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| 1 | Pathogenesis and clinical management of Helicobacter pylori gastric infection显示文摘Helicobacter pylori(H.pylori)is a gram-negative bacterium that infects approximately 4.4 billion individuals worldwide.However,its prevalence varies among different geographic areas,and is influenced by several factors.The infection can be acquired by means of oral-oral or fecal-oral transmission,and the pathogen possesses various mechanisms that improve its capacity of mobility,adherence and manipulation of the gastric microenvironment,making possible the colonization of an organ with a highly acidic lumen.In addition,H.pylori presents a large variety of virulence factors that improve its pathogenicity,of which we highlight cytotoxin associated antigen A,vacuolating cytotoxin,duodenal ulcer promoting gene A protein,outer inflammatory protein and gamma-glutamyl transpeptidase.The host immune system,mainly by means of a Th1-polarized response,also plays a crucial role in the infection course.Although most H.pylori-positive individuals remain asymptomatic,the infection predisposes the development of various clinical conditions as peptic ulcers,gastric adenocarcinomas and mucosa-associated lymphoid tissue lymphomas.Invasive and non-invasive diagnostic methods,each of them with their related advantages and limitations,have been applied in H.pylori detection.Moreover,bacterial resistance to antimicrobial therapy is a major challenge in the treatment of this infection,and new therapy alternatives are being tested to improve H.pylori eradication.Last but not least,the development of effective vaccines against H.pylori infection have been the aim of several research studies. | Breno Bittencourt de Brito Filipe Ant?nio Fran?a da Silva Aline Silva Soares Vinícius Afonso Pereira Maria Luísa Cordeiro Santos Mariana Miranda Sampaio Pedro Henrique Moreira Neves Fabrício Freire de Melo | 2019 | World Journal of Gastroenterology2019，25，37： | 84 |
| 2 | Helicobacter pylori infection: Host immune response, implications on gene expression and microRNAs显示文摘Helicobacter pylori(H. pylori) infection is the most common bacterial infection worldwide. Persistent infection of the gastric mucosa leads to inflammatory processes and may remain silent for decades or progress causing more severe diseases, such as gastric adenocarcinoma. The clinical consequences of H. pylori infection are determined by multiple factors, including host genetic predisposition, gene regulation, environmental factors and heterogeneity of H. pylori virulence factors. After decades of studies of this successful relationship between pathogen and human host, various mechanisms have been elucidated. In this review, we have made an introduction on H. pylori infection and its virulence factors, and focused mainly on modulation of host immune response triggered by bacteria, changes in the pattern of gene expression in H. pylori-infected gastric mucosa, with activation of gene transcription involved in defense mechanisms, inflammatory and immunological response, cell proliferation and apoptosis. We also highlighted the role of bacteria eradication on gene expression levels. In addition, we addressed the recent involvement of different microRNAs in precancerous lesions, gastric cancer, and inflammatory processes induced by bacteria. New discoveries in this field may allow a better understanding of the role of major factors involved in the pathogenic mechanisms of H. pylori. | Aline Cristina Targa Cadamuro Ana Flávia Teixeira Rossi Nathália Maciel Maniezzo Ana Elizabete Silva | 2014 | World Journal of Gastroenterology2014，20，6： | 16 |
| 3 | Proton pump inhibitors therapy and risk of Clostridium difficile infection: Systematic review and meta-analysis显示文摘AIM To perform a systematic review and meta-analysis on proton pump inhibitors(PPIs) therapy and the risk of Clostridium difficile infection(CDI). METHODS We conducted a systematic search of MEDLINE/Pub Med and seven other databases through January 1990 to March 2017 for published studies that evaluated the association between PPIs and CDI. Adult case-control and cohort studies providing information on the association between PPI therapy and the development of CDI were included. Pooled odds ratios(ORs) estimates with 95% confidence intervals(CIs) were calculated using the random effect. Heterogeneity was assessed by I^2 test and Cochran's Q statistic.Potential publication bias was evaluated via funnel plot, and quality of studies by the Newcastle-Otawa Quality Assessment Scale(NOS). RESULTS Fifty-six studies(40 case-control and 16 cohort) involving 356683 patients met the inclusion criteria and were analyzed. Both the overall pooled estimates and subgroup analyses showed increased risk for CDI despite substantial statistical heterogeneity among studies. Meta-analysis of all studies combined showed a significant association between PPI users and the risk of CDI(pooled OR = 1.99, CI: 1.73-2.30, P < 0.001) as compared with non-users. The association remained significant in subgroup analyses: by design-case-control(OR = 2.00, CI: 1.68-2.38, P < 0.0001), and cohort(OR = 1.98, CI: 1.51-2.59, P < 0.0001); adjusted(OR = 1.95, CI: 1.67-2.27, P < 0.0001) and unadjusted(OR = 2.02, CI: 1.41-2.91, P < 0.0001); unicenter(OR = 2.18, CI: 1.72-2.75, P < 0.0001) and multicenter(OR = 1.82, CI: 1.51-2.19, P < 0.0001); age ≥ 65 years(OR = 1.93, CI: 1.40-2.68, P < 0.0001) and < 65 years(OR = 2.06, CI: 1.11-3.81, P < 0.01). No significant differences were found in subgroup analyses(test for heterogeneity): P = 0.93 for case-control vs cohort, P = 0.85 for adjusted vs unadjusted, P = 0.24 for unicenter vs multicenter, P = 0.86 for age ≥ 65 years and < 65 years. There was significant heterogeneity across studies(I^2 = 85.4%, P < 0.001) as well as evidence of publication bias(funnel plot asymmetry test, P = 0.002). CONCLUSION This meta-analysis provides further evidence that PPI use is associated with an increased risk for development of CDI. Further high-quality, prospective studies are needed to assess whether this association is causal. | Anca Trifan Carol Stanciu Irina Girleanu Oana Cristina Stoica Ana Maria Singeap Roxana Maxim Stefan Andrei Chiriac Alin Ciobica Lucian Boiculese | 2017 | World Journal of Gastroenterology2017，23，35： | 15 |
| 4 | Immune checkpoint inhibitor-induced colitis:A comprehensive review显示文摘Immune checkpoint inhibitors(ICIs) are monoclonal antibodies that target downregulators of the anti-cancer immune response: Cytotoxic T-lymphocyte antigen-4, programmed cell death protein-1, and its ligand programmed death-ligand 1.ICIs have revolutionized the treatment of a variety of malignancies. However,many immune-related adverse events have also been described which mainly occurs as the immune system becomes less suppressed, affecting various organs including the gastrointestinal tract and causing diarrhea and colitis. The incidence of immune-mediated colitis(IMC) ranges from 1%-25% depending on the type of ICI and if used in combination. Endoscopically and histologically there is a significant overlap between IMC and inflammatory bowel disease,however more neutrophilic inflammation without chronic inflammation is usually present in IMC. Corticosteroids are recommended for grade 2 or more severe colitis while holding the immunotherapy. About one third to two thirds of patients are steroid refractory and benefit from infliximab. Recently vedolizumab has been found to be efficacious in steroid and infliximab refractory cases. While in grade 4 colitis, the immunotherapy is permanently discontinued, the decision is controversial in grade 3 colitis. | Aniruddh Som Rohan Mandaliya Dana Alsaadi Maham Farshidpour Aline Charabaty Nidhi Malhotra Mark C Mattar | 2019 | World Journal of Clinical Cases2019，7，4： | 14 |
| 5 | Innate lymphoid cells in tissue homeostasis and diseases显示文摘Innate lymphoid cells(ILCs) are the most recently discovered family of innate immune cells. They are a part of the innate immune system, but develop from the lymphoid lineage. They lack pattern-recognition receptors and rearranged receptors, and therefore cannot directly mediate antigen specific responses. The progenitors specifically associated with the ILCs lineage have been uncovered, enabling the distinction between ILCs and natural killer cells. Based on the requirement of specific transcription factors and their patterns of cytokine production, ILCs are categorized into three subsets(ILC1, ILC2 and ILC3). First observed in mucosal surfaces, these cell populations interact with hematopoietic and non-hematopoietic cells throughout the body during homeostasis and diseases, promoting immunity, commensal microbiota tolerance, tissue repair and inflammation. Over the last 8 years, ILCs came into the spotlight as an essential cell type able to integrate diverse host immune responses. Recently, it became known that ILC subsets play a key role in immune responses at barrier surfaces, interacting with the microbiota, nutrients and metabolites. Since the liver receives the venous blood directly from the intestinal vein, the intestine and liver are essential to maintain tolerance and can rapidly respond to infections or tissue damage. Therefore, in this review, we discuss recent findings regarding ILC functions in homeostasis and disease, with a focus on the intestine and liver. | Aline Ignacio Cristiane Naffah Souza Breda Niels Olsen Saraiva Camara | 2017 | World Journal of Hepatology2017，9，23： | 12 |
| 6 | Renin angiotensin system in liver diseases: Friend or foe?显示文摘In the last three decades,the understanding of the renin angiotensin system(RAS)has been changed by the discoveries of functional local systems,novel biologically active peptides,additional specific receptors,alternative pathways of angiotensin(Ang)?Ⅱ?generation,and new roles for enzymes and precursor components other than those in Ang?Ⅱ?synthesis.In this regard,the discovery that Ang-(1-7)opposes the pressor,proliferative,pro-fibrotic,and pro-inflammatory effects mediated by Ang?Ⅱ?has contributed to the realization that the RAS is composed of two axes.The first axis consists of the angiotensin-converting enzyme(ACE),with Ang?Ⅱ?as the end product,and the angiotensin type 1(AT1)receptor as the main effector mediating the biological actions of Ang?Ⅱ.The second axis results from ACE2-mediated hydrolysis of Ang?Ⅱ,leading to the production of Ang-(1-7),with the Mas receptor as the main effector conveying the vasodilatory,antiproliferative,anti-fibrotic,and anti-inflammatory effects of Ang-(1-7).Experimental and clinical studies have shown that both axes of the RAS may take part in the pathogenesis of liver diseases.In this manuscript,we summarize the current evidence regarding the role of RAS in hepatic cirrhosis and its complications,including hemodynamic changes and hepatorenal syndrome.The therapeutic potential of the modulation of RAS molecules in liver diseases is also discussed. | Ana Cristina Simoes e Silva Aline S Miranda Natália P Rocha Antonio L Teixeira | 2017 | World Journal of Gastroenterology2017，23，19： | 12 |
| 7 | 从视听翻译到无障碍传播:实时字幕、口述影像与声音字幕显示文摘近几十年来,视听翻译领域在无障碍传播理念的影响下涌现出一些新形式,全球化所带来的多语言性和多文化性,也促进了视听翻译形式的多元化需求和多元化应用。文章以实时字幕、口述影像和声音字幕为例,探讨了这三种新加入到视听翻译领域的无障碍传播形式的定义、发展历程、制作过程和受众需求等。其中实时字幕不仅包括语种间字幕和同语种的听障者字幕,更多视听障碍者也在呼吁实时翻译的语种间听障者字幕的出现;口述影像作为一种新添加的叙事内容,不仅可以帮助视障观众'收听'影片和理解其内容,对更大范围的受众如老年人观影者等也很有帮助;声音字幕则是将外语电影中的对话或多语言电影中有规律出现的外语对话无障碍化,促进了视障观众的观影体验。与此同时,外语产品和多语种产品也创造出了一种无障碍传播的整合方案——口述影像+翻译+声音字幕,以期帮助视听障碍者无障碍地享受观影过程。 | Aline Remael 丁方舟 | 2014 | 浙江传媒学院学报2014，21，4： | 12 |
| 8 | The enhanced X-ray Timing and Polarimetry mission—eXTP显示文摘In this paper we present the enhanced X-ray Timing and Polarimetry mission—eXTP. eXTP is a space science mission designed to study fundamental physics under extreme conditions of density, gravity and magnetism. The mission aims at determining the equation of state of matter at supra-nuclear density, measuring effects of QED, and understanding the dynamics of matter in strong-field gravity. In addition to investigating fundamental physics, eXTP will be a very powerful observatory for astrophysics that will provide observations of unprecedented quality on a variety of galactic and extragalactic objects. In particular, its wide field monitoring capabilities will be highly instrumental to detect the electro-magnetic counterparts of gravitational wave sources.The paper provides a detailed description of:(1) the technological and technical aspects, and the expected performance of the instruments of the scientific payload;(2) the elements and functions of the mission, from the spacecraft to the ground segment. | ShuangNan Zhang Andrea Santangelo Marco Feroci YuPeng Xu FangJun Lu Yong Chen Hua Feng Shu Zhang Sφren Brandt Margarita Hernanz Luca Baldini Enrico Bozzo Riccardo Campana Alessandra De Rosa YongWei Dong Yuri Evangelista Vladimir Karas Norbert Meidinger Aline Meuris Kirpal Nandra Teng Pan Giovanni Pareschi Piotr Orleanski QiuShi Huang Stephane Schanne Giorgia Sironi Daniele Spiga Jiri Svoboda Gianpiero Tagliaferri Christoph Tenzer Andrea Vacchi Silvia Zane Dave Walton ZhanShan Wang Berend Winter Xin Wu Jean J.M.in't Zand Mahdi Ahangarianabhari Giovanni Ambrosi Filippo Ambrosino Marco Barbera Stefano Basso Jörg Bayer Ronaldo Bellazzini Pierluigi Bellutti Bruna Bertucci Giuseppe Bertuccio Giacomo Borghi XueLei Cao Franck Cadoux Francesco Ceraudo TianXiang Chen Yu Peng Chen Jerome Chevenez Marta Civitani Wei Cui WeiWei Cui Thomas Dauser Ettore Del Monte Sergio Di Cosimo Sebastian Diebold Victor Doroshenko Michal Dovciak YuanYuan Du Lorenzo Ducci QingMei Fan Yannick Favre Fabio Fuschino JoséLuis Ga'lvez Min Gao MingYu Ge Olivier Gevin Marco Grassi QuanYing Gu YuDong Gu DaWei Han Bin Hong Wei Hu Long Ji ShuMei Jia WeiChun Jiang Thomas Kennedy Ingo Kreykenbohm Irfan Kuvvetli Claudio Labanti Luca Latronico Gang Li MaoShun Li Xian Li Wei Li ZhengWei Li Olivier Limousin HongWei Liu XiaoJing Liu Bo Lu Tao Luo Daniele Macera Piero Malcovati Adrian Martindale Malgorzata Michalska Bin Meng Massimo Minuti Alfredo Morbidini Fabio Muleri Stephane Paltani Emanuele Perinati Antonino Picciotto Claudio Piemonte JinLu Qu Alexandre Rachevski Irina Rashevskaya Jerome Rodriguez Thomas Schanz ZhengXiang Shen LiZhi Sheng JiangBo Song LiMing Song Carmelo Sgro Liang Sun Ying Tan Phil Uttley Bo Wang DianLong Wang GuoFeng Wang Juan Wang LangPing Wang YuSa Wang Anna L.Watts XiangYang Wen Jörn Wilms ShaoLin Xiong JiaWei Yang Sheng Yang YanJi Yang Nian Yu WenDa Zhang Gianluigi Zampa Nicola Zampa Andrzej A.Zdziarski AiMei Zhang ChengMo Zhang Fan Zhang Long Zhang Tong Zhang Yi Zhang XiaoLi Zhang ZiLiang Zhang BaoSheng Zhao ShiJie Zheng Yu Peng Zhou Nicola Zorzi J.Frans Zwart | 2019 | Science China(Physics,Mechanics & Astronomy)2019，62，2： | 11 |
| 9 | Pro12Ala polymorphism of the peroxisome proliferator-activated receptor γ2 in patients with fatty liver diseases显示文摘AIM:To test the occurrence of the Pro12Ala mutation of the peroxisome proliferator-activated receptor-γ (PPARγ)2-gene in patients with non-alcoholic fatty liver disease (NAFLD) or alcoholic fatty liver disease (AFLD).METHODS:DNA from a total of 622 specimens including 259 blood samples of healthy blood donors and 363 histologically categorized liver biopsies of patients with NAFLD (n=263) and AFLD (n=100) were analyzed by Real-time polymerase chain reaction using allele-specific probes.RESULTS:In the NAFLD and the AFLD collective,3% of the patients showed homozygous occurrence of the Ala12 PPARγ2-allele,differing from only 1.5% cases in the healthy population.In NAFLD patients,a high incidence of the Ala12 mutant was not associated with the progression of fatty liver disease.However,we observed a significantly higher risk (odds ratio=2.50,CI:1.05-5.90,P=0.028) in AFLD patients carrying the mutated Ala12 allele to develop inflammatory alterations.The linkage of the malfunctioning Ala12-positive PPARγ2 isoform to an increased risk in patients with AFLD to develop severe steatohepatitis and fibrosis indicates a more prominent anti-inflammatory impact of PPARγ2 in progression of AFLD than of NAFLD.CONCLUSION:In AFLD patients,the Pro12Ala single nuclear polymorphism should be studied more extensively in order to serve as a novel candidate in biomarker screening for improved prognosis. | Johannes W Rey Andrea Noetel Aline Hardt Ali Canbay Hakan Alakus Axel zur Hausen Hans Peter Dienes Uta Drebber Margarete Odenthal | 2010 | World Journal of Gastroenterology2010，16，46： | 11 |
| 10 | Early-onset colorectal cancer:A sporadic or inherited disease?显示文摘Colorectal cancer is the third most common cancer diagnosed worldwide.Although epidemiology data show a marked variability around the world,its overall incidence rate shows a slow but steady decrease,mainly in developed countries.Conversely,early-onset colorectal cancer appears to display an opposite trend with an overall prevalence in United States and European Union ranging from 3.0% and 8.6%.Colorectal cancer has a substantial proportion of familial cases.In particular,early age at onset is especially suggestive of hereditary predisposition.The clinicopathological and molecular features of colorectal cancer cases show a marked heterogeneity not only between early- and late-onset cases but also within the early-onset group.Two distinct subtypes of early-onset colorectal cancers can be identified:a 'sporadic' subtype,usually without family history,and an inherited subtype arising in the context of well defined hereditary syndromes.The pathogenesis of the early-onset disease is substantially well characterized in the inherited subtype,which is mainly associated to the Lynch syndrome and occasionally to other rare mendelian diseases,whereas in the 'sporadic' subtype the origin of the disease may be attributed to the presence of various common/rare genetic variants,so far largely unidentified,displaying variable penetrance.These variants are thought to act cumulatively to increase the risk of colorectal cancer,and presumably to also anticipate its onset.Efforts are ongoing in the attempt to unravel the intricate genetic basis of this 'sporadic' early-onset disease.A better knowledge of molecular entities and pathways may impact on family-tailored prevention and clinical management strategies. | Vittoria Stigliano Lupe Sanchez-Mete Aline Martayan Marcello Anti | 2014 | World Journal of Gastroenterology2014，20，35： | 10 |
| 11 | TLR2 and TLR4 polymorphisms influence m RNA and protein expression in colorectal cancer显示文摘AIM: To evaluate the effect of promoter region polymorphisms of toll-like receptor(TLR)2-196 to-174 del and TLR4-1607T/C(rs10759932) on m RNA and protein expression in tumor tissue and of TLR4+896A/G(rs4986790) on colorectal cancer(CRC) risk.METHODS: The TLR2-196 to-174 del polymorphism was investigated using allele-specific polymerase chain reaction(PCR) and the TLR4-1607T/C and TLR4+896A/G by PCR-restriction fragment length p o l y m o r p h i s m( R F L P). W e g e n o t y p e d 4 3 4 D N A samples from 194 CRC patients and 240 healthy individuals. The m RNA relative quantification(RQ) was performed in 40 tumor tissue samples by quantitative PCR Taq Man assay, using specific probes for TLR2 and TLR4 genes, and ACTB and GAPDH reference geneswere used as endogenous controls. Protein expression was analyzed by immunohistochemistry with specific primary antibodies.RESULTS: No association was found for TLR4-1607T/C and TLR4+896A/G by three statistical models(logadditive, dominant and recessive). However, based on dominant and log-additive models, the polymorphic variant TLR2-196 to-174 del was associated with increased CRC risk [dominant: odds ratio(OR) = 1.72, 95%CI: 1.03-2.89; P = 0.038 and log-additive: OR =1.59, 95%CI: 1.02-2.48; P = 0.039]. TLR2 m RNA expression was increased in tumor tissue(RQ = 2.36) when compared to adjacent normal tissue(RQ = 1; P < 0.0001), whereas the TLR4 m RNA showed a basal expression(RQ = 0.74 vs RQ = 1, P = 0.452). Immunohistochemistry analysis of TLR2 and TLR4 protein expression was concordant with the findings of m RNA expression. In addition, the TLR2-196 to-174 del variant carriers showed m RNA relative expression 2.19 times higher than wild-genotype carriers. The TLR2 protein expression was also higher for the TLR2-196 to-174 del variant carriers [117 ± 10 arbitrary unit(a.u.) vs 95 ± 4 a.u., P = 0.03]. However, for the TLR4-1607T/C polymorphism no significant difference was found for both m RNA(P = 0.56) and protein expression(P = 0.26).CONCLUSION: Our findings suggest that TLR2-196 to-174 del polymorphism increases TLR2 m RNA expression and is associated with higher CRC risk, indicating an important role in CRC genetic susceptibility. | Marcela Alcantara Proenca Juliana Garcia de Oliveira Aline Cristina Targa Cadamuro Maysa Succi Joao Gomes Netinho Eny Maria Goloni-Bertolo érika Cristina Pavarino Ana Elizabete Silva | 2015 | World Journal of Gastroenterology2015，21，25： | 9 |
| 12 | Interrelationship between chromosome 8 aneuploidy,C-MYC amplification and increased expression in individuals from northern Brazil with gastric adenocarcinoma显示文摘AIM: To investigate chromosome 8 numerical aberra- tions, C-MYC oncogene alterations and its expression in gastric cancer and to correlate these findings with histo- pathological characteristics of gastric tumors. METHODS: Specimens were collected surgically from seven patients with gastric adenocarcinomas. Immu- nostaining for C-MYC and dual-color fluorescence in situ hybridization (FISH) for C-MYC gene and chromosome 8 centromere were performed. RESULTS: All the cases showed chromosome 8 aneu- ploidy and C-MYC amplification, in both the diffuse and intestinal histopathological types of Lauren. No significant difference (P < 0.05) was observed between the level ofchromosome 8 ploidy and the site, stage or histological type of the adenocarcinomas. C-MYC high amplification, like homogeneously stained regions (HSRs) and double minutes (DMs), was observed only in the intestinal-type. Structural rearrangement of C-MYC, like translocation, was observed only in the diffuse type. Regarding C-MYC gene, a significant difference (P < 0.05) was observed between the two histological types. The C-MYC protein was expressed in all the studied cases. In the intestinal- type the C-MYC immunoreactivity was localized only in the nucleus and in the diffuse type in the nucleus and cytoplasm. CONCLUSION: Distinct patterns of alterations between intestinal and diffuse types of gastric tumors support the hypothesis that these types follow different genetic path- ways. | Danielle Queiroz Calcagno Mariana Ferreira Leal Aline Damaceno Seabra Andre Salim Khayat Elizabeth Suchi Chen Samia Demachki Paulo Pimentel Assumpcao Mario Henrique Girao Faria Silvia Helena Barem Rabenhorst Márcia Valéria Pitombeira Ferreira Marília de Arruda Cardoso Smith Rommel Rodríguez Burbano | 2006 | World Journal of Gastroenterology2006，12，38： | 9 |
| 13 | Psychosocial stress and liver disease status显示文摘'Psychosocial stress' is an increasingly common concept in the challenging and highly-demanding modern society of today. Organic response to stress implicates two major components of the stress system, namely the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system. Stress is anamnestically reported by patients during the course of disease, usually accompanied by a decline in their overall health status. As the mechanisms involving glucocorticoids and catecholamines have been deciphered, and their actions on immune cell function deeper understood, it has become clear that stress has an impact on hepatic inflam-matory response. An increasing number of articles have approached the link between psychosocial stress and the negative evolution of hepatic diseases. This article reviews a number of studies on both human populations and animal models performed in recent years, all linking stress, mainly of psychosocial nature, and the evolution of three important liver-related pathological entities: viral hepatitis, cirrhosis and hepatocellular carcinoma. | Cristin Constantin Vere Costin Teodor Streba Letitia Maria Streba Alin Gabriel Ionescu Felix Sima | 2009 | World Journal of Gastroenterology2009，15，24： | 7 |
| 14 | hsa-miR-29c and hsa-miR-135b differential expression aspotential biomarker of gastric carcinogenesis显示文摘AIM: To investigate the expression profiles of hsa-mi R-29 c and hsa-mi R-135 b in gastric mucosal samples and their values as gastric carcinogenesis biomarkers. METHODS: The expression levels of hsa-mi R-29 c and hsa-mi R-135 b in normal gastric mucosa, non-atrophic chronic gastritis, intestinal metaplasia and intestinaltype gastric adenocarcinoma were analysed using quantitative real-time PCR. The difference between hsa-mi R-29 c and hsa-mi R-135 b expression profiles in the grouped samples was evaluated by ANOVA and Student's t-test tests. The results were adjusted for multiple testing by using Bonferroni's correction. P values ≤ 0.05 were considered statistically significant. To evaluate hsa-mi R-29 c and hsa-mi R-135 b expressions as potential biomarkers of gastric carcinogenesis, we performed a receiver operating characteristic curve analysis and the derived area under the curve, and a Categorical Principal Components Analysis. In silico identification of the genetic targets of hsa-mi R-29 c and hsa-mi R-135 b was performed using different prediction tools, in order to identify possible genes involved in gastric carcinogenesis.RESULTS: The expression levels of hsa-mi R-29 c were higher in normal gastric mucosal samples, and decreased progressively in non-atrophic chronic gastritis samples, intestinal metaplasia samples and intestinal-type gastric adenocarcinoma samples. The expression of hsa-mi R-29 c in the gastric lesions showed that non-atrophic gastritis have an intermediate profile to gastric normal mucosa and intestinal-type gastric adenocarcinoma, and that intestinal metaplasia samples presented an expression pattern similar to that in intestinal-type gastric adenocarcinoma. This micro RNA(mi RNA) has a good discriminatory accuracy between normal gastric samples and(1) intestinal-type gastric adenocarcinoma; and(2) intestinal metaplasia, and regulates the DMNT3 A oncogene. hsa-mi R-135 b is up-regulated in non-atrophic chronic gastritis and intestinal metaplasia samples and down-regulated in normal gastric mucosa and intestinal-type gastric adenocarcinoma samples. Non-atrophic chronic gastritis and intestinal metaplasia are significantly different from normal gastric mucosa samples. hsa-mi R-135 b expression presented a greater discriminatory accuracy between normal samples and gastric lesions. This mi RNA was associated with Helicobacter pylori presence in non-atrophic chronic gastritis samples and regulates the APC and KLF4 tumour suppressor genes.CONCLUSION: Our results provide evidence of epigenetic alterations in non-atrophic chronic gastritis and intestinal metaplasia and suggest that hsa-mi R-29 c and hsa-mi R-135 b are promising biomarkers of gastric carcinogenesis. | Amanda Ferreira Vidal Aline MP Cruz Leandro Magalhães Adenilson L Pereira Ana KM Anaissi Nélisson CF Alves Paulo JBS Albuquerque Rommel MR Burbano Samia Demachki Ândrea Ribeiro-dos-Santos | 2016 | World Journal of Gastroenterology2016，22，6： | 7 |
| 15 | Population-level economic burden of lung cancer in China:Provisional prevalence-based estimations,2017-2030显示文摘Objective:Population-level economic burden is essential for prioritizing healthcare resources and healthcare budget making in the future.However,little is known about the economic burden of lung cancer in China.Methods:A prevalence-based approach was adopted to estimate the economic burden of lung cancer,including direct expenditure(medical and non-medical)and indirect cost(disability and premature death).Data on direct expenditure and work-loss days per patient in each year post-diagnosis were obtained from two primary surveys.Other parameters were obtained from literatures and official reports.Projections were conducted based on varying parameters.All expenditure data were reported in United States dollars(USD)using 2017 value(exchange rate:1 USD=6.760 CNY),with the discount rate of 3%.Results:The total economic burden of lung cancer was estimated to be 25,069 million USD in China in 2017(0.121%of gross domestic productivity,GDP).The estimated direct expenditure was 11,098 million USD,up to1.43%of total healthcare expenditure for China,covering 10,303 million USD and 795 million USD for medical and non-medical expenditure,respectively.The estimated indirect cost was 13,971 million,including 1,517 million USD due to disability and 12,454 million USD due to premature death.Under current assumptions,the projected total economic burden would increase to 30.1 billion USD,40.4 billion USD,and 53.4 billion USD in 2020,2025,and 2030,accounting for 0.121%,0.131%,and 0.146%of China's GDP,respectively.However,if China meets the United Nation sustainable development goal of reducing premature death from non-communicable diseases by one-third by 2030,the total economic burden in 2030 would be 31.9 billion USD,0.087%of China's GDP.Conclusions:The economic burden of lung cancer in China in 2017 is substantial and more likely to increase significantly in the future.Policy makers need to take urgent actions in budget making for health systems.The economic burden could be alleviated by reducing the disease burden of lung cancer via effective control and prevention actions. | Chengcheng Liu Jufang Shi Hong Wang Xinxin Yan Le Wang Jiansong Ren Mark Parascandola Wanqing Chen Alin Dai | 2021 | Chinese Journal of Cancer Research2021，33，1： | 6 |
| 16 | Deciphering the role of PGC-1α in neurological disorders: from mitochondrial dysfunction to synaptic failure显示文摘The onset and mechanisms underlying neurodegenerative diseases remain uncertain. The main features of neurodegenerative diseases have been related with cellular and molecular events like neuronal loss, mitochondrial dysfunction and aberrant accumulation of misfolded proteins or peptides in specific areas of the brain. The most prevalent neurodegenerative diseases belonging to age-related pathologies are Alzheimer's disease, Huntington's disease, Parkinson's disease and amyotrophic lateral sclerosis. Interestingly, mitochondrial dysfunction has been observed to occur during the early onset of several neuropathological events associated to neurodegenerative diseases. The master regulator of mitochondrial quality control and energetic metabolism is the transcriptional coactivator peroxisome proliferator-activated receptor gamma coactivator 1-alpha(PGC-1α). Additionally, it has been observed that PGC-1α appears to be a key factor in maintaining neuronal survival and synaptic transmission. In fact, PGC-1α downregulation in different brain areas(hippocampus, substantia nigra, cortex, striatum and spinal cord) that occurs in function of neurological damage including oxidative stress, neuronal loss, and motor disorders has been seen in several animal and cellular models of neurodegenerative diseases. Current evidence indicates that PGC-1α upregulation may serve as a potent therapeutic approach against development and progression of neuronal damage. Remarkably, increasing evidence shows that PGC-1α deficient mice have neurodegenerative diseases-like features, as well as neurological abnormalities. Finally, we discuss recent studies showing novel specific PGC-1α isoforms in the central nervous system that appear to exert a key role in the age of onset of neurodegenerative diseases and have a neuroprotective function in the central nervous system, thus opening a new molecular strategy for treatment of neurodegenerative diseases. The purpose of this review is to provide an up-to-date overview of the PGC-1α role in the physiopathology of neurodegenerative diseases, as well as establish the importance of PGC-1α function in synaptic transmission and neuronal survival. | Jessica D.Panes Aline Wendt Oscar Ramirez-Molina Patricio A.Castro Jorge Fuentealba | 2022 | Neural Regeneration Research2022，17，2： | 6 |
| 17 | Electrochemical ageing study of mixed lanthanum/praseodymium nickelates La2-xPrxNiO4+δ as oxygen electrodes for solid oxide fuel or electrolysis cells显示文摘The chemical and electrochemical stability of lanthanide nickelates La2 NiO4+δ(LNO),Pr2 NiO4+δ(PNO)and their mixed compounds La(2-x)PrxNiO4+δ(LPNOs)with x=0.5,1 or 1.5 is reported.The aim is to promote these materials as efficient electrodes for solid oxide fuel cell(SOFC)and/or solid oxide electrolysis cell(SOEC).La2 NiO4+δand La1.5Pr0.5NiO4+δcompounds are chemically very stable as powders over one month in the temperature range 600-800℃,while the other materials rich in praseodymium progressively decompose into various perovskite-deriving components with additional Pr6 O11.Despite their uneven properties,all these materials are quite efficient and sustainable as electrodes on top of gadolinium doped ceria(GDCBL)//yttrium doped zirconia(8 YSZ)electrolyte,for one month at 700℃without polarization.Under polarization(300 mA·cm-2),the electrochemical performances of LNO,PNO and La1.5Pr0.5NiO4+δ(LP5 NO)quickly degrade in SOFC mode,i.e.for the oxygen reduction reaction,while they show durability in SOEC mode,i.e.for the oxide oxidation reaction. | Vaibhav Vibhu Aurélien Flura Aline Rougier Clément Nicollet Sébastien Fourcade Teresa Hungria Jean-Claude Grenier Jean-Marc Bassat | 2020 | Journal of Energy Chemistry2020，29，7： | 6 |
| 18 | Estrogen-mediated downregulation of HIF-1αsignaling in B lymphocytes influences postmenopausal bone loss显示文摘In the bone marrow, B cells and bone-resorbing osteoclasts colocalize and form a specific microenvironment. How B cells functionally influence osteoclasts and bone architecture is poorly understood. Using genetically modified mice and highthroughput analyses, we demonstrate that prolonged HIF-1α signaling in B cells leads to enhanced RANKL production and osteoclast formation. In addition, deletion of HIF-1α in B cells prevents estrogen deficiency-induced bone loss in mice.Mechanistically, estrogen controls HIF-1α protein stabilization through HSP70-mediated degradation in bone marrow B cells.The stabilization of HIF-1α protein in HSP70-deficient bone marrow B cells promotes RANKL production and osteoclastogenesis.Induction of HSP70 expression by geranylgeranylacetone(GGA) administration alleviates ovariectomy-induced osteoporosis.Moreover, RANKL gene expression has a positive correlation with HIF1 A expression in human B cells. In conclusion, HIF-1αsignaling in B cells is crucial for the control of osteoclastogenesis, and the HSP70/HIF-1α axis may serve as a new therapeutic target for osteoporosis. | Xianyi Meng Zhen Lin Shan Cao Iga Janowska Koshiro Sonomoto Darja Andreev Knab Katharina Jinming Wen Karl Xaver Knaup Michael Sean Wiesener Gerhard Krönke Marta Rizzi Georg Schett Aline Bozec | 2022 | Bone Research2022，10，2： | 6 |
| 19 | pRB expression in esophageal mucosa of individuals at high risk for squamous cell carcinoma of the esophagus显示文摘AIM: To investigate the pRb expression in a large group of patients with history of chronic exposure to the main risk factors for development of squamous cell carcinoma of the esophagus. METHODS: One hundred and seventy asymptomatic individuals at high risk for esophageal squamous cell carcinoma (consumption of more than 80 g of ethanol and 10 cigarettes/d for at least 10 years) underwent upper gastrointestinal endoscopy with biopsies of the esophageal mucosa. As a control group, specimens of esophageal mucosa obtained from 20 healthy subjects were also studied. Immunohistochemical assessment of the tissues was performed using a monoclonal antibody anti-pRB protein. RESULTS: Absence of the pRB staining, indicating loss of RB function, was observed in 33 (19.4%) of the individuals at risk for esophageal cancer, but in none of the healthy controls (P < 0.02). Loss of pRb expression increased in a stepwise fashion according to the severity of the histological findings (P < 0.005): normal mucosa (11/97 or 11.3%), chronic esophagitis (17/60 or 28.3%), low-grade dysplasia (3/10 or 30%), high-grade dysplasia 1/2 or 50%) and squamous cell carcinoma (1/1 or 100%). CONCLUSION: Our findings suggest that abnormal expression of the pRB protein may be implicated in the process of esophageal carcinogenesis. Additional studies are warranted to define the role of the pRBprotein as a biomarker for development of esophageal squamous cell carcinoma in individuals at high risk for this malignancy. | Simone S Contu Paulo C Contu Daniel C Damin Renato B Fagundes Fabiano Bevilacqua Aline S Rosa Joo C Prolla Luis F Moreira | 2007 | World Journal of Gastroenterology2007，13，11： | 5 |
| 20 | Occurrence of emerging flame retardants from e-waste recycling activities in the northern part of Vietnam显示文摘This study investigated the contamination status of 21 emerging flame retardants(FRs)in soils(n=32)and river sediments(n=8)from an e-waste recycling(EWR)site in the northern part of Vietnam.Among analyzed FRs,higher levels of decabromodiphenyl ethane(DBDPE)(NDe4200 ng/g dw),1,2-bis-(2,4,6-tribromophenoxy)ethane(BTBPE)(NDe350 ng/g dw)and Dechlorane Plus isomers(DPs)(NDe65 ng/g dw)were found in soils near EWR workshops and open burning places.The highest concentrations of DBDPE(20 ng/g dw),BTBPE(5.7 ng/g dw)and DPs(6.7 ng/g dw)were also detected in sediments collected from the middle of the EWR site.The levels decreased concomitantly with increasing distance from the EWR site.These results indicate that these FRs were released to the surrounding environment from improper recycling activities,such as manual dismantling of devices and open burning of e-wastes.Moreover,the estimated daily intakes of those FRs via soil ingestion were approximately ten times higher for children than adults.To our knowledge,this is a first comprehensive study on characterization of soil and sediment contamination by a series of emerging FRs at an EWR site in Vietnam. | Masayuki Someya Go Suzuki Alin C.Ionas Nguyen Minh Tue Fuchao Xu Hidenori Matsukami Adrian Covaci Le Huu Tuyen Pham Hung Viet Shin Takahashi Shinsuke Tanabe Hidetaka Takigami | 2016 | Emerging Contaminants2016，2，2： | 5 |
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