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768篇 您的检索式:作者名="Hussey"
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1MicroRNAs, development of Barrett’s esophagus, and progression to esophageal adenocarcinoma显示文摘Barrett's esophagus is a premalignant condition caused by gastroesophageal reflux. Once developed, it can progress through varying grades of dysplasia to esoph-ageal adenocarcinoma. Whilst it is well accepted that Barrett's esophagus is caused by gastroesophageal reflux, the molecular mechanisms of its pathogenesis and progression to cancer remain unclear. MicroRNAs (miRNAs) are short segments of RNA that have been shown to control the expression of many human genes. They have been implicated in most cellular processes, and the role of miRNAs in disease development is be-coming increasingly evident. Understanding altered miRNA expression is likely to help unravel the molecular mechanisms that underpin the development of Barrett's esophagus and its progression to cancer.Cameron M Smith David I Watson Michael Z Michael Damian J Hussey 2010World Journal of Gastroenterology2010,16,5:23
2miR-200 family expression is downregulated upon neoplastic progression of Barrett's esophagus显示文摘AIM: To investigate miR-200 family expression in Barrett's epithelium, gastric and duodenal epithelia, and esophageal adenocarcinoma. METHODS: Real-time reverse transcriptase-polymerase chain reaction was used to measure miR-200, ZEB1 and ZEB2 expression. Ingenuity Pathway Analysis of miR-200 targets was used to predict biological outcomes. RESULTS: Barrett's epithelium expressed lower levels of miR-141 and miR-200c than did gastric and duodenal epithelia (P < 0.001). In silico analysis indicated roles for the miR-200 family in molecular pathways that distinguish Barrett's epithelium from gastric and duodenalepithelia, and which control apoptosis and proliferation. All miR-200 members were downregulated in adenocarcinoma (P < 0.02), and miR-200c expression was also downregulated in non-invasive epithelium adjacent to adenocarcinoma (P < 0.02). The expression of all miR-200 members was lower in Barrett's epithelium derived high-grade dysplastic cell lines than in a cell line derived from benign Barrett's epithelium. We observed signif icant inverse correlations between miR-200 family expression and ZEB1 and ZEB2 expression in Barrett's epithelium and esophageal adenocarcinoma (P < 0.05). CONCLUSION: miR-200 expression might contribute to the anti-apoptotic and proliferative phenotype of Barrett's epithelium and regulate key neoplastic processes in this epithelium.Cameron M Smith David I Watson Mary P Leong George C Mayne Michael Z Michael Bas PL Wijnhoven Damian J Hussey 2011World Journal of Gastroenterology2011,17,8:13
3MicroRNA signatures in chemotherapy resistant esophageal cancer cell lines显示文摘AIM:To investigate expression of microRNA(miRNA)and potential targets in chemotherapy resistant esoph-ageal cancer cell lines.METHODS:An in-vitro model of acquired chemotherapy resistance in esophageal adeno-(EAC)and squamous cell carcinoma(ESCC)cells was used,and microRNA expression profiles for cisplatin or 5-fluorouracil(5-FU)resistant variants vs chemotherapy sensitive controls were compared using microarray and quantitative real-time polymerase chain reaction(PCR).The expression of chemotherapy-relevant genes potentially targeted by the dysregulated microRNAs in the chemotherapy resistant variants was also evaluated.RESULTS:Chemotherapy resistant sublines were found to have specific miRNA signatures,and these miRNA signatures were different for the cisplatin vs 5-FU resistant cells from the same tumor cell line,and also for EAC vs ESCC cells with resistance to the same specific chemotherapy agent.Amongst others,miR-27b-3p,miR-193b-3p,miR-192-5p,miR-378 a-3p,miR-125a-5p and miR-18a-3p were dysregulated,consistent with negative posttranscriptional control of KRAS,TYMS,ABCC3,CBL-B and ERBB2 expression via these miRNAs.CONCLUSION:The current study supports the hypothesis that microRNA expression has an impact on chemotherapy resistance in esophageal cancer.Richard Hummel Corina Sie David I Watson Tingting Wang Alfiya Ansar Michael Z Michael Mark Van der Hoek Joerg Haier Damian J Hussey 2014World Journal of Gastroenterology2014,20,40:8
4Estrogen,male dominance and esophageal adenocarcinoma:Is there a link?显示文摘Esophageal adenocarcinoma is a cancer with poor prognosis,and its incidence has risen sharply over recent decades.Obesity is a major risk factor for developing this cancer and there is a clear male gender bias in the incidence that cannot be fully explained by known risk factors.It is possible that a difference in the expression of estrogen,or its signaling axes,may contribute to this gender bias.We undertook a comprehensive literature search and analyzed the available data regarding estrogen and estrogen receptor expression,and the possible sex-specific links with esophageal adenocarcinoma development.Potentially relevant associations between visceral vs subcutaneous fat deposition and estrogen expression,and the effect of crosstalk between estrogen and leptin signaling were identified.We also found limited studies suggesting a role for estrogen receptor β expression in esophageal adenocarcinoma development.The current literature supports speculation on an etiological role for estrogen in the male gender bias in esophageal adenocarcinoma,but further studies are required.Huiqi Yang Olga A Sukocheva Damian J Hussey David I Watson 2012World Journal of Gastroenterology2012,18,5:7
5Molecular detection of Helicobacter pylori antibiotic resistance in stool vs biopsy samples显示文摘AIM To compare(1) demographics in urea breath test(UBT) vs endoscopy patients; and(2) the molecular detection of antibiotic resistance in stool vs biopsy samples.METHODS Six hundred and sixteen adult patients undergoing endoscopy or a UBT were prospectively recruited to the study. The Geno Type Helico DR assay was used to detect Helicobacter pylori(H. pylori) and antibiotic resistance using biopsy and/or stool samples from CLOpositive endoscopy patients and stool samples from UBT-positive patients. RESULTS Infection rates were significantly higher in patients referred for a UBT than endoscopy(overall rates: 33% vs 19%; treatment-na?ve patients: 33% vs 14.7%, respectively). H. pylori-infected UBT patients were younger than H. pylori-infected endoscopy patients(41.4 vs 48.4 years, respectively, P < 0.005), with a higher percentage of H. pylori-infected males in the endoscopy-compared to the UBT-cohort(52.6% vs 33.3%, P = 0.03). The Geno Type Helico DR assay was more accurate at detecting H. pylori infection using biopsy samples than stool samples [98.2%(n = 54/55) vs 80.3%(n =53/66), P < 0.005]. Subset analysis using stool and biopsy samples from CLO-positive endoscopy patients revealed a higher detection rate ofresistance-associated mutations using stool samples compared to biopsies. The concordance rates between stool and biopsy samples for the detection of H. pylori DNA, clarithromycin and fluoroquinolone resistance were just 85%, 53% and 35%, respectively. CONCLUSION Differences between endoscopy and UBT patients provide a rationale for non-invasive detection of H. pylori antibiotic resistance. However, the Geno Type Helico DR assay is an unsuitable approach.Denise E Brennan Joseph Omorogbe Mary Hussey Donal Tighe Grainne Holleran Colm O'Morain Sinéad M Smith Deirdre McNamara 2016World Journal of Gastroenterology2016,22,41:6
6Assessment of serum angiogenic factors as a diagnostic aid for small bowel angiodysplasia in patients with obscure gastrointestinal bleeding and anaemia显示文摘AIM To assess the use of serum levels of angiopoietin-1(Ang1), Ang2 and tumor necrosis factor-α(TNFα) as predictive factors for small bowel angiodysplasia(SBA).METHODS Serum samples were collected from patients undergoing capsule endoscopy for any cause of obscure gastrointestinal bleeding(OGIB) or anaemia. Based on small bowel findings patients were divided into 3 groups:(1) SBA;(2) other bleeding causes; and(3) normal, according to diagnosis. Using ELISA technique we measured serum levels of Ang1, Ang2 and TNFα and compared mean and median levels between the groups based on small bowel diagnosis. Using receiver operator curve analysis we determined whether any of the factors were predictive of SBA.RESULTS Serum samples were collected from a total of 120 patients undergoing capsule endoscopy for OGIB or anaemia: 40 with SBA, 40 with other causes of small bowel bleeding, and 40 with normal small bowel findings. Mean and median serum levels were measured and compared between groups; patients with SBA had significantly higher median serum levels of Ang2(3759 pg/mL) compared to both other groups, with no significant differences in levels of Ang1 or TNFα based on diagnosis. There were no differences in Ang2 levels between the other bleeding causes(2261 pg/mL) and normal(2620pg/mL) groups. Using Receiver Operator Curve analysis, an Ang2 level of > 2600 pg/mL was found to be predictive of SBA, with an area under the curve of 0.7. Neither Ang1 or TNFα were useful as predictive markers.CONCLUSION Elevations in serum Ang2 are specific for SBA and not driven by other causes of bleeding and anaemia. Further work will determine whether Ang2 is useful as a diagnostic or prognostic marker for SBA.Grainne Holleran Mary Hussey Sinead Smith Deirdre McNamara 2017World Journal of Gastrointestinal Pathophysiology2017,8,3:3
7MicroRNA profile in neosquamous esophageal mucosa following ablation of Barrett's esophagus显示文摘AIM To investigate the micro RNA expression profile in esophageal neosquamous epithelium from patients who had undergone ablation of Barrett's esophagus.METHODS High throughput screening using Taq Man~ Array Human Micro RNA quantitative PCR was used to determine expression levels of 754 micro RNAs in distal esophageal mucosa(1 cm above the gastro-esophageal junction) from 16 patients who had undergone ablation of non-dysplastic Barrett's esophagus using argon plasma coagulation vs pretreatment mucosa, posttreatment proximal normal non-treated esophageal mucosa, and esophageal mucosal biopsies from 10 controls without Barrett's esophagus. Biopsies of squamous mucosa were also taken from 5 cm above the pre-ablation squamo-columnar junction. Predicted m RNA target pathway analysis was used to investigate the functional involvement of differentially expressed micro RNAs.RESULTS Forty-four micro RNAs were differentially expressed between control squamous mucosa vs post-ablation neosquamous mucosa. Nineteen micro RNAs were differentially expressed between post-ablation neosquamous and post-ablation squamous mucosa obtained from the more proximal non-treated esophageal segment. Twelve microRNAs were differentially expressed in both neosquamous vs matched proximal squamous mucosa and neosquamous vs squamous mucosa from healthy patients. Nine micro RNAs(mi R-424-5p, mi R-127-3p, mi R-98-5p, mi R-187-3p, mi R-495-3p, mi R-34c-5p, mi R-223-5p, mi R-539-5p, mi R-376a-3p, mi R-409-3p) were expressed at higher levels in post-ablation neosquamous mucosa than in matched proximal squamous and healthy squamous mucosa. These micro RNAs were also more highly expressed in Barrett's esophagus mucosa than matched proximal squamous and squamous mucosa from controls. Target prediction and pathway analysis suggests that these micro RNAs may be involved in the regulation of cell survival signalling pathways. Three micro RNAs(mi R-187-3p, mi R-135b-5p and mi R-31-5p) were expressed at higher levels in postablation neosquamous mucosa than in matched proximal squamous and healthy squamous mucosa. These mi RNAs were expressed at similar levels in preablation Barrett's esophagus mucosa, matched proximal squamous and squamous mucosa from controls. Target prediction and pathway analysis suggests that these micro RNAs may be involved in regulating the expression of proteins that contribute to barrier function.CONCLUSION Neosquamous mucosa arising after ablation of Barrett's esophagus expresses micro RNAs that may contribute to decreased barrier function and micro RNAs that may be involved in the regulation of survival signaling pathways.Loveena Sreedharan George C Mayne David I Watson Timothy Bright Reginald V Lord Alfiya Ansar Tingting Wang Jakob Kist David StJ Astill Damian J Hussey 2017World Journal of Gastroenterology2017,23,30:3
8MicroRNAs: Predictors and modifiers of chemo- and radiotherapy in different tumour types显示文摘Richard Hummel Damian J. Hussey Joerg Haier 2009European Journal of Cancer2009,,2:3
9Effect of the specific cyclooxygenase-2 inhibitor meloxicam on tumour growth and cachexia in a murine model显示文摘Hussey H J Tisdale M J 2000Int J Cancer2000,87,1:2
10Androgens and esophageal cancer: What do we know?显示文摘Significant disparities exist between genders for the development and progression of several gastrointestinal(GI) diseases including cancer. Differences in incidence between men vs women for colon, gastric and hepatocellular cancers suggest a role for steroid sex hormones in regulation of GI carcinogenesis. Involvement of intrinsic gender-linked mechanisms is also possible for esophageal adenocarcinoma as its incidence is disproportionally high among men. However, the cause of the observed gender differences and the potential role of androgens in esophageal carcinogenesis remains unclear, even though the cancer-promoting role of androgen receptors(AR) shown in other cancers such as prostate and bladder suggests this aspect warrants exploration. Several studies have demonstrated expression of ARs in esophageal cancer. However, only one study has suggested a potential link between AR signaling and outcome- poorer prognosis. Two groups have analyzed data from cohorts with prostate cancer and one of these found a decreased incidence of esophageal squamous and adenocarcinoma after androgen deprivation therapy. However, very limited information is available about the effects of androgen and AR-initiated signaling on esophageal cancer cell growth in vitro and in vivo. Possible mechanisms for androgens/AR involvement in the regulation of esophageal cancer growth are considered, and the potential use of AR as a prognostic factor and clinical target is highlighted, although insufficient evidence is available to support clinical trials of novel therapies. As esophageal adenocarcinoma is a gender linked cancer with a large male predominance further studies are warranted to clarify the role of androgens and ARs in shaping intracellular signaling and genomic responses in esophageal cancer.Olga A Sukocheva Bin Li Steven L Due Damian J Hussey David I Watson 2015World Journal of Gastroenterology2015,21,20:2
11Vacuolating Cytotoxin and Variants in Atg16L1 That Disrupt Autophagy Promote Helicobacter pylori Infection in Humans显示文摘Deepa Raju Seamus Hussey Michelle Ang Mauricio R. Terebiznik Michal Sibony Esther Galindo–Mata Vijay Gupta Steven R. Blanke Alberto Delgado Judith Romero–Gallo Mahendra Singh Ramjeet Heidi Mascarenhas Richard M. Peek Pelayo Correa Cathy Streutker Georgina 2012Gastroenterology2012,,5:2
12Vesicular-arbuscular mycorrhizae may limit nematode activity and improve plant growth显示文摘 Roncadori R W 1982Plant Dis1982,66,:1
13Aneuploidy detection in single cells using DNA array-based comparative genomic hybridization显示文摘Hu DG Webb G Hussey N 2004Mol Hum Reprod2004,10,4:1
14A new dietary inflammatory index predicts interval changes in serum high-sensitivity C-reactive protein显示文摘Cavicchia P P Steck S E Hurley T G Hussey J R Ma Y Ockene I S 2009J Nutr2009,139,:1
15Serotypes and antimicrobial suscepibility of Haemophilus influenzae antimicrobial显示文摘Hussey G Hitchchoek J Hunslo D 1994Agents Chemother1994,34,6:1
16Analysis of five Duchenne muscular dystrophy exons and gender determination using conventional duplex polymerase chain reaction on single cells 显示文摘Hussey ND Donggui H Froiland DA 1999Mol Hum Reprod1999,5,11:1
17Parasitism genes:what they reveal about parasitism显示文摘DAVIS E L HUSSEY R S BAUM T J 2009Plant Cell Monographs2009,15,:1
18Respiratory syncytial virus infection in clildren hospitalised with acute lower respiratory tract infection显示文摘Hussey GD Apolles P Arerdse Z 2000S Air Med J2000,90,5:1
19Getting to the roots of parasitism by nematodes显示文摘Davis EL Hussey RS Baum TJ 2004TRENDS in Parasitology2004,20,3:1
20Helicobacter pylori infectionand childhood显示文摘Mourad-Baars P Hussey S Jones N L 2010Helicobacter2010,15,1:1
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