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| 1 | Alterations of glutathione S-transferase and matrix metalloproteinase-9 expressions are early events in esophageal carcinogenesis显示文摘AIM: To investigate the role of glutathione S-transferase (GST) and matrix metalloproteinase-9 (MMP-9) expres-sions in the development and progression of reflux es-ophagitis-Barrett’s metaplasia-dysplasia-adenocarcinoma sequence in the esophagus.METHODS: GST and MMP-9 expressions were analyzed in 51 paraffin-embedded tissue samples by immunohisto-chemistry including patients with reflux esophagitis (n = 7), Barrett’s metaplasia (n = 14), Barrett and esophagi-tis (n = 8), Barrett and dysplasia (n = 7), esophageal adenocarcinoma (n = 8) and a control group without any histological changes (n = 7). Immunostaining was determined semiquantitatively. Statistical analysis with one-way ANOVA, LSD test and correlation analysis were performed. P value of < 0.05 was considered significant.RESULTS: GST expression was significantly higher while MMP-9 expression was significantly lower in control group compared to Barrett’s metaplasia and the other groups. No major changes were observed between Bar-rett, esophagitis, and Barrett and concomitant esophagi-tis. Barrett and concomitant dysplasia, and adenocarci-noma revealed a significant lower expression of GST and higher levels of MMP-9 compared to all other groups. Adenocarcinoma showed almost no expression of GST and significantly higher levels of MMP-9 than Barrett and concomitant dysplasia. Alterations of GST and MMP-9 were inversely correlated (r = - 0.82).CONCLUSION: Decreased GST and increased ex-pression of MMP-9 in Barrett’s metaplasia-dysplasia-adenocarcinoma sequence as compared to normal tissue suggest their association with esophageal tumorigenesis. Loss of GST and gain of MMP-9 in Barrett with dyspla-sia compared to non-dysplastic metaplasia indicate that these alterations may be early events in carcinogenesis. Quantification of these parameters in Barrett’s esopha-gus might be useful to identify patients at higher risk for progression to cancer. | Laszlo Herszenyi Istvan Hritz Istvan Pregun Ferenc Sipos Mark Juhasz Bela Molnar Zsolt Tulassay | 2007 | World Journal of Gastroenterology2007，13，5： | 37 |
| 2 | Is rectal indomethacin effective in preventing of post-endoscopic retrograde cholangiopancreatography pancreatitis?显示文摘AIM:To investigate the effectiveness of rectally administered indomethacin in the prophylaxis of post-endoscopic retrograde cholangiopancreatography(ERCP)pancreatitis and hyperamylasaemia in a multicentre study.METHODS:A prospective,randomised,placebocontrolled multicentre study in five endoscopic units was conducted on 686 patients randomised to receive a suppository containing 100 mg indomethacin,or an inert placebo,10-15 min before ERCP.Post-ERCP pancreatitis and hyperamylasaemia were evaluated 24 h following the procedure on the basis of clinical signs and laboratory parameters,and computed tomography/magnetic resonance imaging findings if required.RESULTS:Twenty-one patients were excluded because of incompleteness of their data or because of protocol violation.The results of 665 investigations were evaluated:347 in the indomethacin group and 318 in the placebo group.The distributions of the risk factors in the two groups did not differ significantly.Pancreatitis developed in 42 patients(6.3%):it was mild in34(5.1%)and severe in eight(1.2%)cases.Hyperamylaesemia occurred in 160 patients(24.1%).There was no significant difference between the indomethacin and placebo groups in the incidence of either postERCP pancreatitis(5.8%vs 6.9%)or hyperamylasaemia(23.3%vs 24.8%).Similarly,subgroup analysis did not reveal any significant differences between the two groups.CONCLUSION:100 mg rectal indomethacin administered before ERCP did not prove effective in preventing post-ERCP pancreatitis. | Zoltán Dbrnte Zoltán Szepes Ferenc Izbéki Judit Gervain László Lakatos Gyula Pécsi Miklós Ihász Lilla Lakner Erzsébet Toldy László Czakó | 2014 | World Journal of Gastroenterology2014，20，29： | 16 |
| 3 | Changes of the cytokine profile in inflammatory bowel diseases显示文摘Cytokines are indispensable signals of the mucosaassociated immune system for maintaining normal gut homeostasis.An imbalance of their profile in favour of inflammation initiation may lead to disease states,such as that is observed in inflammatory bowel diseases(IBD).Although Crohn's disease(CD) is often described as a prototype of T-helper 1-type diseases,and ulcerative colitis(UC) is traditionally viewed as a T-helper 2-mediated condition,the classic paradigm,which categorises cytokines into pro-and anti-inflammatory groups,has recently been changed.The inflammation regulatory pathways may not be mutually exclusive as individual cytokines can have diverse and even opposing functions in various clinical and immunological settings.None the less there are many common immunological responses in IBD that are mediated by cytokines.Although they regulate and influence the development,course and recurrence of the inflammatory process,the concrete pathogenic role of these small signaling molecules is sometimes not unambiguous in the subtypes of the disease.Our aim is to review the current information about pro-and anti-inflammatory effects of traditionally studied and recently discovered cytokines in the pathogenesis of UC and CD.The better understanding of their production and functional activity may lead to the development of new therapeutic modalities. | Gyrgyi Mzes Béla Molnár Zsolt Tulassay Ferenc Sipos | 2012 | World Journal of Gastroenterology2012，18，41： | 16 |
| 4 | Epithelial toll-like receptor 9 signaling in colorectal inflammation and cancer: Clinico-pathogenic aspects显示文摘Toll-like receptors (TLRs) recognize specific motifs which are frequently present in bacteria, fungi, prokaryotes and viruses. Amongst TLRs, TLR9 can be activated by such bacterial or viral DNA fragments, immunoglobulin-DNA complexes or synthetic oligonucleotides, which all contain unmethylated cytosineguanine nucleotide sequences (CpGs). Emerging data indicate that TLR9 signaling has a role in, and may influence, colorectal carcinogenesis and colonic inflammation. CpGs are classified into three groups according to their influence on both the antigen-specific humoraland cellular immunity, and the production of type 1 interferons and proinflammatory cytokines. TLR9 activation via CpGs may serve as a new therapeutic target for several cancerous and various inflammatory conditions. Due to its probable anti-cancer effects, the application possibilities of TLR9-signaling modulation may be extremely diverse even in colorectal tumors. In this review we aimed to summarize the current knowledge about TLR-signaling in the pathogenesis and therapy of inflammatory bowel diseases and colorectal cancer. Due to the species-specific differences in TLR9 expression, however, one must be careful in translating the animal model data into the human system, because of the differences between CpG-oligodeoxynucleotide-responsive cells. TLR9 agonist DNA-based immunomodulatory sequences could also represent a promising therapeutic alternative in systemic inflammatory conditions and chronic colonic inflammations as their side effects are not significant. | István Fri Ferenc Sipos Tiana M Germann Alexandra Kalmár Zsolt Tulassay Béla Molnár Gyrgyi Mzes | 2013 | World Journal of Gastroenterology2013，19，26： | 14 |
| 5 | Perianal disease,small bowel disease,smoking,prior steroid or early azathioprine/biological therapy are predictors of disease behavior change in patients with Crohn's disease显示文摘AIM:To assess the combined effect of disease phenotype, smoking and medical therapy [steroid, azathioprine(AZA), AZA/biological therapy] on the probability of disease behavior change in a Caucasian cohort of patients with Crohn's disease(CD).METHODS:Three hundred and forty well-characterized, unrelated, consecutive CD patients were analyzed(M/F:155/185, duration:9.4 ± 7.5 years) with a complete clinical follow-up.Medical records including disease phenotype according to the Montreal classification, extraintestinal manifestations, use of medications and surgical events were analyzed retrospectively.Patients were interviewed on their smoking habits at the time of diagnosis and during the regular follow-up visits.RESULTS:A change in disease behavior was observed in 30.8% of patients with an initially non-stricturing, non-penetrating disease behavior after a mean diseaseduration of 9.0 ± 7.2 years.In a logistic regression analysis corrected for disease duration, perianal disease, smoking, steroid use, early AZA or AZA/ biological therapy use were independent predictors of disease behavior change.In a subsequent Kaplan-Meier survival analysis and a proportional Cox regression analysis, disease location(P = 0.001), presence of perianal disease(P < 0.001), prior steroid use(P = 0.006), early AZA(P = 0.005) or AZA/biological therapy(P = 0.002), or smoking(P = 0.032) were independent predictors of disease behavior change.CONCLUSION:Our data suggest that perianal disease, small bowel disease, smoking, prior steroid use, early AZA or AZA/biological therapy are all predictors of disease behavior change in CD patients. | Peter Laszlo Lakatos Zsofia Czegledi Tamas Szamosi Janos Banai Gyula David Ferenc Zsigmond Tunde Pandur Zsuzsanna Erdelyi Orsolya Gemela Janos Papp Laszlo Lakatos | 2009 | World Journal of Gastroenterology2009，15，28： | 14 |
| 6 | Toll-like receptor 4 and NOD2/CARD15 mutations in Hungarian patients with Crohn's disease: Phenotype-genotype correlations显示文摘AIM: To determine common NOD2/CARD15 mutations and TLR4 D299G polymorphism in Hungarian patients with CD.METHODS: A total of 527 unrelated patients with CD (male/female: 265/262, age: 37.1 (SD 7.6) years) and 200 healthy subjects were included. DNA was screened for possible NOD2/CARD15 mutations by denaturing highperformance liquid chromatography (confirmed by direct sequencing). TLR4 D299G was tested by PCR-RFLP.RESULTS: NOD2/CARD15 mutations were found in 185patients (35.1%) and in 33 controls (16.5%, P<0.0001).SNP8/R702W (10.8% vs 6%, P = 0.02), SNP13/3020insC (19.4% vs 5%, P<0.0001) and exon4 R703C (2.1% vs 0%, P = 0.02) mutations were more frequent in CD, while the frequency of SNP12/G908R was not increased. The frequency of TLR4 D299G was not different (CD: 9.9% vscontrols: 12.0%). Variant NOD2/CARD15 allele was associated with an increased risk for CD (ORhet = 1.71,95%CI = 1.12-2.6, P= 0.0001, ORtwo-riskalleles = 25.2,95%CI = 4.37- , P<0.0001), early disease onset (carrier:26.4 years vs non-carrier: 29.8 years, P = 0.0006), ileal disease (81.9% vs 69.5%, OR = 1.99, 95%CI = 1.29-3.08,P = 0.02, presence of NOD2/CARD15 and TLR4: 86.7% vs64.8%), stricturing behavior (OR = 1.69, 95%CI = 1.13-2.55,P = 0.026) and increased need for resection (OR=1.71,95%CI: 1.13-2.62, P= 0.01), but not with duration, extraintestinal manifestations, familial disease or smoking. TLR4exhibited a modifier effect: age of onset in wt/TLR4 D299G carriers: 27.4 years vs NOD2mut/TLR D299G: 23 years (P= 0.06), in NOD2mut/wt: 26.7 years.CONCLUSION: These results confirm that variant NOD2/CARD15 (R702W, R703C and 3020insC) alleles are associated with earlier disease onset, ileal disease,stricturing disease behavior in Hungarian CD patients. In contrast, although the frequency of TLR4 D299G polymorphism was not different from controls, NOD2/TLR4mutation carriers tended to present at earlier age. | Peter Laszlo Lakatos Laszlo Lakatos Ferenc Szalay Claudia Willheim-Polli Christoph (O|¨)sterreicher Zsolt Tulassay Tamas Molnar Walter Reinisch Janos Papp Gyula Mozsik Hungarian IBD Study Group Peter Ferenci | 2005 | World Journal of Gastroenterology2005，11，10： | 14 |
| 7 | Epithelial-to-mesenchymal and mesenchymal-to-epithelial transitions in the colon显示文摘Epithelial-to-mesenchymal and mesenchymal-to-epithelial transitions are well established biological events which have an important role in not just normal tissue and organ development,but in the pathogenesis of diseases.Increasing evidence has established their presence in the human colon during colorectal carcinogenesis and cancer invasion,chronic inflammation-related fibrosis and in the course of mucosal healing.A large body of evidence supports the role for transforming growth factor-β and its downstream Smad signaling,the phosphatidylinositol 3'-kinase/Akt/mTOR axis,the Ras-mitogen-activated protein kinase/Snail/Slug and FOXC2 pathway,and Hedgehog signaling and microRNAs in the development of colorectal cancers via epithelial-to-mesenchymal transition.C-met and Frizzled-7,among others,seem to be the principle effectors of mesenchymal-to-epithelial transition,hence have a role not just in mucosal regeneration but in the progression of colonic wall fibrosis.Here we discuss a role for these pathways in the initiation and development of the transition events.A better understanding of their induction and regulation may lead to the identification of pathways and factors that could be potent therapeutic targets.The inhibition of epithelial-to-mesenchymal transition using mTOR kinase inhibitors targeting the ATP binding pocket and which inhibit both mTORC1 and mTORC2,RNA aptamers or peptide mimetics,such as a Wnt5A-mimetic,may all be useful in both cancer treatment and delaying fibrosis,while the induction of mesenchymal-to-epithelial transition in induced pluripotent stem cells may enhance epithelial healing in the case of severe mucosal damage.The preliminary results of the current studies are promising,but more clinical investigations are needed to develop new and safe therapeutic strategies for diseases of the colon. | Ferenc Sipos Orsolya Galamb | 2012 | World Journal of Gastroenterology2012，18，7： | 13 |
| 8 | 荧光假单胞菌ZX对采后锦橙绿霉病的防治及其抑菌机制显示文摘【目的】采后柑橘极易受指状青霉(Penicillium digitatum)侵染而发生严重的绿霉病腐烂,生物防治因具有安全、有效、环保等特点近年来备受关注。论文旨在研究荧光假单胞菌(Pseudomonas fluorescens)ZX对采后柑橘绿霉病的防治效果,揭示P.fluorescensZX对P.digitatum可能存在的作用机制。【方法】以'北碚447'锦橙果实为试材,先分别接种20μL拮抗菌培养液、滤液(培养液离心后,上清经0.22μm滤膜过滤)、菌悬液(培养液离心后,菌体用无菌水反复洗涤并用无菌水重悬)和热杀死液(培养液高温高压灭菌),2 h后接种20μL P. digitatum孢子悬浮液(1×10~4spores/m L),所有果实于20oC、90%相对湿度环境下恒温恒湿培养8 d后,测定果实的发病率和病斑直径;制备柑橘皮培养基,进行平板抑菌试验,探索P. fluorescens ZX对P. digitatum孢子发芽情况的影响;采用两板对扣法和生物熏蒸法研究P.fluorescensZX挥发性次级代谢产物的抑菌作用;利用插入式细胞培养皿等分析P.fluorescensZX和P.digitatum之间竞争的营养物质;同时,测定P.fluorescensZX的生长曲线,利用结晶紫染色法评估P. fluorescens ZX的生物膜形成能力。【结果】P. fluorescens ZX不同处理液之间对采后锦橙绿霉病的作用效果差异显著,菌悬液抑菌效果最好,经菌悬液处理的果实,发病率和病斑直径分别仅为40.83%和1.78 cm;不论是在柑橘皮固体培养基上对峙培养还是在液体培养基中混合培养,菌悬液和原液的作用效果较好,固体平板上,相对抑制率达到了35%–45%,液体培养基中,P. digitatum孢子12 h后的发芽率不超过27%;P. fluorescens ZX产生的挥发性物质具有抑菌作用,经P. fluorescensZX熏蒸处理的锦橙果实,发病率和病斑直径都显著降低;营养竞争试验结果表明,P. fluorescens ZX能更快速有效地消耗柑橘皮培养基中的营养,并和P. digitatum竞争葡萄糖、果糖、蔗糖、天冬氨酸、苏氨酸、丝氨酸、亮氨酸、精氨酸和脯氨酸等营养物质;同时,P. fluorescens ZX生命力强,培养4 h后即进入对数生长期,约24 h后形成成熟的生物膜。【结论】P. fluorescens ZX可能通过抑制P. digitatum孢子发芽、营养与空间竞争、形成生物膜、产生抑菌物质等方式抑制P.digitatum的生长繁殖,有效防治采后锦橙绿霉病。 | 王智荣 梅小飞 杜木英 江孟遥 张洪新 汪开拓 Zsolt Zalán Ferenc Hegyi 阚建全 | 2019 | 微生物学报2019，59，5： | 12 |
| 9 | A concept for multiterawatt fibre lasers based on coherent pulse stacking in passive cavities显示文摘Since the advent of femtosecond lasers,performance improvements have constantly impacted on existing applications and enabled novel applications.However,one performance feature bearing the potential of a quantum leap for high-field applications is still not available:the simultaneous emission of extremely high peak and average powers.Emerging applications such as laser particle acceleration require exactly this performance regime and,therefore,challenge laser technology at large.On the one hand,canonical bulk systems can provide pulse peak powers in the multi-terawatt to petawatt range,while on the other hand,advanced solid-state-laser concepts such as the thin disk,slab or fibre are well known for their high efficiency and their ability to emit high average powers in the kilowatt range with excellent beam quality.In this contribution,a compact laser system capable of simultaneously providing high peak and average powers with high wall-plug efficiency is proposed and analysed.The concept is based on the temporal coherent combination(pulse stacking)of a pulse train emitted from a high-repetition-rate femtosecond laser system in a passive enhancement cavity.Thus,the pulse energy is increased at the cost of the repetition rate while almost preserving the average power.The concept relies on a fast switching element for dumping the enhanced pulse out of the cavity.The switch constitutes the key challenge of our proposal.Addressing this challenge could,for the first time,allow the highly efficient dumping of joule-class pulses at megawatt average power levels and lead to unprecedented laser parameters. | Sven Breitkopf Tino Eidam Arno Klenke Lorenz von Grafenstein Henning Carstens Simon Holzberger Ernst Fill Thomas Schreiber Ferenc Krausz Andreas Tunnermann Ioachim Pupeza Jens Limpert | 2014 | Light(Science & Applications)2014，3，1： | 11 |
| 10 | 纳米晶铁钴基软磁材料的研究显示文摘铁钴基纳米晶软磁性材料具有高居里温度的非晶纳米晶两相结构,通过两相结构的匹配完成纳米晶粒间的磁矩交换耦合,使得材料在高温环境下具备优异的软磁性能。通过采用 VSM、TEM、XRD 等技术对材料软磁性能、组织结构以及软磁性能的热稳定性的研究与分析,优化了 FeCoHfBCu 合金成分。试验表明(Fe0.6Co0.4)86Hf7B6Cu1合金在500~600 ℃的工作温度区间范围内具备最佳的饱和磁化强度和较低矫顽力,并且 550 ℃条件下具有优异的软磁性能热稳定性。该材料是高温软磁应用领域的重要候选材料。 | Tadeusz Kulik(波) 梁秀兵 Jaro■saw Ferenc(波) 徐滨士 | 2004 | 中国表面工程2004，17，5： | 10 |
| 11 | Hepatic encephalopathy—Definition, nomenclature, diagnosis, and quantification: Final report of the Working Party at the 11th World Congresses of Gastroenterology, Vienna, 1998显示文摘 | Peter Ferenci Alan Lockwood Kevin Mullen Ralph Tarter Karin Weissenborn Andres T. Blei | 2002 | Hepatology2002，，3： | 10 |
| 12 | Relation of the IGF/IGF1R system to autophagy in colitis and colorectal cancer显示文摘Metabolic syndrome(Met S), as a chronic inflammatory disorder has a potential role in the development of inflammatory and cancerous complications of the colonic tissue. The interaction of DNA damage and inflammation is affected by the insulin-like growth factor 1 receptor(IGF1 R) signaling pathway. The IGF1 R pathway has been reported to regulate autophagy, as well, but sometimes through a bidirectional context. Targeting the IGF1 R-autophagy crosstalk could represent a promising strategy for the development of new antiinflammatory and anticancer therapies, and may help for subjects suffering from Met S who are at increased risk of colorectal cancer. However, therapeutic responses to targeted therapies are often shortlived, since a signaling crosstalk of IGF1 R with other receptor tyrosine kinases or autophagy exists, leading to acquired cellular resistance to therapy. From a pharmacological point of view, it is attractive to speculate that synergistic benefits could be achieved by inhibition of one of the key effectors of the IGF1 R pathway, in parallel with the pharmacological stimulation of the autophagy machinery, but cautiousness is also required, because pharmacologic IGF1 R modulation can initiate additional, sometimes unfavorable biologic effects. | Ferenc Sipos Hajnal Székely Imre Dániel Kis Zsolt Tulassay Gyorgyi Muzes | 2017 | World Journal of Gastroenterology2017，23，46： | 9 |
| 13 | Therapeutic aspects of c-MYC signaling in inflammatory and cancerous colonic diseases显示文摘Colonic inflammation is required to heal infections, wounds, and maintain tissue homeostasis. As the seventh hallmark of cancer, however, it may affect all phases of tumor development, including tumor initiation, promotion, invasion and metastatic dissemination, and also evasion immune surveillance. Inflammation acts as a cellular stressor and may trigger DNA damage or genetic instability, and, further, chronic inflammation can provoke genetic mutations and epigenetic mechanisms that promote malignant cell transformation. Both sporadical and colitis-associated colorectal carcinogenesis are multi-step, complex processes arising from the uncontrolled proliferation and spreading of malignantly transformed cell clones with the obvious ability to evade the host's protective immunity. In cells upon DNA damage several protooncogenes, including c-MYC are activated in parelell with the inactivation of tumor suppressor genes. The target genes of the c-MYC protein participate in different cellular functions, including cell cycle, survival, protein synthesis, cell adhesion, and microRNA expression. The transcriptional program regulated by c-MYC is context dependent, therefore the final cellular response to elevated c-MYC levels may range from increased proliferation to augmented apoptosis. Considering physiological intestinal homeostasis, c-MYC displays a fundamental role in the regulation of cell proliferation and crypt cell number. However, c-MYC gene is frequently deregulated in inflammation, and overexpressed in both sporadic and colitis-associated colon adenocarcinomas. Recent results demonstrated that endogenous c-MYC is essential for efficient induction of p53-dependent apoptosis following DNA damage, but c-MYC function is also involved in and regulated by autophagy-related mechanisms, while its expression is affected by DNA-methylation, or histone acetylation. Molecules directly targeting c-MYC, or agents acting on other genes involved in the c-MYC pathway could be selected for combined regiments. However, due to its context-dependent cellular function, it is clinically essential to consider which cytotoxic drugs are used in combination with c-MYC targeted agents in various tissues. Increasing our knowledge about MYCdependent pathways might provide direction to novel anti-inflammatory and colorectal cancer therapies. | Ferenc Sipos Gábor Firneisz Györgyi Mũzes | 2016 | World Journal of Gastroenterology2016，22，35： | 9 |
| 14 | Contribution of TLR signaling to the pathogenesis of colitisassociated cancer in inflammatory bowel disease显示文摘In the intestine a balance between proinflammatory and repair signals of the immune system is essential for the maintenance of intestinal homeostasis. The innate immunity ensures a primary host response to microbial invasion, which induces an inflammatory process to localize the infection and prevent systemic dissemination of pathogens. The key elements of this process are the germline encoded pattern recognition receptors inclu-ding Toll-like receptors(TLRs). If pathogens cannot be eliminated, they may elicit chronic inflammation, which may be partly mediated via TLRs. Additionally, chronic inflammation has long been suggested to trigger tissue tumorous transformation. Inflammation, the seventh hallmark of cancer, may affect all phases of tumor development, and evade the immune system. Inflammation acts as a cellular stressor and may trigger DNA damage or genetic instability. Furthermore, chronic inflammation can provoke genetic mutations and epigenetic mechanisms that promote malignant cell transformation. Colorectal cancers in inflammatory bowel disease patients are considered typical examples of inflammation-related cancers. Although data regarding the role of TLRs in the pathomechanism of cancer-as-sociated colitis are rather conflicting, functionally these molecules can be classified as 'largely antitumorigenic' and 'largely pro-tumorigenic' with the caveat that the underlying signaling pathways are mainly context(i.e., organ-, tissue-, cell-) and ligand-dependent. | Ferenc Sipos István Fri Miklós Constantinovits Zsolt Tulassay Gyrgyi Mzes | 2014 | World Journal of Gastroenterology2014，20，36： | 9 |
| 15 | The Epithelial-Mesenchymal Transition Generates Cells with Properties of Stem Cells显示文摘 | Sendurai A. Mani Wenjun Guo Mai-Jing Liao Elinor Ng. Eaton Ayyakkannu Ayyanan Alicia Y. Zhou Mary Brooks Ferenc Reinhard Cheng Cheng Zhang Michail Shipitsin Lauren L. Campbell Kornelia Polyak Cathrin Brisken Jing Yang Robert A. Weinberg | 2008 | Cell2008，，4： | 7 |
| 16 | Regulatory T cells in inflammatory bowel diseases and colorectal cancer显示文摘Regulatory T cells(T regs) are key elements in immunological self-tolerance.The number of T regs may alter in both peripheral blood and in colonic mucosa during pathological circumstances.The local cellular,microbiological and cytokine milieu affect immunophenotype and function of T regs.Forkhead box P3+ T regs function shows altered properties in inflammatory bowel diseases(IBDs).This alteration of T regs function can furthermore be observed between Crohn's disease and ulcerative colitis,which may have both clinical and therapeutical consequences.Chronic mucosal inflammation may also influence T regs function,which together with the intestinal bacterial flora seem to have a supporting role in colitis-associated colorectal carcinogenesis.T regs have a crucial role in the immunoevasion of cancer cells in sporadic colorectal cancer.Furthermore,their number and phenotype correlate closely with the clinical outcome of the disease,even if their contribution to carcinogenesis has previously been controversial.Despite knowledge of the clinical relationship between IBD and colitis-associated colon cancer,and the growing number of immunological aspects encompassing sporadic colorectal carcinogenesis,the molecular and cellular links amongst T regs,regulation of the inflammation,and cancer development are still not well understood.In this paper,we aimed to review the current data surrounding the role of T regs in the pathogenesis of IBD,colitis-associated colon cancer and sporadic colorectal cancer. | Gyrgyi Mzes Béla Molnár Ferenc Sipos | 2012 | World Journal of Gastroenterology2012，18，40： | 7 |
| 17 | 荧光假单胞菌ZX对葡萄采后灰霉病的防治显示文摘研究荧光假单胞菌(Pseudomonas fluorescens)ZX对葡萄采后灰霉病的防治效果。以“巨峰”葡萄为试材,测定P.fluorescens ZX的控病效果和生长动态,在离体条件下通过孢子萌发观察、挥发性物质抑菌测试、扫描电镜探究其对灰葡萄孢霉(Botrytis cinerea)的防治。结果表明,使用P.fluorescens ZX处理,葡萄果实的发病率仅为24.8%,明显低于对照组(发病率64.67%),病斑直径最小,可以明显抑制B.cinerea孢子萌发、芽管伸长。P.fluorescens ZX产生的挥发性物质具有较强的抑菌效果,并且能对B.cinerea有重寄生作用,破坏菌丝的正常形态。另外,无论是浸泡还是接种处理,P.fluorescens ZX都能在葡萄果实上快速地定殖生长。由此表明,P.fluorescens ZX通过抑制B.cinerea生长来控制葡萄采后灰霉病,为果实采后防腐保鲜提供一种新的选择。 | 魏雪 江孟遥 钟涛 张曼 王智荣 ZSOLT Zalan FERENC Hegyi KRISZTINA Takacs 杜木英 | 2021 | 食品工业科技2021，42，22： | 6 |
| 18 | Interplay of autophagy and innate immunity in Crohn's disease: A key immunobiologic feature显示文摘Crohn's disease representing a clinical phenotype of inflammatory bowel disease is a polygenic immune disorder with complex multifactor etiology. Recent genome-wide association studies of susceptibility loci have highlighted on the importance of the autophagy pathway, which previously had not been implicated in disease pathology. Autophagy represents an evolutionarily highly conserved multi-step process of cellular self-digestion due to sequestration of excessive, damaged, or aged proteins and intracellular organelles in double-membranous vesicles of autophagosomes, terminally self-digested in lysosomes. Autophagy is deeply involved in regulation of cell development and differentiation, survival and senescence, and it also fundamentally affects the inflammatory pathways, as well as the innate and adaptive arms of immune responses. Autophagy is mainly activated due to sensors of the innate immunity, i.e., by pattern recognition receptor signaling. The interplay of genes regulating immune functions is strongly influenced by the environment, especially gut resident microbiota. The basic challenge for intestinal immune recognition is the requirement of a simultaneous delicate balance between tolerance and responsiveness towards microbes. On the basis of autophagy-related risk genetic polymorphisms (ATG16L1, IRGM , NOD2 , XBP1 ) impaired sensing and handling of intracellular bacteria by innate immunity, closely interrelated with the autophagic and unfolded protein pathways seem to be the most relevant immunobiologic events. Autophagy is now widely considered as a key regulator mechanism with the capacity to integrate several aspects of Crohn's disease pathogenesis. In this review, recent advances in the exciting crosstalk of susceptibility coding variants-related autophagy and innate immunity are discussed. | Gyrgyi Müzes Zsolt Tulassay Ferenc Sipos | 2013 | World Journal of Gastroenterology2013，19，28： | 6 |
| 19 | 不同非酿酒酵母与酿酒酵母混合发酵对脆红李酒品质的影响显示文摘分别采用热带假丝酵母(Candida tropicalis)、东方伊萨酵母(Issatchenkio orientalis)、美极梅奇酵母(Metschnikowia pulcherrima)、葡萄汁有孢汉逊酵母(Hanseniaspora uvarum)与商业酿酒酵母(Saccharomyces cerevisiae)D254混合发酵脆红李酒,比较其在发酵速率、理化指标、有机酸和挥发性成分的差异,并进行感官评价分析,以期为提升脆红李酒品质提供依据。结果表明,与S.cerevisiae单独发酵(10 d)相比,混合发酵延缓了发酵进程(12~13 d)。不同脆红李酒的理化指标均符合国标,混合发酵后酒样中苹果酸、乳酸和乙酸含量显著降低(P<0.05),有利于果酒风味平衡协调。香气成分结合主成分分析表明,Mp-Sc混合发酵香气组分优于其他酒样,其中辛酸乙酯、癸酸乙酯、月桂酸乙酯、芳樟醇显著提高且香气活度值>1,能够增强酒体果香、花香。感官评价结果也表明Mp-Sc混合发酵的果香味和花香味较为浓郁。综上,Mp-Sc混合发酵更适合应用于脆红李酒酿造,有利于增加香气复杂性,提升品质。 | 张曼 钟涛 魏雪 阚建全 武运 FERENC Hegyi 杜木英 | 2021 | 食品与发酵工业2021，47，12： | 6 |
| 20 | Gut barrier failure biomarkers are associated with poor disease outcome in patients with primary sclerosing cholangitis显示文摘AIM To assess the prevalence of a panel of serologic markers that reflect gut barrier dysfunction in a mixed cohort of pediatric and adult primary sclerosing cholangitis(PSC) patients.METHODS Sera of 67 PSC patients [median age(range): 32(5-79) years, concomitant IBD: 67% and cirrhosis: 20%] were assayed for the presence of antibodies against to F-actin(AAA Ig A/Ig G) and gliadin(AGA Ig A/Ig G)] and for serum level of intestinal fatty acid-binding protein(I-FABP) by ELISA. Markers of lipopolysaccharide(LPS) exposure [LPS binding protein(LBP)] and various antimicrobial antibodies [anti-OMP Plus Ig A and endotoxin core Ig A antibody(Endo CAb)] were also determined. Poor disease outcome was defined as orthotopic liver transplantation and/or liver-related death during the follow-up [median: 99(14-106) mo]. One hundred and fifty-three healthy subjects(HCONT) and 172 ulcerative colitis(UC) patients were the controls. RESULTS A total of 28.4%, 28.0%, 9% and 20.9% of PSC patients were positive for AAA Ig A, AAA Ig G, AGA Ig A and AGA Ig G, respectively. Frequencies of AAA Ig A and AAA Ig G(P < 0.001, for both) and AGA Ig G(P = 0.01, for both) but not AGA Ig A were significantly higher compared to both of the HCONT and the UC groups. In survival analysis, AAA Ig A-positivity was revealed as an independent predictor of poor disease outcome after adjusting either for the presence of cirrhosis [HR = 5.15(1.27-20.86), P = 0.022 or for the Mayo risk score(HR = 4.24(0.99-18.21), P = 0.052]. AAA Ig A-positivity was significantly associated with higher frequency of antimicrobial antibodies(P < 0.001 for Endo Cab Ig A and P = 0.012 for anti-OMP Plus Ig A) and higher level of the enterocyte damage marker(median I-FABP_(AAA Ig A pos vs neg): 365 vs 166 pg/m L, P = 0.011), but not with serum LBP level. CONCLUSION Presence of Ig A type AAA identified PSC patients with progressive disease. Moreover, it is associated with enhanced mucosal immune response to various microbial antigens and enterocyte damage further highlighting the importance of the gut-liver interaction in PSC. | Tamas Tornai Eszter Palyu Zsuzsanna Vitalis Istvan Tornai David Tornai Peter Antal-Szalmas Gary L Norman Zakera Shums Gabor Veres Antal Dezsofi Gabriella Par Alajos Par Peter Orosz Ferenc Szalay Peter Laszlo Lakatos Maria Papp | 2017 | World Journal of Gastroenterology2017，23，29： | 5 |
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