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| 1 | Naringenin prevents experimental liver fibrosis by blocking TGFβ-Smad3 and JNK-Smad3 pathways显示文摘AIM To study the molecular mechanisms involved in the hepatoprotective effects of naringenin(NAR)on carbon tetrachloride(CCl4)-induced liver fibrosis.METHODS Thirty-two male Wistar rats(120-150 g)were randomly divided into four groups:(1)a control group(n=8)that received 0.7%carboxy methyl-cellulose(NAR vehicle)1 m L/daily p.o.;(2)a CCl4 group(n=8)that received 400 mg of CCl4/kg body weight i.p.3 times a week for 8 wk;(3)a CCl4+NAR(n=8)group that received 400 mg of CCl4/kg body weight i.p.3times a week for 8 wk and 100 mg of NAR/kg body weight daily for 8 wk p.o.;and(4)an NAR group(n=8)that received 100 mg of NAR/kg body weight daily for 8 wk p.o.After the experimental period,animals were sacrificed under ketamine and xylazine anesthesia.Liver damage markers such as alanine aminotransferase(ALT),alkaline phosphatase(AP),γ-glutamyl transpeptidase(γ-GTP),reduced glutathione(GSH),glycogen content,lipid peroxidation(LPO)and collagen content were measured.The enzymatic activity of glutathione peroxidase(GPx)was assessed.Liver histopathology was performed utilizing Masson’s trichrome and hematoxylin-eosin stains.Zymography assays for MMP-9 and MMP-2 were carried out.Hepatic TGF-β,α-SMA,CTGF,Col-I,MMP-13,NF-κB,IL-1,IL-10,Smad7,Smad3,p Smad3 and p JNK proteins were detected via western blot.RESULTS NAR administration prevented increases in ALT,AP,γ-GTP,and GPx enzymatic activity;depletion of GSH and glycogen;and increases in LPO and collagen produced by chronic CCl4 intoxication(P<0.05).Liver histopathology showed a decrease in collagen deposition when rats received NAR in addition to CCl4.Although zymography assays showed that CCl4 produced an increase in MMP-9 and MMP-2gelatinase activity;interestingly,NAR administration was associated with normal MMP-9 and MMP-2 activity(P<0.05).The anti-inflammatory,antinecrotic and antifibrotic effects of NAR may be attributed to its ability to prevent NF-κB activation and the subsequent production of IL-1 and IL-10(P<0.05).NAR completely prevented the increase in TGF-β,α-SMA,CTGF,Col-1,and MMP-13 proteins compared with the CCl4-treated group(P<0.05).NAR prevented Smad3phosphorylation in the linker region by JNK since this flavonoid blocked this kinase(P<0.05).CONCLUSION NAR prevents CCl4 induced liver inflammation,necrosis and fibrosis,due to its antioxidant capacity as a free radical inhibitor and by inhibiting the NF-κB,TGF-β-Smad3 and JNK-Smad3 pathways. | Erika Hernández-Aquino Natanael Zarco Sael Casas-Grajales Erika Ramos-Tovar Rosa E Flores-Beltrán Jonathan Arauz Mineko Shibayama Liliana Favari Víctor Tsutsumi José Segovia Pablo Muriel | 2017 | World Journal of Gastroenterology2017，23，24： | 10 |
| 2 | Addition of statins to the standard treatment in patients with cirrhosis:Safety and efficacy显示文摘This review summarizes the safety and efficacy of statins in patients with cirrhosis.Due to concerns about the safety of statins in patients with impaired liver function,they have recently been investigated as a potential treatment option in cirrhosis.The most clinically significant adverse event is statin-related myopathy,and this may be related to the high serum statin concentrations in the setting of severely impaired liver function.Rhabdomyolysis is the most serious and potentially life-threatening manifestation.It has recently been demonstrated that the recommended dose of simvastatin in patients with decompensated cirrhosis would be 20 mg/d because higher values,such as 40 mg/d,are associated with many adverse events,especially muscle injury.Likewise,simvastatin should not be administered to patients with Model for End-stage Liver Disease score>12 and/or Child-Pugh class C because of the high risk of severe muscle injury.Due to the pleiotropic effects,the focus on statins has shifted from being considered harmful to something useful.Through these effects,statins could prevent liver-related morbidity and mortality in cirrhotic patients.Observational studies in large populations of patients with cirrhosis have shown that treatment with statins to decrease high cholesterol levels was associated with a reduced risk of hepatic decompensation,hepatocellular carcinoma development and death.The few randomized controlled trials in patients with cirrhosis and portal hypertension showed that statins lower portal pressure,quite likely through a reduction in hepatic resistance.Another large randomized controlled trial in patients with variceal bleeding showed that simvastatin in addition to standard of care did not prevent rebleeding but improved survival rate.Despite these encouraging outcomes,the quality of the evidence regarding the use of statins is low or very low due to the observational characteristics of most of the studies involved.Therefore,it is advisable to perform further randomized controlled trials on a large series of patients with hard clinical endpoints,using different statin types and varying doses.The objectives would be to prevent liver-related morbidity and mortality rather than treating cirrhosis complications to take additional information that makes it possible to add statins to the standard of care of these patients. | Alberto E Muñoz Florencia D Pollarsky Mónica Marino Mariano Cartier Horacio Vázquez Pablo Salgado Gustavo Romero | 2021 | World Journal of Gastroenterology2021，27，28： | 4 |
| 3 | YKL40 expression in CD14^+ liver cells in acute and chronic injury显示文摘AIM:To demonstrate that CD14 + cells are an important source of the growth factor YKL40 in acute and chronic liver damage.METHODS:Rats were inoculated with one dose of CCl4 to induce acute damage.Liver biopsies were obtained at 0,6,12,24,48 and 72 h.For chronic damage,CCl4 was administered three days per week for 6 or 8 wk.Tissue samples were collected,and cellular populations were isolated by liver digestion and purified by cell sorting.YKL40 mRNA and protein expression were evaluated by realtime polymerase chain reaction and western blot.RESULTS:Acute liver damage induced a rapid increase of YKL40 mRNA beginning at 12 h.Expression peaked at 24 h,with a 26fold increase over basal levels.By 72 h however,YKL40 expression levels had nearly returned to control levels.On the other hand,chronic damage induced a sustained increase in YKL40 expression,with 7and 9fold higher levels at 6 and 8 wk,respectively.The pattern of YKL40 expression in different subpopulations showed that CD14+cells,which include Kupffer cells,are a source of YKL40 after acute damage at 72 h[0.09 relative expression units(REU)]as well as after chronic injury at 6 wk(0.11 REU).Hepatocytes,in turn,accounted for 0.06 and 0.01 REU after 72 h(acute)or 6 wk(chronic),respectively.The rest of the CD14cells(including T lymphocytes,B lymphocytes,natural killer and natural killer T cells) yielded 0.07 and 0.15 REU at 72 h and 6 wk,respectively.YKL40 protein expression in liver was detected at 72 h as well as 6 and 8 wk,with the highest expression relative to controls(11fold;P≤0.05)seen at 6 wk.Macrophages were stimulated by lipopolysaccharide.We demonstrate that under these conditions,these cells showed maximum expression of YKL40 at 12 h,with P<0.05 compared with controls.CONCLUSION:Hepatic CD14 + cells are an YKL40 mRNA and protein source in acute and chronic liver injury,with expression patterns similar to growth factors implicated in inflammationfibrogenesis. | Oscar Pizano-Martínez Irinea Yaez-Sánchez Pilar Alatorre-Carranza Alejandra Miranda-Díaz Pablo C Ortiz-Lazareno Trinidad García-Iglesias Adrian Daneri-Navarro Mónica Vázquez-Del Mercado Mary Fafutis-Morris Vidal Delgado-Rizo | 2011 | World Journal of Gastroenterology2011，17，33： | 3 |
| 4 | MicroRNAs contribute to ATP-binding cassette transporter-and autophagy-mediated chemoresistance in hepatocellular carcinoma显示文摘Hepatocellular carcinoma(HCC) has an elevated mortality rate, largely because of high recurrence and metastasis. Additionally, the main obstacle during treatment of HCC is that patients usually develop resistance to chemotherapy.Cancer drug resistance involves many different mechanisms, including alterations in drug metabolism and processing, impairment of the apoptotic machine, activation of cell survival signaling, decreased drug sensitivity and autophagy, among others. Nowadays, miRNAs are emerging as master regulators of normal physiology-and tumor-related gene expression. In HCC,aberrant expression of many miRNAs leads to chemoresistance. Herein, we particularly analyzed miRNA impact on HCC resistance to drug therapy. Certain miRNAs target ABC(ATP-binding cassette) transporter genes. As most of these miRNAs are downregulated in HCC, transporter levels increase and intracellular drug accumulation decrease, turning cells less sensitive to death. Others miRNAs target autophagy-related gene expression, inhibiting autophagy and acting as tumor suppressors. Nevertheless, due to its downregulation in HCC, these miRNAs do not inhibit autophagy or tumor growth and, resistance is favored.Concluding, modulation of ABC transporter and/or autophagy-related gene expression or function by miRNAs could be determinant for HCC cell survival under chemotherapeutic drug treatment. Undoubtedly, more insights on the biological processes, signaling pathways and/or molecular mechanisms regulated by miRNAs are needed. Anyway, miRNA-based therapy together with conventional chemotherapeutic drugs has a great future in cancer therapy. | María V Espelt María L Bacigalupo Pablo Carabias María F Troncoso | 2019 | World Journal of Hepatology2019，11，4： | 3 |
| 5 | Functional topology classification of biological computing networks显示文摘 | Pablo B Itay B Vladislav V | 2005 | Natural Computing2005，4，： | 1 |
| 6 | Effect of an axial magnetic field on the flow pattern in a cylindrical floating zone 显示文摘 | Pablo V D Damian R | 2005 | Advances in Space Research2005，36，1： | 1 |
| 7 | Effect of an Axial Magnetic Field on the Flow Pattern in a Cylindrical Floating Zone显示文摘 | Pablo V Rivas D | 2005 | Advances in Space Research2005，36，1： | 1 |
| 8 | Carbon nanofibres and activated carbon nanofibres as electrodes in supercapacitors 显示文摘 | CESAR M PABLO S EDUARDO V | 2005 | Carbon2005，43，3： | 1 |
| 9 | Use of Mfu-galactoside enzymatic activity as ecotoxicological endpoint on rainbow trout red blood cells 显示文摘 | Pablos M V Boleas S Tarazona J V | 1998 | Bulletin of Environmental Contamination and Toxicology1998，61，6： | 1 |
| 10 | Effect of an Axial Magnetic Field on the Flow Pattern in a Cylindrical Floating Zone显示文摘 | Pablo V Rivas D | 2005 | Advances in Space Research2005，36，1： | 1 |
| 11 | Exclusion of Fluoroscopy Use in Catheter Ablation Procedures: Six Years of Experience at a Single Center显示文摘 | JUAN M. FERNáNDEZ‐GóMEZ PABLO MORI?A‐VáZQUEZ ELENA DEL RIO MORALES JOSé VENEGAS‐GAMERO RAFAEL BARBA‐PICHARDO MANUEL HERRERA CARRANZA | 2014 | J Cardiovasc Electrophysiol2014，，6： | 1 |
| 12 | Delignification of Eucalyptusglobulus saplings in two organosolv systems(formic and acetic acid)-Preliminary analysis of dissolved lignins 显示文摘 | Pablo L Juan J V Alberto de V | 2008 | Industrial crops andproducts2008，7，： | 1 |
| 13 | 'Occult' ectopic ACTH secretion syndrome:a case report显示文摘 | Garcia Puente I Sanchez Moro V de Pablos Velasco P | 2000 | An Med Interna2000，17，： | 1 |
| 14 | Determination of tetracycline residues in soil by pressurized liquid extraction and liquid chromatography tandem mass spectrometry显示文摘 | VICENTE A PABLO V R CRISTINA B YOLANDA P | 2009 | Anal Bioanal Chem2009，394，5： | 1 |
| 15 | A mixture of the exclusion process and the voter model显示文摘 | Vladimir Belitsky Pablo Ferrari A Mikhail Menshikov V Serguei Yu Popov | 2001 | Bernoulli2001，7，1： | 1 |
| 16 | Electrochemical and chemical formation of a low-barrier proton transfer complex between the quinone dianion and hydroquinone显示文摘 | Pablo D A Drochss P V Miguel A G | 2012 | Electrochemical Acta2012，81，： | 1 |
| 17 | Gluten immunogenic peptide excretion detects dietary transgressions in treated celiac disease patients显示文摘BACKGROUND Life-long removal of gluten from the diet is currently the only way to manage celiac disease(CeD). Until now, no objective test has proven useful to objectively detect ingested gluten in clinical practice. Recently, tests that determine consumption of gluten by assessing excretion of gluten immunogenic peptides(GIP) in stool and urine have been developed. Their utility, in comparison with conventional dietary and analytical follow-up strategies, has not been fully established.AIM To assess the performance of enzyme-linked immunosorbent assay(ELISA) and point-of-care tests(PoCTs) for GIP excretion in CeD patients on gluten-free diet(GFD).METHODS We conducted an observational, prospective, cross-sectional study in patients following a GFD for at least two years. Using the Gastrointestinal Symptom Rating Scale questionnaire, patients were classified at enrollment as asymptomatic or symptomatic. Gluten consumption was assessed twice by 3-d dietary recall and GIP excretion(by ELISA in stool and PoCTs(commercial kits for stool and urine) in two consecutive samples. These samples and dietary reports were obtained 10 day apart one from the other. Patients were encouraged to follow their usual GFD during the study period.RESULTS Forty-four patients were enrolled, of which 19(43.2%) were symptomatic despite being on a GFD. Overall, 83 sets of stool and/or urine samples were collected.Eleven out of 44 patients(25.0%) had at least one positive GIP test. The occurrence of at least one positive test was 32% in asymptomatic patients compared with 15.8% in symptomatic patients. GIP was concordant with dietary reports in 65.9% of cases(Cohen′s kappa: 0.317). PoCT detected dietary indiscretions. Both ELISA and PoCT in stool were concordant(concomitantly positive or negative) in 67 out of 74(90.5%) samples. Excretion of GIP was detected in 7(8.4%) stool and/or urine samples from patients considered to be strictly compliant with the GFD by dietary reports.CONCLUSION GIP detects dietary transgressions in patients on long-term GFD, irrespective of the presence of symptoms. PoCT for GIP detection constitutes a simple homebased method for self-assessment of dietary indiscretions. | Ana Florencia Costa Emilia Sugai María de la Paz Temprano Sonia Isabel Niveloni Horacio Vázquez María Laura Moreno M.Remedios Domínguez-Flores Alba Mu?oz-Suano Edgardo Smecuol Juan Pablo Stefanolo Andrea F González Angel Cebolla-Ramirez Eduardo Mauri?o Elena F Verdú Julio César Bai | 2019 | World Journal of Gastroenterology2019，25，11： | 1 |
| 18 | Functional topology classification of biological computing networks显示文摘 | Pablo B Itay B Vladislav V | 2005 | Natural Computing2005，4，： | 1 |
| 19 | Photosynthetic plasticity of Nothofagus pumilio seedlings to light intensity and soil moisture 显示文摘 | GUILLERMO M P MARIA V L PABLO L P | 2007 | Forest Ecology and Management2007，243，： | 1 |
| 20 | Are pteural fluid parameters related to the development of residual pleural thickening in tuberculosis?显示文摘 | Pablo A Villena V Echave SJ | 1997 | Chest1997，112，5： | 1 |
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