Costs must be considered and justified by analyses showing cost-effectiveness. We will use the WHO definitions of cost-effectiveness find more and will calculate the disability-adjusted life year (DALY) for Viet Nam in order to incorporate loss of quality of life as well as actual loss of years of life in our cost-effectiveness analyses. Based on such assessments, decisions can be made about which approaches are the worst and the best values. An expert evaluation team will perform process evaluation for each of the tasks defined here, as well as outcome evaluation for the entire project. Both qualitative information and quantitative data

will be collected, analyzed, and reported by the evaluators for adjustment under formative evaluation and for final report under a formal/summative evaluation. Convenient ubiquitin-Proteasome pathway samples of patients who have been screened or vaccinated for hepatitis B will be acquired from commune health centers, selected clinics, and selected pharmacies and statistically analyzed for effectiveness. Samples of people who have been provided with liver disease education at the gathering points will be selected for pre/post

knowledge, attitude, and practice changes. Evaluation forms at health education training meetings and health professionals’ training sessions will be analyzed to assess training effectiveness and trainers’ performance. Evaluation reports will be submitted during and after the project life to indicate the achievement of project goals and objectives. 1. Henderson DK, Dembry L, Fishman NO et al. SHEA guideline for management of health-care workers who are infected with hepatitis B virus, hepatitis check details C virus, and/or human immunodeficiency virus. Infect. Control Hosp. Epidemiol. 2010; 31: 203–32. “
“Data on the relationship between epidemiological changes in food bolus impaction (FBI) and its relationship to eosinophilic esophagitis (EoE) are limited. The aim of this study was to evaluate changes in the prevalence and etiology of FBI at the Royal Adelaide Hospital over 15 years. Details of all patients who presented with FBI to Royal Adelaide Hospital (1996–2010) were reviewed from a

prospective database. Detailed endoscopic and histological findings were examined for patients admitted under the Gastroenterology team. From 1996–2010, 539 patients were admitted. Prevalence of FBI increased overtime, with a male preponderance. The age at presentation was significantly lower in 2006–2010 (56.2 ± 1.6 years) compared with 2001–2005 (61.6 ± 1.9 years, P = 0.03). There was a reduction in the proportion of patients with peptic-related stricture (from 75% [1996–2000] to 41% [2006–2010] [P < 0.001]) and an increase in the prevalence of EoE (from 0% [1996–2000] to 35% [2006–2010], P < 0.001). The proportion of patients who had esophageal biopsies taken at the index endoscopy also increased (8% [1996–2000] vs 28% [2001–2005] and 61% [2006–2010], P < 0.01).

Most significant effects were observed for BPA doses within one order of magnitude around the current TDI of 50 μg/kg/day. Conversely, virtually no effects were observed at the NOAEL (5,000 μg/kg/day). Agencies for risk assessment have established

a “safe” TDI for BPA at 50 μg/kg/day, but several studies have revealed that exposure to environmentally relevant BPA doses below the TDI alters various biological functions, including reproductive, behavioral, metabolic, and immune systems.4 However, the molecular mechanisms underlying these low-level responses are still unknown. It was proposed that down-regulation of receptors at higher hormone or xenoestrogen levels may contribute to shape these nonmonotonic curves. Some of BPA’s actions, including insulin production by the pancreas, were attributed to its ability to bind to nonclassical membrane estrogen receptor as well as the G-protein coupled-receptor 30 (GPR30) Ibrutinib price and to act through nongenomic pathways.20, 30 Interestingly, we observed that, contrary to lipid metabolism genes, Ugt1a1 expression displayed a dose-dependent increase in response to BPA (Fig. 3E). Human UGT1a1 mRNA expression has been previously reported to be increased by low BPA doses in HepG2 cells.31 This phase II enzyme is involved in the metabolism of endogenous estrogens32 and has also been shown to catalyze BPA

glucuronidation at high substrate concentration.33 Whether the modest increase in Ugt1a1 expression can interfere with Selleck INCB024360 the action of BPA and/or find more endogenous estrogens may be doubtful, but it suggests that different pathways with different sensitivities to BPA are targeted depending on the dose of exposure. The effects of BPA on insulin expression and secretion have been described.17 Our results strongly

suggest that the effects of BPA on insulin production by the pancreas translate to transcriptional and functional consequences in the liver. Indeed, insulin is known to increase glycolysis and lipogenesis by way of both posttranslational protein modifications and transcriptional mechanisms.34 SREBP-1c plays a major role in the regulation of these genes in response to insulin.35 LXR is thought to contribute to the effect of insulin on Srebp-1c gene expression.36 LXR also directly regulates the expression of lipogenic genes.37 Additionally, insulin also stimulates the proteolytic processing of SREBP-1c,38 leading to increased mature nuclear form and subsequent induction of lipogenic gene expression. In addition to insulin, glucose stimulates glycolytic and lipogenic gene expression by activating the ChREBP,29 which is itself under the transcriptional control of LXR.39 Insulin also induces the expression of Spot14, which is required for induction of hepatic lipogenesis by thyroid hormone and insulin40, 41 and of Pnpla3 by way of SREBP1-c.42 SREBP-2 expression and activity are primarily regulated by low sterol levels but were also reported to respond to increased insulin levels.

Initially, sumatriptan was available only in an injectable formulation; using an “autoinjector” specifically designed for the drug, sumatriptan can be delivered subcutaneously (just below the skin surface) via a small needle. Injectable sumatriptan proved to be a revolutionary drug, empowering millions of individuals who experience moderate to severe intensity acute migraine headache. Self-administered injectable sumatriptan has offered such individuals

a safe and rapidly effective therapy far superior to the dismal options of either suffering in silence at home MAPK Inhibitor Library concentration or seeking care at an emergency department or other health care facility. An oral version of sumatriptan soon followed its injectable formulation, ultimately to be joined by 6 additional oral “triptans” and, most recently, an oral compound containing oral sumatriptan and an anti-inflammatory drug, naproxen sodium. While the oral triptans undeniably have benefited many migraine

sufferers, they all are most consistently effective when taken at a relatively early stage in the migraine attack. None is as effective – and as rapidly effective – as injectable sumatriptan in treating migraine headache that has reached the moderate to severe level of intensity. There is now available a “needle-free” delivery system for administering subcutaneous sumatriptan. As with the pre-existing autoinjector (that continues to be marketed), “Sumavel DosePro” delivers sumatriptan Protease Inhibitor Library to the area just beneath the skin’s surface, but it does so selleck kinase inhibitor via a novel technology that uses compressed gas to create a stream of medication that passes through the skin into the subcutaneous tissue. While patients experience a similarly minor degree of (typically brief) pain at the injection site regardless of which delivery system is used, autoinjector

or DosePro, studies have indicated that Sumavel DosePro is well tolerated and simple to use. If Sumavel DosePro is administered into the thigh or abdomen, the dose received (6 mg) is biologically equivalent to an equal dose administered via the needle-based autoinjector. This is not true for the arm, and administration of Sumavel DosePro into the arm consequently is not recommended. In summary, migraine sufferers now have available to them 2 alternatives for administering subcutaneous sumatriptan. The newer of the two, Sumavel DosePro, is needle-free and quite simple to use. No matter which method of administration is chosen, however, subcutaneous sumatriptan may cause a wide variety of side effects that include neck “squeezing,” chest pressure, and palpitations. While these and other side effects typically are short-lived and benign, the drug can cause blood vessel constriction and is not to be used by individuals at particular risk for vascular complications such as heart attack or stroke.

Ten days after consuming the experimental diets, the mice were orally administered maltose dextrin solution (9 g of maltose dextrin/kg of body weight; CTRL

group) or ethanol solution (5 g of Dabrafenib clinical trial ethanol/kg of body weight; EtOH group) at zeitgeber time (ZT) 3 (9 am), and were sacrificed at ZT12, 18, 0, and 6. Serum and livers were collected at each time point. [Results] Serum ALT and AST levels were induced by alcohol at all time points, but with ALT showing a stronger oscillation, which was highest at ZT12 and lowest at ZT0. Serum triglyceride (TG) levels exhibited the highest induction by alcohol at ZT0, which declined to basal levels by ZT12. Interestingly, hepatic TG reached the highest levels in the EtOH group at ZT12, which was gradually decreased to the lowest levels by ZT6. Serum cholesterol levels did not show marked differences in CTRL and EtOH groups, whereas liver cholesterol content was constantly higher in the EtOH group with a moderate rhythm. Consistently, oil red O staining revealed the highest hepatic neutral lipid accumulation at ZT12 and lowest at ZT6 in the EtOH group. Gene expression analysis by qPCR uncovered a striking effect of alcohol on the alteration OSI906 of rhythmic expression of transcription factors E2F1 and

Egr-1, nuclear receptors SHP and RORγ, bile acid synthesis enzyme Cyp7a1, lipid metabolic gene VLDLR, and the key clock gene NPAS2. [Conclusions] The effect of alcohol consumption by chronic and binge ethanol feeding in mice on the disruption of serum and hepatic lipid metabolism is strongly associated with alterations in the expression of key liver circadian clock genes. Disclosures: The following people have nothing to disclose: Hiroyuki Tsuchiya, Sangmin Lee, Yuxia Zhang, Rana Smalling, Li Wang FOXO3 is a multifunctional transcription factor that initiates several different transcriptional programs including oxidative stress resistance, cell proliferation, apoptosis, autophagy, and metabolism. The mechanisms that regulate

transcriptional specificity of FOXO3 are unknown. We have recently shown that ethanol and HCV infection each individually activate FOXO3 but they do so by different post-translational modifications. The AIM of this study was to determine the effects of ethanol on the transcriptional find more specificity and post-translational modifications of FOXO3 and their consequences. METHODS: Huh7.5 cells were transfected with HA-tagged FOXO3, treated with 50 mM ethanol for 48 h and/or infected with HCV strain JFH1. ChiP assays were performed with anti-HA or FOXO3 antibodies. A phospho-specific S574-P_FOXO3 antibody was generated by Epitomics. RESULTS: Ethanol treatment increased mRNA for the apoptotic FOXO3 target protein Bim but not the antioxidant target protein SOD2. HCV-infection, which similarly stimulated FOXO3 reporter activity, had the opposite effect activating SOD2 but not Bim. We performed ChIP assays on Huh7.

Ten days after consuming the experimental diets, the mice were orally administered maltose dextrin solution (9 g of maltose dextrin/kg of body weight; CTRL

group) or ethanol solution (5 g of selleck inhibitor ethanol/kg of body weight; EtOH group) at zeitgeber time (ZT) 3 (9 am), and were sacrificed at ZT12, 18, 0, and 6. Serum and livers were collected at each time point. [Results] Serum ALT and AST levels were induced by alcohol at all time points, but with ALT showing a stronger oscillation, which was highest at ZT12 and lowest at ZT0. Serum triglyceride (TG) levels exhibited the highest induction by alcohol at ZT0, which declined to basal levels by ZT12. Interestingly, hepatic TG reached the highest levels in the EtOH group at ZT12, which was gradually decreased to the lowest levels by ZT6. Serum cholesterol levels did not show marked differences in CTRL and EtOH groups, whereas liver cholesterol content was constantly higher in the EtOH group with a moderate rhythm. Consistently, oil red O staining revealed the highest hepatic neutral lipid accumulation at ZT12 and lowest at ZT6 in the EtOH group. Gene expression analysis by qPCR uncovered a striking effect of alcohol on the alteration SCH727965 cost of rhythmic expression of transcription factors E2F1 and

Egr-1, nuclear receptors SHP and RORγ, bile acid synthesis enzyme Cyp7a1, lipid metabolic gene VLDLR, and the key clock gene NPAS2. [Conclusions] The effect of alcohol consumption by chronic and binge ethanol feeding in mice on the disruption of serum and hepatic lipid metabolism is strongly associated with alterations in the expression of key liver circadian clock genes. Disclosures: The following people have nothing to disclose: Hiroyuki Tsuchiya, Sangmin Lee, Yuxia Zhang, Rana Smalling, Li Wang FOXO3 is a multifunctional transcription factor that initiates several different transcriptional programs including oxidative stress resistance, cell proliferation, apoptosis, autophagy, and metabolism. The mechanisms that regulate

transcriptional specificity of FOXO3 are unknown. We have recently shown that ethanol and HCV infection each individually activate FOXO3 but they do so by different post-translational modifications. The AIM of this study was to determine the effects of ethanol on the transcriptional find more specificity and post-translational modifications of FOXO3 and their consequences. METHODS: Huh7.5 cells were transfected with HA-tagged FOXO3, treated with 50 mM ethanol for 48 h and/or infected with HCV strain JFH1. ChiP assays were performed with anti-HA or FOXO3 antibodies. A phospho-specific S574-P_FOXO3 antibody was generated by Epitomics. RESULTS: Ethanol treatment increased mRNA for the apoptotic FOXO3 target protein Bim but not the antioxidant target protein SOD2. HCV-infection, which similarly stimulated FOXO3 reporter activity, had the opposite effect activating SOD2 but not Bim. We performed ChIP assays on Huh7.

The nodules were located in the VII and VIII segments and had diameters of 24 and 39 mm, respectively. For characterization and staging, CEUS and contrast-enhanced computed tomography were performed. Both techniques showed intense and homogeneous arterial enhancement (Fig. 1A,B) followed by washout in the portal and delayed phases (Fig. 1D,E). In order to complete the genetic and immunochemical study protocol, biopsy was performed on both nodules. The lesion in the VIII segment ERK inhibitor was revealed

to be well-differentiated ICC (Fig. 1C), whereas the other lesion showed features of well-differentiated HCC (Fig. 1F). This case clearly demonstrates the risk of accepting imaging findings as conclusive for HCC in the setting of liver cirrhosis and the risk of considering the largest of multiple nodules to be representative of all others. The AASLD guidelines should be amended with respect to the possible misdiagnosis of lesions whose imaging simulates HCC but that are due to different diseases (e.g., ICC or non-Hodgkin’s lymphoma) and with respect to synchronous nodules occurring in patients with cirrhosis. In conclusion, our case and the results of Vilana et al.1 confirm that aimed biopsy is the most accurate option for a confident diagnosis buy CH5424802 of liver nodules.4 The AASLD diagnostic

criteria increasingly seem to display evidence of low sensitivity and specificity, and this suggests the need for redefinition. Giorgia Ghittoni M.D.*, Eugenio Caturelli M.D.†, Sandro Rossi M.D.*, * Medicina VI, Ecografia Interventistica, Istituto di Ricovero selleckchem e Cura a Carattere, Scientifico Policlinico San Matteo, Pavia, Italy, † Unità Operativa di Gastroenterologia, Ospedale Belcolle,

Viterbo, Italy. “
“We read with interest the study by Solà et al.,1 who found that 39 patients (67%) had a very alarming decrease in their serum sodium levels ≥ 5 mEq/L during terlipressin treatment for acute variceal bleeding (AVB). We, however, feel that some of their observations may require a closer look by the readers. Terlipressin for AVB has been evaluated in a number of studies, but hyponatremia has not been mentioned, has not been found significant, or has not been examined in most. Escorsell et al.2 observed hyponatremia in 4 of 105 patients (3%) treated with terlipressin; similarly, Feu et al.3 observed 5 cases of hyponatremia among 80 patients (6%) with AVB. At our center, 47 patients were treated with band ligation along with terlipressin (2 mg every 6 hours for the first 48 hours and then 1 mg every 6 hours for the next 3 days) over the last 12 months [age = 50.4 ± 11.9 years, hemoglobin level = 8.1 ± 2.1 g %, median total bilirubin level = 2.3 mg % (range = 1.0-27.0 mg %), serum sodium level = 132.2 ± 6.3 mmol/L, serum albumin level = 2.5 ± 0.5 g %, median serum creatinine level = 0.

The nodules were located in the VII and VIII segments and had diameters of 24 and 39 mm, respectively. For characterization and staging, CEUS and contrast-enhanced computed tomography were performed. Both techniques showed intense and homogeneous arterial enhancement (Fig. 1A,B) followed by washout in the portal and delayed phases (Fig. 1D,E). In order to complete the genetic and immunochemical study protocol, biopsy was performed on both nodules. The lesion in the VIII segment www.selleckchem.com/products/Cisplatin.html was revealed

to be well-differentiated ICC (Fig. 1C), whereas the other lesion showed features of well-differentiated HCC (Fig. 1F). This case clearly demonstrates the risk of accepting imaging findings as conclusive for HCC in the setting of liver cirrhosis and the risk of considering the largest of multiple nodules to be representative of all others. The AASLD guidelines should be amended with respect to the possible misdiagnosis of lesions whose imaging simulates HCC but that are due to different diseases (e.g., ICC or non-Hodgkin’s lymphoma) and with respect to synchronous nodules occurring in patients with cirrhosis. In conclusion, our case and the results of Vilana et al.1 confirm that aimed biopsy is the most accurate option for a confident diagnosis this website of liver nodules.4 The AASLD diagnostic

criteria increasingly seem to display evidence of low sensitivity and specificity, and this suggests the need for redefinition. Giorgia Ghittoni M.D.*, Eugenio Caturelli M.D.†, Sandro Rossi M.D.*, * Medicina VI, Ecografia Interventistica, Istituto di Ricovero check details e Cura a Carattere, Scientifico Policlinico San Matteo, Pavia, Italy, † Unità Operativa di Gastroenterologia, Ospedale Belcolle,

Viterbo, Italy. “
“We read with interest the study by Solà et al.,1 who found that 39 patients (67%) had a very alarming decrease in their serum sodium levels ≥ 5 mEq/L during terlipressin treatment for acute variceal bleeding (AVB). We, however, feel that some of their observations may require a closer look by the readers. Terlipressin for AVB has been evaluated in a number of studies, but hyponatremia has not been mentioned, has not been found significant, or has not been examined in most. Escorsell et al.2 observed hyponatremia in 4 of 105 patients (3%) treated with terlipressin; similarly, Feu et al.3 observed 5 cases of hyponatremia among 80 patients (6%) with AVB. At our center, 47 patients were treated with band ligation along with terlipressin (2 mg every 6 hours for the first 48 hours and then 1 mg every 6 hours for the next 3 days) over the last 12 months [age = 50.4 ± 11.9 years, hemoglobin level = 8.1 ± 2.1 g %, median total bilirubin level = 2.3 mg % (range = 1.0-27.0 mg %), serum sodium level = 132.2 ± 6.3 mmol/L, serum albumin level = 2.5 ± 0.5 g %, median serum creatinine level = 0.

14, 28, 39 Hu et al.14 demonstrated that appending tyrosine- or dileucine-based motifs of CFTR to a Tac reporter allows for rapid internalization, indicating that the C-terminus of CFTR contains endocytic signals. However, identifying endocytic signals in a full-length polytopic protein is often difficult because creating mutations in the putative see more sequence by alanine scanning or sequential deletion may lead to misprocessing of the full-length protein and hamper its trafficking to the plasma membrane. For example, in full-length multidrug-resistant 1 (MDR1), mutations of analogous leucine or tyrosine residues led to misprocessing and ER retention, precluding the evaluation

of its targeting function.40 Epacadostat solubility dmso However, we were able to successfully mutate the tyrosines in the C-terminus of full-length

BSEP and observe the same defect in endocytosis that we had demonstrated in TacCterm. To date, there are no known disease-producing point mutations of human BSEP in the identified endocytic signal region; however, there are premature stop codons that lead to deletion of the tyrosine-based motif.3 Deletion of a major portion of the C-terminus in a human disease-causing Bsep mutant in the rat (R1050X) showed proper targeting to the apical membrane of MDCK cells, indicating that a large portion of the C-terminal nucleotide-binding domain is not necessary for biosynthetic processing and apical targeting.41 However, we and others have identified a number of BSEP mutations that cause a reduction of Bsep on the cell surface through increased rate of internalization in heterologous expression systems.30, 41 This loss of Bsep protein from the canalicular membrane is characteristic of some forms of experimental cholestatic liver injury, as well as human cholestatic liver diseases. Cholestasis induced by estradiol-17β-D-glucuronide, taurolithocholic selleck chemicals acid, cyclosporine A, and lipopolycharide all result in redistribution of

Bsep to the subapical cytoplasm.7, 8, 42, 43 Efforts have been made to compensate for the loss of cell surface BSEP with the administration of chemical or pharmacological agents such as MG-132 or sodium phenylbutyrate.30, 41, 44 Although the mechanisms of action are not clearly defined for these agents, one possible explanation for the increase of BSEP cell surface expression is that these compounds limit the extent of ubiquitinylation of BSEP.45 Ubiquitinylation of membrane proteins and endocytic adaptor proteins attenuates signaling of ligand-dependent activation of receptors by targeting these receptors to the endolysosomal pathway for degradation. Hayashi et al.45 showed that attaching short-chain ubiquitin to BSEP shortens the half-life of cell surface BSEP.

14, 28, 39 Hu et al.14 demonstrated that appending tyrosine- or dileucine-based motifs of CFTR to a Tac reporter allows for rapid internalization, indicating that the C-terminus of CFTR contains endocytic signals. However, identifying endocytic signals in a full-length polytopic protein is often difficult because creating mutations in the putative BMN 673 chemical structure sequence by alanine scanning or sequential deletion may lead to misprocessing of the full-length protein and hamper its trafficking to the plasma membrane. For example, in full-length multidrug-resistant 1 (MDR1), mutations of analogous leucine or tyrosine residues led to misprocessing and ER retention, precluding the evaluation

of its targeting function.40 Selleck Idasanutlin However, we were able to successfully mutate the tyrosines in the C-terminus of full-length

BSEP and observe the same defect in endocytosis that we had demonstrated in TacCterm. To date, there are no known disease-producing point mutations of human BSEP in the identified endocytic signal region; however, there are premature stop codons that lead to deletion of the tyrosine-based motif.3 Deletion of a major portion of the C-terminus in a human disease-causing Bsep mutant in the rat (R1050X) showed proper targeting to the apical membrane of MDCK cells, indicating that a large portion of the C-terminal nucleotide-binding domain is not necessary for biosynthetic processing and apical targeting.41 However, we and others have identified a number of BSEP mutations that cause a reduction of Bsep on the cell surface through increased rate of internalization in heterologous expression systems.30, 41 This loss of Bsep protein from the canalicular membrane is characteristic of some forms of experimental cholestatic liver injury, as well as human cholestatic liver diseases. Cholestasis induced by estradiol-17β-D-glucuronide, taurolithocholic selleck chemical acid, cyclosporine A, and lipopolycharide all result in redistribution of

Bsep to the subapical cytoplasm.7, 8, 42, 43 Efforts have been made to compensate for the loss of cell surface BSEP with the administration of chemical or pharmacological agents such as MG-132 or sodium phenylbutyrate.30, 41, 44 Although the mechanisms of action are not clearly defined for these agents, one possible explanation for the increase of BSEP cell surface expression is that these compounds limit the extent of ubiquitinylation of BSEP.45 Ubiquitinylation of membrane proteins and endocytic adaptor proteins attenuates signaling of ligand-dependent activation of receptors by targeting these receptors to the endolysosomal pathway for degradation. Hayashi et al.45 showed that attaching short-chain ubiquitin to BSEP shortens the half-life of cell surface BSEP.

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 selleck chemicals 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 this website 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. click here 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.