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| 1 | How Plants Cope with Cadmium: Staking All on Metabolism and Gene Expression显示文摘Environmental pollution is one of the major problems for human health. Toxic heavy metals are normally present as soil constituents or can also be spread out in the environment by human activity and agricultural techniques. Soil contamination by heavy metals as cadmium, highlights two main aspects: on one side they interfere with the life cycle of plants and therefore reduce crop yields, and on the other hand, once adsorbed and accumulated into the plant tissues, they enter the food chain poisoning animals and humans. Considering this point of view, understanding the mechanism by which plants handle heavy metal exposure, in particular cadmium stress, is a primary goal of plant-biotechnology research or plant breeders whose aim is to create plants that are able to recover high amounts of heavy metals, which can be used for phytoremediation, or identify crop varieties that do not accumulate toxic metal in grains or fruits. In this review we focus on the main symptoms of cadmium toxicity both on root apparatus and shoots. We elucidate the mechanisms that plants activate to prevent absorption or to detoxify toxic metal ions, such as synthesis of phytochelatins, metallothioneins and enzymes involved in stress response. Finally we consider new plant-biotechnology applications that can be applied for phytoremediation. | Giovanni DalCorso Silvia Farinati Silvia Maistri Antonella Furini | 2008 | Journal of Integrative Plant Biology2008，50，10： | 60 |
| 2 | Operative link for gastritis assessment vs operative link on intestinal metaplasia assessment显示文摘AIM:To compare the reliability of gastritis staging sys-tems in ranking gastritis-associated cancer risk in a large series of consecutive patients.METHODS:Gastric mucosal atrophy is the precancer-ous condition in which intestinal-type gastric cancer(GC)most frequently develops.The operative link for gas-tritis assessment(OLGA)staging system ranks the GC risk according to both the topography and the severity of gastric atrophy(as assessed histologically on the ba-sis of the Sydney protocol for gastric mucosal biopsy).Both cross-sectional and long-term follow-up trials have consistently associated OLGA stages Ⅲ-Ⅳ with a higher risk of GC.A recently-proposed modification of the OLGA staging system(OLGIM)basically incorporates the OLGA frame,but replaces the atrophy score with an assessment of intestinal metaplasia(IM)alone.A series of 4552 consecutive biopsy sets(2007-2009)was re-trieved and reassessed according to both the OLGA and the OLGIM staging systems.A set of at least 5 biopsy samples was available for all the cases considered.RESULTS:In 4460 of 4552 cases(98.0%),both the high-risk stages(Ⅲ + Ⅳ)and the low-risk stages(0 +Ⅰ + Ⅱ)were assessed applying the OLGA and OL-GIM criteria.Among the 243 OLGA high-risk stages,14(5.8%)were down-staged to a low risk using OLGIM.The 67(1.5%)incidentally-found neoplastic lesions(intraepithelial or invasive)were consistently associated with high-risk stages,as assessed by both OLGA and OLGIM(P < 0.001 for both).Two of 34 intestinal-type GCs coexisting with a high-risk OLGA stage(stage Ⅲ)were associated with a low-risk OLGIM stage(stage Ⅱ).CONCLUSION:Gastritis staging systems(both OLGA and OLGIM)convey prognostically important informa-tion on the gastritis-associated cancer risk.Because of its clinical impact,the stage of gastritis should be included as a conclusive message in the gastritis histol-ogy report.Since it focuses on IM alone,OLGIM staging is less sensitive than OLGA staging in the identif ication of patients at high risk of gastric cancer. | Massimo Rugge Matteo Fassan Marco Pizzi Fabio Farinati Giacomo Carlo Sturniolo Mario Plebani David Y Graham | 2011 | World Journal of Gastroenterology2011，17，41： | 19 |
| 3 | Oxidative damage in the progression of chronic liver disease to hepatocellular carcinoma:An intricate pathway显示文摘The histo-pathologic and molecular mechanisms leading to initiation and progression of hepatocellular carcinoma(HCC)are still ill-defined;however,there is increasing evidence that the gradual accumulation of mutations,genetic and epigenetic changes which occur in preneoplastic hepatocytes results in the development of dysplastic foci,nodules,and finally,overt HCC.As well as many other neoplasias,liver cancer is considered an'inflammatory cancer',arising from a context of inflammation,and characterized by inflammation-related mechanisms that favor tumor cell survival,proliferation,and invasion.Molecular mechanisms that link inflammation and neoplasia have been widely investigated,and it has been well established that inflammatory cells recruited at these sites with ongoing inflammatory activity release chemokines that enhance the production of reactive oxygen species.The latter,in turn,probably have a major pathogenic role in the continuum starting from hepatitis followed by chronic inflammation,and ultimately leading to cancer.The relationship amongst chronic liver injury,free radical production,and development of HCC is explored in the present review,particularly in the light of the complex network that involves oxidative DNA damage,cytokine synthesis,telomere dysfunction,and microRNA regulation. | Romilda Cardin Marika Piciocchi Marina Bortolami Andromachi Kotsafti Luisa Barzon Enrico Lavezzo Alessandro Sinigaglia Kryssia Isabel Rodriguez-Castro Massimo Rugge Fabio Farinati | 2014 | World Journal of Gastroenterology2014，20，12： | 14 |
| 4 | Role of antiviral therapy in the natural history of hepatitis B virus-related chronic liver disease显示文摘Hepatitis B virus(HBV) infection is a dynamic state ofinteractions among HBV, hepatocytes, and the host immune system. Natural history studies of chronic hepatitis B(CHB) infection have shown an association between active viral replication and adverse clinical outcomes such as cirrhosis and hepatocellular carcinoma. The goal of therapy for CHB is to improve quality of life and survival by preventing progression of the disease to cirrhosis, decompensation, end-stage liver disease, hepatocellular carcinoma(HCC) and death. This goal can be achieved if HBV replication is suppressed in a sustained manner. The accompanying reduction in histological activity of CHB lessens the risk of cirrhosis and of HCC, particularly in non-cirrhotic patients. However, CHB infection cannot be completely eradicated, due to the persistence of covalently closed circular DNA in the nucleus of infected hepatocytes, which may explain HBV reactivation. Moreover, the integration of the HBV genome into the host genome may favour oncogenesis, development of HCC and may also contribute to HBV reactivation. | Francesco Paolo Russo Kryssia Rodríguez-Castro Laura Scribano Giorgia Gottardo Veronica Vanin Fabio Farinati | 2015 | World Journal of Hepatology2015，7，8： | 10 |
| 5 | Autoimmune gastritis:Pathologist's viewpoint显示文摘Western countries are seeing a constant decline in the incidence of Helicobacter pylori-associated gastritis, coupled with a rising epidemiological and clinical impact of autoimmune gastritis. This latter gastropathy is due to autoimmune aggression targeting parietal cells through a complex interaction of auto-antibodies against the parietal cell proton pump and intrinsic factor, and sensitized T cells. Given the specific target of this aggression, autoimmune gastritis is typically restricted to the gastric corpus-fundus mucosa. In advanced cases, the oxyntic epithelia are replaced by atrophic(and metaplastic) mucosa, creating the phenotypic background in which both gastric neuroendocrine tumors and(intestinal-type) adenocarcinomas may develop. Despite improvements in our understanding of the phenotypic changes or cascades occurring in this autoimmune setting, no reliable biomarkers are available for identifying patients at higher risk of developing a gastric neoplasm. The standardization of autoimmune gastritis histology reports and classifications in diagnostic practice is a prerequisite for implementing definitive secondary prevention strategies based on multidisciplinary diagnostic approaches integratingendoscopy, serology, histology and molecular profiling. | Irene Coati Matteo Fassan Fabio Farinati David Y Graham Robert M Genta Massimo Rugge | 2015 | World Journal of Gastroenterology2015，21，42： | 8 |
| 6 | Oxidative damage,pro-inflammatory cytokines,TGF-αand c-myc in chronic HCV-related hepatitis and cirrhosis显示文摘AIM: To assess whether a correlation exists between oxidative DNA damage occurring in chronic HCV-related hepatitis and expression levels of pro-inflammatory cytokines, TGF-αand c-myc. METHODS: The series included 37 patients with chronic active HCV-related hepatitis and 11 with HCV-related compensated cirrhosis. Eight-hydroxydeoxyguanosine in liver biopsies was quantified using an electrochemical detector. The mRNA expression of TIMF-α, IL-1β, TGF-αand c-myc in liver specimens was detected by semi-quantitative comparative RT-PCR. RESULTS: TNF-αlevels were significantly higher in hepatitis patients than in cirrhosis patients (P=0.05). IL-1βwas higher in cirrhosis patients (P=0.05). A significant correlation was found between TNF-αand staging (P=0.05) and between IL-1βlevels and grading (P=0.04). c-myc showed a significantly higher expression in cirrhosis patients (P=0.001). Eight-hydroxydeoxyguanosine levels were significantly higher in cirrhosis patients (P=0.05) and in HCV genotype 1 (P=0.03). Considering all patients, 8-hydroxydeoxyguanosine levels were found to be correlated with genotype (P=0.04) and grading (P=0.007). Also multiple logistic regression analysis demonstrated a significant correlation among the number of DNA adducts, TNF-αexpression and HCV genotype (P=0.02). CONCLUSION: In chronic HCV-related liver damage, oxidative DNA damage correlates with HCV genotype, grading and TNF-αlevels. As HCV-related liver damage progresses, TNF-αlevels drop while IL-1βand c-myc levels increase, which may be relevant to liver carcinogenesis. | Fabio Farinati Romilda Cardin Marina Bortolami Maria Guido Massimo Rugge | 2006 | World Journal of Gastroenterology2006，12，13： | 5 |
| 7 | Survival benefit of liver resection for patients with hepatocellular carcinoma across different Barcelona Clinic Liver Cancer stages: a multicentre study显示文摘 | Alessandro Vitale Patrizia Burra Anna Chiara Frigo Franco Trevisani Fabio Farinati Gaya Spolverato Michael Volk Edoardo G. Giannini Francesca Ciccarese Fabio Piscaglia Gian Lodovico Rapaccini Mariella Di Marco Eugenio Caturelli Marco Zoli Franco Borzio Gi | 2014 | Journal of Hepatology2014，，： | 2 |
| 8 | Prospective validation of the Barcelona Clinic Liver Cancer staging system显示文摘 | Umberto Cillo Alessandro Vitale Francesco Grigoletto Fabio Farinati Alberto Brolese Giacomo Zanus Daniele Neri Patrizia Boccagni Nela Srsen Francesco D’Amico Francesco Antonio Ciarleglio Alessio Bridda Davide Francesco D’Amico | 2006 | Journal of Hepatology2006，，4： | 2 |
| 9 | Barcelona Clinic Liver Cancer staging and transplant survival benefit for patients with hepatocellular carcinoma: a multicentre, cohort study显示文摘 | Alessandro Vitale Rafael Ramirez Morales Giacomo Zanus Fabio Farinati Patrizia Burra Paolo Angeli Anna Chiara Frigo Paolo Del Poggio Gianludovico Rapaccini Maria Anna Di Nolfo Luisa Benvegnù Marco Zoli Franco Borzio Edoardo Giovanni Giannini Eugenio Catur | 2011 | Lancet Oncology2011，，7： | 2 |
| 10 | Helicobacter pylori CagA status,mucosal oxidative damage and gastritis phenotype:a potential pathway to cancer?显示文摘 | Farinati F Cardin R Russo VM | 2003 | Helicobacter2003，8，3： | 1 |
| 11 | TACE treatment in hepatoeellular carcinoma: what should we do now显示文摘 | Farinati F Giacomin A Vanin V | 2012 | J Hep- atol2012，57，1： | 1 |
| 12 | Diagnostic and prognostic role of alpha-fetoprotein in hepatocellular carcinoma:both or neither显示文摘 | Farinati F Marino D De Giorgio M | 2006 | Am J Gastroenterol2006，101，3： | 1 |
| 13 | Usefulness of Noninvasive Predictors of Oesophageal Varices in Black African Cirrhotic Patients in C?te d’Ivoire (West Africa)显示文摘 | Alassan Kouamé Mahassadi Fulgence Yao Bathaix Constant Assi Aboubacar Demba Bangoura Emile Allah-Kouadio Henriette Ya Kissi Abdoulaye Touré Stanislas Doffou Issa Konaté Alain Koffi Attia Mathieu Benoit Camara Thérèse Aya Ndri-Yoman Fabio Farinati | 2012 | Gastroenterology Research and Practice2012，，： | 1 |
| 14 | Cost-effectiveness of semi-annual surveillance for hepatocellular carcinoma in cirrhotic patients of the Italian Liver Cancer population显示文摘 | Alessandro Cucchetti Franco Trevisani Matteo Cescon Giorgio Ercolani Fabio Farinati Paolo Del Poggio Gianludovico Rapaccini Maria Anna Di Nolfo Luisa Benvegnù Marco Zoli Franco Borzio Edoardo Giovanni Giannini Eugenio Caturelli Maria Chiaramonte Antonio D | 2012 | Journal of Hepatology2012，，5： | 1 |
| 15 | How should patients with hepatocellular carcinoma be staged? Validation of a new prognostic system 显示文摘 | Farinati F Rinaldi M Gianni S | 2000 | Cancer2000，89，11： | 1 |
| 16 | Gastric epifhelial dysplasia,how clinico-pathologic background relates to management显示文摘 | Leandto G Farinati F | 1995 | Cancer1995，76，： | 1 |
| 17 | Barcelona Clinic Liver Cancer staging and transplant survival benefit for patients with hepatocellular carcinoma: a multicentre, cohort study显示文摘 | Alessandro Vitale Rafael Ramirez Morales Giacomo Zanus Fabio Farinati Patrizia Burra Paolo Angeli Anna Chiara Frigo Paolo Del Poggio Gianludovico Rapaccini Maria Anna Di Nolfo Luisa Benvegnù Marco Zoli Franco Borzio Edoardo Giovanni Giannini Eugenio Catur | 2011 | Lancet Oncology2011，，7： | 1 |
| 18 | Oxidative DNA damage accumulation in gastric carcinogenesis 显示文摘 | Farinati F Orkixz S Bartel H | 1998 | Gut1998，42，3： | 1 |
| 19 | TACE treatment in hepatocellular carcinoma,what should we do now显示文摘 | Farinati F Giacomin A Vanin V | 2012 | J Hepatol2012，57，： | 1 |
| 20 | Non-invasive neoplasia of the stomach显示文摘 | Rugge M Nitti D Farinati F | 2005 | Eur J Gastroenterol Hepatol2005，17，11： | 1 |
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