“
“Background and Aims:  Researches about blocking angiogenesis to treat tumor have become one of the most promising

and active fields in anticancer research. This study aimed to investigate the eukaryotic expression of extracellular ligand binding domains of murine Tie-2 and its anti-angiogenesis effect. Methods:  A eukaryotic expression vector pcDNA3.1+ integrating with a DNA fragment which encode extracellular ligand binding domains of murine Tie-2 was transfected into Lumacaftor clinical trial SGC-7901 gastric cancer cell line. The protein expression was detected by western blot analysis and immunocytochemistry staining. Following the construction of nude mouse tumor xenograft model with and without transfected cells, tumor microvessel density was determined by counting per high power field in the sections stained with an antibody to CD31 to test its inhibition of angiogenesis. Results:  The extracellular ligand binding domains of murine Tie-2 receptor was highly expressed in SGC-7901 gastric cancer cells with plasmid transfection. The mean tumor sizes of groups with and without transfection were 1.27 ± 0.35 and 1.75 ± 0.17 cm3, respectively (P = 0.025). The mean inhibitory rate of tumor was 27.18 ± 19.93%. The comparison between highest microvessel density of group with transfection (14.00 ± 3.80) and that of group without transfection (22.30 ± 5.91) was statistically significant at P = 0.030. Conclusion:  The

protein of extracellular ligand binding domains of murine Tie-2 can be expressed at high level in the eukaryotic expression system, PD0325901 and the expressed protein may have the anti-angiogenesis

effect. “
“Transdifferentiation of hepatic stellate cells (HSCs) to a myofibroblast-like phenotype is the pivotal event in liver fibrosis. The dramatic change in phenotype associated with transdifferentiation is underpinned by a global change in gene expression. Orchestrated changes in gene expression take place at the level of chromatin packaging which is regulated by enzymatic activity of epigenetic regulators that in turn affect histone modifications. Using expression profiling of epigenetic regulators in quiescent and activated primary HSCs we found a number of histone methyltranferases including MLL1, MLL5, Set1 and ASH1 to be highly up-regulated during transdifferentiation of HSCs. All of these histone methyltranferases Exoribonuclease regulate methylation of lysine 4 of histone H3, which is a signature of actively transcribed genes. We therefore postulated that one or more of these enzymes may be involved in positively influencing expression of profibrogenic genes. Conclusion: We find that ASH1 directly binds to the regulatory regions of alpha smooth muscle actin (αSMA), collagen I, tissue inhibitor of metalloproteinase-1 (TIMP1) and transforming growth factor beta1 (TGFβ1) in activated HSCs while depletion of ASH1 caused broad suppression of fibrogenic gene expression.

Research also indicates that for both migraine and tension-type headache, the judicious combination of headache medications and behavioral therapies provides better outcomes than the

sole use of either therapy alone. The effectiveness Sirtuin inhibitor of behavioral headache therapies is underscored by the numerous professional associations that endorse them (eg, US Headache Consortium, World Health Organization, National Institutes of Health, American Medical Association, American Academy of Neurology, American Headache Society). Relaxation training focuses on helping patients modify headache-related physiological responses, reduce arousal of the nervous system, and decrease muscular tension. A common training procedure (progressive muscle relaxation) teaches Ivacaftor patients to achieve a relaxed state through a series of muscle exercises and controlled breathing. Relaxation training gives a patient increased awareness and control of biological changes that can cause headaches. Biofeedback training uses special monitoring devices that help patients learn to control headache-related physical responses. Biofeedback devices

measure and then “feed back” information about the physical response to the patient. EMG biofeedback can help patients learn to reduce muscular tension, and hand-warming biofeedback can help patients learn to reduce nervous system arousal. Cognitive behavior therapy or stress management training helps patients identify their unique behavioral risk/trigger factors for headache (often including stress, sleep disruption, and skipping meals) and then to develop strategies to minimize the impact of their triggers. Learning to recognize and cope more effectively with headache triggers often assists patients to prevent headaches and reduce headache-related disability. There are other “tried and

true” therapies practiced widely in the United States that eventually may be proven effective for head pain management. These include acupuncture, chiropractic therapy, hypnosis, and physical therapies. While research and clinical experience provide evidence that these treatment approaches can benefit headache sufferers, the science is yet inconclusive – mainly because too few well-designed studies provide the evidence needed to conclusively Interleukin-3 receptor establish their indications and effectiveness. Although the complimentary therapies listed here seldom are harmful, they also are not completely harmless (especially in the hands of unqualified practitioners), and they are not without cost. It’s an excellent idea to consult with your physician about complementary therapies. Be certain you know your headache diagnosis, and be sure that the unlikely possibility that your head pain is due to a life-threatening illness has been ruled out. In this day and age, most physicians are open to consideration of complementary treatments.

pylori infection. In children, especially in the youngest, the usefulness of the diagnostic test based on the detection of H. pylori-specific IgG antibodies (serum, urine, whole blood, saliva) is controversial due to their low sensitivity. Okuda et al. [35] evaluated the accuracy of two urinary IgG antibodies tests (Urine-HpELISA test and Rapid urine-HpAb) obtaining sensitivity and specificity of 91.9% and 96.9% for Urine-HpELISA and 78.4% and 100% for Rapid urine-HpAb and recommended these methods as simple, low cost, rapid, and reliable for screening of H. pylori. Histopathologic https://www.selleckchem.com/products/ABT-263.html studies are still important to identify mucosal lesions. Carvalho et al. analyzed histopathologic lesions in 96 Brazilian

children with H. pylori infection. 70.5% had moderate-to-severe chronic active gastritis. Intestinal metaplasia was not found, selleck chemical and gastric atrophy was not significant. 61.9% had pangastritis, and H. pylori density was higher in the antrum than in the corpus [36]. Molecular methods have been used for different purposes: detection of H. pylori in gastric biopsies compared with conventional methods, detection of virulence genes, both in biopsy specimens and in specimens other than biopsies obtained using less invasive methods (string test) or noninvasive methods (stool samples). Ou et al. [37] found that the fluorescent quantitative PCR test was more sensitive than conventional methods alone or in combination (p<0.01). A nested

PCR had a sensitivity of 93.0% and a specificity of 100% compared with the 13C-urea breath test (UBT) on gastric DNA obtained by a string test in asymptomatic children [2]. Baskovich et al. [38] also detected a surprisingly high number of new cases with H. pylori by PCR, in both the normal biopsies and test cases, suggesting that PCR could detect colonization in asymptomatic patients. The sensitivity and specificity of the glmM gene compared with UBT was 42.6% and 100%, respectively, in stools of patients with dyspepsia [1]. Multilocus sequence typing MLST of total DNA extracted from fecal specimens to genotype H. pylori was successfully Decitabine research buy used by Osaki et al. [21]. Antibiotic resistance is

the major cause of failure in the treatment of H. pylori infection. Most of the studies worldwide confirmed an increase in macrolide resistance, while metronidazole resistance either decreased or remained stable. In a prospective multicentre European study, primarily comprised of adults, Megraud et al. [39] found a 31.8% resistance rate to clarithromycin and 25.7% to metronidazole in the 311 H. pylori isolates from children from eight countries included in the study. The increase in clarithromycin resistance in many countries (especially in Western/Central and Southern Europe) has prohibited its empirical use in standard therapeutic regimens. Hojsak et al. [40] found a 17.9% resistance to azithromycin, 11.9% to clarithromycin, 10.1% to metronidazole, and 0.

Predictable pharmacokinetics and pharmacodynamics allow a fixed dose of rivaroxaban without coagulation monitoring.[2] It has a half-life of up to 12 hours, its absorption is not affected by food, and one-third of the drug is eliminated by the kidneys, while two-thirds undergo metabolism in the liver.[2] Specific labeling restrictions for rivaroxaban regarding impaired hepatic function are based

on both the Child-Pugh classification and liver-related exclusion criteria applied in pivotal trials.[2] It is currently contraindicated in patients with liver disease associated with coagulopathy, cirrhosis Child Class B or C, and clinically relevant bleeding risk.[2] When compared to warfarin, rivaroxaban’s acquisition cost is higher, but this may be counterbalanced by costs of monitoring, patient’s inconvenience, and healthcare provider’s time required for managing test learn more results.[2] Carfilzomib supplier In fact, a recent study showed that rivaroxaban is more cost-effective than warfarin for prevention of recurrent venous thromboembolism.[4] Although major and clinically relevant nonmajor bleeding rates were similar between warfarin and rivaroxaban, the rates of intracranial bleeding were significantly lower in the rivaroxaban group, but significantly higher with regard to gastrointestinal bleed.[5] Current concerns about the lack of an antidote for rivaroxaban may be alleviated

when a promising agent such as Andexanet Alfa (Clinicaltrials.gov: NCT01758432) gains regulatory approval. Premature discontinuation of rivaroxaban, like any anticoagulant, can increase the risk of thrombotic events and therefore documentation of complete clot resolution is essential.[2] “
“Despite standardization of surgical Phospholipase D1 methods in biliary reconstruction, immunosuppression and post-operative management, biliary complications continue to be a major cause of morbidity

and mortality after liver transplantation (LT). Early identification of biliary complications after LT is critical due to the potential for graft and patient injury. Biliary complications include biliary strictures, bile leaks, biliary stones/debris, sphincter of Oddi dysfunction, mucoceles and hemobilia. Many of these complications can be managed with a combination of endoscopic and percutaneous therapy and this has minimized the need for post-transplant biliary surgery. “
“Superior mesenteric artery (SMA) syndrome, a rare form of proximal intestinal obstruction, occurs when the third portion of duodenum passes through a narrowed opening between the SMA and abdominal aorta. It has been described in association with anorexia nervosa, burns as well as severe weight loss due to various etiologies. The mechanism is a loss of the mesenteric fat pad from undue weight loss. The course may be acute or insidious with nonspecific presentations of postprandial epigastric pain, nausea, and vomiting. Panendoscopy usually identifies reflux-related injury.

2B). Costaining of CcnE1 and α-SMA in fibrotic livers revealed an accumulation of CcnE1-expressing cells in areas of fiber formation (Fig. 2C). Using confocal laser scanning microscopy, we demonstrated nuclear CcnE1 localization predominantly in α-SMA-expressing cells (Fig. 2D). These data demonstrated that liver fibrogenesis in humans and mice involves increased cell-cycle activity, potentially driven by CcnE1, and suggested that CcnE1 is especially induced in HSCs during this process. Single CCl4 administration triggers approximately

20-fold CcnE1 messenger RNA (mRNA) expression www.selleckchem.com/p38-MAPK.html in WT mice within 48 hours (Fig. 2A). We recently reported that genetic ablation of CcnE2 results in the overexpression of CcnE1 and excessive hepatocyte proliferation after PH.11 In agreement with our earlier findings, CcnE1 mRNA induction was approximately 5-fold higher in CcnE2−/− mice, compared to WT animals, 48 hours after single CCl4 administration (Fig. 2A). To evaluate the effect of CcnE1 Selinexor for the onset of liver fibrosis, we compared the immediate proliferative response 48 hours after single CCl4 treatment in WT, CcnE1−/−, and CcnE2−/− mice by measuring bromodeoxyuridine

(BrdU) incorporation (specific for DNA synthesis) and the general proliferation marker, cell-cycle–specific protein encoded by the MKI67 gene (Ki-67). Of note, CCl4 induced a similar level of necrotic liver injury in each group, as evidenced by the comparable induction of alanine aminotransferase (ALT) activity (Fig. 3B and Supporting Fig. 1A). WT and CcnE2−/− livers revealed a similar proliferative response with substantial DNA synthesis of hepatic cells, as evidenced by strong

BrdU incorporation (Fig. 3C and Supporting ifoxetine Fig. 1B) and extensive Ki-67 expression. Under these conditions, CcnE1 was localized in the hepatocytes of WT and CcnE2−/− mice (Supporting Fig. 1C). However, elevated CcnE1 levels, as observed in the CcnE2−/− liver, did not result in enhanced hepatocyte proliferation after toxic injury. In contrast, CcnE1 deficiency resulted in a remarkable reduction of hepatocyte proliferation and DNA synthesis after acute CCl4 treatment (Fig. 3C,D). Thus, CcnE1 plays an important role for liver regeneration after CCl4-mediated toxic liver injury. We next investigated the consequences of chronic CCl4 treatment in CcnE1−/− mice, in comparison to WT controls. Repeated injections of CCl4for 4 weeks induced prominent liver fibrosis with septum formation in WT animals, as evidenced by Sirius red staining. In contrast, fiber formation was barely observed in CcnE1−/− mice (Fig. 4A,B), suggesting a functional role of CcnE1. Additionally, WT mice revealed a substantial up-regulation of collagen type I α1 (COL1A1) and α-SMA mRNA expression 4 weeks after CCl4 treatment, which were only moderately induced in CcnE1−/− livers (Fig. 4C,D).

However, it did not completely prevent the onset of latent gastric cancer among those at high risk (i.e., with atrophic gastritis). To prevent deaths

from gastric cancer, it is necessary to eradicate H. pylori infection. We propose a program of risk stratification based on the presence of H. pylori infection with or without atrophic gastritis followed by targeted interventions. Those at no risk for gastric cancer (no H. pylori, no atrophic gastritis) need no therapy or follow-up. Those at low risk (H. pylori infected, nonatrophic gastritis) need only H. pylori eradication therapy. The smaller groups at high or very high risk need eradication and cancer surveillance. We estimated the costs and the benefits of this strategy. Gastric cancer selleck compound screening

by simultaneous measurement of serum pepsinogen and H. pylori antibody combined with eradication of H. pylori in all individuals at risk would initially increase national healthcare expenditure, but this would be offset by markedly reducing the cost of treating gastric cancer. The proposed strategy should prevent about 150,000 deaths from gastric cancer during the 5 years after its adoption. If the loss caused by these deaths is also taken into account, the economic effect of this strategy becomes enormous. It would probably reduce the incidence of gastric cancer by more than 80–90% within 10 years. The Japanese government should take the initiative to implement this strategy as RO4929097 solubility dmso soon as possible. “
“Helicobacter pylori eradication is essential for metachronous gastric cancer prevention in patients undergoing endoscopic mucosectomy (EMR). This study was aimed to determine the optimal biopsy site for H. pylori detection in the 5-Fluoracil cell line atrophic remnant mucosa of EMR patients. Data were analyzed from 91 EMR patients. Three paired biopsies for histology were taken at antrum, corpus lesser (CLC), and greater curve (CGC). Additional specimens were obtained at antrum and CGC for rapid urease test (RUT). H. pylori infection was defined as at least two positive specimens on histology and/or RUT. Serologic atrophy was

determined by pepsinogen levels. Overall H. pylori infection rate was 72.5%. The proportions of moderate-to-marked atrophy/intestinal metaplasia at CGC (5.6/6.6%) were significantly lower than those at antrum (58.6/75.8%) and CLC (60.7/70.0%). Sensitivity of histology in detecting H. pylori was significantly higher at CGC than at antrum and CLC (84.8 vs 30.3 and 47.0%, respectively; p < .001). On RUT, detection at CGC also showed higher sensitivity than at antrum (77.3 vs 33.3%, p < .001). Specificities of all three biopsy sites were more than 90%. Regardless of serologic atrophy, CGC showed consistently higher sensitivities on histology and RUT. In patients with serologic atrophy, antral sensitivities were much lower than those of nonatrophic patients, 9.5 versus 40.0% on histology (p = .012) and 14.3 versus 42.2% on RUT (p = .025). CGC is the optimal biopsy site for H.

205 One potential approach to resolve this is the use of individual patient data across clinical trials, which represents the “gold standard” approach to meta-analysis.206 Although it is impractical to retrieve and combine primary data from all the clinical trials in this field, where large variation in studies over time exists, this approach was pursued with the use of a combined dataset, using pooled primary data from three placebo controlled trials in patients with comparable

measures of disease severity (i.e., an MDF ≥32). The result showed a significant increase in short-term check details survival among treated patients compared to control patients: 84.6% versus 65%.207 This represents a modest absolute reduction in risk, but a 30% relative risk reduction, and translates into a number needed to treat of 5, i.e., five patients need to

be treated to avert one death. This last meta-analysis also excluded a recent trial comparing steroids to a combination of antioxidants, which showed a similar protective effect of corticosteroids among treated patients.208 Although it is possible that antioxidants themselves may be detrimental,209 the doses used seem unlikely to account for the differences in survival, and the consistency of the data suggest a protective effect of steroids. Although the doses and durations Dabrafenib of steroid treatment used in the clinical trials were variable, the best available evidence suggests a dose of prednisolone (40 mg/day Etofibrate for 4 weeks then tapered over 2-4 weeks, or stopped, depending on the clinical situation) should be used in favor of prednisone.210 It is important to recognize that the efficacy of steroids

has not been evaluated in patients with severe alcoholic hepatitis and concomitant pancreatitis, gastrointestinal bleeding, renal failure, or active infection, which were exclusion criteria in many of the early studies of alcoholic hepatitis. An important issue in all studies of medical therapy, and one that has been recognized for some time in this literature, is the possibility that these therapies may not be effective at an advanced stage of disease. Just as there is a threshold for the use of steroids (i.e., identifying patients at high risk of mortality defined by a MDF score ≥32), there may also be a ceiling beyond which medical therapies aimed at decreasing the inflammatory cascade may cause more harm than benefit. One study examined this issue, and suggested that patients with a MDF > 54 were at a higher mortality risk from use of steroids than from not being treated.211 This cutoff, however, needs to be confirmed. One recently derived model used six variables to predict 6-month mortality in patients who were universally treated with steroids (including age, renal insufficiency (serum creatinine > 1.

Moreover, JGH has contributed importantly to the increased quality of clinical practice and scientific research in the field of gastroenterology and hepatology in the Asia-Pacific area. Overall, it has become one of the most prestigious scientific

journals in the gastroenterology field. I am glad to acknowledge that many Japanese scientists and clinician scientists have been engaged in the editorial board of JGH ever since its inauguration. Especially, we have to remember the late Professor Kunio Okuda, late Professor Hiromasa Ishii, and Professor Nobihiro Sato, for their outstanding contributions and efforts as Editors and Editors-in-Chief of JGH for years. I believe Professor Mamoru Watanabe will continue the tradition

of the sincere contribution of Japanese scientists to the further remarkable development of JGH. As a long-time friend and as a JGH Editor, it is my privilege to introduce Dr Watanabe’s career and his scientific achievements to the readers of the Journal. After graduation from Keio University in 1979, Dr Mamoru Watanabe engaged in clinical practice in gastroenterology, and together we experienced care of a variety of intractable GI disorders. At that time, I was really impressed by his superior talent as a resident, one who not only showed a warm-hearted devotion to the care of his patients with his excellent medical knowledge, but also had a keen interest about future medical progress and a great ability to predict

a medical trend. It seems he already had in mind that he should be involved in medical achievements for intractable digestive diseases in the future. Mamoru also recognized the necessity of training himself for basic research to conduct future epoch-making discoveries and innovations in medical treatment. He entered the graduate school of Keio and began research in the area of gastroenterology. Mamoru Watanabe has been working on inflammatory bowel disease (IBD), mucosal immunology and intestinal epithelial PAK6 biology for years, initially under the mentorship of late Professor Masaharu Tsuchiya (Emeritus Professor of Keio University), Professor Hitoshi Asakura (Emeritus Professor of Niigata University) and Professor Toshifumi Hibi (Current Professor of Department of Internal Medicine, School of Medicine, Keio University). It was an exciting and stimulating time at Keio University, given the selleck inhibitor vision and charisma of Dr Tsuchiya, a great chief, intent on building a world-class Division of Gastroenterology. Since then Mamoru’s prodigious body of work has been disseminated in the most respected journals. He has published over 200 original articles in prominent journals including Nature, Nature Medicine, PNAS, JCI, Journal of Experimental Medicine, Cancer Research and Gastroenterology. From 1987 to 1991, Dr Watanabe had been a postdoctoral research fellow in Norman Letvin’s lab at the New England Primate Research Center in Harvard Medical School, Boston.

Any use of the program content, which includes, but is not limited to oral presentations, audiovisual materials used by speakers, and program handouts, without the written consent of AASLD is prohibited. The CME/CE evaluations are electronic and can be completed using the following options: Upon download, use the meeting app to evaluate the sessions in real-time Using your personal device, link to the CME and/or CE evaluation on The Liver Meeting® website Visit Tech Connect to access the evaluation from any available kiosk CME and CE credit will be awarded upon completion of the electronic evaluation. You will have the ability to download and/or

print a certificate for your records once you have completed the CME and/or CE evaluations. Certificates of Attendance IWR-1 ic50 are also available. Certificates may be downloaded and/or printed upon completion of The Liver Meeting® evaluation. A follow-up survey

PD0325901 concentration will be sent to all attendees within three months of the conclusion of the meeting to assess the new skills and competencies learned as a result of participating in this live activity. May 16 – 19 Walter E. Washington Convention Center Washington, DC June 27 – 28 The Westin Chicago River North Chicago, Illinois Spring 2015 Location TBD November 13 – 17 Moscone West Convention Center San Francisco, California Managing Liver Disease – From the Clinic to the Community November 14 Moscone West Convention Center San Francisco, California Meeting-at-a-Glance

2A General Meeting Information 5A Limited License 7A Disclosure Index 8A Oral Sessions   Friday, November 7 32A Saturday, November 8 39A Sunday, November 9 43A Monday, November 10 65A Tuesday, November 11 85A Poster Sessions   Saturday, November 8 92A Sunday, November 9 119A Monday, November 10 146A Tuesday, November 11 169A Abstracts 197A Author Index 1206A Category Index 1256A selleck screening library The Scientific Program Committee has created an exciting and diverse scientific program that highlights new technology, current clinical issues and hot topics facing the hepatology community. Members include: Adrian M. Di Bisceglie, MD, FACP, Co-Chair Gary L. Davis, MD, Co-Chair Carla W. Brady, MD Kenneth D. Chavin, MD, PhD Mark J. Czaja, MD Marc G. Ghany, MD Saul J. Karpen, MD, PhD Keith D. Lindor, MD Gyongyi Szabo, MD, PhD Rebecca T. Wells, MD “
“We congratulate Berzigotti et al.1 for performing an excellent study that raises more questions, just as many post hoc analyses of observational studies do. It is intriguing that obesity may predict future decompensation in patients with compensated cirrhosis and portal hypertension. The potential mechanism is unexplained. The presence of a proinflammatory and proangiogenic state driven by extrahepatic adipose tissue may accelerate existing liver disease. Furthermore, hemodynamic changes linked to metabolic syndrome may affect the development of portal hypertension.

Some of the patients had liver stiffness Bortezomib purchase measurement assessed by transient elastography in our previous study and the last visit was taken as the day of transient elastography.14 Otherwise, the last visit was taken as the last follow-up visit with serum sample available. Detailed analyses were also performed to investigate the changes of HBsAg levels at the time of HBeAg seroconversion and hepatitis flare. For Group 3 patients, the HBsAg levels immediately before and after HBeAg seroconversion were measured and compared. Hepatitis flare was defined as an abrupt elevation of ALT to > 200 IU/L or >3 times the baseline level,

whichever was higher.15 HBsAg levels were determined in the available serum samples at the visits immediately before the flare, at the flare, and immediately after the flare. HBsAg was quantified by Architect HBsAg QT (Abbott Diagnostic, Germany) according to the manufacturer instructions.16 The sensitivity of Architect assay ranged from 0.05 to 250 IU/mL. Samples with HBsAg titer higher than 250 IU/mL were diluted to 1:500 to 1:1000 to bring the reading within the range

of the calibration curve. HBV DNA was quantified by TaqMan real-time polymerase chain reaction assay as described.17 This assay was standardized by serial dilution of EUROHEP genotype D HBV standard, which contained 2.7 × 109 viral copies per mL and was validated by the World Health Organization HBV standard. The range of HBV DNA detection was from 102 to 109 copies/mL with correlation coefficient of the standard curve routinely greater than 0.990. For samples with HBV DNA > 109 copies/mL, PD0325901 mouse HBV DNA assay would be repeated after dilution to 1:100. In this assay, 4.86 copies/mL equaled 1 IU/mL. HBV genotyping was determined by restriction fragment length polymorphism and was confirmed by direct sequencing in case of doubt in the residual serum sample at initial visit, as described.18 Statistical analysis was performed by SPSS (version 15.0; SPSS, Inc., Chicago, IL). Continuous variables were expressed as mean ± standard deviation click here or median (range) as appropriate. HBV DNA (IU/mL) and HBsAg

(IU/mL) were logarithmically transformed for analysis. For patients with undetectable HBV DNA and negative HBsAg, the results were taken as the lower limit of detection (20.6 IU/mL for HBV DNA and 0.05 IU/mL for HBsAg) for calculation. Ratio of HBsAg (log IU/mL) to HBV DNA (log IU/mL) was determined to reflect the proportion of subviral particles to virions. Continuous variables including HBV DNA and HBsAg were compared by Student t test or Mann-Whitney U test as appropriate. Wilcoxon signed rank test was used to compare the reduction in log HBV DNA and log HBsAg levels during the longitudinal follow-up. The annual decline of HBsAg was computed by dividing the HBsAg decline from the first to the last follow-up visit by the total duration of follow-up.