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157 results on '"HORN, PAUL"'

11. PREDICT identifies precipitating events associated with the clinical course of acutely decompensated cirrhosis

Author

Maschmeier, Miriam, Semela, David, Elkrief, Laure, Elsharkawy, Ahmed, Tornai, Tamas, Tornai, Istvan, Altorjay, Istvan, Antognoli, Agnese, Baldassarre, Maurizio, Gagliardi, Martina, Bertoli, Eleonora, Mareso, Sara, Brocca, Alessandra, Campion, Daniela, Saracco, Giorgio Maria, Rizzo, Martina, Lehmann, Jennifer, Pohlmann, Alessandra, Brol, Maximilian J., Chang, Johannes, Schierwagen, Robert, Solà, Elsa, Amari, Nesrine, Rodriguez, Miguel, Nevens, Frederik, Clemente, Ana, Janicko, Martin, Markwardt, Daniel, Mandorfer, Mattias, Welsch, Christoph, Welzel, Tanja M., Ciraci, Emanuela, Patel, Vish, Ripoll, Cristina, Herber, Adam, Horn, Paul, Bendtsen, Flemming, Gluud, Lise Lotte, Schaapman, Jelte, Riggio, Oliviero, Rainer, Florian, Moritz, Jörg Tobiasch, Mesquita, Mónica, Alvarado-Tapias, Edilmar, Akpata, Osagie, Aamann, Luise, Samuel, Didier, Tresson, Sylvie, Strnad, Pavel, Amathieu, Roland, Simón-Talero, Macarena, Smits, Francois, van den Ende, Natalie, Martinez, Javier, Garcia, Rita, Rupprechter, Harald, Engelmann, Cornelius, Özdogan, Osman Cavit, Trebicka, Jonel, Fernandez, Javier, Papp, Maria, Caraceni, Paolo, Laleman, Wim, Gambino, Carmine, Giovo, Ilaria, Uschner, Frank Erhard, Jansen, Christian, Jimenez, Cesar, Mookerjee, Rajeshwar, Gustot, Thierry, Albillos, Agustin, Bañares, Rafael, Jarcuska, Peter, Steib, Christian, Reiberger, Thomas, Acevedo, Juan, Gatti, Pietro, Shawcross, Debbie L., Zeuzem, Stefan, Zipprich, Alexander, Piano, Salvatore, Berg, Thomas, Bruns, Tony, Danielsen, Karen Vagner, Coenraad, Minneke, Merli, Manuela, Stauber, Rudolf, Zoller, Heinz, Ramos, José Presa, Solé, Cristina, Soriano, Germán, de Gottardi, Andrea, Gronbaek, Henning, Saliba, Faouzi, Trautwein, Christian, Kani, Haluk Tarik, Francque, Sven, Ryder, Stephen, Nahon, Pierre, Romero-Gomez, Manuel, Van Vlierberghe, Hans, Francoz, Claire, Manns, Michael, Garcia-Lopez, Elisabet, Tufoni, Manuel, Amoros, Alex, Pavesi, Marco, Sanchez, Cristina, Praktiknjo, Michael, Curto, Anna, Pitarch, Carla, Putignano, Antonella, Moreno, Esau, Bernal, William, Aguilar, Ferran, Clària, Joan, Ponzo, Paola, Vitalis, Zsuzsanna, Zaccherini, Giacomo, Balogh, Boglarka, Gerbes, Alexander, Vargas, Victor, Alessandria, Carlo, Bernardi, Mauro, Ginès, Pere, Moreau, Richard, Angeli, Paolo, Jalan, Rajiv, and Arroyo, Vicente

Published
2021
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12. Metabolic reprogramming in liver fibrosis.

Author

Horn, Paul and Tacke, Frank

Abstract

Chronic liver diseases, primarily metabolic dysfunction-associated steatotic liver disease (MASLD), harmful use of alcohol, or viral hepatitis, may result in liver fibrosis, cirrhosis, and cancer. Hepatic fibrogenesis is a complex process with interactions between different resident and non-resident heterogeneous liver cell populations, ultimately leading to deposition of extracellular matrix and organ failure. Shifts in cell phenotypes and functions involve pronounced transcriptional and protein synthesis changes that require metabolic adaptations in cellular substrate metabolism, including glucose and lipid metabolism, resembling changes associated with the Warburg effect in cancer cells. Cell activation and metabolic changes are regulated by metabolic stress responses, including the unfolded protein response, endoplasmic reticulum stress, autophagy, ferroptosis, and nuclear receptor signaling. These metabolic adaptations are crucial for inflammatory and fibrogenic activation of macrophages, lymphoid cells, and hepatic stellate cells. Modulation of these pathways, therefore, offers opportunities for novel therapeutic approaches to halt or even reverse liver fibrosis progression. Horn and Tacke review how cellular adaptations in substrate metabolism, metabolic stress responses, and nuclear receptor signaling shape inflammatory and fibrogenic cell states in liver fibrosis. Our increasing understanding provides promising therapeutic avenues to halt or reverse liver disease progression. [ABSTRACT FROM AUTHOR]

Published
2024
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14. The PREDICT study uncovers three clinical courses of acutely decompensated cirrhosis that have distinct pathophysiology

Author

Maschmeier, Miriam, Semela, David, Elkrief, Laure, Elsharkawy, Ahmed, Tornai, Tamas, Tornai, Istvan, Altorjay, Istvan, Antognoli, Agnese, Baldassarre, Maurizio, Gagliardi, Martina, Bertoli, Eleonora, Mareso, Sara, Brocca, Alessandra, Campion, Daniela, Saracco, Giorgio Maria, Rizzo, Martina, Lehmann, Jennifer, Pohlmann, Alessandra, Praktiknjo, Michael, Schierwagen, Robert, Solà, Elsa, Amari, Nesrine, Rodriguez, Miguel, Nevens, Frederik, Clemente, Ana, Jarcuska, Peter, Gerbes, Alexander, Mandorfer, Mattias, Welsch, Christoph, Ciraci, Emanuela, Patel, Vish, Ripoll, Cristina, Herber, Adam, Horn, Paul, Danielsen, Karen Vagner, Gluud, Lise Lotte, Schaapman, Jelte, Riggio, Oliviero, Rainer, Florian, Moritz, Jörg Tobiasch, Mesquita, Mónica, Alvarado-Tapias, Edilmar, Akpata, Osagie, Lykke Eriksen, Peter, Samuel, Didier, Tresson, Sylvie, Strnad, Pavel, Amathieu, Roland, Simón-Talero, Macarena, Smits, Francois, van den Ende, Natalie, Martinez, Javier, Garcia, Rita, Markwardt, Daniel, Rupprechter, Harald, Engelmann, Cornelius, Trebicka, Jonel, Fernandez, Javier, Papp, Maria, Caraceni, Paolo, Laleman, Wim, Gambino, Carmine, Giovo, Ilaria, Uschner, Frank Erhard, Jimenez, Cesar, Mookerjee, Rajeshwar, Gustot, Thierry, Albillos, Agustin, Bañares, Rafael, Janicko, Martin, Steib, Christian, Reiberger, Thomas, Acevedo, Juan, Gatti, Pietro, Bernal, William, Zeuzem, Stefan, Zipprich, Alexander, Piano, Salvatore, Berg, Thomas, Bruns, Tony, Bendtsen, Flemming, Coenraad, Minneke, Merli, Manuela, Stauber, Rudolf, Zoller, Heinz, Ramos, José Presa, Solè, Cristina, Soriano, Germán, de Gottardi, Andrea, Gronbaek, Henning, Saliba, Faouzi, Trautwein, Christian, Özdogan, Osman Cavit, Francque, Sven, Ryder, Stephen, Nahon, Pierre, Romero-Gomez, Manuel, Van Vlierberghe, Hans, Francoz, Claire, Manns, Michael, Garcia, Elisabet, Tufoni, Manuel, Amoros, Alex, Pavesi, Marco, Sanchez, Cristina, Curto, Anna, Pitarch, Carla, Putignano, Antonella, Moreno, Esau, Shawcross, Debbie, Aguilar, Ferran, Clària, Joan, Ponzo, Paola, Jansen, Christian, Vitalis, Zsuzsanna, Zaccherini, Giacomo, Balogh, Boglarka, Vargas, Victor, Montagnese, Sara, Alessandria, Carlo, Bernardi, Mauro, Ginès, Pere, Jalan, Rajiv, Moreau, Richard, Angeli, Paolo, and Arroyo, Vicente

Published
2020
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43. Pediatric reference intervals for 32 routine biochemical markers using the siemens healthineers atellica® CH assays in healthy children and adolescents.

Author

Bohn, Mary Kathryn, Horn, Paul, League, Donna, Steele, Paul, Hall, Alexandra, and Adeli, Khosrow

Subjects
*TEENAGERS, *BIOMARKERS, *LDL cholesterol, *AGE differences, *REFERENCE values, *TEENAGE girls
Abstract

• Pediatric reference intervals were determined for 32 Siemens Atellica® CH assays. • Of 32 parameters, 26 required age partitioning and 18 required sex partitioning. • Assay reference distributions mirrored those on other systems with few exceptions. Pediatric reference intervals are essential for test interpretation. With development of newer analytical systems, de novo reference interval establishment is of necessary importance. In the current study, pediatric reference intervals were determined for 32 analytes using Siemens Healthineers Atellica® CH assays in the CALIPER cohort of healthy children and adolescents. Approximately 600 healthy children and adolescents were recruited with informed consent and collected serum samples were analyzed on the Siemens Healthineers Atellica® CH platform. Assays studied included enzymes, proteins, lipids, electrolytes, and additional markers Reference intervals were established according to Clinical and Laboratory Standards Institute (CLSI) guidelines. Of the 32 parameters, 26 required age partitioning and 18 required sex partitioning. Reference value distributions included consistent increases, decreases, and dynamic variation across the age continuum. Chloride, LDL cholesterol, glucose, lipase, sodium, and triglyceride demonstrated no age or sex-specific differences. The current study expands the clinical utility of the CALIPER database to include 32 Siemens Atellica® chemistry assays. Reference value distributions for Siemens assays mirrored those observed on other comparable assays/systems with few exceptions (e.g. lipase, direct and total bilirubin). These finding support the robustness of previously derived reference intervals in the CALIPER cohort and other global cohorts. [ABSTRACT FROM AUTHOR]

Published
2022
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48. Racial, Ethnic, and Socioeconomic Disparities in Pediatric Aquaporin-4-Positive Neuromyelitis Optica Spectrum Disorder.

Author

Poisson, Kelsey E., Nguyen, Linda, Horn, Paul S., Beck, Andrew F., Wu, Helen, Wesselkamper, Kris, Ness, Jayne M., and Wheeler, Yolanda S.

Subjects
*MEDICAL care use, *SOCIAL determinants of health, *PEDIATRIC therapy, *DEMYELINATION, *INSTITUTIONAL racism, *NEUROMYELITIS optica
Abstract

Only 5% of aquaporin-4-positive neuromyelitis optica spectrum disorder (AQP4+ NMOSD) cases emerge during childhood. Poorer outcomes have been suggested in black/African American (AA) adults with NMOSD; however, conflicting and limited data exist for pediatric-onset NMOSD. This study evaluates racial, ethnic, and socioeconomic disparities in pediatric AQP4+ NMOSD outcomes. Thirty-eight pediatric patients with AQP4+ NMOSD cared for at three pediatric tertiary care centers between 2009 and 2021 were identified. Patient addresses connected to socioeconomic measures available from the US Census. Demographic characteristics, pertinent clinical outcomes, and health care utilization in the two years following diagnosis were captured. Compared with non-Hispanic White children, Black/AA children had a significantly higher Expanded Disability Status Scale (EDSS) (2.46 vs 0.33, P = 0.003), 2.37 more hospital admissions (P = 0.002), and 28.40 additional inpatient days (P = 0.002) in the two years following their NMOSD diagnosis. Additionally, children with public insurance had higher relapse rates than those with private insurance (P = 0.046). At two years and at the most recent follow-up, a significantly higher EDSS was correlated with children living in census tracts with a lower median income, higher deprivation index, and higher proportion of population on assisted income, in poverty, and with vacant housing (all P < 0.05). We identified racial, ethnic, and socioeconomic disparities in clinical outcomes and health care utilization in pediatric AQP4+ NMOSD. Further prospective and household-level data are needed to dissect the interplay of genetics, structural racism, and social determinants of health so that interventions to optimize care and outcomes for this population may be developed. [ABSTRACT FROM AUTHOR]

Published
2024
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