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| 1 | Immunopathogenesis of chronic hepatitis B显示文摘Chronic hepatitis B(CHB) is a widespread infectious disease with unfavorable outcomes and life-threatening consequences for patients, in spite of modern vaccination and antiviral treatment modalities. Cutting-edge experimental approaches have demonstrated key pathways that involve cross-talk between viral particles and host immune cells. All events, including penetration of hepatitis B virus(HBV) particles into host cells, establishing persistence, and chronization of CHB infection, and possibility of complete elimination of HBV particles are controlled by the immune system. Researchers have paid special attention to the replication capacity of HBV in host cells, which is associated with cellular changes that reflect presentation of viral antigens and variability of HBV antigen features. In addition, specific HBV proteins have an immune-modulating ability to initiate molecular mechanisms that 'avoid' control by the immune system. The relationship between immunological shifts and chronic infection stages has been intensively studied since it was recognized that the immune system is a direct participant in the recurrent(cyclic) nature of CHB. Understanding the wide diversity of molecular pathways and the crosstalk between innate and adaptive immune system components will provide fresh insight into CHB immune pathogenesis and the possibilities of developing new treatment strategies for this disease. | Irina P Balmasova Nikolay D Yushchuk Ospan A Mynbaev Nageswara R Alla Elena S Malova Zhongjie Shi Chang-Lu Gao | 2014 | World Journal of Gastroenterology2014，20，39： | 15 |
| 2 | Negative capsule endoscopy in patients with obscure gastrointestinal bleeding reliable: Recurrence of bleeding on long-term follow-up显示文摘AIM: To assess the rate of recurrent bleeding of the small bowel in patients with obscure bleeding already undergone capsule endoscopy (CE) with negative results. METHODS: We reviewed the medical records related to 696 consecutive CE performed from December 2002 to January 2011, focusing our attention on patients with recurrence of obscure bleeding and negative CE. Evaluating the patient follow-up, we analyzed the recurrence rate of obscure bleeding in patient with a negative CE. Actuarial rates of rebleeding during follow-up were calculated, and factors associated with rebleeding were assessed through an univariate and multivariate analysis. A P value of less than 0.05 was regarded as statistically significant. The sensitivity, specificity, and positive and negative predictive values (PPV and NPV) of negative CE were calculated. RESULTS: Two hundred and seven out of 696 (29.7%) CE studies resulted negative in patient with obscure/overt gastrointestinal bleeding. Overall, 489 CE (70.2%) were positive studies. The median follow-up was 24 mo (range 12-36 mo). During follow-up, recurrence of obscure bleeding was observed only in 34 out of 207 negative CE patients (16.4%); 26 out of 34 with obscure overt bleeding and 8 out of 34 with obscure occult bleeding. The younger age (< 65 years) and the onset of bleeding such as melena are independent risk factors of rebleeding after a negative CE (OR = 2.6703, 95%CI: 1.1651-6.1202, P = 0.0203; OR 4.7718, 95%CI: 1.9739-11.5350, P = 0.0005). The rebleeding rate (CE+ vs CE-) was 16.4% vs 45.1% (χ 2 test, P = 0.00001). The sensitivity, specificity, and PPV and NPV were 93.8%, 100%, 100%, 80.1%, respectively. CONCLUSION: Patients with obscure gastrointestinal bleeding and negative CE had a significantly lower rebleeding rate, and further invasive investigations can be deferred. | Maria Elena Riccioni Riccardo Urgesi Rossella Cianci Gianluca Rizzo Luca D'Angelo Riccardo Marmo Guido Costamagna | 2013 | World Journal of Gastroenterology2013，19，28： | 14 |
| 3 | Fat:A matter of disturbance for the immune system显示文摘Obesity is increasingly being recognized as a risk factor for a number of benign and malignant gastrointestinal conditions. However, literature on the underlying pathophysiological mechanisms is sparse and ambiguous. There is compelling evidence that both overnutrition and undernutrition negatively interfere with the immune system. Overnutrition has been found to increase susceptibility to the development of inflammatory diseases, autoimmune diseases and cancer. In the regulation of immune and in? ammatory processes, white adipose tissue plays a critical role, not only as an energy store but also as an important endocrine organ. The obese state is characterised by a low-grade systemic in? ammation, mainly as a result of increased adipocytes as well as fat resident-and recruited-macrophage activity. In the past few years, various products of adipose tissue including adipokines and cytokines have been characterised and a number of pathways linking adipose tissue metabolism with the immune system have been identified. Activation of the innate immune system plays a major role in hepatic steatosis. Non-alcoholic fatty liver disease includes a wide spectrum of diseases, from pure steatosis to non-alcoholic steato-hepatitis in the absence of signif icant alcohol consumption. Although steatosis is considered a non-progressive disease, non-alcoholic steatohepatitis may deteriorate in advanced chronic liver diseases, cirrhosis, and hepatocellular carcinoma. An important parallel between obesityrelated pathology of adipose tissue and liver pertains to the emerging role of macrophages, and growing evidence suggests that Kupffer cells critically contribute to progression of non-alcoholic fatty liver disease. Moreover, a close link between specif ic immune activation and atherosclerosis has been well established, suggesting that fat can directly trigger immune responses. This review discusses the role of fat as 'a matter of disturbance for the immune system' with a focus on hepatic steatosis. | Alessandro Federico Elena D’Aiuto Francesco Borriello Giusi Barra Antonietta Gerarda Gravina Marco Romano Raffaele De Palma | 2010 | World Journal of Gastroenterology2010，16，38： | 12 |
| 4 | Role of endoscopic ultrasonography in the loco-regional staging of patients with rectal cancer显示文摘The prognosis of rectal cancer(RC) is strictly related to both T and N stage of the disease at the time of diagnosis. RC staging is crucial for choosing the best multimodal therapy: patients with high risk locally advanced RC(LARC) undergo surgery after neoadjuvant chemotherapy and radiotherapy(NAT); those with low risk LARC are operated on after a preoperative short-course radiation therapy; finally, surgery alone is recommended only for early RC. Several imaging methods are used for staging patients with RC: computerized tomography, magnetic resonance imaging, positron emission tomography, and endoscopic ultrasound(EUS). EUS is highly accurate for the loco-regional staging of RC, since it is capable to evaluate precisely the mural infiltration of the tumor(T), especially in early RC. On the other hand, EUS is less accurate in restaging RC after NAT and before surgery. Finally, EUS is indicated for follow-up of patients operated on for RC, where there is a need for the surveillance of the anastomosis. The aim of this review is to highlight the impact of EUS on the management of patients with RC, evaluating its role in both preoperative staging and follow-up of patients after surgery. | Pietro Marone Mario de Bellis Valentina D'Angelo Paolo Delrio Valentina Passananti Elena Di Girolamo Giovanni Battista Rossi Daniela Rega Maura Claire Tracey Alfonso Mario Tempesta | 2015 | World Journal of Gastrointestinal Endoscopy2015，7，7： | 11 |
| 5 | Pharmacogenetics of the systemic treatment in advanced hepatocellular carcinoma显示文摘Hepatocellular carcinoma (HCC) accounts for the majority of primary liver cancers. To date, most patients with HCC are diagnosed at an advanced tumor stage, excluding them from potentially curative therapies (i.e., resection, liver transplantation, percutaneous ablation). Treatments with palliative intent include chemoembolization and systemic therapy. Among systemic treatments, the small-molecule multikinase inhibitor sorafenib has been the only systemic treatment available for advanced HCC over 10 years. More recently, other smallmolecule multikinase inhibitors (e.g., regorafenib, lenvatinib, cabozantinib) have been approved for HCC treatment. The promising immune checkpoint inhibitors (e.g., nivolumab, pembrolizumab) are still under investigation in Europe while in the US nivolumab has already been approved by FDA in sorafenib refractory or resistant patients. Other molecules, such as the selective CDK4/6inhibitors (e.g., palbociclib, ribociclib), are in earlier stages of clinical development, and the c- MET inhibitor tivantinib did not show positive results in a phase III study. However, even if the introduction of targeted agents has led to great advances in patient response and survival with an acceptable toxicity profile, a remarkable inter-individual heterogeneity in therapy outcome persists and constitutes a significant problem in disease management. Thus, the identification of biomarkers that predict which patients will benefit from a specific intervention could significantly affect decision-making and therapy planning. Germ-line variants have been suggested to play an important role in determining outcomes of HCC systemic therapy in terms of both toxicity and treatment efficacy. Particularly, a number of studies have focused on the role of genetic polymorphisms impacting the drug metabolic pathway and membrane translocation as well as the drug mechanism of action as predictive/prognostic markers of HCC treatment. The aim of this review is to summarize and critically discuss the pharmacogenetic literature evidences, with particular attention to sorafenib and regorafenib, which have been used longer than the others in HCC treatment. | Elena De Mattia Erika Cecchin Michela Guardascione Luisa Foltran Tania Di Raimo Francesco Angelini Mario D’Andrea Giuseppe Toffoli | 2019 | World Journal of Gastroenterology2019，25，29： | 8 |
| 6 | High levels of homocysteine downregulate apolipoprotein E expression via nuclear factor kappa B显示文摘AIM: To investigate the effect of high homocysteine(Hcy) levels on apolipoprotein E(apoE) expression and the signaling pathways involved in this gene regulation.METHODS: Reverse transcriptase polymerase chain reaction(RT-PCR) and Western blot were used to assess apo E expression in cells treated with various concentrations(50-500 μmol/L) of Hcy. Calcium phosphatetransient transfections were performed in HEK-293 and RAW 264.7 cells to evaluate the effect of Hcy on apoE regulatory elements [promoter and distal multienhancer 2(ME2)]. To this aim, plasmids containing the proximal apoE promoter [(-500/+73)apoE construct] alone or in the presence of ME2 [ME2/(-500/+73)apoE construct] to drive the expression of the reporter luciferase gene were used. Co-transfection experiments were carried out to investigate the downstream effectors of Hcymediated regulation of apoE promoter by using specific inhibitors or a dominant negative form of IKβ. In other co-transfections, the luciferase reporter was under the control of synthetic promoters containing multiple specific binding sites for nuclear factor kappa B(NF-κB), activator protein-1(AP-1) or nuclear factor of activated T cells(NFAT). Chromatin immunoprecipitation(ChI P)assay was accomplished to detect the binding of NF-κB p65 subunit to the apoE promoter in HEK-293 treated with 500 μmol/L Hcy. As control, cells were incubated with similar concentration of cysteine. NF-κB p65 proteins bound to DNA were immunoprecipitated with anti-p65 antibodies and DNA was identified by PCR using primers amplifying the region-100/+4 of the apoE gene. RESULTS: RT-PCR revealed that high levels of Hcy(250-750 μmol/L) induced a 2-3 fold decrease in apoE m RNA levels in HEK-293 cells, while apo E gene expression was not significantly affected by treatment with lower concentrations of Hcy(100 μmol/L). Immunoblotting data provided additional evidence for the negative role of Hcy in apoE expression. Hcy decreased apoE promoter activity, in the presence or absence of ME2, in a dose dependent manner, in both RAW 264.7 and HEK-293 cells, as revealed by transient transfection experiments. The downstream effectors of the signaling pathways of Hcy were also investigated. The inhibitory effect of Hcy on the apo E promoter activity was counteracted by MAPK/ERK kinase 1/2(MEK1/2) inhibitor U0126, suggesting that MEK1/2 is involved in the downregulation of apoE promoter activity by Hcy. Our data demonstrated that Hcy-induced inhibition of apoE took place through activation of NF-κB. Moreover, we demonstrated that Hcy activated a synthetic promoter containing three NF-κB binding sites, but did not affect promoters containing AP-1 or NFAT binding sites. ChI P experiments revealed that NF-κB p65 subunit is recruited to the apoE promoter following Hcy treatment of cells.CONCLUSION: Hcy-induced stress negatively modulates apoE expression via MEK1/2 and NF-κB activation. The decreased apo E expression in peripheral tissues may aggravate atherosclerosis, neurodegenerative diseases and renal dysfunctions. | Violeta G Trusca Adina D Mihai Elena V Fuior Ioana M Fenyo Anca V Gafencu | 2016 | World Journal of Biological Chemistry2016，7，1： | 6 |
| 7 | Percutaneous coronary intervention in nonagenarians: pros and cons显示文摘Percutaneous coronary intervention is a mainstay in the management of symptomatic or high-risk coronary artery disease. The bulk of clinical evidence and experience underlying this fact relies, however, on relatively young patients. Indeed, few data of very limited quality are available which adequately define the risk-benefit and cost-benefit profile of coronary angioplasty and stenting in very old subjects, such as those of 90 years of age or older (i.e., nonagenarians). The aim of this review is to provide a concise, yet practical, synthesis of the available evidence on percutaneous coronary revascularization in the very elderly. The main arguments elaborated upon are to what extent we can extrapolate findings from studies including younger patients to nonagenarians, whether we should provide higher priority to prognosis or quality of life in such patients, and whether we can afford to allocate vast resources to care for such subjects in an era of financial constraints. Our review of 18 studies and 1082 patients suggest that percutaneous coronary intervention is feasible and associated with acceptable short- and long-term results in this population, which is nonetheless fraught with a high mortality risk irrespective of the revascularization procedure. Accordingly, the pros and cons of percutaneous coronary intervention should be carefully weighed when considering this treatment in nonagenarians. | Giuseppe Biondi Zoccai Antonio Abbate Fabrizio D'Ascenzo Davide Presutti Mariangela Peruzzi Elena Cavarretta Antonino G.M. Marullo Marzia Lotrionte Giacomo Frati | 2013 | Journal of Geriatric Cardiology2013，10，1： | 6 |
| 8 | High prevalence of viable Mycobacterium avium subspecies paratuberculosis in Crohn's disease显示文摘AIM:To examine the detection rate of viable Mycobacterium avium subspecies paratuberculosis(MAP) in patients with inflammatory bowel disease [Crohn's disease(CD) and ulcerative colitis(UC)].METHODS:Thirty patients with CD(15 with at least one NOD2/CARD15 mutation),29 with UC,and 10 with no inflammatory bowel disease(IBD).were tested for MAP by polymerase chain reaction(specific IS900 fragment) and blood culture.RESULTS:MAP DNA was detected in all original blood samples and 8-wk blood cultures(CD,UC and non-IBD).Positive MAP DNA status was confirmed by dot blot assays.All 69 cultures were negative by acid-fast Ziehl-Neelsen staining.Viable MAP,in spheroplast form,was isolated from the 18-mo blood cultures of all 30 CD patients,one UC patient,and none of the non-IBD controls.No association was found between positive MAP cultures and use of immunosuppressive drugs or CDassociated single nucleotide polymorphisms.CONCLUSION:MAP is widely present in our area and MAP DNA can be recovered from the blood of CD,UC and non-IBD patients.However,MAP spheroplasts were only found in CD patients. | Juan L Mendoza Amparo San-Pedro Esther Culebras Raquel Cíes Carlos Taxonera Raquel Lana Elena Urcelay Fernando de la Torre Juan J Picazo Manuel Díaz-Rubio | 2010 | World Journal of Gastroenterology2010，16，36： | 5 |
| 9 | IBD5 polymorphisms in inflammatory bowel disease: Association with response to infliximab显示文摘AIM: Inflammatory bowel diseases (IBD) are multifactorial pathologies of unknown etiology. One susceptibility locus,IBD5, has been mapped to chromosome 5q31. We analyzed our Spanish cohorts of Crohn's disease (CD)and ulcerative colitis (UC) patients to determine whether this locus is associated with IBD, and to ascertain the main clinical phenotype influenced by this risk factor. The kind of interaction, either genetic heterogeneity or epistasis, between this IBD5 susceptibility region and the NOD2/CARD15 gene mutations was studied as well.Finally, ve assessed whether this locus can predict response to infliximab therapy.METHODS: A case control study was performed with 274CD and 211 UC patients recruited from a single center and 511 healthy ethnically matched controls. Two polymorphisms were genotyped in the IBD5 locus and three in the CARD15/NOD2 gene.RESULTS: Our results evidence association only with CD especially with the fistulizing phenotype and in the absence of NOD2/CARD15 variants (mutant allele frequency in patients vscontrols: OR = 2.03, 95% CI = 1.35-3.06,P<0.01). The frequency of the IBD5 homozygous mutant genotype significantly increased in CD patients lacking response to infliximab (RR = 3.88, 95% CI = 1.18-12.0,P<0.05). UC patients overall do not show association with 5q31 polymorphisms, although a similar trend to the one observed in CD is found within the worse prognosis group.CONCLUSION: The IBD5 variants may enhance an individual carrier's risk for CD, mainly in the absence of the NOD2/CARD15 mutations and in fistulizing patients.The data presented suggest the potential role of the 5q31polymorphisms as markers of response to infiiximab. | Elena Urcelay Juan Luis Mendoza Alfonso Martínez Laura Fernández Carlos Taxonera Manuel Díaz-Rubio Emilio G.de la Concha | 2005 | World Journal of Gastroenterology2005，11，8： | 4 |
| 10 | Energy metabolism and the skeleton:Reciprocal interplay显示文摘The relation between bone remodelling and energy expenditure is an intriguing,and yet unexplained,challenge of the past ten years. In fact,it was only in the last few years that the skeleton was found to function,not only in its obvious roles of body support and protection,but also as an important part of the endocrine system. In particular,bone produces different hormones,like osteocalcin(OC),which influences energy expenditure in humans. The undercarboxylated form of OC has a reduced affinity for hydroxyapatite; hence it enters the systemic circulation more easily and exerts its metabolic functions for the proliferation of pancreatic β-cells,insulin secretion,sensitivity,and glucose tolerance. Leptin,a hormone synthesized by adipocytes,also has an effect on both bone remodelling and energy expenditure; in fact it inhibits appetite through hypothalamic influence and,in bone,stimulates osteoblastic differentiation and inhibits apoptosis. Leptin and serotonin exert opposite influences on bone mass accrual,but several features suggest that they might operate in the same pathway through a sympathetic tone. Serotonin,in fact,acts via two opposite pathways in controlling bone remodelling: central and peripheral. Serotonin product by the gastrointestinal tract(95%) augments bone formation by osteoblast,whereas brain-derived serotonin influences low bone mineral density and its decrease leads to an increase in boneresorption parameters. Finally,amylin(AMY) acts as a hormone that alters physiological responses related to feeding,and plays a role as a growth factor in bone. In vitro AMY stimulates the proliferation of osteoblasts,and osteoclast differentiation. Here we summarize the evidence that links energy expenditure and bone remodelling,with particular regard to humans. | Patrizia D'Amelio Anna Panico Elena Spertino Giovanni Carlo Isaia | 2012 | World Journal of Orthopedics2012，3，11： | 2 |
| 11 | Helicobacter pylori secreted peptidyl prolyl cis , trans -isomerase drives Th17 inflammation in gastric adenocarcinoma显示文摘 | Amedeo Amedei Fabio Munari Chiara Della Bella Elena Niccolai Marisa Benagiano Lapo Bencini Fabio Cianchi Marco Farsi Giacomo Emmi Giuseppe Zanotti Marina Bernard Manikuntala Kundu Mario Milco D’Elios | 2014 | Internal and Emergency Medicine2014，，3： | 2 |
| 12 | T cell responses to allogeneic human mesenchymal stem cells: immunogenicity, tolerance, and suppression显示文摘 | Elena Klyushnenkova Joseph D Mosca Valentina Zernetkina Manas K Majumdar Kirstin J Beggs Donald W Simonetti Robert J Deans Kevin R McIntosh | 2005 | Journal of Biomedical Science2005，，1： | 2 |
| 13 | Antitumor activity of pimasertib, a selective MEK 1/2 inhibitor, in combination with PI3K/mTOR inhibitors or with multi‐targeted kinase inhibitors in pimasertib‐resistant human lung and colorectal cancer cells显示文摘 | Erika Martinelli Teresa Troiani Elena D’Aiuto Floriana Morgillo Donata Vitagliano Anna Capasso Sarah Costantino Loreta Pia Ciuffreda Francesco Merolla Loredana Vecchione Veerle Vriendt Sabine Tejpar Anna Nappi Vincenzo Sforza Giulia Martini Liberato Berri | 2013 | Int J Cancer2013，，9： | 2 |
| 14 | Effective bowel cleansing before colonoscopy: a randomized study of split-dosage versus non-split dosage regimens of high-volume versus low-volume polyethylene glycol solutions显示文摘 | Riccardo Marmo Gianluca Rotondano Giovanni Riccio Armando Marone Maria Antonia Bianco Italo Stroppa Anna Caruso Nicola Pandolfo Stefano Sansone Elena Gregorio Giuseppe D’Alvano Nicoletta Procaccio Pina Capo Clelia Marmo Livio Cipolletta | 2010 | Gastrointestinal Endoscopy2010，，2： | 2 |
| 15 | Ultrasound evaluation of liver fibrosis: preliminary experience with acoustic structure quantification (ASQ) software显示文摘 | Paolo Ricci Chiara Marigliano Vito Cantisani Andrea Porfiri Andrea Marcantonio Pietro Lodise Ugo D’Ambrosio Giancarlo Labbadia Elena Maggini Ester Mancuso Giovanna Panzironi Mattia Segni Caterina Furlan Raffaele Masciangelo Gloria Taliani | 2013 | La radiologia medica2013，，6： | 2 |
| 16 | Gut microbiota disturbance during antibiotic therapy: a multi-omic approach显示文摘 | Ana Elena Pérez-Cobas María José Gosalbes Anette Friedrichs Henrik Knecht Alejandro Artacho Kathleen Eismann Wolfgang Otto David Rojo Rafael Bargiela Martin von Bergen Sven C Neulinger Carolin D?umer Femke-Anouska Heinsen Amparo Latorre Coral Barbas Jana | 2013 | Gut2013，，11： | 2 |
| 17 | Ex vivo analysis of pancreatic cancer-infiltrating T lymphocytes reveals that ENO-specific Tregs accumulate in tumor tissue and inhibit Th1/Th17 effector cell functions显示文摘 | Amedeo Amedei Elena Niccolai Marisa Benagiano Chiara Della Bella Fabio Cianchi Paolo Bechi Antonio Taddei Lapo Bencini Marco Farsi Paola Cappello Domenico Prisco Francesco Novelli Mario Milco D’Elios | 2013 | Cancer Immunology, Immunotherapy2013，，7： | 2 |
| 18 | EUS-guided single-incision needle-knife biopsy: description and results of a new method for tissue sampling of subepithelial GI tumors (with video)显示文摘 | Carlos de la Serna-Higuera Manuel Pérez-Miranda Pilar Díez-Redondo Paula Gil-Simón Teresa Herranz Elena Pérez-Martín C. Ochoa Agustín Caro-Patón | 2011 | Gastrointestinal Endoscopy2011，，3： | 2 |
| 19 | Pharmacogenetics of ABC and SLC transporters in metastatic colorectal cancer patients receiving first-line FOLFIRI treatment显示文摘 | Elena De Mattia Giuseppe Toffoli Jerry Polesel Mario D’Andrea Giuseppe Corona Vittorina Zagonel Angela Buonadonna Eva Dreussi Erika Cecchin | 2013 | Pharmacogenetics and Genomics2013，，10： | 2 |
| 20 | p63 identifies keratinocyte stem cells 显示文摘 | Graziella P Elena D Osvaldo G | 2001 | Proc Natl Acad Sci USA2001，98，6： | 1 |
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