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| 1 | 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 |
| 2 | Determination of drug,excipients and coating distribution in pharmaceutical tablets using NIR-CI显示文摘The growing interest of the pharmaceutical industry in Near Infrared-Chemical Imaging (NIR-CI) is a result of its high usefulness for quality control analyses of drugs throughout their production process (particularly of its non-destructive nature and expeditious data acquisition).In this work,the concentration and distribution of the major and minor components of pharmaceutical tablets are determined and the spatial distribution from the internal and external sides has been obtained.In addition,the same NIR-CI allowed the coating thickness and its surface distribution to be quantified.Images were processed to extract the target data and calibration models constructed using the Partial Least Squares (PLS) algorithms.The concentrations of Active Pharmaceutical Ingredient (API) and excipients obtained for uncoated cores were essentially identical to the nominal values of the pharmaceutical formulation.But the predictive ability of the calibration models applied to the coated tablets decreased as the coating thickness increased. | Anna Palou Jordi Cruz Marcelo Blanco Jaume Tomàs Joaquín de los Ríos Manel Alcalà | 2012 | Journal of Pharmaceutical Analysis2012，2，2： | 4 |
| 3 | Treatment of chronic hepatitis C with direct-acting antivirals: The role of resistance显示文摘The use of direct-acting antivirals(DAAs) to treat chronic hepatitis C has resulted in a significant increase in rates of sustained viral response(around 90%-95%) as compared with the standard treatment of peginterferon/ribavirin. Despite this, however, the rates of therapeutic failure in daily clinical practice range from 10%-15%. Most of these cases are due to the presence of resistant viral variants, resulting from mutations produced by substitutions of amino acids in the viral target protein that reduce viral sensitivity to DAAs, thus limiting the efficacy of these drugs. The high genetic diversity of hepatitis C virus has resulted in the existence of resistance-associated variants(RAVs), sometimes even before starting treatment with DAAs, though generally at low levels. These preexisting RAVs do not appear to impact on the sustained viral response, whereas those that appear after DAA therapy could well be determinant in virological failure with future treatments. As well as the presence of RAVs, virological failure to treatment with DAAs is generally associated with other factors related with a poor response, such as the degree of fibrosis, the response to previous therapy, the viral load or the viral genotype. Nonetheless, viral breakthrough and relapse can still occur in the absence of detectable RAVs and after the use of highly effective DAAs, so that the true clinical impact of the presence of RAVs in therapeutic failure remains to be determined. | Miguel Jiménez-Pérez Rocío González-Grande Pilar Espana Contreras Isabel Pinazo Martínez Jesús de la Cruz Lombardo Raúl Olmedo Martín | 2016 | World Journal of Gastroenterology2016，22，29： | 3 |
| 4 | Prophylaxis with ketotifen in rats with portal hypertension:involvement of mast cell and eicosanoids显示文摘BACKGROUND:Since we have previously shown an increase of mast cells in the small bowel and in the mesenteric lymph nodes in the rats with prehepatic portal hypertension,it can be hypothesized that this essential inflammatory cell would be involved in the pathogeny of the splanchnic changes related to portal hypertension. METHODS:To verify this hypothesis,we first studied mast cell infiltration in the ileum and in the mesenteric lymph nodes in sham-operated male Wistar rats(n=12) and in short-term prehepatic portal hypertensive rats (n=12),and the serum levels of rat mast cell protease Ⅱ(RMCP-Ⅱ)by ELISA.In a second set of experiments ketotifen,a mast cell stabilizer drug,was administered to sham-operated(n=10)and portal hypertensive(n=12) rats 24 hours before the intervention and prostanoids (PGE2,PGI2,TXB2)and leukotrienes(LTC4,LTB4)were assayed by RIA,mast cell infiltration in the ileum and in the mesenteric lymph nodes and the serum levels of RMCP-Ⅱwere also studied,to show its effectiveness to prevent the mesenteric alterations produced by the inflammatory mediators released by the mast cell. RESULTS:Forty-eight hours after the intervention RMCP-Ⅱ (P<0.05),PGE2(P<0.001)and LTC4 serum levels decreased and mast cell number and RMCP-Ⅱlevels increased in mesenteric lymph nodes in portal hypertensive rats.Prophylactic administration of ketotifen reduced portal pressure(P<0.001),serum levels of PGE2(P<0.001)and RMCP-Ⅱ(P<0.001)in mesenteric lymph nodes. CONCLUSIONS:In acute portal hypertension in the rat,the mast cell translocation from intestinal mucosa to mesenteric lymph nodes,where they are activated and degranulates,would represent a defence mechanism to avoid the activation of an acute and massive inflammatory response in this location.Prophylactic administration of ketotifen is able to reduce the splanchnic inflammatory changes related to acute portal hypertension in the rat. | Fernando Sánchez-Patán Raquel Anchuelo Elena Vara Cruz García Yolanoa Saavedra Patri Vergara Carmen Cuellar Marta Rodero Maria-Angeles Aller Jaime Arias | 2008 | Hepatobiliary & Pancreatic Diseases International2008，7，4： | 2 |
| 5 | Insulin resistance impairs sustained response rate to peginterferon plus ribavirin in chronic hepatitis C patients显示文摘 | Manuel Romero-Gómez Maria Del Mar Viloria Raúl J. Andrade Javier Salmerón Moisés Diago Conrado M. Fernández-Rodríguez Raquel Corpas Marina Cruz Lourdes Grande Luis Vázquez Paloma Mu?oz-de-Rueda Pilar López-Serrano Ana Gila María L. Gutiérrez Celia Pérez A | 2005 | Gastroenterology2005，，3： | 2 |
| 6 | Percutaneous fixation of displaced proximal humeral fractures: Indications based on the correlation between clinical and radiographic results显示文摘 | Emilio Calvo Ignacio de Miguel Juan J. de la Cruz Néstor López-Martín | 2007 | Journal of Shoulder and Elbow Surgery2007，，6： | 2 |
| 7 | Laparoscopy-assisted versus open colectomy for treatment of colon cancer in the elderly: morbidity and mortality outcomes in 545 patients显示文摘 | Francesc Vallribera Valls Filippo Landi Eloy Espín Basany José Luis Sánchez García Luis Miguel Jiménez Gómez Marc Martí Gallostra Luis Salgado Cruz Manuel Armengol Carrasco | 2014 | Surgical Endoscopy2014，，12： | 2 |
| 8 | Hepatic lipid metabolism changes in short-and long-term prehepatic portal hypertensive rats显示文摘AIM: To verify the impairment of the hepatic lipid metabolism in prehepatic portal hypertension. METHODS: The concentrations of free fatty acids, diacylglycerol, triglycerides, and phospholipids were assayed by using D-[U-14C] glucose incorporation in the different lipid fractions and thin-layer chromatography and cholesterol was measured by spectrophotometry, in liver samples of Wistar rats with partial portal vein ligation at short- (1 mo) and long-term (1 year) (i.e. portal hypertensive rats) and the control rats. RESULTS: In the portal hypertensive rats, liver phospholipid synthesis significantly decreased (7.42 ± 0.50 vs 4.70 ± 0.44 nCi/g protein; P < 0.01) and was associated with an increased synthesis of free fatty acids (2.08 ± 0.14 vs 3.36 ± 0.33 nCi/g protein; P < 0.05), diacylglycerol (1.93 ± 0.2 vs 2.26 ± 0.28 nCi/g protein), triglycerides (2.40 ± 0.30 vs 4.49 ± 0.15 nCi/g protein) and cholesterol (24.28 ± 2.12 vs 57.66 ± 3.26 mg/g protein; P < 0.01). CONCLUSION: Prehepatic portal hypertension in rats impairs the liver lipid metabolism. This impairment consists in an increase in lipid deposits (triglycerides,diacylglycerol and cholesterol) in the liver, accompanied by a decrease in phospholipid synthesis. | Maria-Angeles Aller Elena Vara Cruz García Maria-Paz Nava Alejandra Angulo Fernando Sánchez-Patán Ana Calderón Patri Vergara Jaime Arias | 2006 | World Journal of Gastroenterology2006，12，42： | 2 |
| 9 | Contrasted effect of biochar and earthworms on rice growth and resource allocation in different soils显示文摘 | Diana Noguera Marco Rondón Kam-Rigne Laossi Valerio Hoyos Patrick Lavelle Maria Helena Cruz de Carvalho Sébastien Barot | 2010 | Soil Biology and Biochemistry2010，，7： | 2 |
| 10 | Measurement of the integrated luminosity of the Phase 2 data of the Belle Ⅱ experiment显示文摘From April to July 2018,a data sample at the peak energy of the T(4 S) resonance was collected with the Belle Ⅱ detector at the SuperKEKB electron-positron collider.This is the first data sample of the Belle Ⅱ experiment.Using Bhabha and digamma events,we measure the integrated luminosity of the data sample to be(496.3±0.3±3.0) pb-1,where the first uncertainty is statistical and the second is systematic.This work provides a basis for future luminosity measurements at Belle Ⅱ. | F.Abudinén I.Adachi P.Ahlburg H.Aihara N.Akopov A.Aloisio F.Ameli L.Andricek N.Anh Ky D.M.Asner H.Atmacan T.Aushev V.Aushev T.Aziz K.Azmi V.Babu S.Baehr S.Bahinipati A.M.Bakich P.Bambade Sw.Banerjee S.Bansal V.Bansal M.Barrett J.Baudot A.Beaulieu J.Becker P.K.Behera J.V.Bennett E.Bernieri F.U.Bernlochner M.Bertemes M.Bessner S.Bettarini V.Bhardwaj F.Bianchi T.Bilka S.Bilokin D.Biswas G.Bonvicini A.Bozek M.Bračko P.Branchini N.Braun T.E.Browder A.Budano S.Bussino M.Campajola L.Cao G.Casarosa C.Cecchi D.Červenkov M.-C.Chang P.Chang R.Cheaib V.Chekelian Y.Q.Chen Y.-T.Chen B.G.Cheon K.Chilikin H.-E.Cho K.Cho S.Cho S.-K.Choi S.Choudhury D.Cinabro L.Corona L.M.Cremaldi S.Cunliffe T.Czank F.Dattola E.De La Cruz-Burelo G.De Nardo M.De Nuccio G.De Pietro R.de Sangro M.Destefanis S.Dey A.De Yta-Hernandez F.Di Capua S.Di Carlo J.Dingfelder Z.Doležal I.Domínguez Jiménez T.V.Dong K.Dort S.Dubey S.Duell S.Eidelman M.Eliachevitch T.Ferber D.Ferlewicz G.Finocchiaro S.Fiore A.Fodor F.Forti A.Frey B.G.Fulsom M.Gabriel E.Ganiev M.Garcia-Hernandez R.Garg A.Garmash V.Gaur A.Gaz U.Gebauer A.Gellrich J.Gemmler T.Geßler R.Giordano A.Giri B.Gobbo R.Godang P.Goldenzweig B.Golob P.Gomis P.Grace W.Gradl E.Graziani D.Greenwald C.Hadjivasiliou S.Halder K.Hara T.Hara O.Hartbrich K.Hayasaka H.Hayashii C.Hearty M.T.Hedges I.Heredia de la Cruz M.Hernández Villanueva A.Hershenhorn T.Higuchi E.C.Hill H.Hirata M.Hoek S.Hollitt T.Hotta C.-L.Hsu Y.Hu K.Huang T.Iijima K.Inami G.Inguglia J.Irakkathil Jabbar A.Ishikawa R.Itoh M.Iwasaki Y.Iwasaki S.Iwata P.Jackson W.W.Jacobs D.E.Jaffe E.-J.Jang H.B.Jeon S.Jia Y.Jin C.Joo J.Kahn H.Kakuno A.B.Kaliyar G.Karyan Y.Kato T.Kawasaki H.Kichimi C.Kiesling B.H.Kim C.-H.Kim D.Y.Kim S.-H.Kim Y.K.Kim Y.Kim T.D.Kimmel K.Kinoshita C.Kleinwort B.Knysh P.Kodyš T.Koga I.Komarov T.Konno S.Korpar D.Kotchetkov N.Kovalchuk T.M.G.Kraetzschmar P.Križan R.Kroeger J.F.Krohn P.Krokovny W.Kuehn T.Kuhr M.Kumar R.Kumar K.Kumara S.Kurz A.Kuzmin Y.-J.Kwon S.Lacaprara Y.-T.Lai C.La Licata K.Lalwani L.Lanceri J.S.Lange K.Lautenbach I.-S.Lee S.C.Lee P.Leitl D.Levit P.M.Lewis C.Li L.K.Li S.X.Li Y.M.Li Y.B.Li J.Libby K.Lieret L.Li Gioi J.Lin Z.Liptak Q.Y.Liu D.Liventsev S.Longo A.Loos F.Luetticke T.Luo C.MacQueen Y.Maeda M.Maggiora S.Maity E.Manoni S.Marcello C.Marinas A.Martini M.Masuda K.Matsuoka D.Matvienko J.McNeil J.C.Mei F.Meier M.Merola F.Metzner M.Milesi C.Miller K.Miyabayashi H.Miyata R.Mizuk G.B.Mohanty H.Moon T.Morii H.-G.Moser F.Mueller F.J.Müller Th.Muller R.Mussa K.R.Nakamura E.Nakano M.Nakao H.Nakayama H.Nakazawa M.Nayak G.Nazaryan D.Neverov M.Niiyama N.K.Nisar S.Nishida K.Nishimura M.Nishimura M.H.A.Nouxman B.Oberhof S.Ogawa Y.Onishchuk H.Ono Y.Onuki P.Oskin H.Ozaki P.Pakhlov G.Pakhlova A.Paladino T.Pang E.Paoloni H.Park S.-H.Park B.Paschen A.Passeri S.Patra S.Paul T.K.Pedlar I.Peruzzi R.Peschke R.Pestotnik M.Piccolo L.E.Piilonen P.L.M.Podesta-Lerma V.Popov C.Praz E.Prencipe M.T.Prim M.V.Purohit P.Rados M.Remnev P.K.Resmi I.Ripp-Baudot M.Ritter M.Ritzert G.Rizzo L.B.Rizzuto S.H.Robertson D.Rodríguez Pérez J.M.Roney C.Rosenfeld A.Rostomyan N.Rout G.Russo D.Sahoo Y.Sakai D.A.Sanders S.Sandilya A.Sangal L.Santelj P.Sartori Y.Sato V.Savinov B.Scavino M.Schram H.Schreeck J.Schueler C.Schwanda A.J.Schwartz B.Schwenker R.M.Seddon Y.Seino A.Selce K.Senyo M.E.Sevior C.Sfienti C.P.Shen H.Shibuya J.-G.Shiu A.Sibidanov F.Simon S.Skambraks R.J.Sobie A.Soffer A.Sokolov E.Solovieva S.Spataro B.Spruck M.Starič S.Stefkova Z.S.Stottler R.Stroili J.Strube M.Sumihama T.Sumiyoshi D.J.Summers W.Sutcliffe M.Tabata M.Takizawa U.Tamponi S.Tanaka K.Tanida H.Tanigawa N.Taniguchi Y.Tao P.Taras F.Tenchini E.Torassa K.Trabelsi T.Tsuboyama N.Tsuzuki M.Uchida I.Ueda S.Uehara T.Uglov K.Unger Y.Unno S.Uno P.Urquijo Y.Ushiroda S.E.Vahsen R.van Tonder G.S.Varner K.E.Varvell A.Vinokurova L.Vitale A.Vossen E.Waheed H.M.Wakeling K.Wan W.Wan Abdullah B.Wang M.-Z.Wang X.L.Wang A.Warburton M.Watanabe S.Watanuki J.Webb S.Wehle N.Wermes C.Wessel J.Wiechczynski P.Wieduwilt H.Windel E.Won S.Yamada W.Yan S.B.Yang H.Ye J.Yelton J.H.Yin M.Yonenaga Y.M.Yook C.Z.Yuan Y.Yusa L.Zani J.Z.Zhang Z.Zhang V.Zhilich Q.D.Zhou X.Y.Zhou V.I.Zhukova V.Zhulanov A.Zupanc | 2020 | Chinese Physics C2020，44，2： | 2 |
| 11 | Allergic rhinitis and its im- pact on asthma (ARIA)2008 update (in collaboration with the World Health Organization,GA(2)LEN and AllerGen)显示文摘 | Bousquet J Khaltaev N Cruz AA | 2008 | Allergy2008，，： | 1 |
| 12 | Cutaneous squamous cell carcinoma:Defining the high -risk variant显示文摘 | Martorell - Calatayud A Sanmartín O Cruz J | 2013 | Actas Dermosifiliogr2013，104，5： | 1 |
| 13 | Erlotinib inhibits progression to dysplasia in a colitis-associated colon cancer model显示文摘AIM:To investigate the role of epidermal growth factor receptor(EGFR) in colitis-associated dysplasia using the EGFR tyrosine kinase inhibitor erlotinib.METHODS:Sprague-Dawley rats received trinitrobenzene sulfonic acid(TNBS;30 mg in 50% ethanol,ic),followed 6 wk later by reactivation with TNBS(5 mg/kg,iv) for 3 d.To induce colitis-associated dysplasia,rats then received TNBS(iv) twice a week for 10 wk.One group received erlotinib(10 mg/kg,ip) for 1 wk before the start of the reactivation of the colitis and 2 wk after(21 d);the rest received the vehicle.After rats were euthanized,the colons were removed and analyzed for damage and expression of the EGFR downstream effectors Erk1/2 and c-Myc.RESULTS:Ninety percent of the vehicle-treated animals had dysplasia in any region of the colon.Erlotinib-treated animals had a significant decrease in the incidence of dysplasia compared to vehicle-treated animals in all regions of the colon(50.00% ± 11.47% vs 90.00% ± 10.00% in proximal,P < 0.05;15.00% ± 8.19% vs 50.00% ± 16.67% in mid,P < 0.05;and 20.00% ± 9.17% vs 70.00% ± 15.28% in distal,P < 0.01).Erlotinib-treated animals also had reduced cell proliferation,reduced active Erk1/2,and reduced c-Myc in colon epithelium compared with the vehicle-treated animals.In vitro,erlotinib treatment was shown to markedly decrease c-Myc and pErk1/2 levels in rat epithelial cells.Proliferation of rat epithelial cells was stimulated by epidermal growth factor and inhibited by erlotinib(P < 0.05).CONCLUSION:Erlotinib can decrease the development of colitis-associated dysplasia,suggesting a potential therapeutic use for erlotinib in patients with long-standing colitis. | Beatriz Pagán Angel A Isidro Myrella L Cruz Domenico Coppola Caroline B Appleyard | 2011 | World Journal of Gastroenterology2011，17，44： | 1 |
| 14 | Allergic rhinitis and its impact on Asthma(ARIA) 2008 update (in collaboration with the World Health Organization,GA(2)LEN and AllerGen) 显示文摘 | BOUSQUET J KHALTAEV N CRUZ A A | 2008 | Allergy2008，6386，： | 1 |
| 15 | Allergic rhinitis and its impact on asthma ( ARIA ) 2008 update ( in collaboration with the World Health Organization ) 显示文摘 | Bousquet J Khaltaev N Cruz KA | 2009 | J Rev Alerg Mex2009，56，2： | 1 |
| 16 | Allergic Rhinitis and its Impact on Asthma(ARIA) 2008 update (in collaboration with the World Health Organization,GA2LEN and AllerGen) 显示文摘 | BOUSQUET J KHALTAEV N CRUZ A A | 2008 | Allergy2008，63，： | 1 |
| 17 | Allergic rhinitis and its impact on asthma (ARIA) 2008 update显示文摘 | Bousquet J Khaltaev N Cruz AA | 2008 | Allergy2008，63，86： | 1 |
| 18 | Hospital-acquired Acute Kidney Injury in the Elderly显示文摘 | Chronopoulos A Cruz D N Roneo C | 2010 | Nat Rev Nephrol2010，6，3： | 1 |
| 19 | The influence of employee motivation on knowledge transfer 显示文摘 | Cruz N M Perez V M Gantero C T | 2009 | Journal of Knowledge Management2009，13，6： | 1 |
| 20 | World incidence of AKI: a meta-analysis显示文摘 | SUSANTITAPHONG P CRUZ D N CERDA J | 2013 | Clin J Am SocNephrol2013，8，9： | 1 |
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