respectively. Multivariate analysis revealed that being part of group Aa (P < 0.001) or group Ab (P < 0.001) and having albumin levels of 4.0 g/dL or more (P = 0.040) were significantly associated with 上海皓元 OS, while HCC stage (P = 0.001) and hepatitis B e-antigen positivity (P < 0.001) were independent predictors linked to RFS. NA therapy in patients with HBV-related HCC may improve survival after curative therapy. "
“High-quality artifact-free ultrasound images can now be produced by a portable machine. Being relatively cheap and non-invasive, ultrasound is widely accepted as the first-line investigation for patients with abdominal symptoms. A negative ultrasound is often regarded as the absence of major

abdominal conditions. Positive findings on ultrasound can guide further imaging (CT/MRI) for better characterization and delineation of the underlying disease. Specific diagnosis of certain disease entities can sometimes be made based on characteristic ultrasound features. The real-time nature of ultrasound can assist correlation with clinical symptoms and provide imaging guidance to obtain tissue biopsy. New advances in technique (contrast-enhanced ultrasound and ultrasound elastography) not only provide morphological but also functional assessment. “
“We investigated left ventricular diastolic dysfunction (LVDD) and its relationship with circulatory function and prognosis in cirrhosis with portal hypertension and normal creatinine.

05 Leaf samples were also collected from non-inoculated plants a

05. Leaf samples were also collected from non-inoculated plants at the same time-points above. Leaf samples were kept in liquid nitrogen during sampling and then stored at −80°C until further analysis. For enzyme extracts of peroxidases (POX, EC 1.11.1.7), 1 g fresh leaf segments were ground into a fine powder using a pestle and mortar with liquid nitrogen and the fine power was homogenized in an ice bath in 20 ml 100 mm potassium BMS-777607 phosphate buffer (pH 6.8) containing 1 mm phenylmethylsulfonyl fluoride (PMSF), 1 mm ethylenediaminetetraacetic acid (EDTA), and 200 mg polyvynilpolypyrrolidone (PVPP). The homogenate was centrifuged at 12 000 g for 15 min at 4°C and the supernatant

was used as crude enzyme extract. The POX activity was assayed following the colorimetric determination of pyrogallol oxidation according to Kar and Mishra (1976). A substrate mixture containing SAR245409 950 μl distilled water, 750 μl 100 mm potassium phosphate buffer (pH 6.8), 600 μl 100 mm pyrogallol, and 600 μl 100 mm hydrogenous peroxide was added to 100 μl of crude enzyme extract. Absorbance of the colored purpurogalin was recorded at 420 nm between the 2nd and 5th minute after adding the crude enzyme extract to the substrate mixture. An extinction coefficient of 2.47/mm/cm was used to calculate POX activity. The POX activity was expressed as m of purpurogalin produced per minute per milligram protein. For enzyme extracts of polyphenoloxidases

(PPO, EC 1.10.3.1), a total of 0.5 g of fresh leaf segments were ground into a fine powder in a pestle and mortar with liquid nitrogen and the fine powder was homogenized in an ice bath in 5 ml 100 mm potassium phosphate buffer (pH 6.8) containing 1 mm PMSF, 1 mm EDTA, and 50 mg PVPP. The homogenate was centrifuged at 12 000 g for

15 min at 4°C and the supernatant was used as crude enzyme extract. The PPO activity was determined as the same as for POX activity except that hydrogenous peroxide was not used in the substrate mixture. For enzyme extracts of chitinases (CHI, EC 3.2.1.14), 1 g of fresh leaf segments were ground into a fine powder with a pestle and mortar with liquid nitrogen and the fine powder was homogenized in MCE an ice bath in 3 ml 50 mm sodium phosphate buffer (pH 6.5) containing 1 mm PMSF and 30 mg PVPP. The homogenate was centrifuged at 20 000 g for 25 min at 4°C and the supernatant was used as crude enzyme extract. The CHI activity was assayed following the colorimetric determination of p-nitrophenyl cleaved from a chitin-analogous substrate p-nitrophenyl-β-D-N,N′-diacetylchitobiose (PNP) (Sigma-Aldrich, St Louis, MO, USA) (Harman et al., 1993). The reaction was started after addition of 20 μl crude enzyme extract to a mixture containing 470 μl 50 mm sodium acetate buffer (pH 5.0) and 10 μl of PNP at 2 mg/ml. The reaction mixture was incubated in a water bath at 37°C for 2 h. The reaction was terminated by adding 0.5 ml of 0.2 m sodium carbonate.

Human liver samples were available from routine liver biopsies or

Human liver samples were available from routine liver biopsies or from explanted cirrhotic livers this website resulting from transplantation, as described recently.13 The study protocol was approved by the local ethics committee (ethics committee of University Hospital Aachen, RWTH Aachen, Aachen, Germany), and the study was conducted according to the principles expressed

in the Declaration of Helsinki. Animal husbandry and procedures were approved by the authority for environment conservation and consumer protection of the state of North Rhine–Westfalia (LANUV, Germany) and the University Hospital Aachen Animal Care Facility’s guidelines. For our study, we used mice of Carfilzomib concentration male gender with constitutive deletion of CcnE1 (CcnE1−/−) and CcnE2 (CcnE2−/−)

and wild-type (WT) littermates from heterozygous breeding couples, as recently reported.9, 11 HSCs were prepared from adult male mice (weighing approximately 25 g), according to the collagenase method,14 as described in the Supporting Materials. Data are expressed as mean ± standard deviation of the mean. Statistical significance was determined by two-way analysis of variance, followed by a Student t test. E-type cyclins CcnE1 and CcnE2 control the transition of quiescent cells into the S phase and subsequent cell 上海皓元 proliferation.4 We hypothesized that liver fibrogenesis involves the cell proliferation of hepatic cell populations and determines overall CcnE expression in liver biopsies from patients

with liver fibrosis of different etiologies (see Supporting Table 1). CcnE1 mRNA expression was significantly up-regulated in patients with advanced hepatic fibrosis (F3) and liver cirrhosis (F4), compared to healthy control livers (F0) or patients with mild (F1) fibrosis (Fig. 1A). In contrast, CcnE2 was not aberrantly expressed in liver fibrosis at any stage (Fig. 1B). Immunostaining of liver biopsies confirmed the overexpression of CcnE1 in liver cirrhosis (Fig. 1C). Detailed analysis revealed the substantial nuclear expression of CcnE1 in nonparenchymal cells (NPCs), but also in hepatocytes of cirrhotic livers, which was not observed in healthy liver samples (Fig. 1D). We next investigated the involvement of CcnE1 in experimental liver fibrosis in WT mice subjected to repetitive CCl4 injections. In agreement with the human samples, mRNA expression of CcnE1, but not of CcnE2, was induced in murine liver after CCl4 treatment and correlated with fibrosis progression (Fig. 2A).


“Summary  Currently, patients with severe haemophilia can


“Summary.  Currently, patients with severe haemophilia can expect

to lead a relatively normal life including prevention of disabling arthropathy as a result of the development of factor replacement therapy and advances in the understanding of the use of such therapy given prophylactically. Unfortunately, a subset of patients develops neutralizing antibodies termed inhibitors rendering such therapy ineffective. These patients frequently develop recurrent joint bleeding resulting in arthropathy. Until recently, prophylactic SB525334 therapy was not considered for patients with inhibitors because of the perceived lack of an effective therapeutic agent. However, an accumulation of case reports and a recent prospective study have suggested that prophylaxis with the currently

available bypassing agents could be effective and appears to be safe in selected cases. This report will review the current data on prophylaxis with bypassing agents and suggest specific situations in which prophylaxis in inhibitor patients could be considered. “
“Summary.  For patients with haemophilia, gastrointestinal (GI) bleeding is a life-threatening complication and can be caused by the Helicobacter pylori infection. Among children with haemophilia who had visited with GI bleeding, the prevalence of H. pylori infection and the recurrence rate after H. pylori eradication was investigated. Seven children with haemophilia A with hematemesis (age: 5.3–17.0 years) were evaluated for the causes MAPK Inhibitor Library in vivo of GI bleeding and the detection of H. pylori. Gastroendoscopy was done to find the bleeding focus and for further evaluation including rapid

urease test and mucosal biopsy. Four patients had dyspepsia and abdominal pain for several weeks or months prior to hematemesis. Three patients MCE did not show any symptoms of bleeding. From gastroendoscopy, four patients were diagnosed as duodenal ulcer, one as H. pylori associated chronic gastritis and one as haemorrhagic gastritis. One patient showing a normal finding was diagnosed with adenoid haemorrhage after nasopharyngoscopy. Helicobacter pylori infection was found in four of six patients with GI bleeding (3, duodenal ulcer; 1, H. pylori associated chronic gastritis). The patients with H. pylori infection had an eradication treatment of triple therapy and no recurrence happened. In children with haemophilia, H. pylori should also be considered as an important cause of GI bleeding. The recurrence of the infection and GI bleeding can be prevented with eradication of H. pylori. Screening test for H. pylori would be needed in children with haemophilia in endemic area. “
“Effective healthcare delivery necessitates evaluation of the effect of interventions in the form of outcome assessment.

Furthermore, iPSC-derived hepatocytes produced and secreted the p

Furthermore, iPSC-derived hepatocytes produced and secreted the plasma proteins, fibrinogen, fibronectin, transthyretin, and alpha-fetoprotein, an essential feature for functional HE. Additionally iPSC-derived HE supported both CYP1A2 and CYP3A4 metabolism, which is essential for drug and toxicology testing. Conclusion: This work is first to demonstrate the efficient generation of hepatic endodermal lineage from human iPSCs that exhibits key attributes of

hepatocytes, and the AT9283 cell line potential application of iPSC-derived HE in studying human liver biology. In particular, iPSCs from individuals representing highly polymorphic variants in metabolic genes and different ethnic groups will provide pharmaceutical development and toxicology studies a unique opportunity to revolutionize predictive drug toxicology assays and allow the creation of in vitro hepatic disease models. (HEPATOLOGY 2009.) Human induced pluripotent stem cells (iPSCs) are reprogrammed mature somatic fibroblasts which represent a pluripotent cell population able to generate all primary cell types in vitro.1–3 The ability to derive iPSCs from an indefinite range of genotypes makes them an attractive resource on which to model liver function reflecting the complexity of polygenic influences on metabolism in vitro. Another Crizotinib ic50 facet of iPSC technology

is the ability to study the impact of gene polymorphisms in a native chromatin setting and model gene interactions with precision. Therefore iPSC-derived models hold great potential to develop a detailed understanding of human liver disease and metabolism including drug toxicity (for a review, see Dalgetty et al.4). Any methods which might streamline and standardize the process of drug and toxicology testing, which currently relies on primary human hepatocytes (PHHs), would represent a significant development. Therefore, an iPSC resource representative of polymorphic 上海皓元医药股份有限公司 variants and ethnic groups, unhindered by quality and supply, would revolutionize predictive drug toxicology assays and

have an effect on drug attrition. Presently, PHHs are the gold standard cell type used in predictive drug toxicology. Unfortunately, PHHs are a scarce, heterogeneous, and expensive resource which function only short-term in vitro. The generation of hepatic endoderm (HE) from iPSCs has the potential to fulfill the major challenge to acquire the reliable and clonal source of functional human hepatocyte cells for biotechnology purposes. To date, efficient models of deriving HE from iPSCs have not been described or developed. Capitalizing on our recent investigations that human embryonic stem cells (hESCs) can be stimulated to form HE,5 we have developed a parallel methodology for iPSCs; here, we describe the generation of functional HE from multiple human iPSC lines that can potentially model human drug metabolism.

However, small numbers of events limit the strength of inferences

However, small numbers of events limit the strength of inferences. “
“(Headache 2010;50:1328-1334) Background.— Religious fasting is associated with headache. This has been documented as “Yom Kippur Headache” and “First-of-Ramadan Headache.” Rofecoxib (Vioxx®), a cyclooxygenase-2 (Cox-2) inhibitor with a find more 17-hour half-life, has been shown to be effective in preventing fasting headache when taken just prior to the 25-hour Yom Kippur fast. Unfortunately for fasters rofecoxib is no longer available. We hypothesized that etoricoxib, another Cox-2 inhibitor with a longer half-life, would also be effective in preventing fasting headache. Methods.—

We performed a double-blind randomized prospective trial of etoricoxib 120 mg vs placebo, taken just prior to the onset of fasting, Yom Kippur 2008. Healthy

adults aged 18-65 years were enrolled from the community. Subjects completed a demographic data form and questions regarding headache history and a post-fast survey on headache during the fast. We compared incidence, time of onset and intensity of headache, general ease of fasting, and side effects in control and treatment groups. Results.— We enrolled 211 patients and 195 completed the post-fast questionnaire (92%). Of those subjects receiving etoricoxib buy INK 128 (n = 99), 36 or 36.4% vs 65 or 67.7% of the placebo group (n = 96) 上海皓元医药股份有限公司 developed any headache during the fast (P < .0001). Median

severity of headache in the treatment group was significantly lower for the treatment group (3.0 vs 5.0 on a visual analog scale of 10; P = .024). Also, participants in the treatment group reported an easier fast than the placebo group, as compared with previous fasting experience (4.0 vs 3.5 on a scale of 1-5; P < .0001). Conclusion.— Etoricoxib 120 mg taken prior to a 25-hour ritual fast decreases incidence of and attenuates fasting headache. NCT number is NCTT00752921. "
“(Headache 2011;51:995-998) “
“Objectives.— The goal of this study was to measure the effect of biofeedback therapy on pediatric headache and to identify factors associated with response to biofeedback therapy. Background.— In the United States, 17% of children have frequent or severe headaches. Biofeedback therapy (BFT) appears to be an effective treatment for headaches in adults and is often recommended for children with headaches, but there are few data in the pediatric population. It is also not clear which patients are most likely to benefit from biofeedback therapy. Methods.— We examined the records of patients, aged 8 to 18 years old, who were referred to a pediatric BFT clinic for management of headache between 2004 and 2008.

Results: In NAs group the response rate in 3 months was 397%, in

Results: In NAs group the response rate in 3 months was 39.7%, in 3 year was 61.3%, and in 5 year was 49.1%. Nevertheless, in Peg-IFN-NAs sequential group, the response rate in 3 months was 50.0%, in 3 year was 67.5%, and in 5 year was 67.6%. 2-year and 5-year cumulative

survival rates in antiviral therapy group were 97.3%, 73.5%, significantly higher than control group (88.2%, 43.5%), P < 0.01. And 2-year and 5-year cumulative recurrence rates in antiviral therapy group were JQ1 cost 13.3% and 76.5%, which were significantly lower than control group (P < 0.05). Than in NAs group, the 5-year cumulative survival rate in Peg-IFN-NAs sequential group (94.4%) was higher, P < 0.01. and the 2-year

and 5-year cumulative recurrence rates (5.1%, 68.3%) were lower, P < 0.01. However, in both NAs group and Peg-IFN-NAs sequential group, the disease progression rates were no significant difference. Conclusion: Antiviral therapy could effectively improve the prognosis of patients with HCC after liver resection / interventional treatment, and the Peg-IFN- NAs sequential therapy could significantly improve the patient's 5-year survival and 2-year and 5-year cumulative recurrence compared with NAs. Key Word(s): 1. pegylated interferon; 2. nucleoside Raf inhibitor analog; 3. HCC; 4. sequential therapy; Presenting Author: YUNTAO BING Additional Authors: ZHISU LIU, QUANYAN LIU Corresponding Author: QUANYAN LIU Affiliations: Zhongnan hospital Objective: Hepatitis B virus (HBV) infection can cause severe liver diseases, including chronic hepatitis and hepatocellular carcinoma (HCC). Glucocorticoids (Gcs) are commonly used to treat various cancers and immunosuppression, which is based on Glucocorticoid receptor (GR)-mediated mechanisms that trigger cell death. However, HBV patients treated with Gcs lead to severe acute hepatitis. The mechanisms that Gcs play the opposite effect on HBV patients are not fully understood. Methods: We studied MAT1A expression

by real-time quantitative polymerase chain reaction and immunobloting. Key Word(s): 1. MCE GR; 2. MAT1A; 3. HBV; 4. HCC; Presenting Author: TANGYIN HUA Corresponding Author: TANGYIN HUA Affiliations: The First Affiliated Hospital of Harbin Medical University Objective: To study the effects of As2O3 on invasion and metastasis of hepatoma tumor model. Methods: Hepatoma cell line (Bel-7402 cells) was established. After treated by different density As2O3. The size and weighty of tumor were observed, inhibition ratio of tumor weight were calculated and AFP was detected. The pathology of tumor tissue and lung were examined. Pulmonary metastasis tubercle were counted. The expression of MIF, IL-8, bFGF and HIF-1α were detected by immunohistochemical. Results: We established a tumor model in nude mice of hepatoma cell line.