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| 1 | 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 |
| 2 | Impact of an acute hemodynamic response-guided protocol for primary prophylaxis of variceal bleeding显示文摘AIM To evaluate the long-term outcome of an acute hemodynamic response-guided protocol in which acute responders to intravenous propranolol received traditional nonselective beta-blockers(NSBBs) and acute nonresponders received carvedilol.METHODS Retrospective review of a protocol for primary prophylaxis of variceal bleeding guided by the acute hemodynamic response to intravenous propranolol. Fifty-two acute responders treated with traditional NSBB(i.e. propranolol or nadolol) were compared with 24 acute nonresponders receiving carvedilol. A second hemodynamic study was performed in 27 and 13 patients, respectively. The primary endpoint was development of first or further decompensation. Secondary endpoints included death from any cause, association between acute and chronic hemodynamic response, and baseline clinical and laboratory variables related to the acute hemodynamic response.RESULTS Acute responders and acute nonresponders presented similar 1, 2, and 3-year probabilities of first decompensation(NSBB: 0%, 13.7%, 26.1% vs carvedilol: 0%, 20%, 20%, P = 0.968) or further decompensation(21.2%, 26.1%, 40.9% vs 21.2%, 50.0%, 50.0%, P = 0.525). A previous episode of hepatic encephalopathy was the only independent predictor of decompensation [hazard ratio(95% confidence interval): 8.03(2.76-23.37)]. Mortality rates were similar in acute responders and acute nonresponders with compensated(P = 0.428) or decompensated cirrhosis(P = 0.429). No clinical, laboratory, endoscopic or hemodynamic parameter predicted the acute hemodynamic response. In patients receiving traditional NSBB, the acute and chronic changes of hepatic venous pressure gradient were correlated(r = 0.59, P = 0.001). Up to 69.2% of acute nonresponders gained chronic response with carvedilol.CONCLUSION Early identification and treatment with carvedilol of acute nonresponders to intravenous propranolol improves the clinical outcome of this high-risk group of patients, probably due to its greater effects for reducing portal pressure. | José Ignacio Fortea ángela Puente Patricia Ruiz Iranzu Ezcurra Javier Vaquero Antonio Cuadrado María Teresa Arias-Loste Joaquín Cabezas Susana Llerena Paula Iruzubieta Carlos Rodríguez-Lope Patricia Huelin Fernando Casafont Emilio Fábrega Javier Crespo | 2018 | World Journal of Clinical Cases2018，6，13： | 6 |
| 3 | Double-layer graphene for enhanced tunable infrared plasmonics显示文摘Graphene is emerging as a promising material for photonic applications owing to its unique optoelectronic properties.Graphene supports tunable,long-lived and extremely confined plasmons that have great potential for applications such as biosensing and optical communications.However,in order to excite plasmonic resonances in graphene,this material requires a high doping level,which is challenging to achieve without degrading carrier mobility and stability.Here,we demonstrate that the infrared plasmonic response of a graphene multilayer stack is analogous to that of a highly doped single layer of graphene,preserving mobility and supporting plasmonic resonances with higher oscillator strength than previously explored single-layer devices.Particularly,we find that the optically equivalent carrier density in multilayer graphene is larger than the sum of those in the individual layers.Furthermore,electrostatic biasing in multilayer graphene is enhanced with respect to single layer due to the redistribution of carriers over different layers,thus extending the spectral tuning range of the plasmonic structure.The superior effective doping and improved tunability of multilayer graphene stacks should enable a plethora of future infrared plasmonic devices with high optical performance and wide tunability. | Daniel Rodrigo Andreas Tittl Odeta Limaj F Javier García de Abajo Valerio Pruneri Hatice Altug | 2017 | Light(Science & Applications)2017，6，1： | 3 |
| 4 | Liver fat deposition and mitochondrial dysfunction in morbid obesity:An approach combining metabolomics with liver imaging and histology显示文摘AIM: To explore the usefulness of magnetic resonance imaging(MRI) and spectroscopy(MRS) for assessment of non-alcoholic fat liver disease(NAFLD) as compared with liver histological and metabolomics findings. METHODS: Patients undergoing bariatric surgery following procedures involved in laparoscopic sleeve gastrectomy were recruited as a model of obesityinduced NAFLD in an observational, prospective, singlesite, cross-sectional study with a pre-set duration of 1 year. Relevant data were obtained prospectively and surrogates for inflammation, oxidative stress and lipid and glucose metabolism were obtained through standard laboratory measurements. To provide reliable data from MRI and MRS, novel procedures were designed to limit sampling variability and other sources of error using a 1.5T Signa HDx scanner and protocols acquired from the 3D or 2D Fat SAT FIESTA prescription manager. We used our previously described 1H NMRbased metabolomics assays. Data were obtained immediately before surgery and after a 12-mo period including histology of the liver and measurement of metabolites. Values from 1H NMR spectra obtained after surgery were omitted due to technical limitations.RESULTS: MRI data showed excellent correlation with the concentration of liver triglycerides, other hepatic lipid components and the histological assessment, w h i c h e xc l u d e d t h e p r e s e n c e o f n o n-a l c o h o l i c steatohepatitis(NASH). MRI was sufficient to follow up NAFLD in obese patients undergoing bariatric surgery and data suggest usefulness in other clinical situations. The information provided by MRS replicated that obtained by MRI using the-CH3 peak(0.9 ppm), the-CH2- peak(1.3 ppm, mostly triglyceride) and the-CH=CH- peak(2.2 ppm). No patient depicted NASH. After surgery all patients significantly decreased their body weight and steatosis was virtually absent even in patients with previous severe disease. Improvement was also observed in the serum concentrations of selected variables. The most relevant findings using metabolomics indicate increased levels of triglyceride and monounsaturated fatty acids in severe steatosis but those results were accompanied by a significant depletion of diglycerides, polyunsaturated fatty acids, glucose-6-phosphate and the ATP/AMP ratio. Combined data indicated the coordinated action on mitochondrial fat oxidation and glucose transport activity and may support the consideration of NAFLD as a likely mitochondrial disease. This concept may helpto explain the dissociation between excess lipid storage in adipose tissue and NAFLD and may direct the search for plasma biomarkers and novel therapeutic strategies. A limitation of our study is that data were obtained in a relatively low number of patients.CONCLUSION: MRI is sufficient to stage NAFLD in obese patients and to assess the improvement after bariatric surgery. Other data were superfluous for this purpose. | Nahum Calvo Raúl Beltrán-Debón Esther Rodríguez-Gallego Anna Hernández-Aguilera Maria Guirro Roger Mariné-Casadó Lidón Millá Josep M Alegret Fàtima Sabench Daniel del Castillo María Vinaixa Miguelàngel Rodríguez Xavier Correig Roberto García-álvarez Javier A Menendez Jordi Camps Jorge Joven | 2015 | World Journal of Gastroenterology2015，21，24： | 2 |
| 5 | Functional Heterogeneity of Cancer-Associated Fibroblasts from Human Colon Tumors Shows Specific Prognostic Gene Expression Signature显示文摘 | Mercedes Herrera Abul B.M.M.K. Islam Alberto Herrera Paloma Martín Vanesa García Javier Silva Jose M. Garcia Clara Salas Ignacio Casal Antonio García de Herreros Félix Bonilla Cristina Pe?a | 2013 | Clinical Cancer Research2013，，21： | 2 |
| 6 | 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 |
| 7 | Molecular genetics of berry colour variation in table grape显示文摘 | Diego Lijavetzky Leonor Ruiz-García José A. Cabezas María T. Andrés Gemma Bravo Ana Ibá?ez Juan Carre?o Félix Cabello Javier Ibá?ez José M. Martínez-Zapater | 2006 | Molecular Genetics and Genomics2006，，5： | 2 |
| 8 | Theoreti- cal studies of Nz O adsorption and reactivity to Nz and NOon Rh(111)显示文摘 | Paul J F Javier P R Francisco A | 2004 | J Phys Chem B2004，108，17： | 1 |
| 9 | Genetic variability related to serum uric acid concentration and risk of Parkinson’s disease显示文摘 | Isabel González‐Aramburu Pascual Sánchez‐Juan Silvia Jesús Ana Gorostidi Eduardo Fernández‐Juan Fátima Carrillo María Sierra Pilar Gómez‐Garre María T. Cáceres‐Redondo José Berciano Javier Ruiz‐Martínez Onofre Combarros Pablo Mir Jon Infante | 2013 | Mov Disord2013，，： | 1 |
| 10 | A posteriori error estimates for fully discrete nonlinear parabolic problems显示文摘 | Javier F Bosco G A Julia N | 2007 | Comput Methods Appl Mech Engrg2007，196，： | 1 |
| 11 | To adipocyte: a model for integration of endocrine and metabolic signaling, in energy metabolism regulation 显示文摘 | Gema F Javier G A Francisco J M | 2001 | Am J Physiol Endocrinol Metab2001，280，： | 1 |
| 12 | Optical properties of platinum-coated gold nanorods 显示文摘 | Marek Grzelczak Jorge Pe'rez-Juste F Javier Garci'a de Abajo | 2007 | J Phys Chem C2007，111，： | 1 |
| 13 | An economic assessment of proteins recovery from fish meal effluents by uhrafiltration显示文摘 | Marai D A Javier F Rodrigo B | 2004 | Trends in Food Science & Technology2004，15，10： | 1 |
| 14 | Antimicrobial activity of reuterin in combination with nisin against food-borne pathogens显示文摘 | JUAN L A JAVIER F PILAR G | 2004 | International Journal of Food Microbiology2004，95，2： | 1 |
| 15 | Xylanase production by a new alkalitolerant isolate of Bacillus显示文摘 | L'opez C Blanco A Javier Pastor F I | 1998 | Biotechnology Letters1998，20，3： | 1 |
| 16 | Kernel-oriented algorithm for transmission expansion planning显示文摘 | Javier C Felix F Wu A | 2000 | IEEE Trans on Power Systems2000，15，4： | 1 |
| 17 | Antimicrobial activity of reuterin in combination with nisin against food-borne pathogens显示文摘 | Juan L A Javier F Pilar G | 2004 | International Journal of Food Microbiology2004，95，2： | 1 |
| 18 | Rejection after conversion to a proliferation signal inhibitor in chronic heart transplantation显示文摘 | Francisco González‐Vílchez José A. Vázquez de Prada María J. Paniagua Luis Almenar Sonia Mirabet Manuel Gómez‐Bueno Beatriz Díaz‐Molina Jose M. Arizón Juan Delgado Félix Pérez‐Villa María G. Crespo‐Leiro Luis Martínez‐Dolz Eulalia Roig Javier Segovia José | 2013 | Clin Transplant2013，，6： | 1 |
| 19 | Inhibition of angiotensin converting enzyme activity by flavanol-rich foods显示文摘 | Lucas A G Javier I O Cesar G F | 2006 | Journal of Agricultural and Food Chemistry2006，54，1： | 1 |
| 20 | Inflammatory parameters are independently associated with urinary albumin in type 2 diabetes mellitus显示文摘 | Juan F Navarro Carmen Mora Manuel Mac??a Javier Garc??a | 2003 | American Journal of Kidney Diseases2003，，1： | 1 |
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