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| 1 | Helicobacter pylori in human health and disease:Mechanisms for local gastric and systemic effects显示文摘Helicobacter pylori(H. pylori) is present in roughly 50% of the human population worldwide and infection levels reach over 70% in developing countries. The infection has classically been associated with different gastro-intestinal diseases, but also with extra gastric diseases. Despite such associations, the bacterium frequently persists in the human host without inducing disease, and it has been suggested that H. pylori may also play a beneficial role in health. To understand how H. pylori can produce such diverse effects in the human host, several studies have focused on understanding the local and systemic effects triggered by this bacterium. One of the main mechanisms by which H. pylori is thought to damage the host is by inducing local and systemic inflammation. However, more recently, studies are beginning to focus on the effects of H. pylori and its metabolism on the gastric and intestinal microbiome. The objective of this review is to discuss how H. pylori has co-evolved with humans, how H. pylori presence is associated with positive and negative effects in human health and how inflammation and/or changes in the microbiome are associated with the observed outcomes. | Denisse Bravo Anilei Hoare Cristopher Soto Manuel A Valenzuela Andrew FG Quest | 2018 | World Journal of Gastroenterology2018，24，28： | 32 |
| 2 | Helicobacter pylori-induced inflammation and epigenetic changes during gastric carcinogenesis显示文摘The sequence of events associated with the development of gastric cancer has been described as 'the gastric precancerous cascade'. This cascade is a dynamic process that includes lesions, such as atrophic gastritis, intestinal metaplasia and dysplasia. According to this model, Helicobacter pylori(H. pylori) infection targets the normal gastric mucosa causing non-atrophic gastritis, an initiating lesion that can be cured by clearing H. pylori with antibiotics or that may then linger in the case of chronic infection and progress to atrophic gastritis. The presence of virulence factors in the infecting H. pylori drives the carcinogenesis process. Independent epidemiological and animal studies have confirmed the sequential progression of these precancerous lesions. Particularly long-term follow-up studies estimated a risk of 0.1% for atrophic gastritis/intestinal metaplasia and 6% in case of dysplasia for the long-term development of gastric cancer. With this in mind, a better understanding of the genetic and epigenetic changes associated with progression of the cascade is critical in determining the risk of gastric cancer associated with H. pylori infection. In this review, we will summarize some of the mostrelevant mechanisms and focus predominantly but not exclusively on the discussion of gene promoter methylation and mi RNAs in this context. | Manuel A Valenzuela Jimena Canales Alejandro H Corvalán Andrew FG Quest | 2015 | World Journal of Gastroenterology2015，21，45： | 33 |
| 3 | Endoscopic management of esophageal varices显示文摘The rupture of gastric varices results in variceal hemorrhage, which is one the most lethal complications of cirrhosis. Endoscopic therapies for varices aim to reduce variceal wall tension by obliteration of the varix. The two principal methods available for esophageal varices are endoscopic sclerotherapy (EST) and band ligation (EBL). The advantages of EST are that it is cheap and easy to use, and the injection catheter fits through the working channel of a diagnostic gastroscope. Endoscopic variceal ligation obliterates varices by causing mechanical strangulation with rubber bands. The following review aims to describe the utility of EBL and EST in different situations, such as acute bleeding, primary and secondary | Joaquin Poza Cordon Consuelo Froilan Torres Aurora Burgos García Francisco Gea Rodriguez Jose Manuel Suárez de Parga | 2012 | World Journal of Gastrointestinal Endoscopy2012，4，7： | 27 |
| 4 | Alcoholic liver disease:Utility of animal models显示文摘Alcoholic liver disease(ALD) is a major cause of acute and chronic liver injury. Extensive evidence has been accumulated on the pathological process of ALD during the past decades. However, effective treatment options for ALD are very limited due to the lack of suitable in vivo models that recapitulate the full spectrum of ALD. Experimental animal models of ALD, particularly rodents, have been used extensively to mimic human ALD. An ideal animal model should recapitulate all aspects of the ALD process, including significant steatosis, hepatic neutrophil infiltration, and liver injury. A better strategy against ALD depends on clear diagnostic biomarkers, accurate predictor(s) of its progression and new therapeutic approaches to modulate stop or even reverse the disease. Numerous models employing rodent animals have been established in the last decades to investigate the effects of acute and chronic alcohol exposure on the initiation and progression of ALD. Although significant progress has been made in gaining better knowledge on the mechanisms and pathology of ALD, many features of ALD are unknown, and require further investigation, ideally with improved animal models that more effectively mimic human ALD. Although differences in the degree and stages of alcoholic liver injury inevitably exist between animal models and human ALD, the acquisition and translational relevance will be greatly enhanced with the development of new and improved animal models of ALD. | Arantza Lamas-Paz Fengjie Hao Leonard J Nelson Maria Teresa Vázquez Santiago Canals Manuel Gómez del Moral Eduardo Martínez-Naves Yulia A Nevzorova Francisco Javier Cubero | 2018 | World Journal of Gastroenterology2018，24，45： | 26 |
| 5 | Epidemiological Evolution of Lung Cancer in the South of Spain from 1990 to 2010显示文摘Background: Changes in lung cancer has been characterized by the increase of cases among women and the increase in adenocarcinomas among other histological subtypes.Methods: Descriptive analysis of cases diagnosed with lung cancer in Hospital Virgen de las Nieves(Spain) from 1990 to 2010,based on five variables(age, sex, smoking, histology and pathological anatomy). The study establishes associations between these variables and compares the results with the literature.Results: 2,026 patients were diagnosed with lung cancer in this period; 1,838 were males(90.7%) and 188 women(9.3%); 1,892 patients(93.4%) were smokers or ex-smokers and 134(6.6%) had never smoked; the most frequent non-small cell histology types were squamous cell carcinoma and adenocarcinoma and it was the most frequent neoplasia in women and were associated with a lower tobacco consumption.Conclusion: The large majority of lung cancer cases is associated with a history of smoking tobacco and there are histopathological differences according to gender and cumulative tobacco smoke load. | Alberto Caballero Vázquez Ana Dolores Romero Ortiz Jose Manuel González de Vega San Román Raimundo García del Moral Bernardino Alcázar Navarrete | 2018 | 中国肺癌杂志2018，21，1： | 17 |
| 6 | Update on pathogenesis and clinical management of acute pancreatitis显示文摘Acute pancreatitis (AP), defined as the acute nonbacterial inflammatory condition of the pancreas, is derived from the early activation of digestive enzymes found inside the acinar cells, with variable compromise of the gland itself, nearby tissues and other organs. So, it is an event that begins with pancreatic injury, elicits an acute inflammatory response, encompasses a variety of complications and generally resolves over time. Different conditions are known to induce this disorder, although the innermost mechanisms and how they act to develop the disease are still unknown. We summarize some well established aspects. A phase sequence has been proposed: etiology factors generate other conditions inside acinar cells that favor the AP development with some systemic events; genetic factors could be involved as susceptibility and modifying elements. AP is a disease with extremely different clinical expressions. Most patients suffer a mild and limited disease, but about one fifth of cases develop multi organ failure, accompanied by high mortality. This great variability in presentation, clinical course and complications has given rise to the confusion related to AP related terminology. However, consensus meetings have provided uniform definitions, including the severity of the illness. The clinical management is mainly based on the disease′s severity and must be directed to correct the underlying predisposing factors and control the inflammatory process itself. The first step is to determine if it is mild or severe. We review the principal aspects to be considered in this treatment, as reflected in several clinical practice guidelines. For the last 25 years, there has been a global increase in incidence of AP, along with many advances in diagnosis and treatment. However, progress in knowledge of its pathogenesis is scarce. | Dulce M Cruz-Santamaría Carlos Taxonera Manuel Giner | 2012 | World Journal of Gastrointestinal Pathophysiology2012，3，3： | 16 |
| 7 | Tenofovir vs lamivudine plus adefovir in chronic hepatitis B:TENOSIMP-B study显示文摘AIM To demonstrate the non-inferiority(15% non-inferiority limit) of monotherapy with tenofovir disoproxil fumarate(TDF) vs the combination of lamivudine(LAM) plus adefovir dipivoxil(ADV) in the maintenance of virologic response in patients with chronic hepatitis B(CHB) and prior failure with LAM.METHODS This study was a Phase IV prospective, randomized, open, controlled study with 2 parallel groups(TDF and LAM+ADV) of adult patients with hepatitis B e antigen(HBe Ag)-negative CHB, prior failure with LAM, on treatment with LAM+ADV for at least 6 mo, without prior resistance to ADV and with an undetectable viral load at the start of the study, in 14 Spanish hospitals. The follow-up time for each patient was 48 wk after randomization, with quarterly visits in which the viral load, biochemical and serological parameters, adverse effects, adherence to treatment and consumption of hospital resources were analysed.RESULTS Forty-six patients were evaluated [median age: 55.4 years(30.2-75.2); 84.8% male], including 22 patients with TDF and 24 with LAM+ADV. During study development, hepatitis B virus DNA(HBV-DNA) remained undetectable, all patients remained HBe Ag negative, and hepatitis B surface antigen(HBs Ag) positive. Alanine aminotransferase(ALT) values at the end of the study were similar in the 2 groups(25.1± 7.65, TDF vs 24.22 ± 8.38, LAM+ADV, P = 0.646). No significant changes were observed in creatinine or serum phosphorus values in either group. No significant differences between the 2 groups were noted in the identification of adverse effects(AEs)(53.8%, TDF vs 37.5%, LAM+ADV, P = 0.170), and none of the AEs which occurred were serious. Treatment adherence was 95.5% and 83.3% in the TDF and the LAM+ADV groups, respectively(P = 0.488). The costs associated with hospital resource consumption were significantly lower with the TDF treatment than the LAM+ADV treatment(€4943 ± 1059 vs €5811 ± 1538, respectively, P < 0.001).CONCLUSION TDF monotherapy proved to be safe and not inferior to the LAM+ADV combination therapy in maintaining virologic response in patients with CHB and previous LAM failure. In addition, the use of TDF generated a significant savings in hospital costs. | Manuel Rodríguez Juan Manuel Pascasio Enrique Fraga Javier Fuentes Martín Prieto Gloria Sánchez-Antolín Jose Luis Calleja Esther Molina María Luisa García-Buey María Angeles Blanco Javier Salmerón María Lucía Bonet Jose Antonio Pons Jose Manuel González Miguel Angel Casado Francisco Jorquera 无 | 2017 | World Journal of Gastroenterology2017，23，41： | 16 |
| 8 | Hepatoprotective effect of silymarin显示文摘The use of medicinal plants in treating illnesses has been reported since ancestral times.In the case of hepatic diseases,several species such as Silybum marianum,Phyllanthus niruri,and Panus giganteus(Berk.)have been shown to ameliorate hepatic lesions.Silymarin is a natural compound derived from the species Silybum marianum,which is commonly known as Milk thistle.This plant contains at least seven flavoligands and the flavonoid taxifolin.The hepatoprotective and antioxidant activity of silymarin is caused by its ability to inhibit the free radicals that are produced from the metabolism of toxic substances such as ethanol,acetaminophen,and carbon tetrachloride.The generation of free radicals is known to damage cellular membranes and cause lipoperoxidation.Silymarin enhances hepatic glutathione and may contribute to the antioxidant defense of the liver.It has also been shown that silymarin increases protein synthesis in hepatocytes by stimulating RNA polymerase I activity.A previous study on humans reported that silymarin treatment caused a slight increase in the survival of patients with cirrhotic alcoholism compared with untreated controls. | Nancy Vargas-Mendoza Eduardo Madrigal-Santillán ngel Morales-González Jaime Esquivel-Soto Cesar Esquivel-Chirino Manuel García-Luna y González-Rubio Juan A Gayosso-de-Lucio José A Morales-González | 2014 | World Journal of Hepatology2014，6，3： | 12 |
| 9 | Review of natural products with hepatoprotective effects显示文摘The liver is one of the most important organs in the body,performing a fundamental role in the regulationof diverse processes,among which the metabolism,secretion,storage,and detoxification of endogenous and exogenous substances are prominent.Due to these functions,hepatic diseases continue to be among the main threats to public health,and they remain problems throughout the world.Despite enormous advances in modern medicine,there are no completely effective drugs that stimulate hepatic function,that offer complete protection of the organ,or that help to regenerate hepatic cells.Thus,it is necessary to identify pharmaceutical alternatives for the treatment of liver diseases,with the aim of these alternatives being more effective and less toxic.The use of some plants and the consumption of different fruits have played basic roles in human health care,and diverse scientific investigations have indicated that,in those plants and fruits so identified,their beneficial effects can be attributed to the presence of chemical compounds that are called phytochemicals.The present review had as its objective the collecting of data based on research conducted into some fruits(grapefruit,cranberries,and grapes)and plants[cactus pear(nopal)and cactus pear fruit,chamomile,silymarin,and spirulina],which are consumed frequently by humans and which have demonstrated hepatoprotective capacity,as well as an analysis of a resin(propolis)and some phytochemicals extracted from fruits,plants,yeasts,and algae,which have been evaluated in different models of hepatotoxicity. | Eduardo Madrigal-Santillán Eduardo Madrigal-Bujaidar Isela álvarez-González María Teresa Sumaya-Martínez José Gutiérrez-Salinas Mirandeli Bautista ángel Morales-González Manuel García-Luna y González-Rubio J Leopoldo Aguilar-Faisal José A Morales-González | 2014 | World Journal of Gastroenterology2014，20，40： | 10 |
| 10 | Acute necrotizing pancreatitis: Surgical indications and technical procedures显示文摘Necrosis of pancreatic parenchyma or extrapancreatic tissues is present in 10%-20% of patients with acute pancreatitis, defining the necrotizing presentation frequently associated with high morbidity and mortality rates. During the initial phase of acute necrotizing pancreatitis the most important pillars of medical treatment are fluid resuscitation, early enteral nutrition, endoscopic retrograde colangiopancreatography if associated cholangitis and intensive care unit support. When infection of pancreatic or extrapancreatic necrosis occurs, surgical approach constitutes the most accepted therapeutic option. In this context, we have recently assited to changes in time for surgery(delaying the indication if possible to around 4 wk to deal with 'walledoff' necrosis) and type of access for necrosectomy: from a classical open approach(with closure over large-bore drains for continued postoperative lavage or semiopen techniques with scheduled relaparotomies), trends have changed to a 'step-up' philosophy with initial percutaneous drainage and posterior minimally invasive or endoscopic access to the retroperitoneal cavity for necrosectomy if no improvement has been previously achieved. These approaches are progressively gaining popularity and morbidity and mortality rates have decreased significantly. Therefore, a staged, multidisciplinary, step-up approach with minimally invasive or endoscopic access for necrosectomy is widely accepted nowadays for management of pancreatic necrosis. | José Manuel Aranda-Narváez Antonio Jesús González-Sánchez María Custodia Montiel-Casado Alberto Titos-García Julio Santoyo-Santoyo | 2014 | World Journal of Clinical Cases2014，2，12： | 10 |
| 11 | Hepatobiliary manifestations in inflammatory bowel disease: The gut,the drugs and the liver显示文摘Abnormal liver biochemical tests are present in up to30%of patients with inflammatory bowel disease(IBD),and therefore become a diagnostic challenge.Liver and biliary tract diseases are common extraintestinal manifestations for both Crohn’s disease and ulcerative colitis(UC),and typically do not correlate with intestinal activity.Primary sclerosing cholangitis(PSC)is the most common hepatobiliary manifestation of IBD,and is more prevalent in UC.Approximately 5%of patients with UC develop PSC,with the prevalence reaching up to 90%.Cholangiocarcinoma and colon cancer risks are increased in these patients.Less common disorders include autoimmune hepatitis/PSC overlap syndrome,IgG4-associated cholangiopathy,primary biliary cirrhosis,hepatic amyloidosis,granulomatous hepatitis,cholelithiasis,portal vein thrombosis,liver abscess,and non-alcoholic fatty liver disease.Hepatitis B reactivation during immunosuppressive therapy is a major concern,with screening and vaccination being recommended in serologically negative cases for patients with IBD.Reactivation prophylaxis with entecavir or tenofovir for 6to 12 mo after the end of immunosuppressive therapy is mandatory in patients showing as hepatitis B surface antigen(HBsAg)positive,independently from viral load.HBsAg negative and anti-HBc positive patients,with or without anti-HBs,should be closely monitored,measuring alanine aminotransferase and hepatitis B virus DNA within 12 mo after the end of therapy,and should be treated if the viral load increases.On the other hand,immunosuppressive therapy does not seem to promote reactivation of hepatitis C,and hepatitis C antiviral treatment does not influence IBD natural history either.Most of the drugs used for IBD treatment may induce hepatotoxicity,although the incidence of serious adverse events is low.Abnormalities in liver biochemical tests associated with aminosalicylates are uncommon and are usually not clinically relevant.Methotrexaterelated hepatotoxicity has been described in 14%of patients with IBD,in a dose-dependent manner.Liver biopsy is not routinely recommended.Biologics-related hepatotoxicity is rare,but has been shown most frequently in patients treated with infliximab.Thiopurines have been associated with veno-occlusive disease,regenerative nodular hyperplasia,and liver peliosis.Routine liver biochemical tests are recommended,especially during the first month of treatment.All these conditions should be considered in IBD patients with clinical or biochemical features suggestive of hepatobiliary involvement.Diagnosis and management of these disorders usually involve hepatologists and gastroenterologists due to its complexity. | María Rojas-Feria Manuel Castro Emilio Suárez Javier Ampuero Manuel Romero-Gómez | 2013 | World Journal of Gastroenterology2013，19，42： | 9 |
| 12 | Steatosis and insulin resistance in hepatitis C: A way out for the virus?显示文摘The hepatitis C virus (HCV) induces lipid accumulation in vitro and in vivo. The pathogenesis of steatosis is due to both viral and host factors. Viral steatosis is mostly reported in patients with genotype 3a, whereas meta-bolic steatosis is often associated with genotype 1 and metabolic syndrome. Several molecular mechanisms responsible for steatosis have been associated with the HCV core protein, which is able to induce gene expres-sion and activity of sterol regulatory element binding protein 1 (SREBP1) and peroxisome proliferator-activat-ed receptor γ (PPARγ), increasing the transcription of genes involved in hepatic fatty acid synthesis. Steatosis has been also implicated in viral replication. In infected cells, HCV core protein is targeted to lipid droplets which serve as intracellular storage organelles. These studies have shown that lipid droplets are essential for virus assembly. Thus, HCV promotes steatosis as an eff icient mechanism for stable viral replication. Chronic HCV in-fection can also induce insulin resistance. In patients with HCV, insulin resistance is more strongly associated with viral load than visceral obesity. HCV seems to lead to insulin resistance through interference of intracellular insulin signalling by HCV proteins, mainly, the serine phosphorylation of insulin receptor-1 (IRS-1) and im-pairment of the downstream Akt signalling pathway. The HCV core protein interferes with in vitro insulin signal-ling by genotype-specif ic mechanisms, where the role of suppressor of cytokine signal 7 (SOCS-7) in genotype 3aand mammalian target of rapamycin (mTOR) in geno-type 1 in IRS-1 downregulation play key roles. Steatosis and insulin resistance have been associated with f ibrosis progression and a reduced rate of sustained response to peginterferon plus ribavirin. | José A Del Campo Manuel Romero-Gómez | 2009 | World Journal of Gastroenterology2009，15，40： | 8 |
| 13 | Soluble ST2:A new and promising activity marker in ulcerative colitis显示文摘AIM:To correlate circulating soluble ST2(sST2) levels with the severity of ulcerative colitis(UC) and serum levels of pro-inflammatory cytokines,and to demonstrate the predictive power of sST2 levels for differentiation between active and inactive UC.METHODS:We recruited 153 patients:82 with UC,26 with Crohn's disease(CD) and 43 disease controls [non-inflammatory bowel disease(IBD)].Subjects were excluded if they had diagnosis of asthma,autoimmune diseases or hypertension.The serum levels of sST2 and pro-inflammatory cytokines [pg/mL;median(25th-75th)] as well as clinical features,endoscopic and histological features,were subjected to analyses.The sST2 performance for discrimination between active and inactive UC,non-IBD and healthy controls(HC) was determined with regard to sensitivity and specificity,and Spearman's rank correlation coefficient(r).To validate the method,the area under the curve(AUC) of receiver-operator characteristic(ROC) was determined(AUC,95% CI) and the total ST2 content of the colonic mucosa in UC patients was correlated with circulating levels of sST2.RESULTS:The serum sST2 value was significantly higher in patients with active [235.80(90.65-367.90) pg/mL] rather than inactive UC [33.19(20.04-65.32) pg/mL],based on clinical,endoscopic and histopathological characteristics,as well as compared with non-IBD and HC(P < 0.001).The median level of sST2 in CD patients was 54.17(35.02-122.0) pg/mL,significantly higher than that of the HC group only(P < 0.01).The cutoff was set at 74.87 pg/mL to compare active with inactive UC in a multicenter cohort of patients.Values of sensitivity,specificity,and ability to correctly classify UC,according to activity,were 83.33%,83.33% and 83.33%,respectively.The AUC of the ROC curve to assess the ability of this molecule to discriminate between active vs inactive UC was 0.92(0.86-0.97,P < 0.0001).The serum levels of sST2 in patients with UC significantly correlated with endoscopic and histo-pathological scores(r = 0.76 and r = 0.67,P < 0.0001,respectively),and with the pro-inflammatory cytokine,tumor necrosis factor-α(r = 0.69 and r = 0.61,respectively,P < 0.0001).Interestingly,we found a direct correlation between total intestinal ST2 content and serum levels of sST2,adjusted to endoscopic activity score in patients with mild(r = 0.44,P = 0.004),moderate(r = 0.59,P = 0.002) and severe disease(r = 0.82,P = 0.002).Only patients with inactive UC showed no significant correlation(r = 0.45,P = 0.267).CONCLUSION:sST2 levels correlated with disease severity and inflammatory cytokines,are able to differentiate active from inactive UC and might have a role as a biomarker. | David Díaz-Jiménez Lucía E Núez Caroll J Beltrán Enzo Candia Cristóbal Suazo Manuel varez-Lobos María-Julieta González Marcela A Hermoso Rodrigo Quera | 2011 | World Journal of Gastroenterology2011，17，17： | 8 |
| 14 | Modulation of faecal metagenome in Crohn's disease:Role of microRNAs as biomarkers显示文摘BACKGROUND The gut microbiota plays a key role in the maintenance of intestinal homeostasis and the development and activation of the host immune system. It has been shown that commensal bacterial species can regulate the expression of host genes. 16 S rRNA gene sequencing has shown that the microbiota in inflammatory bowel disease(IBD) is abnormal and characterized by reduced diversity. Micro RNAs(miRNAs) have been explored as biomarkers and therapeutic targets, since they are able to regulate specific genes associated with Crohn's disease(CD). In this work, we aim to investigate the composition of gut microbiota of active treatment-na?ve adult CD patients, with miRNA profile from gut microbiota.AIM To investigate the composition of gut microbiota of active treatment-na?ve adult CD patients, with miRNA profile from gut microbiota.METHODS Patients attending the outpatient clinics at Valme University Hospital without relevant co-morbidities were matched according to age and gender. Faecal samples of newonset CD patients, free of treatment, and healthy controls were collected. Faecal samples were homogenized, and DNA was amplified by PCR using primers directed to the 16 S bacterial rRNA gene. Pyrosequencing was performed using GS-Junior platform. For sequence analysis, MGRAST server with the database Ribosomal Project was used. MiRNA profile and their relative abundance were analyzed by quantitative PCR.RESULTS Microbial community was characterized using 16 S rRNA gene sequencing in 29 samples(n = 13 CD patients, and n = 16 healthy controls). The mean Shannon diversity was higher in the healthy control population compared to CD group(5.5 vs 3.7). A reduction in Firmicutes and an increase in Bacteroidetes were found. Clostridia class was also significantly reduced in CD. Principal components analysis showed a grouping pattern, identified in most of the subjects in both groups, showing a marked difference between control and CD groups. A functional metabolic study showed that a lower metabolism of carbohydrates(P = 0.000) was found in CD group, while the metabolism of lipids was increased. In CD patients, three miRNAs were induced in affected mucosa: mir-144(6.2 ± 1.3 fold), mir-519(21.8 ± 3.1) and mir-211(2.3 ± 0.4). CONCLUSION Changes in microbial function in active non-treated CD subjects and three miRNAs in affected vs non-affected mucosa have been found. miRNAs profile may serve as a biomarker. | María Rojas-Feria Teresa Romero-García Jose Angel Fernández Caballero-Rico Helena Pastor Ramírez Marta Avilés-Recio Manuel Castro-Fernandez Natalia Chueca Porcuna Manuel Romero-Gomez Federico García Lourdes Grande JoséA Del Campo | 2018 | World Journal of Gastroenterology2018，24，46： | 7 |
| 15 | Peritoneal metastases of colorectal origin treated by cytoreduction and HIPEC: An overview显示文摘Colorectal peritoneal carcinomatosis was considered a terminal condition with a merely palliative treatment that included only supportive care, palliative surgery and the best systemic chemotherapy. Since the birth of a new approach, cytoreductive surgery with peritonectomy procedures together with hyperthermic intraperitoneal chemotherapy and/or early postoperative intraperitoneal chemotherapy to treat peritoneal carcinomatosis, many research groups contributed with promising results using this procedure being up to date this strategy the only one that has shown curative benefits on colorectal peritoneal carcinomatosis achieving reported overall survival rates up to 64 mo and fiveyear survival rates up to 51%. The aim of this paper is to expose an updated overview of the therapeutic possibilities of these procedures in colorectal peritoneal metastases in the same way that our Unit of Oncologic Surgery has performed since 1997 with more than four hundred procedures. | Alvaro Arjona-Sánchez Francisco Javier Medina-Fernández Francisco Cristobal Mu?oz-Casares Angela Casado-Adam Juan Manuel Sánchez-Hidalgo Sebastián Rufián-Pe?a | 2014 | World Journal of Gastrointestinal Oncology2014，6，10： | 7 |
| 16 | SIRT3-mediated inhibition of FOS through histone H3 deacetylation prevents cardiac fibrosis and inflammation显示文摘Sirtuin 3(SIRT3)is a deacetylase that modulates proteins that control metabolism and protects against oxidative stress.Modulation of SIRT3 activity has been proposed as a promising therapeutic target for ameliorating metabolic diseases and associated cardiac disturbances.In this study,we investigated the role of SIRT3 in inflammation and fibrosis in the heart using male mice with constitutive and systemic deletion of SIRT3 and human cardiac AC16 cells.SIRT3 knockout mice showed cardiac fibrosis and inflammation that was characterized by augmented transcriptional activity of AP-1.Consistent with this,SIRT3 overexpression in human and neonatal rat cardiomyocytes partially prevented the inflammatory and profibrotic response induced by TNF-α.Notably,these effects were associated with a decrease in the mRNA and protein levels of FOS and the DNA-binding activity of AP-1.Finally,we demonstrated that SIRT3 inhibits FOS transcription through specific histone H3 lysine K27 deacetylation at its promoter.These findings highlight an important function of SIRT3 in mediating the often intricate profibrotic and proinflammatory responses of cardiac cells through the modulation of the FOS/AP-1 pathway.Since fibrosis and inflammation are crucial in the progression of cardiac hypertrophy,heart failure,and diabetic cardiomyopathy,our results point to SIRT3 as a potential target for treating these diseases. | Xavier Palomer MSilvia Román-Azcona Javier Pizarro-Delgado Ana Planavila Francesc Villarroya Brenda Valenzuela-Alcaraz Fátima Crispi Álvaro Sepúlveda-Martínez Irene Miguel-Escalada Jorge Ferrer JFrancisco Nistal Raquel García Mercy MDavidson Emma Barroso Manuel Vázquez-Carrera | 2020 | Signal Transduction and Targeted Therapy2020，5，1： | 7 |
| 17 | Tumor infiltrating lymphocytes in triple negative breast cancer receiving neoadjuvant chemotherapy显示文摘AIM To determine influence of neoadjuvant-chemotherapy(NAC) over tumor-infiltrating-lymphocytes(TIL) intriple-negative-breast-cancer(TNBC).METHODS TILs were evaluated in 98 TNBC cases who came to Instituto Nacional de Enfermedades Neoplasicas from 2005 to 2010. Immunohistochemistry staining for CD3, CD4, CD8 and FOXP3 was performed in tissue microarrays(TMA) sections. Evaluation of H/E in full-face and immunohistochemistry in TMA sections was performed in pre and post-NAC samples. STATA software was used and P value < 0.05 was considered statistically significant. RESULTS Higher TIL evaluated in full-face sections from pre-NAC tumors was associated to pathologic-complete-response(pCR)(P = 0.0251) and outcome(P = 0.0334). TIL evaluated in TMA sections showed low level of agreement with full-face sections(ICC = 0.017-0.20) and was not associated to pCR or outcome. TIL in post-NAC samples were not associated to response or outcome. PostNAC lesions with pC R had similar TIL levels than those without pCR(P = 0.6331). NAC produced a TIL decrease in full-face sections(P < 0.0001). Percentage of TIL subpopulations was correlated with their absolute counts. Higher counts of CD3, CD4, CD8 and FOXP3 in pre-NAC samples had longer disease-free-survival(DFS). Higher counts of CD3 in pre-NAC samples had longer overallsurvival. Higher ratio of CD8/CD4 counts in pre-NAC was associated with pCR. Higher ratio of CD4/FOXP3 counts in pre-NAC was associated with longer DFS. Higher counts of CD4 in post-NAC samples were associated with pCR.CONCLUSION TIL in pre-NAC full-face sections in TNBC are correlated to longer survival. TIL in full-face differ from TMA sections, absolute count and percentage analysis of TIL subpopulation closely related. | Carlos A Castaneda Elizabeth Mittendorf Sandro Casavilca Yun Wu Miluska Castillo Patricia Arboleda Teresa Nunez Henry Guerra Carlos Barrionuevo Ketty Dolores-Cerna Carolina Belmar-Lopez Julio Abugattas Gabriela Calderon Miguel De La Cruz Manuel Cotrina Jorge Dunstan Henry L Gomez Tatiana Vidaurre | 2016 | World Journal of Clinical Oncology2016，7，5： | 6 |
| 18 | Reduced Exposure to Calcineurin Inhibitors Early After Liver Transplantation Prevents Recurrence of Hepatocellular Carcinoma显示文摘 | Manuel Rodríguez-Perálvarez Emmanuel Tsochatzis María Carmen Naveas Giulia Pieri Carmen García-Caparrós James O’Beirne Antonio Poyato-González Gustavo Ferrín-Sánchez Jose Luis Montero-álvarez David Patch Douglas Thorburn Javier Brice?o Manuel De la Mata A | 2013 | Journal of Hepatology2013，，： | 5 |
| 19 | Role of microglial cells in photoreceptor degeneration显示文摘Inherited photoreceptor degeneration in humans constitutes a major cause of irreversible blindness in the world.They comprise various diseases,but retinitis pigmentosa is the most frequently observed.Retinitis pigmentosa is commonly limited to the eye,where there is progressive photoreceptor degeneration,rods and secondarily cones.The mechanisms of cone and rod degeneration continue to be investigated,since most of the mutations causing retinitis pigmentosa affect rods and thus,the secondary death of cones is an intriguing question but,ultimately,the cause of blindness.Understanding the mechanisms of rod and cone degeneration could help us to develop therapies to stop or,at least,slow down the degeneration process.Secondary cone degeneration has been attributed to the trophic dependence between rods and cones,but microglial cell activation could also have a role.In this review,based on previous work carried out in our laboratory in early stages of photoreceptor degeneration in two animal models of retinitis pigmentosa,we show that microglial cell activation is observed prior to the the initiation of photoreceptor death.We also show that there is an increase of the retinal microglial cell densities and invasion of the outer retinal layers by microglial cells.The inhibition of the microglial cells improves photoreceptor survival and morphology,documenting a role for microglial cells in photoreceptor degeneration.Furthermore,these results indicate that the modulation of microglial cell reactivity can be used to prevent or diminish photoreceptor death in inherited photoreceptor degenerations. | Johnny Di Pierdomenico Diego García-Ayuso Marta Agudo-Barriuso Manuel Vidal-Sanz María Paz Villegas-Pérez | 2019 | Neural Regeneration Research2019，14，7： | 4 |
| 20 | Clinicopathological predictors of long-term benefit in breast cancer treated with neoadjuvant chemotherapy显示文摘AIM To investigate the survival impact of clinicopathological factors, including pathological complete response(p CR) and tumor-infiltrating lymphocytes(s TIL) levels according to subtypes, in breast cancer(BC) patients who received neo-adjuvant chemotherapy(NAC).METHODS We evaluated 435 BC patients who presented and received NAC at the Instituto Nacional de Enfermedades Neoplasicas from 2003 to 2014. s TIL was analyzed as the proportion of tumor stroma occupied by lymphocytes, and was prospectively evaluated on hematoxylin and eosin-stained sections of the preN AC core biopsy. p CR was considered in the absence of infiltrating cancer cells in primary tumor and axillary lymph nodes. Analysis of statistical association between clinical pathological features, s TIL, p CR and survival were carried out using SPSSvs19.RESULTS Median age was 49 years(range 24-84 years) and the most frequent clinical stage was ⅢB(58.3%). Luminal A, Luminal B, HER2-enriched and(triple-negative) TN phenotype was found in 24.6%, 37.9%, 17.7% and 19.8%, respectively. p CR was observed in 11% and median percentage of s TIL was 40%(2%-95%) in the whole population. p CR was associated to Ct1-2(P = 0.045) and to high s TIL(P = 0.029) in the whole population. There was a slight trend towards significance for s TIL(P = 0.054) in Luminal A. s TIL was associated with grade Ⅲ(P < 0.001), no-Luminal A subtype(P < 0.001), RE-negative(P < 0.001), PgR-negative(P < 0.001), HER2-positive(P = 0.002) and p CR(P = 0.029) in the whole population. Longer disease-free survival was associated with grade Ⅰ-Ⅱ(P = 0.006), cN 0(P < 0.001), clinical stage Ⅱ(P = 0.004), ER-positive(P < 0.001), Pg R-positive(P < 0.001), luminal A(P < 0.001) and p CR(P = 0.002). Longer disease-free survival was associated with grade Ⅰ-Ⅱ in Luminal A(P < 0.001), N0-1 in Luminal A(P = 0.045) and TNBC(P = 0.01), clinical stage Ⅱ in Luminal A(P = 0.003) and TNBC(P = 0.038), and pC R in TNBC(P < 0.001). Longer overall survival was associated with grade Ⅰ-Ⅱ(P < 0.001), ER-positive(P < 0.001), PgR-positive(P < 0.001), Luminal A(P < 0.001), cN 0(P = 0.002) and p CR(P = 0.002) in the whole population. Overall survival was associated with clinical stage Ⅱ(P = 0.017) in Luminal A, older age(P = 0.042) in Luminal B, and pC R in TNBC(P = 0.005).CONCLUSION Predictive and prognostic values of clinicopathological features, like p CR and s TIL, differ depending on the evaluated molecular subtype. | Marco Galvez Carlos A Castaneda Joselyn Sanchez Miluska Castillo Lia Pamela Rebaza Gabriela Calderon Miguel De La Cruz Jose Manuel Cotrina Julio Abugattas Jorge Dunstan Henry Guerra Omar Mejia Henry L Gomez | 2018 | World Journal of Clinical Oncology2018，9，2： | 4 |
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