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| 1 | How antibiotic resistances could change Helicobacter pylori treatment:A matter of geography?显示文摘Therapeutic management of Helicobacter pylori(H.pylori)remains an unsolved issue.Indeed,no therapeutic regimen is able to cure the infection in all treated patients,and in many the infection persists despite the administration of several consecutive standard therapies.Although antibiotic resistance reports describe alarming results,the outcome of therapeutic regimens does not seem to parallel this scenario in most cases,since a successful performance is often reached in more than 80%of cases.However,the phenomenon of increasing antibiotic resistance is being closely studied,and the results show controversial aspects even in the same geographic area.For the continents of Europe,America,Asia,Africa,and Oceania,minimal and maximal values of resistance to the main antibiotics(clarithromycin,amoxicillin,metronidazole,and levofloxacin)feature wide ranges in different countries.The real enigma is therefore linked to the several different therapeutic regimens,which show results that often do not parallel the in vitro findings even in the same areas.A first aspect to be emphasized is that some regimens are limited by their use in very small geographic districts.Moreover,not all therapeutic trials have considered bacterial and host factors affecting the therapeutic outcome.The additional use of probiotics may help to reduce adverse events,but their therapeutic impact is doubtful.In conclusion,the'ideal therapy',paradoxically,appears to be a'utopia',despite the unprecedented volume of studies in the field and the real breakthrough in medical practice made by the discovery and treatment of H.pylori.The ample discrepancies observed in the different areas do not encourage the development of therapeutic guidelines that could be valid worldwide.On these bases,one of the main challenges for the future might be identifying a successful solution to overcome antibiotic resistances.In this context,geography must be considered a relevant matter. | Enzo Ierardi Floriana Giorgio Giuseppe Losurdo Alfredo Di Leo Mariabeatrice Principi | 2013 | World Journal of Gastroenterology2013，19，45： | 23 |
| 2 | The use of virtual surgical planning and navigation in the treatment of orbital trauma显示文摘 | Alan Scott Herford Meagan Miller Floriana Lauritano Gabriele Cervino Fabrizio Signorino Carlo Maiorana | 2017 | Chinese Journal of Traumatology2017，20，1： | 19 |
| 3 | Implication of the Hedgehog pathway in hepatocellular carcinoma显示文摘The prognosis for patients who are diagnosed with advanced stage hepatocellular carcinoma(HCC)is poor because there are few treatment options.Recent research has focused on the identification of novel molecular entities that can be targeted to inhibit oncogenic signals that are involved in the carcinogenesis,proliferation and progression of HCC.Among all of the pathways that are involved in the development of HCC,Hedgehog(HH)signalling has demonstrated a substantial role in hepatocarcinogenesis and HCC progression.HH plays a physiological role in embryogenesis,through the induction of the differentiation of hepatocytes from endodermal progenitors.The re-activation of the HH pathway in chronic damaged liver is a mechanism of fibrotic degeneration and is implicated in various stages of HCC development.HH activation sustains the subpopulation of immature liver epithelial cells that are involved in the pathogenesis of cirrhosis and HCC,and HH itself is a mediator of the alcohol-derived malignant transformation of liver cells.High levels of expression of HH protein markers in liver tumour tissues are correlated with aggressive histological and biological features and a poor clinical outcome.In vitro and in vivo inhibition models of the HH pathway confirm that HH is essential in maintaining tumour growth,metastasis and a mesenchymal phenotype. | Carminia Maria Della Corte Giuseppe Viscardi Federica Papaccio Giovanna Esposito Giulia Martini Davide Ciardiello Erika Martinelli Fortunato Ciardiello Floriana Morgillo | 2017 | World Journal of Gastroenterology2017，23，24： | 10 |
| 4 | Mechanisms of Helicobacter pylori antibiotic resistance:An updated appraisal显示文摘Helicobacter pylori(H. pylori) antibiotic resistance is the main factor affecting the efficacy of the current eradicating therapies. The aim of this editorial is to report on the recent information about the mechanisms accounting for the resistance to the different antibiotics currently utilized in H. pylori eradicating treatments. Different mechanisms of resistance to clarithromycin,metronidazole,quinolones,amoxicillin and tetracycline are accurately detailed(point mutations,redox intracellular potential,pump efflux systems,membrane permeability) on the basis of the most recent data available from the literature. The next hope for the future is that by improving the knowledge of resistance mechanisms,the elaboration of rational and efficacious associations for the treatment of the infection will be possible. Another auspicious progress might be the possibility of a cheap,feasible and reliable laboratory test to predict the outcome of a therapeutic scheme. | Vincenzo De Francesco Angelo Zullo Cesare Hassan Floriana Giorgio Rosa Rosania Enzo Ierardi | 2011 | World Journal of Gastrointestinal Pathophysiology2011，2，3： | 10 |
| 5 | 主要 clarithromycin 抵抗到 Helicobacter pylori : 这是为三倍的治疗失败的主要原因?显示文摘 Conventional triple therapies for Helicobacter pylori (H. pylori ) eradication have recently shown a disappointing reduction in effectiveness in many countries. The main reason for failure was found to be bacterial resistance to one of the most commonly used antibiotics, clarithromycin. An additional problem for conventional triple therapy is the high rate of resistance to metronidazole found in Europe, America and Asia. In Italy, in the last 15 years a 2-fold increase in resistance has occurred. A recent study of the whole of Italy included about 20 patients from each region at the first endoscopic diagnosis of H. pylori infection. The most surprising result was the patchy distribution of resistance, which was almost absent in two regions (one northern and one southern), although the highest prevalence was found in some regions of the South. In the paediatricpopulation we found a 25% prevalence of resistance in a sample of H. pylori positive children observed between 2002 and 2007, mirroring data obtained in southern European countries. Clarithromycin resistance assessment is currently based on phenotypic detection performed after culture the agar dilution method or E-test, and genotypic methods based on polymerase chain reaction (PCR). In a recent comparative study we found a 71.2% agreement between the two methods. Culture-free techniques are highly accurate in finding even minimal traces of genotypically resistant strains. Moreover, PCR-based tools are accurate in detecting a heteroresistant status, defined as the co-existence of some strains that are susceptible and some resistant to the same antibiotic in an individual patient. Three point mutations, namely A2143G , A2142G and A2142C , are responsible for 90% of cases of primary clarithromycin resistance in H. pylori strains isolated in Western countries, although we previously demonstrated that the presence of the A2143G mutation, but not A2142G or A2142C , significantly lowered the H. pylori eradication rate. Treatment failure has considerable cost/benefit implications because of 'waste' of National Health System and patient resources, in terms of drugs, further diagnostic tests and medical examination expenses. Therefore, in future it would be very useful to be able to test for clarithromycin resistance before starting conventional triple therapy. Hopefully, fast, effective noninvasive tests may soon be devised to determine this condition. | Floriana Giorgio Mariabeatrice Principi Vincenzo De Francesco Angelo Zullo Giuseppe Losurdo Alfredo Di Leo Enzo Ierardi | 2013 | World Journal of Gastrointestinal Pathophysiology2013，4，3： | 10 |
| 6 | Targeted therapies in metastatic gastric cancer: Current knowledge and future perspectives显示文摘Gastric cancer(GC)represents a leading cause of cancer related morbidity and mortality worldwide accounting for more than 1 million of newly diagnosed cases and thousands of deaths every year.In the last decade,the development of targeted therapies and the optimization of already available chemotherapeutic drugs has expanded the available treatment options for advanced GC and granted better survival expectations to the patients.At the same time,global efforts have been undertaken to investigate in detail the genomic and epigenomic heterogeneity of this disease,resulting in the identification of new specific and sensitive predictive and prognostic biomarkers and in innovative molecular classifications based on gene expression profiling.Nonetheless,several randomized studies aimed at exploring new innovative agents,such as immune checkpoint inhibitors,failed to demonstrate clinically meaningful survival advantages.Therefore,it is essential to further improve the molecular characterization of GC subgroups in order to provide researchers and medical oncologists with new tools for patients’selection and stratification in future clinical development programs and subsequent trials.The aim of the present manuscript is to provide a global overview of the recent molecular classifications from The Cancer Genome Atlas and the Asian Cancer Research Group and to present key promising developments in the field of immunotherapy and targeted therapies in metastatic GC. | Antonio Pellino Erika Riello Floriana Nappo Stefano Brignola Sabina Murgioni Selma Ahcene Djaballah Sara Lonardi Vittorina Zagonel Massimo Rugge Fotios Loupakis Matteo Fassan | 2019 | World Journal of Gastroenterology2019，25，38： | 9 |
| 7 | Present and future of metastatic colorectal cancer treatment: A review of new candidate targets显示文摘In the last two decades, great efforts have been made in the treatment of metastatic colorectal cancer(m CRC) due to the approval of new target agents for cytotoxic drugs. Unfortunately, a large percentage of patients present with metastasis at the time of diagnosis or relapse after a few months. The complex molecular heterogeneity of this disease is not completely understood; to date, there is a lack of predictive biomarkers that can be used to select subsets of patients who may respond to target drugs. Only the RAS-mutation status is used to predict resistance to anti-epidermal growth factor receptor agents in patients with m CRC. In this review, we describe approved targeted therapies for the management of metastatic m CRC and discuss new candidate targets on the horizon. | Giulia Martini Teresa Troiani Claudia Cardone Pietropaolo Vitiello Vincenzo Sforza Davide Ciardiello Stefania Napolitano Carminia Maria Della Corte Floriana Morgillo Antonio Raucci Antonio Cuomo Francesco Selvaggi Fortunato Ciardiello Erika Martinelli | 2017 | World Journal of Gastroenterology2017，23，26： | 7 |
| 8 | New fecal test for non-invasive Helicobacter pylori detection:A diagnostic accuracy study显示文摘AIM To assess the diagnostic accuracy of a new fecal test for detecting Helicobacter pylori(H. pylori), using ^(13)Curea breath test as the reference standard, and explore bacterial antibiotic resistance. METHODS We conducted a prospective two-center diagnostic test accuracy study. We enrolled consecutive people≥ 18 years without previous diagnosis of H. pylori infection, referred for dyspepsia between February and October 2017. At enrollment, all participants underwent 13 C-urea breath test. Participants aged over 50 years were scheduled to undergo upper endoscopy with histology. Participants collected stool samples 1-3 d after enrollment for a new fecal investigation(THD fecal test). The detection of bacterial 23 S rRNA subunit gene indicated H. pylori infection. We also used the index diagnostic test to examine mutations conferring resistance to clarithromycin and levofloxacin. Independent investigators analyzed index test and reference test standard results blinded to the other test findings. We estimated sensitivity, specificity, positive(PPV) and negative(NPV) predictive value, diagnostic accuracy, positive and negative likelihood ratio(LR), together with 95% confidence intervals(CI).RESULTS We enrolled 294 consecutive participants(age: Median 37.0 years, IQR: 29.0-46.0 years; men: 39.8%). Ninetyfive(32.3%) participants had a positive ^(13)C-urea breath test. Twenty-three(7.8%) participants underwent upper endoscopy with histology, with a full concordance between ^(13)C-urea breath test and histology in detecting H. pylori infection. Four(1.4%) out of the 294 participants withdrew from the study after the enrollment visit and did not undergo THD fecal testing. In the 290 participants who completed the study, the THD fecal test sensitivity was 90.2%(CI: 84.2%-96.3%), specificity 98.5%(CI:96.8%-100%), PPV 96.5%(CI: 92.6%-100%), NPV 95.6%(CI: 92.8%-98.4%), accuracy 95.9%(CI: 93.6%-98.2%), positive LR 59.5(CI: 19.3-183.4), negative LR 0.10(CI: 0.05-0.18). Out of 83 infected participants identified with the THD fecal test, 34(41.0%) had bacterial genotypic changes consistent with antibiotic-resistant H. pylori infection. Of these, 27(32.5%) had bacterial strains resistant to clarithromycin, 3(3.6%) to levofloxacin, and 4(4.8%) to both antibiotics. CONCLUSION The THD fecal test has high performance for the non-invasive diagnosis of H. pylori infection while additionally enabling the assessment of bacterial antibiotic resistances. | Andrea Iannone Floriana Giorgio Francesco Russo Giuseppe Riezzo Bruna Girardi Maria Pricci Suetonia C Palmer Michele Barone Mariabeatrice Principi Giovanni FM Strippoli Alfredo Di Leo Enzo Ierardi | 2018 | World Journal of Gastroenterology2018，24，27： | 5 |
| 9 | The deubiquitinase OTUB1 augments NF-κB-dependent immune responses in dendritic cells in infection and inflammation by stabilizing UBC13显示文摘Dendritic cells(DCs)are indispensable for defense against pathogens but may also contribute to immunopathology.Activation of DCs upon the sensing of pathogens by Toll-like receptors(TLRs)is largely mediated by pattern recognition receptor/nuclear factor-κB(NF-κB)signaling and depends on the appropriate ubiquitination of the respective signaling molecules.However,the ubiquitinating and deubiquitinating enzymes involved and their interactions are only incompletely understood.Here,we reveal that the deubiquitinase OTU domain,ubiquitin aldehyde binding 1(OTUB1)is upregulated in DCs upon murine Toxoplasma gondii infection and lipopolysaccharide challenge.Stimulation of DCs with the TLR11/12 ligand T.gondii profilin and the TLR4 ligand lipopolysaccharide induced an increase in NF-κB activation in OTUB1-competent cells,resulting in elevated interleukin-6(IL-6),IL-12,and tumor necrosis factor(TNF)production,which was also observed upon the specific stimulation of TLR2,TLR3,TLR7,and TLR9.Mechanistically,OTUB1 promoted NF-κB activity in DCs by K48-linked deubiquitination and stabilization of the E2-conjugating enzyme UBC13,resulting in increased K63-linked ubiquitination of IRAK1(IL-1 receptor-associated kinase 1)and TRAF6(TNF receptor-associated factor 6).Consequently,DC-specific deletion of OTUB1 impaired the production of cytokines,in particular IL-12,by DCs over the first 2 days of T.gondii infection,resulting in the diminished production of protective interferon-γ(IFN-γ)by natural killer cells,impaired control of parasite replication,and,finally,death from chronic T.encephalitis,all of which could be prevented by low-dose IL-12 treatment in the first 3 days of infection.In contrast,impaired OTUB1-deficient DC activation and cytokine production by OTUB1-deficient DCs protected mice from lipopolysaccharide-induced immunopathology.Collectively,these findings identify OTUB1 as a potent novel regulator of DCs during infectious and inflammatory diseases. | Floriana Mulas Xu Wang Shanshan Song Gopala Nishanth Wenjing Yi Anna Brunn Pia-Katharina Larsen Berend Isermann Ulrich Kalinke Antonio Barragan Michael Naumann Martina Deckert Dirk Schlüter | 2021 | Cellular & Molecular Immunology2021，18，6： | 4 |
| 10 | Noninvasive molecular analysis of Helicobacter pylori : Is it time for tailored first-line therapy?显示文摘The main problem of Helicobacter pylori(H. pylori) infection management is linked to antibiotic resistances. This phenomenon has grown in the last decade, inducing a dramatic decline in conventional regimen effectiveness. The causes of resistance are point mutations in bacterial DNA, which interfere with antibiotic mechanism of action, especially clarithromycin and levofloxacin. Therefore, international guidelines have recently discouraged their use in areas with a relevant resistance percentage, suggesting first-line schedules with expected high eradication rates, i.e., bismuth containing or non-bismuth quadruple therapies. These regimens require the daily assumption of a large number of tablets. Consequently, a complete adherence is expected only in subjects who may be motivated by the presence of major disorders. However, an incomplete adherence to antibiotic therapies may lead to resistance onset, since sub-inhibitory concentrations could stimulate the selection of resistant mutants. Of note, a recent meta-analysis suggests that susceptibility tests may be more useful for the choice of first than second-line or rescue treatment. Additionally, susceptibility guided therapy has been demonstrated to be highly effective and superior to empiric treatments by both meta-analyses and recent clinical studies. Conventional susceptibility test is represented by culture and antibiogram. However, the method is not available everywhere mainly for methodology-related factors and fails to detect hetero-resistances. Polymerase chain reaction(PCR)-based, culture-free techniques on gastric biopsy samples are accurate in finding even minimal traces of genotypic resistant strains and hetero-resistant status by the identification of specific point mutations. The need for an invasive endoscopic procedure has been the most important limit to their spread. A further step has, moreover, been the detection of point mutations in bacterial DNA fecal samples. Few studies on clarithromycin susceptibility have shown an overall high sensitivity and specificity when compared with culture or PCR on gastric biopsies. On these bases, two commercial tests are now available although they have shown some controversial findings. A novel PCR method showed a full concordance between tissue and stool results in a preliminary experience. In conclusion, despite poor validation, there is increasing evidence of a potential availability of noninvasive investigations able to detect H. pylori resistances to antibiotics. These kinds of analysis are currently at a very early phase of development and caution should be paid about their clinical application. Only further studies aimed to evaluate their sensitivity and specificity will afford novel data for solid considerations. Nevertheless, noninvasive molecular tests may improve patient compliance, time/cost of infection management and therapeutic outcome. Moreover, the potential risk of a future increase of resistance to quadruple regimens as a consequence of their use on large scale and incomplete patient adherence could be avoided. | Enzo Ierardi Floriana Giorgio Andrea Iannone Giuseppe Losurdo Mariabeatrice Principi Michele Barone Antonio Pisani Alfredo Di Leo | 2017 | World Journal of Gastroenterology2017，23，14： | 3 |
| 11 | Histomorhological and clinical evaluation of maxillary alveolar ridge reconstruction after craniofacial trauma by applying combination of allogeneic and autogenous bone graft显示文摘 | Francesco Saverio De Ponte Roberto Falzea Michele Runci Enrico Nastro Siniscalchi Floriana Lauritano Ennio Bramanti Gabriele Cervino Marco Cicciu | 2017 | Chinese Journal of Traumatology2017，20，1： | 2 |
| 12 | Evolution of nonspecific duodenal lymphocytosis over 2 years of follow-up显示文摘AIM: To assess the evolution of duodenal lymphocytosis(DL), a condition characterized by increased intraepithelial lymphocytes(IELs), over 2 years of follow-up.METHODS: Consecutive patients undergoing upper endoscopy/histology for abdominal pain, diarrhea, weight loss, weakness or other extraintestinal features compatible with celiac disease(CD) were included. Evaluation of IELs infiltrate in duodenal biopsy sampleswas carried out by CD3-immunohistochemistry and expressed as number of positive cells/100 enterocytes. Diagnostic agreement on the IELs count was tested by calculating the weighted k coefficient. All patients underwent serological detection of autoantibodies associated with CD: Ig G and Ig A anti-tissue transglutaminase and endomysium. Each patient underwent further investigations to clarify the origin of DL at baseline and/or in the course of 2 years of follow-up every six months. Autoimmune thyroiditis, intestinal infections, parasitic diseases, bacterial intestinal overgrowth, hypolactasia and wheat allergy were detected. Colonoscopy and enteric magnetic resonance i m a g i n g w e r e p e r f o r m e d w h e n n e c e s s a r y. R i s k factors affecting the final diagnosis were detected by multinomial logistic regression and expressed as OR.RESULTS: Eighty-five patients(16 males, 69 females, aged 34.1 ± 12.5 years) were followed up for a mean period of 21.7 ± 11.7 mo. At baseline, endoscopy/duodenal biopsy, CD3 immunohistochemistry revealed: > 25 IELs/100 enterocytes in 22 subjects, 15-25 IELs in 37 and < 15 IELs in 26. They all had negative serum anti-transglutaminase and anti-endomysium, whilst 5 showed Ig G anti-gliadin positivity. In the course of follow-up, 23 developed CD seropositivity and gluten sensitivity(GS) was identified in 19. Other diagnoses were: 5 Helicobacter pylori infections, 4 jejunal Crohn's disease, 1 lymphocytic colitis and 1 systemic sclerosis. The disease in the remaining 32 patients was classified as irritable bowel syndrome because of the lack of diagnostic evidence. At multivariate analysis, the evolution towards CD was associated with an IELs infiltrate > 25(OR = 1640.4) or 15-25(OR = 16.95), human leukocyte antigen(HLA) DQ2/8(OR = 140.85) or DQA1*0501(OR = 15.36), diarrhea(OR = 5.56) and weakness(OR = 11.57). GS was associated with IELs 15-25(OR = 28.59), autoimmune thyroiditis(OR = 87.63), folate deficiency(OR = 48.53) and diarrhea(OR = 54.87).CONCLUSION: DL may have a multifactorial origin but the IELs infiltrate and HLA are strong predictive factors for CD development and a clinical diagnosis of GS. | Giuseppe Losurdo Domenico Piscitelli Antonio Giangaspero Mariabeatrice Principi Francesca Buffelli Floriana Giorgio Lucia Montenegro Claudia Sorrentino Annacinzia Amoruso Enzo Ierardi Alfredo Di Leo | 2015 | World Journal of Gastroenterology2015，21，24： | 2 |
| 13 | Management of single pulmonary metastases from colorectal cancer:State of the art显示文摘Colorectal cancer(CRC)is one of the most common causes of death from cancer.Lung seeding occurs in approximately 10%of patients surgically treated for primary CRC with radical intent:the lung is the most common site of metastases after the liver.While surgical treatment of liver metastases is widely accepted to affect long-term outcomes,more controversial and not standardized is the therapy for CRC patients developing lung metastases.Experience suggests the potential curative role of pulmonary metastasectomy,especially in oligometastatic disease.However,the optimal strategy of care and the definition of prognostic factors after treatment still need to be defined.This review focused on the uncommon scenario of single pulmonary metastases from CRC.We explored pertinent literature and provide an overview of the epidemiology,clinical characteristics and imaging of single pulmonary metastases from CRC.Additionally,we identified the best available evidence for overall management.In particular,we analyzed the role and results of locoregional approaches(surgery,radiotherapy or ablative procedures)and their integration with systemic therapy. | Marco Chiappetta Lisa Salvatore Maria Teresa Congedo Maria Bensi Viola De Luca Leonardo PetraccaCiavarella Floriana Camarda Jessica Evangelista Vincenzo Valentini Giampaolo Tortora StefanoMargaritora Filippo Lococo | 2022 | World Journal of Gastrointestinal Oncology2022，14，4： | 2 |
| 14 | 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 |
| 15 | From chronic liver disorders to hepatocellular carcinoma: Molecular and genetic pathways显示文摘Hepatocarcinogenesis is a process attributed to progressive genomic changes that alter the hepatocellular phenotype producing cellular intermediates that evolve into hepatocellular carcinoma (HCC). During the preneoplastic phase, the liver is often the site of chronic hepatitis and/or cirrhosis, and these conditions induce liver regeneration with accelerated hepatocyte cycling in an organ that is otherwise proliferatively at rest. Hepatocyte regeneration is accelerated by upregulation of mitogenic pathways involving molecular and genetic mechanisms. Hepatic growth factors, inhibitors and triggers may also play a role. This process leads to the production of monoclonal populations of aberrant and dysplastic hepatocytes that have telomerase reexpression, microsatellite instability, and occasionally structural aberrations in genes and chromosomes. Development of dysplastic hepatocytes in foci and nodules and the emergence of HCC are associated with the accumulation of irreversible structural alterations in genes and chromosomes even if the genomic basis of the malignant phenotype is largely heterogeneous. Therefore, a malignant hepatocyte phenotype may be produced by changes in genes acting through different regulatory pathways, thus producing several molecular variants of HCC. On these bases, a key point for future research will be to determine whether the deletions are specific, due to particular loci in the minimally deleted regions of affected chromosome arms, or whether they are nonspecific with loss of large portions of chromosomes or entire chromosome arms leading to passive deletion of loci. The final aim is the possibility of identifying a step where carcinogenetic processes could be terminated. | Enzo Ierardi Rosa Rosania Mariangela Zotti Floriana Giorgio Simonetta Prencipe Nicola Della Valle Vincenzo De Francesco Carmine Panella | 2010 | World Journal of Gastrointestinal Oncology2010，2，6： | 2 |
| 16 | Altered molecular pattern of mucosal healing in Crohn's disease fibrotic stenosis显示文摘AIM: To investigate tumor necrosis factor-α (TNF-α), syndecan 1 and basic fibroblast growth factor (bFGF) balance in Crohn's disease (CD) strictures. METHODS: Our study was performed on 24 surgical specimens of CD fibrotic stenosis. Ten histological normal surgical samples were retrieved for both the large and small bowel from patients with benign conditions and healthy tissue represented control collection. Sex and age in controls did not differ from CD group. Three endoscopic biopsy specimens taken after informed consent in subjects with normal colon were also used as negative controls. TNF-α, syndecan 1 and bFGF were detected by both reverse transcriptase reverse transcriptase polymerase chain reaction after mRNA extraction (results expressed as fold-change) and immunohistochemistry.RESULTS: TNF-α did not show any significant difference between CD and control specimens (1.54 ± 1.19; P > 0.05). Very high levels of bFGF were observed in CD (11.76 ± 4.65; P < 0.001) unlike syndecan 1 which showed a moderate increase (5.53 ± 2.18; P < 0.005). analysis of variance (ANOVA) plus Student-NeumannKeuls showed: bFGF > syndecan 1 > TNF-α = control. Immunoreactivity for bFGF was observed in epithelial, stromal, endothelial cells and even in the muscular layer, whilst in normal tissue it was almost unexpressed. Syndecan 1 and TNF-α staining was confined to mucosal epithelial and stromal cells, while in controls syndecan 1 was found in its normal site, i.e. , basolateral area of the crypts and TNF-α very poorly expressed. CONCLUSION: Fibrotic stenosis of CD may be the final result of an irreversible transformation of different cells into fibrogenic phenotype no longer inhibited by posttranscriptional regulation. | Enzo Ierardi Floriana Giorgio Domenico Piscitelli Mariabeatrice Principi Santina Cantatore Maria Grazia Fiore Roberta Rossi Michele Barone Alfredo Di Leo Carmine Panella | 2013 | World Journal of Gastrointestinal Pathophysiology2013，4，3： | 2 |
| 17 | 在煽动性的肠疾病的 Fibrogenesis 和纤维变性: 一样的硬币的好、坏的方面?显示文摘 Fibrogenesis in inflammatory bowel diseases is a complex phenomenon aimed at mucosal repair. However, it may provoke intestinal fibrosis with the development of strictures which require surgery. Therefore, fibrogenesis may be considered as a 'two-faced' process when related to chronic intestinal inflammation. Many types of cells may be converted into the fibrogenic phenotype at different levels of the intestinal wall. A complex interaction of cytokines, adhesion molecules and growth factors is involved in the process. We report an overview of recent advances in molecular mechanisms of stricturizing Crohn’s disease(CD) including the potential role of trasforming growth factor beta, protein kinase C and Ras, Raf and ERK proteins. Fibrotic growth factors such as vascular endothelial growth factor and platelet-derived growth factor, as well as the Endothelial-to-Mesenchymal Transition induced by transforming growth factor-β, are considered. Finally, our experience, focused on tumor necrosis factor α(the main cytokine of inflammatory bowel diseases) and the link between syndecan 1(a heparan sulphate adhesion molecule) and basic fibroblast growth factor(a strong stimulator of collagen synthesis) is described. We hypothesize a possible molecular pattern for mucosal healing as well as how its deregulation could be involved in fibrotic complications of CD. A final clinical point is the importance of performing an accurate evaluation of the presence of fibrotic strictures before starting anti-tumor necrosis α treatment, which could worsen the lesions. | Mariabeatrice Principi Floriana Giorgio Giuseppe Losurdo Viviana Neve Antonella Contaldo Alfredo Di Leo Enzo Ierardi | 2013 | World Journal of Gastrointestinal Pathophysiology2013，4，4： | 2 |
| 18 | A comparative analysis of methods for pruning decision tree显示文摘 | Floriana Esposito Donato Malerba Giovanni Semeraro | 1997 | IEEE Tranactions of Pattern Analysis and Machine Intelligence1997，19，5： | 1 |
| 19 | Expression of CD52 mRNA in the rat embryo显示文摘 | Ermini L Aldi S Floriana R | 2008 | Dev Growth Differ2008，50，7： | 1 |
| 20 | Role of concomitant therapy for Helicobacter pylori eradication: A technical note显示文摘We read with interest the recent meta-analysis by Lin et al who evaluated the effectiveness of concomitant regimen for Helicobacter pylori(H. pylori) in Chinese regions. They found that 7-d concomitant regimen is undoubtedly superior to 7-d triple therapy(91.2% vs 77.9%, P < 0.0001). However, it is a common belief that a triple therapy lasting 7 d should be definitively removed from the clinical practice for its ineffectiveness. Only its prolongation to 14 d may give satisfactory success rate. Thus, the assessment of an old and outdated treatment versus a more recent and successful one does not seem to bring novel and useful information. Moreover, a 7-d duration has not been ascertained for concomitant regimen, as main guidelines recommend a 10-d schedule for this scheme. Therefore, only studies comparing 10-d concomitant versus 14-d triple seem to be appropriate according to current Guidelines and would clarify which regimen is the most suitable worldwide. Additionally, in this metaanalysis concomitant and sequential therapy showed similar performances, despite it is common opinion that sequential is more prone than concomitant therapy to fail when metronidazole resistance occurs, and China is characterized by high rate of resistance to this antibiotic. None of the included studies evaluated a priori antibiotic resistances, and the lack of this detail hampers the unveiling of this apparent contradiction. In conclusion, the lack of the evaluation of the quality of included trials as well as their high heterogeneity constitute a burdensome limit to draw solid conclusions in this meta-analysis. On the bases of these considerations and the low number of examined trials, we believe that further studies and the knowledge of antibiotic resistances will support with high quality evidence which is the best regimen and its optimal duration. | Giuseppe Losurdo Floriana Giorgio Andrea Iannone Mariabeatrice Principi Michele Barone Alfredo Di Leo Enzo Ierardi | 2016 | World Journal of Gastroenterology2016，22，38： | 1 |
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