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Your search keyword '"F. Acosta Villegas"' showing total 9 results
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9 results on '"F. Acosta Villegas"'

1. N-terminal pro-BNP predicts mortality better than procalcitonin in abdominal severe sepsis and septic shock

Author

MJ Antolino-Martinez, Carlos García-Palenciano, F Acosta-Villegas, N Ruiz-Vera, Ada Gonzalez-Lisorge, and T Sansano-Sanchez

Subjects
medicine.medical_specialty, Septic shock, business.industry, macromolecular substances, bacterial infections and mycoses, Critical Care and Intensive Care Medicine, medicine.disease, Procalcitonin, nervous system, Poster Presentation, parasitic diseases, medicine, Intensive care medicine, N-terminal pro-BNP, business, hormones, hormone substitutes, and hormone antagonists, Severe sepsis
Abstract

N-terminal pro-BNP (pBNP) could be useful to predict outcome in severe sepsis. We have conducted a study to compare pBNP and procalcitonin (PCT) in the setting of abdominal severe sepsis or septic shock.

Published
2011
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3. Procalcitonin as prognostic marker in severe sepsis of abdominal origin

Author

T Sansano-Sanchez, Carlos García-Palenciano, M. Campos Aranda, F Acosta Villegas, Ada Gonzalez-Lisorge, and Giovanni Alessandro Ercole

Subjects
medicine.medical_specialty, Sicus, biology, business.industry, bacterial infections and mycoses, Critical Care and Intensive Care Medicine, biology.organism_classification, medicine.disease, Gastroenterology, Procalcitonin, Sepsis, Internal medicine, Poster Presentation, parasitic diseases, medicine, Intensive care medicine, business, hormones, hormone substitutes, and hormone antagonists, Severe sepsis
Abstract

We evaluated the utility of procalcitonin (PCT) as a marker of outcome in severe sepsis of abdominal origin (SSAO). SSAO is one of the most prevalent pathologies in surgical ICUs (sICUs). Mortality from 19 to 70% has been reported. Biomarkers are basic tools for diagnosis, follow-up and outcome of sepsis. One of the most studied in last decades has been PCT. Its levels and kinetics could be useful to evaluate the outcome of septic patients.

Published
2015
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6. P2X7 receptor induces mitochondrial failure in monocytes and compromises NLRP3 inflammasome activation during sepsis.

Author

Martínez-García JJ, Martínez-Banaclocha H, Angosto-Bazarra D, de Torre-Minguela C, Baroja-Mazo A, Alarcón-Vila C, Martínez-Alarcón L, Amores-Iniesta J, Martín-Sánchez F, Ercole GA, Martínez CM, González-Lisorge A, Fernández-Pacheco J, Martínez-Gil P, Adriouch S, Koch-Nolte F, Luján J, Acosta-Villegas F, Parrilla P, García-Palenciano C, and Pelegrin P

Subjects
Adult, Aged, Aged, 80 and over, Animals, Disease Models, Animal, Female, Follow-Up Studies, Humans, Hypoxia-Inducible Factor 1, alpha Subunit immunology, Hypoxia-Inducible Factor 1, alpha Subunit metabolism, Inflammasomes metabolism, Macrophages immunology, Macrophages metabolism, Male, Mice, Middle Aged, Mitochondria immunology, Mitochondria metabolism, Mitochondrial Dynamics immunology, Monocytes cytology, NLR Family, Pyrin Domain-Containing 3 Protein immunology, Receptors, Purinergic P2X7 immunology, Sepsis blood, Sepsis microbiology, Sepsis mortality, Up-Regulation immunology, Inflammasomes immunology, Monocytes immunology, NLR Family, Pyrin Domain-Containing 3 Protein metabolism, Receptors, Purinergic P2X7 metabolism, Sepsis immunology
Abstract

Sepsis is characterized by a systemic inflammatory response followed by immunosuppression of the host. Metabolic defects and mitochondrial failure are common in immunocompromised patients with sepsis. The NLRP3 inflammasome is important for establishing an inflammatory response after activation by the purinergic P2X7 receptor. Here, we study a cohort of individuals with intra-abdominal origin sepsis and show that patient monocytes have impaired NLRP3 activation by the P2X7 receptor. Furthermore, most sepsis-related deaths are among patients whose NLRP3 activation is profoundly altered. In monocytes from sepsis patients, the P2X7 receptor is associated with mitochondrial dysfunction. Furthermore, activation of the P2X7 receptor results in mitochondrial damage, which in turn inhibits NLRP3 activation by HIF-1α. We show that mortality increases in a mouse model of sepsis when the P2X7 receptor is activated in vivo. These data reveal a molecular mechanism initiated by the P2X7 receptor that contributes to NLRP3 impairment during infection.

Published
2019
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