14 results on '"Serrano-Macia, Marina"'
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2. SUMOylation controls Hu antigen R posttranscriptional activity in liver cancer
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Lachiondo-Ortega, Sofia, Rejano-Gordillo, Claudia M., Simon, Jorge, Lopitz-Otsoa, Fernando, C. Delgado, Teresa, Mazan-Mamczarz, Krystyna, Goikoetxea-Usandizaga, Naroa, Zapata-Pavas, L. Estefanía, García-del Río, Ana, Guerra, Pietro, Peña-Sanfélix, Patricia, Hermán-Sánchez, Natalia, Al-Abdulla, Ruba, Fernandez-Rodríguez, Carmen, Azkargorta, Mikel, Velázquez-Cruz, Alejandro, Guyon, Joris, Martín, César, Zalamea, Juan Diego, Egia-Mendikute, Leire, Sanz-Parra, Arantza, Serrano-Maciá, Marina, González-Recio, Irene, Gonzalez-Lopez, Monika, Martínez-Cruz, Luis Alfonso, Pontisso, Patrizia, Aransay, Ana M., Barrio, Rosa, Sutherland, James D., Abrescia, Nicola G.A., Elortza, Félix, Lujambio, Amaia, Banales, Jesus M., Luque, Raúl M., Gahete, Manuel D., Palazón, Asís, Avila, Matias A., G. Marin, Jose J., De, Supriyo, Daubon, Thomas, Díaz-Quintana, Antonio, Díaz-Moreno, Irene, Gorospe, Myriam, Rodríguez, Manuel S., and Martínez-Chantar, María Luz
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- 2024
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3. Anti-miR-873-5p improves alcohol-related liver disease by enhancing hepatic deacetylation via SIRT1
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Rodríguez-Agudo, Rubén, González-Recio, Irene, Serrano-Maciá, Marina, Bravo, Miren, Petrov, Petar, Blaya, Delia, Herranz, Jose María, Mercado-Gómez, María, Rejano-Gordillo, Claudia María, Lachiondo-Ortega, Sofía, Gil-Pitarch, Clàudia, Azkargorta, Mikel, Van Liempd, Sebastiaan Martijn, Martinez-Cruz, Luis Alfonso, Simão, A.L., Elortza, Félix, Martín, César, Nevzorova, Yulia A., Cubero, Francisco Javier, Delgado, Teresa C., Argemi, Josepmaria, Bataller, Ramón, Schoonjans, Kristina, Banales, Jesús M., Castro, Rui E., Sancho-Bru, Pau, Avila, Matías A., Julve, Josep, Jover, Ramiro, Mabe, Jon, Simon, Jorge, Goikoetxea-Usandizaga, Naroa, and Martínez-Chantar, María L.
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- 2024
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4. Neddylation of phosphoenolpyruvate carboxykinase 1 controls glucose metabolism
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Gonzalez-Rellan, María J., Fernández, Uxía, Parracho, Tamara, Novoa, Eva, Fondevila, Marcos F., da Silva Lima, Natalia, Ramos, Lucía, Rodríguez, Amaia, Serrano-Maciá, Marina, Perez-Mejias, Gonzalo, Chantada-Vazquez, Pilar, Riobello, Cristina, Veyrat-Durebex, Christelle, Tovar, Sulay, Coppari, Roberto, Woodhoo, Ashwin, Schwaninger, Markus, Prevot, Vincent, Delgado, Teresa C., Lopez, Miguel, Diaz-Quintana, Antonio, Dieguez, Carlos, Guallar, Diana, Frühbeck, Gema, Diaz-Moreno, Irene, Bravo, Susana B., Martinez-Chantar, Maria L., and Nogueiras, Ruben
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- 2023
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5. Hepatic levels of S-adenosylmethionine regulate the adaptive response to fasting
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Capelo-Diz, Alba, Lachiondo-Ortega, Sofía, Fernández-Ramos, David, Cañas-Martín, Jorge, Goikoetxea-Usandizaga, Naroa, Serrano-Maciá, Marina, González-Rellan, Maria J., Mosca, Laura, Blazquez-Vicens, Joan, Tinahones-Ruano, Alberto, Fondevila, Marcos F., Buyan, Mason, Delgado, Teresa C., Gutierrez de Juan, Virginia, Ayuso-García, Paula, Sánchez-Rueda, Alejandro, Velasco-Avilés, Sergio, Fernández-Susavila, Héctor, Riobello-Suárez, Cristina, Dziechciarz, Bartlomiej, Montiel-Duarte, Cristina, Lopitz-Otsoa, Fernando, Bizkarguenaga, Maider, Bilbao-García, Jon, Bernardo-Seisdedos, Ganeko, Senra, Ana, Soriano-Navarro, Mario, Millet, Oscar, Díaz-Lagares, Ángel, Crujeiras, Ana B., Bao-Caamano, Aida, Cabrera, Diana, van Liempd, Sebastiaan, Tamayo-Caro, Miguel, Borzacchiello, Luigi, Gomez-Santos, Beatriz, Buqué, Xabier, Sáenz de Urturi, Diego, González-Romero, Francisco, Simon, Jorge, Rodríguez-Agudo, Rubén, Ruiz, Asier, Matute, Carlos, Beiroa, Daniel, Falcon-Perez, Juan M., Aspichueta, Patricia, Rodríguez-Cuesta, Juan, Porcelli, Marina, Pajares, María A., Ameneiro, Cristina, Fidalgo, Miguel, Aransay, Ana M., Lama-Díaz, Tomas, Blanco, Miguel G., López, Miguel, Villa-Bellosta, Ricardo, Müller, Timo D., Nogueiras, Rubén, Woodhoo, Ashwin, Martínez-Chantar, María Luz, and Varela-Rey, Marta
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- 2023
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6. Arachidyl amido cholanoic acid improves liver glucose and lipid homeostasis in nonalcoholic steatohepatitis via AMPK and mTOR regulation
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Fernández-Ramos, David, Lopitz-Otsoa, Fernando, Delacruz-Villar, Laura, Bilbao, Jon, Pagano, Martina, Mosca, Laura, Bizkarguenaga, Maider, Serrano-Macia, Marina, Azkargorta, Mikel, Iruarrizaga-Lejarreta, Marta, Sot, Jesús, Tsvirkun, Darya, van Liempd, Sebastiaan Martijn, Goni, Felix M, Alonso, Cristina, Martínez-Chantar, María Luz, Elortza, Felix, Hayardeny, Liat, Lu, Shelly C, and Mato, José M
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Digestive Diseases ,Liver Disease ,Nutrition ,Hepatitis ,Chronic Liver Disease and Cirrhosis ,AMP-Activated Protein Kinases ,Animals ,Cholic Acids ,Disease Models ,Animal ,Glucose ,Homeostasis ,Humans ,Lipid Metabolism ,Lipids ,Liver ,Male ,Methionine ,Mice ,Mice ,Inbred C57BL ,Non-alcoholic Fatty Liver Disease ,TOR Serine-Threonine Kinases ,Nonalcoholic fatty liver disease ,Steatohepatitis ,Methionine and choline deficient diet ,Tricarboxylic acid cycle ,Hemoglobin A1c ,Stearoyl-CoA desaturase 1 ,Clinical Sciences ,Gastroenterology & Hepatology - Abstract
BackgroundArachidyl 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.AimTo 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.MethodsIsolated primary mouse hepatocytes were incubated with 20 μmol/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.ResultsCombination 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 [P-ACCα/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 13C-uniformely 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.ConclusionAramchol exerts its effect on glucose and lipid metabolism in NASH through activation of AMPK and inhibition of mTORC1, which in turn activate FA β-oxidation and oxidative phosphorylation.
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- 2020
7. Targeting Hepatic Glutaminase 1 Ameliorates Non-alcoholic Steatohepatitis by Restoring Very-Low-Density Lipoprotein Triglyceride Assembly
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Simon, Jorge, Nuñez-García, Maitane, Fernández-Tussy, Pablo, Barbier-Torres, Lucía, Fernández-Ramos, David, Gómez-Santos, Beatriz, Buqué, Xabier, Lopitz-Otsoa, Fernando, Goikoetxea-Usandizaga, Naroa, Serrano-Macia, Marina, Rodriguez-Agudo, Rubén, Bizkarguenaga, Maider, Zubiete-Franco, Imanol, Gutiérrez-de Juan, Virginia, Cabrera, Diana, Alonso, Cristina, Iruzubieta, Paula, Romero-Gomez, Manuel, van Liempd, Sebastiaan, Castro, Azucena, Nogueiras, Ruben, Varela-Rey, Marta, Falcón-Pérez, Juan Manuel, Villa, Erica, Crespo, Javier, Lu, Shelly C, Mato, Jose M, Aspichueta, Patricia, Delgado, Teresa C, and Martínez-Chantar, María Luz
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Biochemistry and Cell Biology ,Biological Sciences ,Hepatitis ,Chronic Liver Disease and Cirrhosis ,Liver Disease ,Nutrition ,Digestive Diseases ,2.1 Biological and endogenous factors ,Aetiology ,Adult ,Animals ,Choline ,Disease Models ,Animal ,Female ,Glutaminase ,Hepatocytes ,Humans ,Lipid Metabolism ,Lipoproteins ,VLDL ,Liver ,Male ,Methionine ,Mice ,Inbred C57BL ,Non-alcoholic Fatty Liver Disease ,Oxidative Stress ,Phospholipids ,Triglycerides ,GLS1 ,GLS2 ,NAFLD ,NASH ,TCA cycle ,VLDL ,folate cycle ,glutaminase ,methionine cycle ,phospholipids ,Medical Biochemistry and Metabolomics ,Endocrinology & Metabolism ,Biochemistry and cell biology ,Medical biochemistry and metabolomics - Abstract
Non-alcoholic steatohepatitis (NASH) is characterized by the accumulation of hepatic fat in an inflammatory/fibrotic background. Herein, we show that the hepatic high-activity glutaminase 1 isoform (GLS1) is overexpressed in NASH. Importantly, GLS1 inhibition reduces lipid content in choline and/or methionine deprivation-induced steatotic mouse primary hepatocytes, in human hepatocyte cell lines, and in NASH mouse livers. We suggest that under these circumstances, defective glutamine fueling of anaplerotic mitochondrial metabolism and concomitant reduction of oxidative stress promotes a reprogramming of serine metabolism, wherein serine is shifted from the generation of the antioxidant glutathione and channeled to provide one-carbon units to regenerate the methionine cycle. The restored methionine cycle can induce phosphatidylcholine synthesis from the phosphatidylethanolamine N-methyltransferase-mediated and CDP-choline pathways as well as by base-exchange reactions between phospholipids, thereby restoring hepatic phosphatidylcholine content and very-low-density lipoprotein export. Overall, we provide evidence that hepatic GLS1 targeting is a valuable therapeutic approach in NASH.
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- 2020
8. miR-873-5p targets mitochondrial GNMT-Complex II interface contributing to non-alcoholic fatty liver disease
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Fernández-Tussy, Pablo, Fernández-Ramos, David, Lopitz-Otsoa, Fernando, Simón, Jorge, Barbier-Torres, Lucía, Gomez-Santos, Beatriz, Nuñez-Garcia, Maitane, Azkargorta, Mikel, Juan, Virginia Gutiérrez-de, Serrano-Macia, Marina, Rodríguez-Agudo, Rubén, Iruzubieta, Paula, Anguita, Juan, Castro, Rui E, Champagne, Devin, Rincón, Mercedes, Elortza, Felix, Arslanow, Anita, Krawczyk, Marcin, Lammert, Frank, Kirchmeyer, Mélanie, Behrmann, Iris, Crespo, Javier, Lu, Shelly C, Mato, José M, Varela-Rey, Marta, Aspichueta, Patricia, Delgado, Teresa C, and Martínez-Chantar, María L
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Liver Disease ,Biotechnology ,Hepatitis ,Digestive Diseases ,Complementary and Integrative Health ,Chronic Liver Disease and Cirrhosis ,Aetiology ,2.1 Biological and endogenous factors ,Oral and gastrointestinal ,Metabolic and endocrine ,Good Health and Well Being ,Adult ,Animals ,Antagomirs ,Disease Models ,Animal ,Electron Transport Complex II ,Female ,Glycine N-Methyltransferase ,Hepatocytes ,Humans ,Lipid Peroxidation ,Liver ,Male ,Mice ,Mice ,Inbred C57BL ,MicroRNAs ,Middle Aged ,Mitochondria ,Non-alcoholic Fatty Liver Disease ,Up-Regulation ,NASH ,GNMT ,beta-oxidation ,Metabolism ,microRNA ,β-oxidation ,Biochemistry and Cell Biology ,Physiology - Abstract
OBJECTIVE:Non-alcoholic fatty liver disease (NAFLD) is a complex pathology in which several dysfunctions, including alterations in metabolic pathways, mitochondrial functionality and unbalanced lipid import/export, lead to lipid accumulation and progression to inflammation and fibrosis. The enzyme glycine N-methyltransferase (GNMT), the most important enzyme implicated in S-adenosylmethionine catabolism in the liver, is downregulated during NAFLD progression. We have studied the mechanism involved in GNMT downregulation by its repressor microRNA miR-873-5p and the metabolic pathways affected in NAFLD as well as the benefit of recovery GNMT expression. METHODS:miR-873-5p and GNMT expression were evaluated in liver biopsies of NAFLD/NASH patients. Different in vitro and in vivo NAFLD murine models were used to assess miR-873-5p/GNMT involvement in fatty liver progression through targeting of the miR-873-5p as NAFLD therapy. RESULTS:We describe a new function of GNMT as an essential regulator of Complex II activity in the electron transport chain in the mitochondria. In NAFLD, GNMT expression is controlled by miR-873-5p in the hepatocytes, leading to disruptions in mitochondrial functionality in a preclinical murine non-alcoholic steatohepatitis (NASH) model. Upregulation of miR-873-5p is shown in the liver of NAFLD/NASH patients, correlating with hepatic GNMT depletion. Importantly, NASH therapies based on anti-miR-873-5p resolve lipid accumulation, inflammation and fibrosis by enhancing fatty acid β-oxidation in the mitochondria. Therefore, miR-873-5p inhibitor emerges as a potential tool for NASH treatment. CONCLUSION:GNMT participates in the regulation of metabolic pathways and mitochondrial functionality through the regulation of Complex II activity in the electron transport chain. In NAFLD, GNMT is repressed by miR-873-5p and its targeting arises as a valuable therapeutic option for treatment.
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- 2019
9. Neddylation inhibition ameliorates steatosis in NAFLD by boosting hepatic fatty acid oxidation via the DEPTOR-mTOR axis
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Serrano-Maciá, Marina, Simón, Jorge, González-Rellan, Maria J., Azkargorta, Mikel, Goikoetxea-Usandizaga, Naroa, Lopitz-Otsoa, Fernando, De Urturi, Diego Saenz, Rodríguez-Agudo, Rubén, Lachiondo-Ortega, Sofia, Mercado-Gomez, Maria, Gutiérrez de Juan, Virginia, Bizkarguenaga, Maider, Fernández-Ramos, David, Buque, Xabier, Baselli, Guido A., Valenti, Luca V.C., Iruzubieta, Paula, Crespo, Javier, Villa, Erica, Banales, Jesus M., Avila, Matias A., Marin, Jose J.G., Aspichueta, Patricia, Sutherland, James, Barrio, Rosa, Mayor, Ugo, Elortza, Félix, Xirodimas, Dimitris P., Nogueiras, Rubén, Delgado, Teresa C., and Martínez-Chantar, María Luz
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- 2021
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10. Boosting mitochondria activity by silencing MCJ overcomes cholestasis-induced liver injury
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Iruzubieta, Paula, Goikoetxea-Usandizaga, Naroa, Barbier-Torres, Lucía, Serrano-Maciá, Marina, Fernández-Ramos, David, Fernández-Tussy, Pablo, Gutiérrez-de-Juan, Virginia, Lachiondo-Ortega, Sofia, Simon, Jorge, Bravo, Miren, Lopitz-Otsoa, Fernando, Robles, Mercedes, Ferre-Aracil, Carlos, Varela-Rey, Marta, Elguezabal, Natalia, Calleja, José Luis, Lu, Shelly C., Milkiewicz, Malgorzata, Milkiewicz, Piotr, Anguita, Juan, Monte, María J., Marin, José J.G., López-Hoyos, Marcos, Delgado, Teresa C., Rincón, Mercedes, Crespo, Javier, and Martínez-Chantar, María Luz
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- 2021
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11. miR-873-5p targets mitochondrialGNMT-Complex II interface contributing tonon-alcoholic fatty liver disease
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Fernández-Tussy, Pablo, Fernández-Ramos, David, Lopitz-Otsoa, Fernando, Simón, Jorge, Barbier-Torres, Lucía, Gomez-Santos, Beatriz, Nuñez-Garcia, Maitane, Azkargorta, Mikel, Gutiérrez-de Juan, Virginia, Serrano-Macia, Marina, Rodríguez-Agudo, Rubén, Iruzubieta, Paula, Anguita, Juan, Castro, Rui Eduardo, Champagne, Devin, Rincón, Mercedes, Elortza, Felix, Arslanow, Anita, Krawczyk, Marcin, Lammert, Frank, Kirchmeyer, Mélanie, Behrmann, Iris, Crespo, Javier, Lu, Shelly, Mato, José, Varela-Rey, Marta, Aspichueta, Patricia, Cardoso Delgado, Teresa, Martinez_Chantar, Maria, Fernández-Tussy, Pablo, Fernández-Ramos, David, Lopitz-Otsoa, Fernando, Simón, Jorge, Barbier-Torres, Lucía, Gomez-Santos, Beatriz, Nuñez-Garcia, Maitane, Azkargorta, Mikel, Gutiérrez-de Juan, Virginia, Serrano-Macia, Marina, Rodríguez-Agudo, Rubén, Iruzubieta, Paula, Anguita, Juan, Castro, Rui Eduardo, Champagne, Devin, Rincón, Mercedes, Elortza, Felix, Arslanow, Anita, Krawczyk, Marcin, Lammert, Frank, Kirchmeyer, Mélanie, Behrmann, Iris, Crespo, Javier, Lu, Shelly, Mato, José, Varela-Rey, Marta, Aspichueta, Patricia, Cardoso Delgado, Teresa, and Martinez_Chantar, Maria
- Abstract
Objective:Non-alcoholic fatty liver disease (NAFLD) is a complex pathology in which several dysfunctions, including alterations in metabolicpathways, mitochondrial functionality and unbalanced lipid import/export, lead to lipid accumulation and progression to inflammation andfibrosis.The enzyme glycine N-methyltransferase (GNMT), the most important enzyme implicated in S-adenosylmethionine catabolism in the liver, isdownregulated during NAFLD progression. We have studied the mechanism involved in GNMT downregulation by its repressor microRNA miR-873-5p and the metabolic pathways affected in NAFLD as well as the benefit of recovery GNMT expression.Methods:miR-873-5p and GNMT expression were evaluated in liver biopsies of NAFLD/NASH patients. Differentin vitroandin vivoNAFLD murinemodels were used to assess miR-873-5p/GNMT involvement in fatty liver progression through targeting of the miR-873-5p as NAFLD therapy.Results:We describe a new function of GNMT as an essential regulator of Complex II activity in the electron transport chain in the mitochondria.In NAFLD, GNMT expression is controlled by miR-873-5p in the hepatocytes, leading to disruptions in mitochondrial functionality in a preclinicalmurine non-alcoholic steatohepatitis (NASH) model. Upregulation of miR-873-5p is shown in the liver of NAFLD/NASH patients, correlating withhepatic GNMT depletion. Importantly, NASH therapies based on anti-miR-873-5p resolve lipid accumulation, inflammation andfibrosis byenhancing fatty acidb-oxidation in the mitochondria. Therefore, miR-873-5p inhibitor emerges as a potential tool for NASH treatment.Conclusion:GNMT participates in the regulation of metabolic pathways and mitochondrial functionality through the regulation of Complex II activityin the electron transport chain. In NAFLD, GNMT is repressed by miR-873-5p and its targeting arises as a valuable therapeutic option for treatment.
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- 2019
- Full Text
- View/download PDF
12. miR-873-5p targets mitochondrial GNMT-Complex II interface contributing to non-alcoholic fatty liver disease
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Fernández-Tussy, Pablo, primary, Fernández-Ramos, David, additional, Lopitz-Otsoa, Fernando, additional, Simón, Jorge, additional, Barbier-Torres, Lucía, additional, Gomez-Santos, Beatriz, additional, Nuñez-Garcia, Maitane, additional, Azkargorta, Mikel, additional, Gutiérrez-de Juan, Virginia, additional, Serrano-Macia, Marina, additional, Rodríguez-Agudo, Rubén, additional, Iruzubieta, Paula, additional, Anguita, Juan, additional, Castro, Rui E., additional, Champagne, Devin, additional, Rincón, Mercedes, additional, Elortza, Felix, additional, Arslanow, Anita, additional, Krawczyk, Marcin, additional, Lammert, Frank, additional, Kirchmeyer, Mélanie, additional, Behrmann, Iris, additional, Crespo, Javier, additional, Lu, Shelly C., additional, Mato, José M., additional, Varela-Rey, Marta, additional, Aspichueta, Patricia, additional, Delgado, Teresa C., additional, and Martínez-Chantar, María L., additional
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- 2019
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13. The Balance between Mono- and NEDD8-Chains Controlled by NEDP1 upon DNA Damage Is a Regulatory Module of the HSP70 ATPase Activity
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Bailly, Aymeric P., primary, Perrin, Aurelien, additional, Serrano-Macia, Marina, additional, Maghames, Chantal, additional, Leidecker, Orsolya, additional, Trauchessec, Helene, additional, Martinez-Chantar, M.L., additional, Gartner, Anton, additional, and Xirodimas, Dimitris P., additional
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- 2019
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14. SUMOylation regulates LKB1 localization and its oncogenic activity in liver cancer
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Zubiete-Franco, Imanol, primary, García-Rodríguez, Juan L., additional, Lopitz-Otsoa, Fernando, additional, Serrano-Macia, Marina, additional, Simon, Jorge, additional, Fernández-Tussy, Pablo, additional, Barbier-Torres, Lucía, additional, Fernández-Ramos, David, additional, Gutiérrez-de-Juan, Virginia, additional, López de Davalillo, Sergio, additional, Carlevaris, Onintza, additional, Beguiristain Gómez, Adolfo, additional, Villa, Erica, additional, Calvisi, Diego, additional, Martín, César, additional, Berra, Edurne, additional, Aspichueta, Patricia, additional, Beraza, Naiara, additional, Varela-Rey, Marta, additional, Ávila, Matias, additional, Rodríguez, Manuel S., additional, Mato, José M., additional, Díaz-Moreno, Irene, additional, Díaz-Quintana, Antonio, additional, Delgado, Teresa C., additional, and Martínez-Chantar, María L., additional
- Published
- 2019
- Full Text
- View/download PDF
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