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| 1 | Efficacy and safety of tenofovir in chronic hepatitis B: Australian real world experience显示文摘AIM To evaluate the long-term treatment outcomes of tenofovir therapy in patients in a real world Australian tertiary care setting.METHODS We performed a retrospective analysis of treatment outcomes among treatment-na?ve and treatment-experienced patients receiving a minimum 3 mo tenofovir therapy through St Vincent's Hospital Melbourne, Australia. We included patients receiving tenofovir [tenofovir disoproxil fumarate(TDF)] monotherapy, as well as patients treated with TDF in combination with a second antiviral agent. Patients were excluded if they demonstrated human immune-deficiency virus/hepatitis C virus/hepatitis delta virus coinfection or were less than 18 years of age. We considered virological and biochemicalresponse, as well as safety outcomes. Virological response was determined by measurement of hepatitis B virus(HBV) DNA using sensitive assays; biochemical response was determined via serum liver function tests; histological response was determined from liver biopsy and fibroscan; safety analysis focused on glomerular renal function and bone mineral density. The primary efficacy endpoint was complete virological suppression over time, defined by HBV DNA < 20 IU/m L. Secondary efficacy endpoints included rates of biochemical response, and HB e antigen(HBe Ag)/HB surface antigen loss and seroconversion over time.RESULTS Ninety-two patients were identified who fulfilled the enrolment criteria. Median follow-up was 26 mo(range 3-114). Mean age was 46(24-78) years, 64(70%) were male and 77(84%) were of Asian origin. 55(60%) patients were treatment-na?ve and 62 patients(67%) were HBe Ag-negative. Complete virological suppression was achieved by 45/65(71%) patients at 12 mo, 37/46(80%) at 24 mo and 25/28(89%) at 36 mo. Partial virological response(HBV DNA 20-2000 IU/m L) was achieved by 89/92(96.7%) of patients. Multivariate analysis showed a significant relationship between virological suppression at end of follow-up and baseline HBV DNA level(OR = 0.897, 95%CI: 0.833-0.967, P = 0.0046) and HBe Ag positive status(OR = 0.373, 95%CI: 0.183-0.762, P = 0.0069). There was no difference in response comparing treatment-na?ve and treatment-experienced patients. Three episodes of virological breakthrough occurred in the setting of noncompliance. Tenofovir therapy was well tolerated.CONCLUSION Tenofovir is an efficacious, safe and well-tolerated treatment in an Australian real-world tertiary care setting. Our data are similar to the reported experience from registration trials. | Grace C Lovett Tin Nguyen David M Iser Jacinta A Holmes Robert Chen Barbara Demediuk Gideon Shaw Sally J Bell Paul V Desmond Alexander J Thompson | 2017 | World Journal of Hepatology2017，9，1： | 7 |
| 2 | Aging related methylation influences the gene expression of key control genes in colorectal cancer and adenoma显示文摘AIM To analyze colorectal carcinogenesis and age-related DNA methylation alterations of gene sequences associated with epigenetic clock CpG sites. METHODS In silico DNA methylation analysis of 353 epigenetic clock Cp G sites published by Steve Horvath was performed using methylation array data for a set of 123 colonic tissue samples [64 colorectal cancer(CRC), 42 adenoma, 17 normal; GEO accession number: GSE48684]. Among the differentially methylated agerelated genes, secreted frizzled related protein 1(SFRP1) promoter methylation was further investigated in colonic tissue from 8 healthy adults, 19 normal children, 20 adenoma and 8 CRC patients using bisulfite-specific PCR followed by methylation-specific high resolution melting(MS-HRM) analysis. m RNA expression of age-related 'epigenetic clock' genes was studied using Affymetrix HGU133 Plus2.0 whole transcriptome data of 153 colonic biopsy samples(49 healthy adult, 49 adenoma, 49 CRC, 6 healthy children)(GEO accession numbers: GSE37364, GSE10714, GSE4183, GSE37267). Whole promoter methylation analysis of genes showing inverse DNA methylationgene expression data was performed on 30 colonic samples using methyl capture sequencing.RESULTS Fifty-seven age-related Cp G sites including hypermethylated PPP1R16 B, SFRP1, SYNE1 and hypomethylated MGP, PIPOX were differentially methylated between CRC and normal tissues(P < 0.05, ?β≥ 10%). In the adenoma vs normal comparison, 70 CpG sites differed significantly, including hypermethylated DKK3, SDC2, SFRP1, SYNE1 and hypomethylated CEMIP, SPATA18(P < 0.05, ?β≥ 10%). In MS-HRM analysis, the SFRP1 promoter region was significantly hypermethylated in CRC(55.0% ± 8.4 %) and adenoma tissue samples(49.9% ± 18.1%) compared to normal adult(5.2% ± 2.7%) and young(2.2% ± 0.7%) colonic tissue(P < 0.0001). DNA methylation of SFRP1 promoter was slightly, but significantly increased in healthy adults compared to normal young samples(P < 0.02). This correlated with significantly increased SFRP1 m RNA levels in children compared to normal adult samples(P < 0.05). In CRC tissue the mR NA expression of 117 agerelated genes were changed, while in adenoma samples 102 genes showed differential expression compared with normal colonic tissue(P < 0.05, logF C > 0.5). The change of expression for several genes including SYNE1, CLEC3 B, LTBP3 and SFRP1, followed the same pattern in aging and carcinogenesis, though not for all genes(e.g., MGP). CONCLUSION Several age-related DNA methylation alterations can be observed during CRC development and progression affecting the m RNA expression of certain CRC- and adenoma-related key control genes. | Orsolya Galamb Alexandra Kalmár Barbara Kinga Barták árpád V Patai Katalin Leiszter Bálint Péterfia Barnabás Wichmann Gábor Valcz Gábor Veres Zsolt Tulassay Béla Molnár | 2016 | World Journal of Gastroenterology2016，22，47： | 7 |
| 3 | Thiopurine-methyltransferase variants in inflammatory bowel disease:Prevalence and toxicity in Brazilian patients显示文摘AIM:To analyze the prevalence of thiopurine-methyltransferase(TPMT)genotypes and their associationwith drug toxicity in inflammatory bowel disease(IBD)patients from southeastern Brazil.METHODS:A total of 219 consecutive patients with IBD,of which 146 had Crohn’s disease and 73 had ulcerative colitis,regularly seen at the outpatient unit of the Division of Gastroenterology at the University Hospital Pedro Ernesto of the State University of Rio de Janeiro,a tertiary referral center,were enrolled in this study from February 2009 to January 2011.We analyzed the presence of major TPMT genetic variants(TPMT*2,*3A,*3C)in IBD patients by means of a specific allele and RFLP-PCR.Genomic DNA was isolated from peripheral blood leukocytes by proteinase-K/Sodium Dodecyl Sulfate digestion and phenol-chloroform extraction.TPMT*2(C238G),TPMT*3A(G460A/A719G),and TPMT*3C(A719G)genotypes were detected by real-time polymerase chain reaction followed by direct sequencing with specific primers.Clinical data were systematically recorded,and correlated with the genotype results.RESULTS:The distribution of the selected TPMT gene polymorphism TPMT*2(C238G),TPMT*3A(G460A/A719G),and TPMT*3C(A719G)genotypes was 3.6%,5.4%,and 7.7%of the patients,respectively.Among the side effects recorded from patients taking azathioprine,14 patients presented with pancreatitis and/or an elevation of pancreatic enzymes,while 6 patients had liver toxicity,and 2 patients exhibited myelosuppression/neutropenia.TPMT polymorphisms were detected in 37/219 patients(8 heterozygous for*2,11 heterozygous for*3A,and 18 heterozygous for*3C).No homozygotic polymorphisms were found.Despite the prevalence of the TPMT*3C genotype,no differences among the genotype frequencies were significant.Although no association was detected regarding myelotoxicity or hepatotoxicity,a trend towards the elevation of pancreatic enzymes was observed for TPMT*2 and TPMT*3C genotypes.CONCLUSION:The prevalence of TPMT genotypes was high among Brazilian patients.Variants genes*2and*3C may be associated with azathioprine pancreatic toxicity in a IBD southeastern Brazilian population. | Ana Teresa P Carvalho Barbara C Esberard Renata S B Fróes Davy C M Rapozo Ana B Grinman Tatiana A Simo Juliana C V C Santos Antonio José V Carneiro Luis Felipe Ribeiro-Pinto Heitor S P de Souza | 2014 | World Journal of Gastroenterology2014，20，12： | 3 |
| 4 | Mechanisms involved in the inhibition of myoblast proliferation and differentiation by myostatin显示文摘 | Dominique Joulia Henri Bernardi Véronique Garandel Fanjaniriana Rabenoelina Barbara Vernus Gérard Cabello | 2003 | Experimental Cell Research2003，，2： | 3 |
| 5 | Trabecular Bone Score: A Noninvasive Analytical Method Based Upon the DXA Image显示文摘 | Barbara C Silva William D Leslie Heinrich Resch Olivier Lamy Olga Lesnyak Neil Binkley Eugene V McCloskey John A Kanis John P Bilezikian | 2014 | J Bone Miner Res2014，，3： | 2 |
| 6 | Health Promotion in Adolescents: A Review of Pender's Health Promotion Model显示文摘 | Brenda J S Barbara V F | 2006 | Nurs Sci Q2006，19，4： | 1 |
| 7 | Evaluation of a candidate International Standard for Meningococcal Group C poly- saeeharide 显示文摘 | CAROLINE V BARBARA M PETER R | 2012 | Biologlcals2012，40，5： | 1 |
| 8 | Mast cell - depend- ent excitation of visceral - nociceptive sensory neurons in irrita- ble bowel syndrome 显示文摘 | Barbara G Wang B Stanghellni V | 2007 | Gastroenterology2007，132，1： | 1 |
| 9 | Enteric neuroplasticity evoked by inflammation 显示文摘 | Vasina V Barbara G Talamonti L | 2006 | Auton Neurosci2006，，： | 1 |
| 10 | Dyspeptic symp- toms and gastric emptying in the irritable bowel syndrome 显示文摘 | Stanghellini V Tosetti C Barbara G | 2002 | Am J Gastroenterol2002，97，： | 1 |
| 11 | Functional gastrointestinal disorders and mast ceils : Lmplications for therapy 显示文摘 | Barbara G Stanghellini V de Giorgio R | 2006 | Neuogastroenterol Motil2006，18，1： | 1 |
| 12 | A role for inflammation in irritable bowel syndrome? 显示文摘 | Barbara G De Giorgio R StangheUini V | 2002 | Gut2002，51，1： | 1 |
| 13 | A role for inflammation in irritable bowel syndrome显示文摘 | Barbara G De Giorgio R Stanghellini V | 2002 | Gut2002，51，1： | 1 |
| 14 | Use of filter paper for the collection and analysis of human whole blood specimens 显示文摘 | Joanne V Richard J Barbara W | 2001 | J Nutr2001，131，： | 1 |
| 15 | New pathophysiological mechanisms in irritable bowel syndrome 显示文摘 | Barbara C Giorgio RD Stanghellini V | 2004 | Aliment Pharmacol Ther2004，20，： | 1 |
| 16 | Activatedmast cells in proximity to colonic nervers correlate with ab-dominal pain in irritable bowel syndrome 显示文摘 | Barbara G Stanghellini V De Giorgio | 2004 | Gastroenterology ’2004，126，3： | 1 |
| 17 | A role for inflammation in irritabre bowel syndrome? 显示文摘 | Barbara G De Giorgio R Stanghellini V | 2002 | Gut2002，51，1： | 1 |
| 18 | Inhibin resistance is associated with aggressive tumorigenicity of ovarian cancer cells显示文摘 | MICHAEL D S TANYA J S BARBARA C V | 2005 | Molecular Cancer Research2005，3，1： | 1 |
| 19 | Diagnosis and therapy of irritable bowel syndrome 显示文摘 | De Giorgio R Barbara G Stanghellini V | 2004 | Aliment Pharmacnl Ther2004，20，2： | 1 |
| 20 | A role for inflammation in Irritable bowel syndrome?显示文摘 | Barbara G De Giorgio R Stanghellini V | 2005 | Gut2005，51，1： | 1 |
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