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| 1 | Alcoholic liver disease and the gut-liver axis显示文摘Alcoholic liver disease (ALD) is one of the leading causes of liver diseases and liver-related death worldwide. Of the many factors that contribute to the pathogenesis of ALD, gut-derived lipopolysaccharide (LPS) plays a central role in induction of steatosis, inflammation, and fi brosis in the liver. In this review, we discuss the mechanisms by which alcohol contributes to increased gut permeability, the activation of Kupffer cells, and the infl ammatory cascade by LPS. The role of the Toll-like receptor 4 (TLR4) complex in LPS recognition and the importance of the TLR4-induced signaling pathways are evaluated in ALD. | Gyongyi Szabo Shashi Bala | 2010 | World Journal of Gastroenterology2010，16，11： | 50 |
| 2 | Emerging role of microRNAs in liver diseases显示文摘MicroRNAs are a class of small non-coding RNAs that are found in plants, animals, and some viruses. They modulate the gene function at the post-transcriptional level and act as a fine tuner of various processes, such as development, proliferation, cell signaling, and apopto-sis. They are associated with different types and stages of cancer. Recent studies have shown the involvement of microRNAs in liver diseases caused by various factors, such as Hepatitis C, Hepatitis B, metabolic disorders, and by drug abuse. This review highlights the role of microRNAs in liver diseases and their potential use as therapeutic molecules. | Shashi Bala Miguel Marcos Gyongyi Szabo | 2009 | World Journal of Gastroenterology2009，15，45： | 25 |
| 3 | Genetic update on inflammatory factors in ulcerative colitis: Review of the current literature显示文摘Ulcerative colitis(UC) is one of the main types of inflammatory bowel disease, which is caused by dysregulated immune responses in genetically predisposed individuals. Several genetic factors, including interleukin and interleukin receptor gene polymorphisms and other inflammation-related genes play central role in mediating and modulating the inflammation in the human body, thereby these can be the main cause of development of the disease. It is clear these data are very important for understanding the base of the disease, especially in terms of clinical utility and validity, but summarized literature is exiguous for challenge health specialist that can used in the clinical practice nowadays. This review summarizes the current literature on inflammationrelated genetic polymorphisms which are associated with UC. We performed an electronic search of Pubmed Database among publications of the last 10 years, using the following medical subject heading terms: UC, ulcerative colitis, inflammation, genes, polymorphisms, and susceptibility. | Patricia Sarlos Erzsebet Kovesdi Lili Magyari Zsolt Banfai Andras Szabo Andras Javorhazy Bela Melegh | 2014 | World Journal of Gastrointestinal Pathophysiology2014，5，3： | 15 |
| 4 | Lipopolysaccharide induces and activates the Nalp3 inflammasome in the liver显示文摘AIM:To examine the activation of the Nalp3 inflammasome and its downstream targets following lipopolysaccharide(LPS) -induced stimulation in the liver. METHODS:Six-to-eight-week-old C57BL/6 chow fed mice were injected intraperitoneally with 0.5μg/g bodyweight LPS and sacrificed 2,4,6,18 or 24 h later. LPS-induced liver damage was confirmed by a biochemical assay to detect alanine aminotransferase(ALT) levels.To determine if LPS stimulation in the liver led to activation of the inflammasome,real-time quantitative polymerase chain reaction was used to evaluate the mRNA expression of components of the Nalp3 inflammasome.Enzyme-linked immunosorbent assays were used to determine the protein expression levels of several downstream targets of the Nalp3 inflammasome,including caspase-1 and two cytokine targets of caspase-1,interleukin(IL) -1βand IL-18. RESULTS:We found that LPS injection resulted in liver damage as indicated by elevated ALT levels.This was associated with a significant increase in both mRNA and protein levels of the proinflammatory cy-tokine tumor necrosis factor(TNF) -αin the liver,as well as increased levels of TNFs in serum.We showed that LPS stimulation led to upregulation of mRNA levels in the liver for all the receptor components of the inflammasome,including Nalp3,Nalp1,pannexin-1 and the adaptor molecule apoptosis-associated specklike,caspase recruitment domain-domain containing protein.We also found increased levels of mRNA and protein for caspase-1,a downstream target of the inflammasome.In addition,LPS challenge led to increased levels of both mRNA and protein in the liver for two cytokine targets of caspase-1,IL-1βand IL-18. Interestingly,substantial baseline expression of pre-IL1βand pre-IL-18 was found in the liver.Inflammasome and caspase-1 activation was indicated by the significant increase in the active forms of IL-1βand IL-18 after LPS stimulation. CONCLUSION:Our results show that the Nalp3 inflammasome is upregulated and activated in the liver in response to LPS stimulation. | Michal Ganz Timea Csak Bharath Nath Gyongyi Szabo | 2011 | World Journal of Gastroenterology2011，17，43： | 14 |
| 5 | Immunopathobiology and therapeutic targets related to cytokines in liver diseases显示文摘Chronic liver injury with any etiology can progress to fibrosis and the end-stage diseases cirrhosis and hepatocellular carcinoma.The progression of liver disease is controlled by a variety of factors,including liver injury,inflammatory cells,inflammatory mediators,cytokines,and the gut microbiome.In the current review,we discuss recent data on a large number of cytokines that play important roles in regulating liver injury,inflammation,fibrosis,and regeneration,with a focus on interferons and T helper(Th)1,Th2,Th9,Th17,interleukin(IL)-1 family,IL-6 family,and IL-20 family cytokines.Hepatocytes can also produce certain cytokines(such as IL-7,IL-11;and IL-33),and the functions of these cytokines in the liver are briefly summarized.Several cytokines have great therapeutic potential,and some are currently being tested as therapeutic targets in clinical trials for the treatment of liver diseases,which are also described. | Yong He Seonghwan Hwang Yeni Ait Ahmed Dechun Feng Na Li Marcelle Ribeiro Fouad Lafdil Tatiana Kisseleva Gyongyi Szabo Bin Gao | 2021 | Cellular & Molecular Immunology2021，18，1： | 14 |
| 6 | In vitro and in vivo models of acute alcohol exposure显示文摘Alcohol abuse is a global problem due to the financial burden on society and the healthcare system. While the harmful health effects of chronic alcohol abuse are well established, more recent data suggest that acute alcohol consumption also affects human wellbeing. Thus, there is a need for research models in order to fully understand the effect of acute alcohol abuse on different body systems and organs. The present manuscript summarizes the interdisciplinary advantages and disadvantages of currently available human and non-human models of acute alcohol abuse, and identifi es their suitability for biomedical research. | Angela Dolganiuc Gyongyi Szabo | 2009 | World Journal of Gastroenterology2009，15，10： | 9 |
| 7 | High fat diet feeding results in gender specific steatohepatitis and inflammasome activation显示文摘AIM:To develop an animal model that encompasses the different facets of non-alcoholic steatohepatitis(NASH),which has been a challenge.METHODS:In this study,we used a high fat diet(HFD)feeding supplemented with fructose and sucrose in the water mimicking the high-fructose corn syrup that is abundant in the diet in the United States.We used C57Bl/6 wild-type mice for short and long-term feedings of 6 and 16 wk respectively,and evaluated the extent of liver damage,steatosis,and inflammasome activation.Our methods included histopathological analysis to assess liver damage and steatosis,which involved H and E and oil-red-o staining;biochemical studies to look at ALT and triglyceride levels;RNA analysis using quantitative polymerase chain reaction;and cytokine analysis,which included the enzyme-linked immunosorbent assay method to look at interleukin(IL)-1βand tumor necrosis factor-α(TNFα)levels.Furthermore,at each length of feeding we also looked at insulin resistance and glucose tolerance using insulin tolerance tests(ITT)and glucose tolerance tests.RESULTS:There was no insulin resistance,steatosis,or inflammasome activation at 6 wk.In contrast,at16 wk we found significant insulin resistance demonstrated by impaired glucose and ITT in male,but not female mice.In males,elevated alanine aminotransferase and triglyceride levels,indicated liver damage and steatosis,respectively.Increased liver TNFαand monocyte chemoattractant protein-1 mRNA and protein,correlated with steatohepatitis.The inflammasome components,adaptor molecule,Aim2,and NOD-like receptor 4,increased at the mRNA level,and functional inflammasome activation was indicated by increased caspase-1 activity and IL-1βprotein levels in male mice fed a long-term HFD.Male mice on HFD had increasedα-smooth muscle actin and pro-collagen-1 mRNA indicating evolving fibrosis.In contrast,female mice displayed only elevated triglyceride levels,steatosis,and no fibrosis.CONCLUSION:Our data indicate gender differences in NASH.Male mice fed a long-term HFD display steatohepatitis and inflammasome activation,whereas female mice have steatosis without inflammation. | Michal Ganz Timea Csak Gyongyi Szabo | 2014 | World Journal of Gastroenterology2014，20，26： | 8 |
| 8 | Microwave Plasma Sintering of Nanocrystalline Alumina显示文摘Sintering of nanocrystalline alumina by microwave plasma has been studied. The relative density,microhardness of the samples with different grain sizes by microwave plasma and other sintering techniques have been | Peng, Jinhui Hong, Pinjie Dai, Shushan Vollath, D. Szabo, D.V. | 1998 | Journal of Materials Science & Technology1998，14，2： | 8 |
| 9 | Enhanced Photocatalytic Activity of TiO2 Nanofibers and Their Flexible Composite Films: Decomposition of Organic Dyes and Efficient H2 Generation from Ethanol-Water Mixtures显示文摘与磅和 Pd nanoparticles 装饰的 TiO2 nanofibers 在各种各样的 photocatalytic 过程被综合了并且学习。在水里的器官的染料的分解的优秀 photocatalytic 行为,灵活独立纤维素 / 催化剂的表面上的器官的污点的降级合成电影并且在从乙醇用的氢的产生推迟了并且使不能调动催化剂被表明。基于 nanofiber 的 TiO2 材料的表演是在某情况 outperformstheir 的竞争 withand 常规基于 nanoparticle 的对应物。在所有情况中,装饰 Pd 的 TiO2 nanoparticles 和 nanofibers 证明了比他们的基于磅的对应物更有效,它能在在 TiO2 和金属 nanoparticles 之间的接触根据缩放 nano 的 Schottky 接口的形成被解释。形成纤维素 / 催化剂 composites 的可行性提供在大区域的涂层和独立电影利用光催化剂材料的一个新奇方法。 | Ming-Chung Wu Andras Sapi Anna Avila Maria Szabo Jussi Hiltunen Mika Huuhtanen Geza Toth Akos Kukovecz Zoltan Konya Riitta Keiski Wei-Fang Su Heli Jantunen Krisztian Kordas | 2011 | Nano Research2011，4，4： | 7 |
| 10 | 细支气管肺泡癌^18F—FDG PET/CT显像的代谢和形态特征显示文摘目的分析细支气管肺泡癌(BAC)在^18F-脱氧葡萄糖(FDG)PET/CT图像中的代谢和形态结构特征,并与非细支气管肺泡型腺癌(non—BAC AC)的显像结果进行比较,探讨PET/CT在BAC诊断及鉴别诊断中的价值。方法回顾性分析经病理检查确诊的32例BAC及55例non—BAC AC的FDG PET/CT显像资料。测量病灶最大标准摄取值(SUVmax),分析病灶位置、形态及边界、密度分布及其他典型CT结构征象。统计分析比较2组的平均SUVmax,评价与肿瘤分型有关的CT征象,比较单独PET、CT及PET和CT联合诊断的准确性。采用SPSS12.0软件对数据行t检验、McNemar检验、Fisher精确检验等。结果BAC组共47个病灶,non—BACAC组共63个病灶,组间SUVmax差异有统计学意义(1.51±0.17与6.28±3.04,t=-10.374,P〈0.0001)。BAC组纯磨玻璃密度影(45%的病灶,21/47)是相关的CT征象(Fisher精确检验,P〈0.0001)。结合PET代谢和CT解剖结构特征的联合诊断准确性与单独PET或CT对比,差异均有统计学意义(P=0.001和0.039),诊断准确性分别为88%(28/32)、47%(15/32)和66%(21/32)。结论理解FDG PET/CT显像中BAC的代谢和形态结构特征,有利于提高诊断准确性。如动态观察中呈持续的CT磨玻璃密度影,即使低FDG摄取,也要考虑BAC可能。 | 高永举 Zsolt Szabo | 2009 | 中华核医学杂志2009，29，4： | 7 |
| 11 | Distinct toll-like receptor expression in monocytes and T cells in chronic HCV infection显示文摘瞄准:丙肝病毒经常建立长期的感染。最近的研究建议病毒、细菌的感染在与控制相比的感染 HCV 的病人是更普通的。病原体被像使用费的受体(TLR ) 认出塑造适应、天生的有免疫力的回答。方法:在这研究,估计感染 HCV 的主人的能力认识到入侵病原体,我们调查了像使用费的受体表示在天生(单核白血球) 并且适应(T 房间) 由即时 PCR 的有免疫力的房间。结果:我们决定 RNA 为 TLR 铺平 2, 6。7, 8, 9 和 10 个 mRNA 层次起来与控制相比在感染 HCV 的病人在单核白血球和 T 房间调整了。TLR4 在 T 淋巴细胞在仅仅上面被调整,当 TLR5 有选择地在感染 HCV 的病人的单核白血球被增加时。MD-2, TLR4 合作受体,当 CD14 和 MyD88 仅仅在单核白血球被增加时,在病人的单核白血球和 T 房间被增加。结论:我们的数据在多半在感染 HCV 的个人联系到病原体和有免疫力的防卫的天生的识别的 TLR 表示上披露新奇详情。 | Angela Dolganiuc Catherine Garcia Karen Kodys Gyongyi Szabo | 2006 | World Journal of Gastroenterology2006，12，8： | 7 |
| 12 | Plasma microRNA profiles distinguish lethal injury in acetaminophen toxicity: A research study显示文摘AIM: To investigate plasma microRNA (miRNA) profiles indicative of hepatotoxicity in the setting of lethal acetaminophen (APAP) toxicity in mice. METHODS: Using plasma from APAP poisoned mice, either lethally (500 mg/kg) or sublethally (150 mg/kg) dosed, we screened commercially available murine microRNA libraries (SABiosciences, Qiagen Sciences, MD) to evaluate for unique miRNA profiles between these two dosing parameters. RESULTS: We distinguished numerous, unique plasma miRNAs both up- and downregulated in lethally compared to sublethally dosed mice. Of note, many of the greatest up- and downregulated miRNAs, namely 574-5p, 466g, 466f-3p, 375, 29c, and 148a, have been shown to be associated with asthma in prior studies. Interestingly, a relationship between APAP and asthma has been previously well described in the literature, with an as yet unknown mechanism of pathology. There was a statistically significant increase in alanine aminotransferase levels in the lethal compared to sublethal APAP dosing groups at the 12 h time point (P < 0.001). There was 90% mortality in the lethally compared to sublethally dosed mice at the 48 h time point (P = 0.011). CONCLUSION: We identified unique plasma miRNAs both up- and downregulated in APAP poisoning which are correlated to asthma development. | Jeanine Ward Shashi Bala Jan Petrasek Gyongyi Szabo | 2012 | World Journal of Gastroenterology2012，18，22： | 6 |
| 13 | Protein and non-protein sulfhydryls and disulfides in gastric mucosa and liver after gastrotoxic chemicals and sucralfate: Possible new targets of pharmacologic agents显示文摘瞄准:在化学上导致的胃的出血性的粘膜损害(HML ) 和 sucralfate 的胃的保护的效果的机制调查主要非蛋白质和蛋白质 sulfhydryls 和二硫化物的角色。方法:老鼠 intragastrically 被给 75% 乙醇, 25% NaCl, 0.6 mol/L HCl, 0.2 mol/L NaOH 或 1% 氨溶液的 1 mL (i.g ) 并且牺牲了 1, 3, 6 或 12 min 以后。全部(减少并且氧化) 谷胱甘肽(GSH + GSSG ) ,谷胱甘肽二硫化物(GSSG ) ,蛋白质免费 sulfhydryls (PSH ) ,蛋白质谷胱甘肽混合了二硫化物(PSSG ) ,蛋白质胱氨酸二硫化物(PSSP ) 在胃粘膜和肝被测量。结果:当氧化谷胱甘肽(GSSG ) 集中增加了时,减少的谷胱甘肽(GSH ) 在乙醇, HCl 或 NaCl 暴露以后在胃粘膜被弄空,除了由 HCl 和 NaOH 暴露。在到乙醇的暴露以后的 PSH 的减少的层次被观察, NaCl 或 NaOH 当全部的蛋白质二硫化物被增加时。比率归结为氧化谷胱甘肽或到二硫化物的 sulfhydrils 被所有化学药品减少。在 i.g 缩写第一次应该这里被拼出以后,在巯基动态平衡的变化都没在肝被检测乙醇的管理。Sucralfate 增加了 GSH 和 PSH 的集中并且在胃的粘膜巯基集中阻止了导致乙醇的变化。结论:我们的修改方法现在在胃粘膜或肝对主要蛋白质和非蛋白质 thiols/disulfides 的直接大小合适。在化学上导致的 HML 的致病并且在胃的保护的药的机制的一个普通元素似乎是象蛋白质 sulfhydryls 和二硫化物一样的减少并且氧化的谷胱甘肽的减少的比率。 | Lajos Nagy Miki Nagata Sandor Szabo | 2007 | World Journal of Gastroenterology2007，13，14： | 6 |
| 14 | Gut–Liver Axis in Alcoholic Liver Disease显示文摘 | Gyongyi Szabo | 2014 | Gastroenterology2014，，： | 5 |
| 15 | Inflammasomes in liver diseases显示文摘 | Gyongyi Szabo Timea Csak | 2012 | Journal of Hepatology2012，，3： | 5 |
| 16 | Finding a fairy in the forest: ELF4, a novel and critica element of type I interferon responses显示文摘 | Attila Szabo Eva Rajnavolgyi | 2014 | Cellular & Molecular Immunology2014，11，3： | 5 |
| 17 | IL-1 receptor antagonist ameliorates inflammasome-dependent alcoholic steatohepatitis in mice显示文摘 | Petrasek Jan Bala Shashi Csak Timea Lippai Dora Kodys Karen Menashy Victoria Barrieau Matthew Min So-Yun Kurt-Jones Evelyn A Szabo Gyongyi | 2012 | EN2012，，10： | 4 |
| 18 | Proton pump inhibitors increase the severity of hepatic encephalopathy in cirrhotic patients显示文摘BACKGROUND Liver cirrhosis is the late stage of hepatic fibrosis and is characterized by portal hypertension that can clinically lead to decompensation in the form of ascites,esophageal/gastric varices or encephalopathy.The most common sequelae associated with liver cirrhosis are neurologic and neuropsychiatric impairments labeled as hepatic encephalopathy(HE).Well established triggers for HE include infection,gastrointestinal bleeding,constipation,and medications.Alterations to the gut microbiome is one of the leading ammonia producers in the body,and therefore may make patients more susceptible to HE.AIM To investigate the relationship between the use of proton pump inhibitors(PPIs)and HE in patients with cirrhosis.METHODS This is a single center,retrospective analysis.Patients were included in the study with an admitting diagnosis of HE.The degree of HE was determined from subjective and objective portions of hospital admission notes using the West Haven Criteria.The primary outcome of the study was to evaluate the grade of HE in PPI users versus non-users at admission to the hospital and throughout their hospital course.Secondary outcomes included rate of infection,gastrointestinal bleeding within the last 12 mo,mean ammonia level,and model for end-stage liver disease scores at admission.RESULTS The HE grade at admission using the West Haven Criteria was 2.3 in the PPI group compared to 1.7 in the PPI nonuser group(P=0.001).The average length of hospital stay in PPI group was 8.3 d compared to 6.5 d in PPI nonusers(P=0.046).Twenty-seven(31.8%)patients in the PPI user group required an Intensive Care Unit admission during their hospital course compared to 6 in the PPI nonuser group(16.7%)(P=0.138).Finally,10(11.8%)patients in the PPI group expired during their hospital stay compared to 1 in the PPI nonuser group(2.8%)(P=0.220).CONCLUSION Chronic PPI use in cirrhotic patients is associated with significantly higher average West Haven Criteria for HE compared to patients that do not use PPIs. | Matthew Fasullo Prashanth Rau Dong-Qi Liu Erik Holzwanger Jomol P Mathew Yurima Guilarte-Walker Gyongyi Szabo | 2019 | World Journal of Hepatology2019，11，6： | 4 |
| 19 | Adult mouse model of early hepatocellular carcinoma promoted by alcoholic liver disease显示文摘AIM: To establish a mouse model of alcohol-driven hepatocellular carcinoma(HCC) that develops in livers with alcoholic liver disease(ALD).METHODS: Adult C57BL/6 male mice received multiple doses of chemical carcinogen diethyl nitrosamine(DEN) followed by 7 wk of 4% Lieber-De Carli diet. Serum alanine aminotransferase(ALT), alpha fetoprotein(AFP) and liver Cyp2e1 were assessed. Expression of F4/80, CD68 for macrophages and Ly6 G, MPO, E-selectin for neutrophils was measured. Macrophage polarization was determined by IL-1β/i NOS(M1) and Arg-1/IL-10/CD163/CD206(M2) expression. Liver steatosis and fibrosis were measured by oil-red-O and Sirius red staining respectively. HCC development was monitored by magnetic resonance imaging, confirmed by histology. Cellular proliferation was assessed by proliferating cell nuclear antigen(PCNA).RESULTS: Alcohol-DEN mice showed higher ALTs than pair fed- DEN mice throughout the alcohol feeding without weight gain. Alcohol feeding resulted in increased ALT, liver steatosis and inflammation compared to pair-fed controls. Alcohol-DEN mice had reduced steatosis and increased fibrosis indicatingadvanced liver disease. Molecular characterization showed high estlevels of both neutrophil and macrophage markers in alcohol-DEN livers. Importantly, M 2 macrophages were edominantly higher in alcohol-DEN livers. Magnetic resonance imaging revealed increased numbers of intrahepatic cysts and liver histology confirmed the presence of early HCC in alcohol-DEN mice compared to al l other groups. This correlated with increased serum alphafetoprotein, a marker of HCC, in alcohol-DEN mice. PCNA immunostaining revealed significantly increased hepatocyte proliferation in livers from alcohol-DEN compared to pair fed-DEN or alcohol-fed mice.CONCLUSION: We describe a new 12-wk HCC model in adult mice that develops in livers with alcoholic hepatitis and defines ALD as co-factor in HCC. | Aditya Ambade Abhishek Satishchandran Benedek Gyongyosi Patrick Lowe Gyongyi Szabo | 2016 | World Journal of Gastroenterology2016，22，16： | 4 |
| 20 | Ion Channels in Plant Bioenergetic Organelles, Chloroplasts and Mitochondria: From Molecular Identification to Function显示文摘在 electrophysiological 大小,指向细胞器的荧光成像,和细胞器 proteomics 的最近的技术进展推了离子运输的研究在植物 bioenergetic 细胞器,叶绿体和线粒体的情况中前面的步,在最近的年里导致分子的鉴定和几个离子运输系统的功能的描述。这里,我们在调停的隧道上集中相对高率的离子和水流动并且在这个领域里总结当前的知识,集中于指向机制, proteomics, electrophysiology,和生理的功能。自从从一位 cyanobacterial 祖先发展的叶绿体,另外,我们给在 cyanobacterial 离子隧道附近可得到的信息的概述并且讨论叶绿体隧道的进化起源。一些这些离子隧道的最近的分子的鉴定允许他们的生理的功能用遗传上修改的 Arabidopsis 植物和 cyanobacteria 被学习。看法正在出现叶绿体和 mitochondrial 离子动态平衡的那改变导致细胞器机能障碍,它显著地接着影响整个有机体的精力新陈代谢。然而,为隧道编码为这些细胞器的基因的清晰鉴定在这个很快发展中的领域里仍然是主要挑战。包括生物信息学,房间生物学, electrophysiology,指向细胞器的离子敏感的探针的使用,遗传,和越过细胞器膜得到特定的离子流动的信号的鉴定的多重策略应该提供到以后在植物表明小径的 organellar 隧道和他们的贡献的生理的角色的更好的理解。 | Luca Carraretto Enrico Teardo Vanessa Checchetto Giovanni Finazzi Nobuyuki Uozumi Ildiko Szabo | 2016 | Molecular Plant2016，9，3： | 4 |
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