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| 1 | Acute-on-chronic liver failure:Pathogenesis,prognostic factors and management显示文摘Acute-on-chronic liver failure(ACLF) is increasingly recognized as a complex syndrome that is reversiblein many cases. It is characterized by an acute deterioration of liver function in the background of a pre-existing chronic liver disease often associated with a high short-term mortality rate. Organ failure(OF) is always associated, and plays a key role in determining the course, and the outcome of the disease. The definition of ACLF remains controversial due to its overall ambiguity, with several disparate criteria among various associations dedicated to the study of liver diseases. Although the precise pathogenesis needs to be clarified, it appears that an altered host response to injury might be a contributing factor caused by immune dysfunction, ultimately leading to a pro-inflammatory status, and eventually to OF. The PIRO concept(Predisposition, Insult, Response and Organ Failure) has been proposed to better approach the underlying mechanisms. It is accepted that ACLF is a different and specific form of liver failure, where a precipitating event is always involved, even though it cannot always be ascertained. According to several studies, infections and active alcoholism often trigger ACLF. Viral hepatitis, gastrointestinal haemorrhage, or drug induced liver injury, which can also provoke the syndrome. This review mainly focuses on the physiopathology and prognostic aspects. We believe these features are essential to further understanding and providing the rationale for improveddisease management strategies. | Sara Blasco-Algora José Masegosa-Ataz María Luisa Gutiérrez-García Sonia Alonso-López Conrado M Fernández-Rodríguez | 2015 | World Journal of Gastroenterology2015，21，42： | 45 |
| 2 | Assessment of drug-induced hepatotoxicity in clinical practice: A challenge for gastroenterologists显示文摘Currently, pharmaceutical preparations are serious contributors to liver disease; hepatotoxicity ranking as the most frequent cause for acute liver failure and post-commercialization regulatory decisions. The diagnosis of hepatotoxicity remains a difficult task because of the lack of reliable markers for use in general clinical practice. To incriminate any given drug in an episode of liver dysfunction is a step-by-step process that requires a high degree of suspicion, compatible chronology, awareness of the drug’s hepatotoxic potential, the exclusion of alternative causes of liver damage and the ability to detect the presence of subtle data that favors a toxic etiology. This process is time-consuming and the final result is frequently inaccurate. Diagnostic algorithms may add consistency to the diagnostic process by translating the suspicion into a quantitative score. Such scales are useful since they provide a framework that emphasizes the features that merit attention in cases of suspected hepatic adverse reaction as well. Current efforts in collecting bona fide cases of drug-induced hepatotoxicity will make refinements of existing scales feasible. It is now relatively easy to accommodate relevant data within the scoring system and to delete low-impact items. Efforts should also be directed toward the development of an abridged instrument for use in evaluating suspected drug-induced hepatotoxicity at the very beginning of the diagnosis and treatment process when clinical decisions need to be made. The instrument chosen would enable a confident diagnosis to be made on admission of the patient and treatment to be fine-tuned as further information is collected. | Raúl J Andrade Mercedes Robles Alejandra Fernández-Castaer Susana López-Ortega M Carmen López-Vega M Isabel Lucena | 2007 | World Journal of Gastroenterology2007，13，3： | 18 |
| 3 | Contrast-enhanced ultrasound in diagnosis and characterization of focal hepatic lesions显示文摘The extensive use of imaging techniques in differential diagnosis of abdominal conditions and screening of hepatocellular carcinoma in patients with chronic hepatic diseases,has led to an important increase in identification of focal liver lesions.The development of contrastenhanced ultrasound(CEUS) opens a new window in the diagnosis and follow-up of these lesions.This technique offers obvious advantages over the computed tomography and magnetic resonance,without a decrease in its sensitivity and specificity.The new second generation contrast agents,due to their intravascular distribution,allow a continuous evaluation of the enhancement pattern,which is crucial in characterization of liver lesions.The dual blood supply in the liver shows three different phases,namely arterial,portal and late phases.The enhancement during portal and late phases can give important information about the lesion's behavior.Each liver lesion has a different enhancement pattern that makes possible an accurate approach to their diagnosis.The role of emerging techniques as a contrastenhanced three-dimensional US is also discussed.In this article,the advantages,indications and technique employed during CEUS and the different enhancement patterns of most benign and malignant focal liver lesions are discussed. | Inés Gómez Molins Juan Manuel Fernández Font Juan Carrero álvaro Jose Luís Lledó Navarro Marta Fernández Gil Conrado M Fernández Rodríguez | 2010 | World Journal of Radiology2010，2，12： | 14 |
| 4 | Insulin resistance is associated with subclinical vascular disease in humans显示文摘Insulin resistance is associated with subclinical vascular disease that is not justified by conventional cardiovascular risk factors,such as smoking or hypercholesterolemia.Vascular injury associated to insulin resistance involves functional and structural damage to the arterial wall that includes impaired vasodilation in response to chemical mediators,reduced distensibility of the arterial wall(arterial stiffness),vascular calcification,and increased thickness of the arterial wall.Vascular dysfunction associated to insulin resistance is present in asymptomatic subjects and predisposes to cardiovascular diseases,such as heart failure,ischemic heart disease,stroke,and peripheral vascular disease.Structural and functional vascular disease associated to insulin resistance is highly predictive of cardiovascular morbidity and mortality.Its pathogenic mechanisms remain undefined.Prospective studies have demonstrated that animal protein consumption increases the risk of developing cardiovascular disease and predisposes to type 2 diabetes(T2D)whereas vegetable protein intake has the opposite effect.Vascular disease linked to insulin resistance begins to occur early in life.Children and adolescents with insulin resistance show an injured arterial system compared with youth free of insulin resistance,suggesting that insulin resistance plays a crucial role in the development of initial vascular damage.Prevention of the vascular dysfunction related to insulin resistance should begin early in life.Before the clinical onset of T2D,asymptomatic subjects endure a long period of time characterized by insulin resistance.Latent vascular dysfunction begins to develop during this phase,so that patients with T2D are at increased cardiovascular risk long before the diagnosis of the disease. | María M Adeva-Andany Eva Ameneiros-Rodríguez Carlos Fernández-Fernández Alberto Domínguez-Montero Raquel Funcasta-Calderón | 2019 | World Journal of Diabetes2019，10，2： | 14 |
| 5 | Helicobacter pylori infection as a cause of iron deficiency anaemia of unknown origin显示文摘AIM: To assess the aetiological role of Helicobacter pylori (H. pylori) infection in adult patients with ironrefractory or iron-dependent anaemia of previously unknown origin. METHODS: Consecutive patients with chronic irondeficient anaemia (IDA) with H. pylori infection and a negative standard work-up were prospectively evaluated. All of them had either iron refractoriness or iron dependency. Response to H. pylori eradication was assessed at 6 and 12 mo from follow-up. H. pylori infection was considered to be the cause of the anaemia when a complete anaemia resolution without iron supplements was observed after eradication. RESULTS: H. pylori was eradicated in 88 of the 89 patients. In the non-eradicated patient the four eradicating regimens failed. There were violations of protocol in 4 patients, for whom it was not possible to ascertain the cause of the anaemia. Thus, 84 H. pylori eradicated patients (10 men; 74 women) were available to assess the effect of eradication on IDA. H. pylori infection was considered to be the aetiology of IDA in 32 patients (38.1%; 95%CI: 28.4%-48.8%). This was more frequent in men/postmenopausal women than in premenopausal women (75% vs 23.3%; P < 0.0001) with an OR of 9.8 (95%CI: 3.3-29.6). In these patients, anaemia resolution occurred in the first follow-up visit at 6 mo, and no anaemia or iron deficiency relapse was observed after a mean follow-up of 21 ± 2 mo. CONCLUSION: Gastric H. pylori infection is a frequent cause of iron-refractory or iron-dependent anaemia of previously unknown origin in adult patients. | Helena Monzón Montserrat Forné Maria Esteve Mercé Rosinach Carme Loras Jorge C Espinós Josep M Viver Antonio Salas Fernando Fernández-Baares | 2013 | World Journal of Gastroenterology2013，19，26： | 13 |
| 6 | Prevention of hepatocellular carcinoma in patients with chronic hepatitis B显示文摘Patients with chronic hepatitis B are at significant risk for hepatocellular carcinoma(HCC). Globally,over half a million people each year are diagnosed with HCC,with marked geographical variations. Despite overwhelming evidence for a causal role of hepatitis B virus(HBV) infection in the development of HCC and a well-established relationship between high baseline hepatitis B viral load and cumulative risk of HCC,the molecular basis for this association has not been fully elucidated. In addition,a beneficial role for antiviral therapy in preventing the development of HCC has been difficult to establish. This review examines the biological and molecular mechanisms of HBV-related hepatocarcinogenesis,recent results on the effect of modern nucleos(t)ides on the rate of HCC development in high risk HBV cohorts and the potential mechanisms by which long-term antiviral therapy with potent inhibitors of HBV replication might reduce the risk of HCC in patients with chronic hepatitis B. Although evidence from randomized controlled trials shows the favourable effects of antiviral agentsin achieving profound and durable suppression of HBV DNA levels while improving liver function and histology,robust evidence of other long-term clinical outcomes,such as prevention of HCC,are limited. | Conrado M Fernández-Rodríguez María Luisa Gutiérrez-García | 2014 | World Journal of Gastrointestinal Pharmacology and Therapeutics2014，5，3： | 9 |
| 7 | Gut epithelial barrier dysfunction in humanimmunodeficiency virus-hepatitis C virus coinfectedpatients:Influence on innate and acquired immunity显示文摘Even in cases where viral replication has been controlled by antiretroviral therapy for long periods of time, human immunodeficiency virus(HIV)-infected patients have several non-acquired immunodeficiency syndrome(AIDS) related co-morbidities, including liver disease, cardiovascular disease and neurocognitive decline, which have a clear impact on survival. It has been considered that persistent innate and acquired immune activation contributes to the pathogenesis of these non-AIDS related diseases. Immune activation has been related with several conditions, remarkably with the bacterial translocation related with the intestinal barrier damage by the HIV or by hepatitis C virus(HCV)-related liver cirrhosis. Consequently, increased morbidity and mortality must be expected in HIV-HCV coinfected patients. Disrupted gut barrier lead to an increased passage of microbial products and to an activation of the mucosal immune system and secretion of inflammatory mediators, which in turn might increase barrier dysfunction. In the present review, the intestinal barrier structure, measures of intestinal barrier dysfunction and the modifications of them in HIV monoinfection and in HIV-HCV coinfection will be considered. Both pathogenesis and the consequences for the progression of liver disease secondary to gut microbial fragment leakage and immune activation will be assessed. | Mercedes Márquez Clotilde Fernández Gutiérrez delÁlamo JoséAntonio Girón-González | 2016 | World Journal of Gastroenterology2016，22，4： | 7 |
| 8 | Arachidyl amido cholanoic acid improves liver glucose and lipid homeostasis in nonalcoholic steatohepatitis via AMPK and mTOR regulation显示文摘BACKGROUND Arachidyl amido cholanoic acid(Aramchol)is a potent downregulator of hepatic stearoyl-CoA desaturase 1(SCD1)protein expression that reduces liver triglycerides and fibrosis in animal models of steatohepatitis.In a phase IIb clinical trial in patients with nonalcoholic steatohepatitis(NASH),52 wk of treatment with Aramchol reduced blood levels of glycated hemoglobin A1c,an indicator of glycemic control.AIM To assess lipid and glucose metabolism in mouse hepatocytes and in a NASH mouse model[induced with a 0.1%methionine and choline deficient diet(0.1MCD)]after treatment with Aramchol.METHODS Isolated primary mouse hepatocytes were incubated with 20μmol/L Aramchol or vehicle for 48 h.Subsequently,analyses were performed including Western blot,proteomics by mass spectrometry,and fluxomic analysis with 13C-uniformly labeled glucose.For the in vivo part of the study,male C57BL/6J mice were randomly fed a control or 0.1MCD for 4 wk and received 1 or 5 mg/kg/d Aramchol or vehicle by intragastric gavage for the last 2 wk.Liver metabolomics were assessed using ultra-high-performance liquid chromatography-time of flight-MS for the determination of glucose metabolism-related metabolites.RESULTS Combination of proteomics and Western blot analyses showed increased AMPK activity while the activity of nutrient sensor mTORC1 was decreased by Aramchol in hepatocytes.This translated into changes in the content of their downstream targets including proteins involved in fatty acid(FA)synthesis and oxidation[PACCα/β(S79),SCD1,CPT1A/B,HADHA,and HADHB],oxidative phosphorylation(NDUFA9,NDUFB11,NDUFS1,NDUFV1,ETFDH,and UQCRC2),tricarboxylic acid(TCA)cycle(MDH2,SUCLA2,and SUCLG2),and ribosome(P-p70S6K[T389]and P-S6[S235/S236]).Flux experiments with 13Cuniformely labeled glucose showed that TCA cycle cataplerosis was reduced by Aramchol in hepatocytes,as indicated by the increase in the number of rounds that malate remained in the TCA cycle.Finally,liver metabolomic analysis showed that glucose homeostasis was improved by Aramchol in 0.1MCD fed mice in a dose-dependent manner,showing normalization of glucose,G6P,F6P,UDP-glucose,and Rbl5P/Xyl5P.CONCLUSION Aramchol exerts its effect on glucose and lipid metabolism in NASH through activation of AMPK and inhibition of mTORC1,which in turn activate FAβ-oxidation and oxidative phosphorylation. | David Fernández-Ramos Fernando Lopitz-Otsoa Laura Delacruz-Villar Jon Bilbao Martina Pagano Laura Mosca Maider Bizkarguenaga Marina Serrano-Macia Mikel Azkargorta Marta Iruarrizaga-Lejarreta Jesús Sot Darya Tsvirkun Sebastiaan Martijn van Liempd Felix M Goni Cristina Alonso María Luz Martínez-Chantar Felix Elortza Liat Hayardeny Shelly C Lu JoséM Mato | 2020 | World Journal of Gastroenterology2020，26，34： | 5 |
| 9 | Enhancing survival, engraftment, and osteogenic potential of mesenchymal stem cells显示文摘Mesenchymal stem cells(MSCs)are promising candidates for bone regeneration therapies due to their plasticity and easiness of sourcing.MSC-based treatments are generally considered a safe procedure,however,the long-term results obtained up to now are far from satisfactory.The main causes of these therapeutic limitations are inefficient homing,engraftment,and osteogenic differentiation.Many studies have proposed modifications to improve MSC engraftment and osteogenic differentiation of the transplanted cells.Several strategies are aimed to improve cell resistance to the hostile microenvironment found in the recipient tissue and increase cell survival after transplantation.These strategies could range from a simple modification of the culture conditions,known as cell-preconditioning,to the genetic modification of the cells to avoid cellular senescence.Many efforts have also been done in order to enhance the osteogenic potential of the transplanted cells and induce bone formation,mainly by the use of bioactive or biomimetic scaffolds,although alternative approaches will also be discussed.This review aims to summarize several of the most recent approaches,providing an up-to-date view of the main developments in MSCbased regenerative techniques. | Daniel García-Sánchez Darío Fernández JoséC Rodríguez-Rey Flor M Pérez-Campo | 2019 | World Journal of Stem Cells2019，11，10： | 4 |
| 10 | Systemic, renal, and hepatic hemodynamic derangement in cirrhotic patients with spontaneous bacterial peritonitis显示文摘 | Luis Ruiz-del-Arbol Jesús Urman Javier Fernández Mónica González Miguel Navasa Alberto Monescillo Agustín Albillos Wladimiro Jiménez Vicente Arroyo | 2003 | Hepatology2003，，5： | 4 |
| 11 | Preclinical evaluation of azathioprine plus buthionine sulfoximine in the treatment of human hepatocarcinoma and colon carcinoma显示文摘AIM: To evaluate the efficacy and the safety of azathioprine (AZA) and buthionine sulfoximine (BSO) bylocalized application into HepG2 tumor in vivo.METHODS: Different hepatoma and colon carcinoma cell lines (HepG2, HuH7, Chang liver, LoVo, RKO, SW-48, SW-480) were grown in minimal essencial medium supplemented with 10% fetal bovine serum and 1% antibiotic/antimycotic solution and maintained in a humidified 37 ℃ incubator with 5% CO2. These cells were pretreated with BSO for 24 h and then with AZA for different times. We examined the effects of this combination on some proteins and on cellular death. We also studied the eff icacy and the safety of AZA (6 mg/kg per day) and BSO (90 mg/kg per day) in HepG2 tumor growth in vivo using athymic mice. We measured safety by serological markers such as aminotransferases and creatine kinase.RESULTS: The in vitro studies revealed a new mechanism of action for the AZA plus BSO combination in the cancer cells compared with other thiopurines (6-mercaptopurine, 6-methylmercaptopurine, 6-thioguanine and 6-methylthioguanine) in combination with BSO. The cytotoxic effect of AZA plus BSO in HepG2 cells resulted from necroptosis induction in a mitochondrial-dependent manner. From kinetic studies we suggest that glutathione (GSH) depletion stimulates c-Jun amino-terminal kinase and Bax translocation in HepG2 cells with subsequent deregulation of mitochondria (cytochrome c release, loss of membrane potential), and proteolysis activation leading to loss of membrane integrity, release of lactate dehydrogenase and DNA degradation. Some of this biochemical and cellular changes could be reversed by N-acetylcysteine (a GSH replenisher). In vivo studies showed that HepG2 tumor growth was inhibited when AZA was combined with BSO.CONCLUSION: Our studies suggest that a combination of AZA plus BSO could be useful for localizedtreatment of hepatocellular carcinoma as in the currently used transarterial chemoembolization method. | Borja Hernández-Breijo Jorge Monserrat Sara Ramírez-Rubio Eva P Cuevas Diana Vara Inés Díaz-Laviada M Dolores Fernández-Moreno Irene D Román Javier P Gisbert Luis G Guijarro | 2011 | World Journal of Gastroenterology2011，17，34： | 2 |
| 12 | Susceptibility Genetic Variants Associated With Colorectal Cancer Risk Correlate With Cancer Phenotype显示文摘 | Anna Abulí Xavier Bessa Juan Ramón González Clara Ruiz–Ponte Alejandro Cáceres Jenifer Mu?oz Victoria Gonzalo Francesc Balaguer Ceres Fernández–Rozadilla Dolors González Luisa de Castro Juan Clofent Luís Bujanda Joaquín Cubiella Josep M a Re?é Juan Diego | 2010 | Gastroenterology2010，，3： | 2 |
| 13 | Renal Failure in Patients With Cirrhosis and Sepsis Unrelated to Spontaneous Bacterial Peritonitis: Value of MELD Score显示文摘 | Carlos Terra Mónica Guevara Aldo Torre Rosa Gilabert Javier Fernández Marta Martín-Llahí Maria E. Baccaro Miquel Navasa Conxita Bru Vicente Arroyo Juan Rodés Pere Ginès | 2005 | Gastroenterology2005，，6： | 2 |
| 14 | Dendritic cell deficiencies persist seven months after SARS-CoV-2 infection显示文摘Severe Acute Respiratory Syndrome Coronavirus(SARS-CoV)-2 infection induces an exacerbated inflammation driven by innate immunity components.Dendritic cells(DCs)play a key role in the defense against viral infections,for instance plasmacytoid DCs(pDCs),have the capacity to produce vast amounts of interferon-alpha(IFN-α).In COVID-19 there is a deficit in DC numbers and IFN-αproduction,which has been associated with disease severity.In this work,we described that in addition to the DC deficiency,several DC activation and homing markers were altered in acute COVID-19 patients,which were associated with multiple inflammatory markers.Remarkably,previously hospitalized and nonhospitalized patients remained with decreased numbers of CD1c+myeloid DCs and pDCs seven months after SARS-CoV-2 infection.Moreover,the expression of DC markers such as CD86 and CD4 were only restored in previously nonhospitalized patients,while no restoration of integrinβ7 and indoleamine 2,3-dyoxigenase(IDO)levels were observed.These findings contribute to a better understanding of the immunological sequelae of COVID-19. | Alberto Pérez-Gómez Joana Vitallé Carmen Gasca-Capote Alicia Gutierrez-Valencia María Trujillo-Rodriguez Ana Serna-Gallego Esperanza Muñoz-Muela María de los Reyes Jiménez-Leon Mohamed Rafii-El-Idrissi Benhnia Inmaculada Rivas-Jeremias Cesar Sotomayor Cristina Roca-Oporto Nuria Espinosa Carmen Infante-Domínguez Juan Carlos Crespo-Rivas Alberto Fernández-Villar Alexandre Pérez-González Luis Fernando López-Cortés Eva Poveda Ezequiel Ruiz-Mateos JoséMiguel Cisneros Sonsoles Salto-Alejandre Judith Berastegui-Cabrera Pedro Camacho-Martínez Carmen Infante-Domínguez Marta Carretero-Ledesma Juan Carlos Crespo-Rivas Eduardo Márquez JoséManuel Lomas Claudio Bueno Rosario Amaya JoséAntonio Lepe Jerónimo Pachón Elisa Cordero Javier Sánchez-Céspedes Manuela Aguilar-Guisado Almudena Aguilera Clara Aguilera Teresa Aldabo-Pallas Verónica Alfaro-Lara Cristina Amodeo Javier Ampuero María Dolores Avilés Maribel Asensio Bosco Barón-Franco Lydia Barrera-Pulido Rafael Bellido-Alba Máximo Bernabeu-Wittel Candela Caballero-Eraso Macarena Cabrera Enrique Calderón Jesús Carbajal-Guerrero Manuela Cid-Cumplido Yael Corcia-Palomo Juan Delgado Antonio Domínguez-Petit Alejandro Deniz Reginal Dusseck-Brutus Ana Escoresca-Ortega Fátima Espinosa Nuria Espinosa Michelle Espinoza Carmen Ferrándiz-Millón Marta Ferrer Teresa Ferrer Ignacio Gallego-Texeira Rosa Gámez-Mancera Emilio García Horacio García-Delgado Manuel García-Gutiérrez María Luisa Gascón-Castillo Aurora González-Estrada Demetrio González Carmen Gómez-González Rocío González-León Carmen Grande-Cabrerizo Sonia Gutiérrez Carlos Hernández-Quiles Inmaculada Concepción Herrera-Melero Marta Herrero-Romero Luis Jara Carlos Jiménez-Juan Silvia Jiménez-Jorge Mercedes Jiménez-Sánchez Julia Lanseros-Tenllado Carmina López Isabel López Álvaro López-Barrios Luis F.López-Cortés Rafael Luque-Márquez Daniel Macías-García Guillermo Martín-Gutiérrez Luis Martín-Villén JoséMolina Aurora Morillo María Dolores Navarro-Amuedo Dolores Nieto-Martín Francisco Ortega María Paniagua-García Amelia Peña-Rodríguez Esther Pérez Manuel Poyato Julia Praena-Segovia Rafaela Ríos Cristina Roca-Oporto Jesús F.Rodríguez María Jesús Rodríguez-Hernández Santiago Rodríguez-Suárez Ángel Rodríguez-Villodres Nieves Romero-Rodríguez Ricardo Ruiz Zida Ruiz de Azua Celia Salamanca Sonia Sánchez Víctor Manuel Sánchez-Montagut César Sotomayor Alejandro Suárez Benjumea Javier Toral | 2021 | Cellular & Molecular Immunology2021，18，9： | 2 |
| 15 | 短期常压低氧步行训练对肥胖成年人运动能力和步态的影响显示文摘为了比较以个人喜好的步行速度(preferred walking speed,PWS)短期低氧与常氧训练对肥胖患者的能量、力学、效率和代谢风险标志物的影响,Fernández Menéndez等纳入肥胖患者23例,在缺氧[海拔3km,n=12;体质量指数(body mass index,BMI)(34.0±0.8)kg/m2]或常氧[海拔360m,n=11;BMI(32.9±0.8)kg/m2]情况下. | 刘青 叶鹏 Fernández Menéndez A Saudan G Sperisen L Hans D Saubade M Millet GP Malatesta D | 2018 | 中华高血压杂志2018，26，6： | 2 |
| 16 | Diabetes mellitus, revascularization and outcomes in elderly patients with myocardial infarction-related cardiogenic shock显示文摘Background The prognostic role of diabetes mellitus(DM)in elderly patients with myocardial infarction-related cardiogenic shock(MI-CS)remains controversial.Little information exists about the impact of intensive cardiac care unit(ICCU)and revascularization on outcomes of elderly patients with MI-CS.We aimed to assess the prognostic impact of DM according to age in patients with MI-CS,and to analyze the impact ICCU management and revascularization on in-hospital mortality in MI-CS patients at older ages.Methods Discharge episodes with diagnosis of CS associated with MI were selected from the Spanish National Health System’s Basic Data Set.Centers were classified according to their availability of ICCU.Main outcome measured was in-hospital mortality.Results A total of 23,590 episodes of MI-CS were identified,of whom 12,447(52.8%)were in patients aged≥75 years.The impact of DM on in-hospital mortality was different among age subgroups.While in younger patients,DM was associated to a higher mortality risk(0.52 vs.0.47,OR=1.12,95%CI:1.06–1.18,χ^2<0.001),this association became non-significant in older patients(0.76 vs.0.81,χ^2=0.09).Adjusted mortality rate of MI-CS aged≥75 years was lower in patients admitted to hospitals with ICCU(adjusted mortality rate:74.2%vs.77.7%,P<0.001)and in patients undergoing revascularization(74.9%vs.77.3%,P<0.001).Conclusions Prognostic impact of DM in patients with MI-CS was different according to age,with a significantly lower impact at older ages.The availability of ICCU and revascularization were associated with better outcomes in these complex patients. | Miquel Gual Albert Ariza-Solé María García Márquez Cristina Fernández JoséL Bernal Francesc Formiga María-Isabel Barrionuevo JoséC Sánchez-Salado Victòria Lorente Júlia Pascual Isaac Llaó Oriol Alegre Angel Cequier Javier Elola | 2020 | Journal of Geriatric Cardiology2020，17，10： | 2 |
| 17 | Blatella germanica as a possible cockroach vector of micro-organisms in a hospital显示文摘 | G. Risco Oliva C. Díaz O. Fuentes González M.D. Martínez C. Fernández R. Cordoví P. Más Lago N. Herrera | 2009 | Journal of Hospital Infection2009，，1： | 2 |
| 18 | Alcohol liver disease: A review of current therapeutic approaches to achieve long-term abstinence显示文摘Harmful alcohol drinking may lead to significant damage on any organ or system of the body.Alcoholic liver disease(ALD) is the most prevalent cause of advanced liver disease in Europe.In ALD,only alcohol abstinence was associated with a better long-term survival.Therefore,current effective therapeutic strategy should be oriented towards achieving alcohol abstinence or a significant reduction in alcohol consumption.Screening all primary care patients to detect those cases with alcohol abuse has been proposed as population-wide preventive intervention in primary care.It has been suggested that in patients with mild alcohol use disorder the best approach is brief intervention in the primary care setting with the ultimate goal being abstinence,whereas patients with moderate-to-severe alcohol use disorder must be referred to specialized care where detoxification and medical treatment of alcohol dependence must be undertaken. | María Luisa Gutiérrez García Sara Blasco-Algora Conrado M Fernández-Rodríguez | 2015 | World Journal of Gastroenterology2015，21，28： | 2 |
| 19 | Albumin for bacterial infections other than spontaneous bacterial peritonitis in cirrhosis. A randomized, controlled study显示文摘 | Mónica Guevara Carlos Terra André Nazar Elsa Solà Javier Fernández Marco Pavesi Vicente Arroyo Pere Ginès | 2012 | Journal of Hepatology2012，，4： | 2 |
| 20 | Molecular recognition in a propazine-imprinted polymer and its application to the determination of triazines in environmental samples 显示文摘 | Turiel E Esteban A M Fernández P | 2001 | Anal Chem2001，75，21： | 2 |
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