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1,061 results on '"Halvorsen, Bente"'

3. Efficacy and safety of baricitinib in hospitalized adults with severe or critical COVID-19 (Bari-SolidAct): a randomised, double-blind, placebo-controlled phase 3 trial

Author

Trøseid, Marius, Arribas, José R., Assoumou, Lambert, Holten, Aleksander Rygh, Poissy, Julien, Terzić, Vida, Mazzaferri, Fulvia, Baño, Jesús Rodríguez, Eustace, Joe, Hites, Maya, Joannidis, Michael, Paiva, José-Artur, Reuter, Jean, Püntmann, Isabel, Patrick-Brown, Thale D. J. H., Westerheim, Elin, Nezvalova-Henriksen, Katerina, Beniguel, Lydie, Dahl, Tuva Børresdatter, Bouscambert, Maude, Halanova, Monika, Péterfi, Zoltán, Tsiodras, Sotirios, Rezek, Michael, Briel, Matthias, Ünal, Serhat, Schlegel, Martin, Ader, Florence, Lacombe, Karine, Amdal, Cecilie Delphin, Rodrigues, Serge, Tonby, Kristian, Gaudet, Alexandre, Heggelund, Lars, Mootien, Joy, Johannessen, Asgeir, Møller, Jannicke Horjen, Pollan, Beatriz Diaz, Tveita, Anders Aune, Kildal, Anders Benjamin, Richard, Jean-Christophe, Dalgard, Olav, Simensen, Victoria Charlotte, Baldé, Aliou, de Gastines, Lucie, del Álamo, Marta, Aydin, Burç, Lund-Johansen, Fridtjof, Trabaud, Mary-Anne, Diallo, Alpha, Halvorsen, Bente, Røttingen, John-Arne, Tacconelli, Evelina, Yazdanpanah, Yazdan, Olsen, Inge C., and Costagliola, Dominique

Published
2023
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6. T cells with increased responsiveness cause obesity in mice without diet intervention

Author

Gregersen, Ida, Kong, Xiang Y., Kooijman, Sander, Foyn, Håvard, Grannes, Helene, Olsen, Maria B., Lone, Anna M., Yang, Kuan, Quiles-Jiménez, Ana, Tran, Marianne, Øgaard, Jonas, Segers, Filip M., Rashidi, Azita, Sagen, Ellen Lund, Lauritzen, Knut H., Pronk, Amanda C.M., de Boer, Jan Freark, Holven, Kirsten B., Melum, Espen, Aukrust, Pål, Taskén, Kjetil, Holm, Sverre, Rensen, Patrick C.N., Dahl, Tuva B., and Halvorsen, Bente

Published
2024
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10. Microbial-derived imidazole propionate links the heart failure-associated microbiome alterations to disease severity

Author

Raju, Sajan C., Molinaro, Antonio, Awoyemi, Ayodeji, Jørgensen, Silje F., Braadland, Peder R., Nendl, Andraz, Seljeflot, Ingebjørg, Ueland, Per M., McCann, Adrian, Aukrust, Pål, Vestad, Beate, Mayerhofer, Cristiane, Broch, Kaspar, Gullestad, Lars, Lappegård, Knut T., Halvorsen, Bente, Kristiansen, Karsten, Hov, Johannes R., and Trøseid, Marius

Published
2024
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11. SMUG1 regulates fat homeostasis leading to a fatty liver phenotype in mice

Author

Carracedo, Sergio, Lirussi, Lisa, Alsøe, Lene, Segers, Filip, Wang, Changliang, Bartosova, Zdenka, Bohov, Pavol, Tekin, Nuriye B., Kong, Xiang Yi, Esbensen, Q. Ying, Chen, Liang, Wennerström, Anna, Kroustallaki, Penelope, Ceolotto, Deborah, Tönjes, Anke, Berge, Rolf Kristian, Bruheim, Per, Wong, Garry, Böttcher, Yvonne, Halvorsen, Bente, and Nilsen, Hilde

Published
2022
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12. SLAMF1-derived peptide exhibits cardio protection after permanent left anterior descending artery ligation in mice

Author

Olsen, Maria Belland, primary, Kong, Xiang Yi, additional, Louwe, Mieke C., additional, Lauritzen, Knut H., additional, Schanke, Ylva, additional, Kaasbøll, Ole Jørgen, additional, Attramadal, Håvard, additional, Øgaard, Jonas, additional, Holm, Sverre, additional, Aukrust, Pål, additional, Ryan, Liv, additional, Espevik, Terje, additional, Yurchenko, Maria, additional, and Halvorsen, Bente, additional

Published
2024
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14. Effects of liraglutide vs. lifestyle changes on soluble suppression of tumorigenesis-2 (sST2) and galectin-3 in obese subjects with prediabetes or type 2 diabetes after comparable weight loss

Author

Simeone, Paola, Tripaldi, Romina, Michelsen, Annika, Ueland, Thor, Liani, Rossella, Ciotti, Sonia, Birkeland, Kåre I., Gulseth, Hanne L., Di Castelnuovo, Augusto, Cipollone, Francesco, Aukrust, Pål, Consoli, Agostino, Halvorsen, Bente, and Santilli, Francesca

Published
2022
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18. Alveolar hypoxia induces organ‐specific inflammasome‐related inflammation in male mouse lungs.

Author

Udjus, Camilla, Halvorsen, Bente, Kong, Xiang Yi, Sagen, Ellen Lund, Martinsen, Marita, Yang, Kuan, Løberg, Else Marit, Christensen, Geir, Skjønsberg, Ole Henning, and Larsen, Karl‐Otto

Subjects
*LUNGS, *HYPOXEMIA, *PULMONARY hypertension, *INFLAMMATION, *EPITHELIAL cells
Abstract

Inflammation through activation of caspase‐1, seems to play a role in pulmonary hypertension induced by alveolar hypoxia. Whether alveolar hypoxia induces caspase‐1‐mediated inflammation and influx of leukocytes in other organs than the lungs, is not known. Our aim was to explore sites of caspase‐1‐related inflammation in alveolar hypoxia. Wild type (WT) mice were exposed to environmental hypoxia or room‐air, and organs were analyzed. Right heart catheterization was performed after 14 days of alveolar hypoxia in WT mice and mice transplanted with WT or caspase‐1−/− bone marrow. Hypoxia induced leukocyte accumulation and increased caspase‐1 protein in the lungs, not in other organs. WT mice transplanted with WT or caspase‐1−/− bone marrow showed no difference in pulmonary leukocyte accumulation or development of pulmonary hypertension after alveolar hypoxia. Caspase‐1 and IL‐18 were detected in bronchial epithelium in WT mice, and hypoxia induced IL‐18 secretion from bronchial epithelial cells. IL‐18 stimulation generated IL‐6 mRNA in monocytes. Phosphorylated STAT3 was increased in hypoxic lungs, not in other organs. Alveolar hypoxia induces caspase‐1 activation and leukocyte accumulation specific to the lungs, not in other organs. Caspase‐1 activation and IL‐18 secretion from bronchial epithelial cells might initiate hypoxia‐induced inflammation, leading to pulmonary hypertension. [ABSTRACT FROM AUTHOR]

Published
2024
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19. Extracellular matrix remodelling pathway in peripheral blood mononuclear cells from severe COVID-19 patients: an explorative study.

Author

Murphy, Sarah Louise, Balzer, Nora Reka, Ranheim, Trine, Sagen, Ellen Lund, Huse, Camilla, Bjerkeli, Vigdis, Michelsen, Annika E., Finbråten, Ane-Kristine, Heggelund, Lars, Dyrhol-Riise, Anne Ma, Tveita, Anders, Holten, Aleksander Rygh, Trøseid, Marius, Ueland, Thor, Ulas, Thomas, Aukrust, Pål, Barratt-Due, Andreas, Halvorsen, Bente, and Dahl, Tuva Børresdatter

Subjects
MONONUCLEAR leukocytes, COVID-19, EXTRACELLULAR matrix, TALL-1 (Protein), RNA sequencing
Abstract

There is a reciprocal relationship between extracellular matrix (ECM) remodelling and inflammation that could be operating in the progression of severe COVID-19. To explore the immune-driven ECM remodelling in COVID-19, we in this explorative study analysed these interactions in hospitalised COVID-19 patients. RNA sequencing and flow analysis were performed on peripheral blood mononuclear cells. Inflammatory mediators in plasma were measured by ELISA and MSD, and clinical information from hospitalised COVID-19 patients (N=15) at admission was included in the analysis. Further, we reanalysed two publicly available datasets: (1) lung tissue RNA-sequencing dataset (N=5) and (2) proteomics dataset from PBCM. ECM remodelling pathways were enriched in PBMC from COVID-19 patients compared to healthy controls. Patients treated at the intensive care unit (ICU) expressed distinct ECM remodelling gene profiles compared to patients in the hospital ward. Several markers were strongly correlated to immune cell subsets, and the dysregulation in the ICU patients was positively associated with plasma levels of inflammatory cytokines and negatively associated with B-cell activating factors. Finally, our analysis of publicly accessible datasets revealed (i) an augmented ECM remodelling signature in inflamed lung tissue compared to non-inflamed tissue and (ii) proteomics analysis of PBMC from severe COVID-19 patients demonstrated an up-regulation in an ECM remodelling pathway. Our results may suggest the presence of an interaction between ECM remodelling, inflammation, and immune cells, potentially initiating or perpetuating pulmonary pathology in severe COVID-19. [ABSTRACT FROM AUTHOR]

Published
2024
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20. Escalated complement activation during hospitalization is associated with higher risk of 60‐day mortality in SARS‐CoV‐2‐infected patients.

Author

Barratt‐Due, Andreas, Pettersen, Kristin, Børresdatter‐Dahl, Tuva, Holter, Jan Cato, Grønli, Renathe H., Dyrhol‐Riise, Anne Ma, Lerum, Tøri Vigeland, Holten, Aleksander Rygh, Tonby, Kristian, Trøseid, Marius, Skjønsberg, Ole H., Granerud, Beathe Kiland, Heggelund, Lars, Kildal, Anders Benjamin, Schjalm, Camilla, Aaløkken, Trond Mogens, Aukrust, Pål, Ueland, Thor, Mollnes, Tom Eirik, and Halvorsen, Bente

Subjects
COMPLEMENT activation, COVID-19, INTENSIVE care units, HOSPITAL care, COMPUTED tomography
Abstract

Background: The complement system, an upstream recognition system of innate immunity, is activated upon SARS‐CoV‐2 infection. To gain a deeper understanding of the extent and duration of this activation, we investigated complement activation profiles during the acute phase of COVID‐19, its persistence post‐recovery and dynamic changes in relation to disease severity. Methods: Serial blood samples were obtained from two cohorts of hospitalized COVID‐19 patients (n = 457). Systemic complement activation products reflecting classical/lectin (C4d), alternative (C3bBbP), common (C3bc) and terminal pathway (TCC and C5a) were measured during hospitalization (admission, days 3–5 and days 7–10), at 3 months and after 1 year. Levels of activation and temporal profiles during hospitalization were related to disease severity defined as respiratory failure (PO2/FiO2 ratio <26.6 kPa) and/or admission to intensive care unit, 60‐day total mortality and pulmonary pathology after 3 months. Findings: During hospitalization, TCC, C4d, C3bc, C3bBbP and C5a were significantly elevated compared to healthy controls. Severely ill patients had significantly higher levels of TCC and C4d (p < 0.001), compared to patients with moderate COVID‐19. Escalated levels of TCC and C4d during hospitalization were associated with a higher risk of 60‐day mortality (p < 0.001), and C4d levels were additionally associated with chest CT changes at 3 months (p < 0.001). At 3 months and 1 year, we observed consistently elevated levels of most complement activation products compared to controls. Conclusion: Hospitalized COVID‐19 patients display prominent and long‐lasting systemic complement activation. Optimal targeting of the system may be achieved through enhanced risk stratification and closer monitoring of in‐hospital changes of complement activation products. [ABSTRACT FROM AUTHOR]

Published
2024
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21. Systemic complement activation is associated with respiratory failure in COVID-19 hospitalized patients

Author

Holter, Jan C., Pischke, Soeren E., de Boer, Eline, Lind, Andreas, Jenum, Synne, Holten, Aleksander R., Tonby, Kristian, Barratt-Due, Andreas, Sokolova, Marina, Schjalm, Camilla, Chaban, Viktoriia, Kolderup, Anette, Tran, Trung, Gjølberg, Torleif Tollefsrud, Skeie, Linda G., Hesstvedt, Liv, Ormåsen, Vidar, Fevang, Børre, Austad, Cathrine, Müller, Karl Erik, Fladeby, Cathrine, Holberg-Petersen, Mona, Halvorsen, Bente, Müller, Fredrik, Aukrust, Pål, Dudman, Susanne, Ueland, Thor, Andersen, Jan Terje, Lund-Johansen, Fridtjof, Heggelund, Lars, Dyrhol-Riise, Anne M., and Mollnes, Tom E.

Published
2020

22. Plasma legumain in familial hypercholesterolemia: associations with statin use and cardiovascular risk markers

Author

Gregersen, Ida, primary, Narverud, Ingunn, additional, Christensen, Jacob Juel, additional, Hovland, Anders, additional, Øyri, Linn K. L., additional, Ueland, Thor, additional, Retterstøl, Kjetil, additional, Bogsrud, Martin P., additional, Aukrust, Pål, additional, Halvorsen, Bente, additional, and Holven, Kirsten B., additional

Published
2024
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23. CD38 deficient mice are not protected from atherosclerosis

Author

Kong, Xiang Yi, primary, Lauritzen, Knut H., additional, Dahl, Tuva Børresdatter, additional, Holm, Sverre, additional, Olsen, Maria Belland, additional, Skjelland, Mona, additional, Nielsen, Christopher, additional, Michelsen, Annika E., additional, Ueland, Thor, additional, Aukrust, Pål, additional, Halvorsen, Bente, additional, and Sandanger, Øystein, additional

Published
2024
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24. Bacterial Brain Abscesses Expand Despite Effective Antibiotic Treatment: A Process Powered by Osmosis Due to Neutrophil Cell Death

Author

Dahlberg, Daniel, primary, Holm, Sverre, additional, Sagen, Ellen Margaret Lund, additional, Michelsen, Annika Elisabet, additional, Stensland, Maria, additional, de Souza, Gustavo Antonio, additional, Müller, Ebba Gløersen, additional, Connelly, James Patrick, additional, Revheim, Mona-Elisabeth, additional, Halvorsen, Bente, additional, and Hassel, Bjørnar, additional

Published
2023
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27. DNA glycosylase Neil3 regulates vascular smooth muscle cell biology during atherosclerosis development

Author

Quiles-Jiménez, Ana, Gregersen, Ida, Segers, Filip M., Skarpengland, Tonje, Kroustallaki, Penelope, Yang, Kuan, Kong, Xiang Yi, Lauritzen, Knut H., Olsen, Maria B., Karlsen, Tom Rune, Nyman, Tuula A., Sagen, Ellen L., Bjerkeli, Vigdis, Suganthan, Rajikala, Nygård, Ståle, Scheffler, Katja, Prins, Jurriën, Van der Veer, Eric, Øgaard, Jonas DS., Fløisand, Yngvar, Jørgensen, Helle F., Holven, Kirsten B., Biessen, Erik A., Nilsen, Hilde, Dahl, Tuva B., Holm, Sverre, Bennett, Martin R., Aukrust, Pål, Bjørås, Magnar, and Halvorsen, Bente

Published
2021
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29. High viral loads combined with inflammatory markers predict disease severity in hospitalized COVID‐19 patients: Results from the NOR‐Solidarity trial.

Author

Viermyr, Hans‐Kittil, Halvorsen, Bente, Sagen, Ellen Lund, Michelsen, Annika E, Barrat‐Due, Andreas, Kåsine, Trine, Nezvalova‐Henriksen, Katerina, Dyrhol‐Riise, Anne Ma, Lerum, Tøri Vigeland, Müller, Fredrik, Tonby, Kristian, Tveita, Anders, Aukrust, Pål, Trøseid, Marius, Ueland, Thor, and Dahl, Tuva Børresdatter

Abstract

Objectives: To investigate temporal changes in the association between SARS‐CoV2 viral load (VL) and markers of inflammation during hospitalization, as well as the ability of these markers alone or in combination to predict severe outcomes. Methods: Serial oropharyngeal and blood samples were obtained from hospitalized COVID‐19 patients (n = 160). Levels of inflammatory markers and oropharyngeal VL were measured during hospitalization (admission, days 3–5, and days 7–10) and related to severe outcomes (respiratory failure/intensive care unit admission). Results: Elevated admission levels of IL (interleukin)‐6, IL‐33, IL‐8, monocyte chemoattractant protein‐1 (MCP‐1), interferon‐γ‐induced protein 10 (IP‐10), IL‐1β, and IL‐1Ra were associated with severe outcomes during hospitalization. Although no inflammatory markers correlated with VL at baseline, there was a significant correlation between VL and levels of IP‐10 and MCP‐1 at days 3–5, accompanied by IL‐8 and IL‐6 at days 7–10. Finally, there was a seemingly additive effect of IP‐10, MCP‐1, and IL‐6 in predicting severe outcomes when combined with high VL at baseline. Conclusions: An increasing number of inflammatory markers were associated with VL during the first 10 days of hospitalization, and several of these markers were associated with severe outcomes, in particular when combined with elevated VL. Future studies should assess the potential for combining antiviral and immunomodulatory treatment, preferably guided by viral and inflammatory biomarkers, for the selection of high‐risk patients. [ABSTRACT FROM AUTHOR]

Published
2024
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30. Absence of NLRP3 Inflammasome in Hematopoietic Cells Reduces Adverse Remodeling After Experimental Myocardial Infarction

Author

Louwe, Mieke C., Olsen, Maria B., Kaasbøll, Ole J., Yang, Kuan, Fosshaug, Linn E., Alfsnes, Katrine, Øgaard, Jonas D.S., Rashidi, Azita, Skulberg, Vidar M., Yang, Mingyi, de Miranda Fonseca, Davi, Sharma, Animesh, Aronsen, Jan Magnus, Schrumpf, Elisabeth, Ahmed, Muhammad Shakil, Dahl, Christen Peder, Nyman, Tuula A., Ueland, Thor, Melum, Espen, Halvorsen, Bente E., Bjørås, Magnar, Attramadal, Håvard, Sjaastad, Ivar, Aukrust, Pål, and Yndestad, Arne

Published
2020
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31. Relationship between fibroblast growth factor in plasma and carotid plaque neovascularization: a pilot study.

Author

Zamani, Mahtab, Skagen, Karolina, Lindberg, Beate, Bjerkeli, Vigdis, Aukrust, Pål, Halvorsen, Bente, and Skjelland, Mona

Subjects
ATHEROSCLEROTIC plaque, FIBROBLAST growth factors, CAROTID artery ultrasonography, NEOVASCULARIZATION, DISEASE risk factors, ISCHEMIC stroke
Abstract

Background: Unstable atherosclerotic carotid plaques with intraplaque neovascularization (IPN) carry a substantial risk for ischemic stroke. Conventional ultrasound methods fall short in detecting IPN, where superb microvascular imaging (SMI) has emerged as a promising tool for both visualizing and quantification. High levels of fibroblast growth factor 23 (FGF-23) have, in observational studies, been suggested as related to cardiovascular morbidity and mortality. The association of FGF-23 to atherosclerotic carotid plaque instability remains relatively unexplored. Methods: A cohort of twenty-nine patients with ≥50% atherosclerotic carotid stenosis underwent conventional carotid ultrasound, SMI, and blood tests, including measurement of FGF-23 in plasma. Nineteen patients were characterized as symptomatic and ten as asymptomatic. Results: Our major findings were: i) Higher FGF-23 levels were strongly correlated with increased SMI-assessed IPN. ii) Neo-vessel count recorded by quantitative SMI was positively correlated to increased FGF-23 levels, but not with basic FGF levels. (iii) In contrast, traditional risk factors for plaque instability exhibited no noteworthy associations with SMI-assessed IPN or with FGF-23 levels. Conclusion: This pilot study suggest the potential of FGF-23 as a valuable marker for neovascularization and atherosclerotic carotid plaque instability as a risk factor for ischemic stroke. Further research involving larger cohorts and prospective data is necessary to understand FGF-23's role in this context comprehensively. [ABSTRACT FROM AUTHOR]

Published
2024
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35. Legumain is upregulated in acute cardiovascular events and associated with improved outcome - potentially related to anti-inflammatory effects on macrophages

Author

Lunde, Ngoc Nguyen, Gregersen, Ida, Ueland, Thor, Shetelig, Christian, Holm, Sverre, Kong, Xiang Yi, Michelsen, Annika E., Otterdal, Kari, Yndestad, Arne, Broch, Kaspar, Gullestad, Lars, Nyman, Tuula A., Bendz, Bjørn, Eritsland, Jan, Hoffmann, Pavel, Skagen, Karolina, Gonçalves, Isabel, Nilsson, Jan, Grenegård, Magnus, Poreba, Marcin, Drag, Marcin, Seljeflot, Ingebjørg, Sporsheim, Bjørnar, Espevik, Terje, Skjelland, Mona, Johansen, Harald Thidemann, Solberg, Rigmor, Aukrust, Pål, Björkbacka, Harry, Andersen, Geir Øystein, and Halvorsen, Bente

Published
2020
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42. Interleukin-6 receptor inhibition with tocilizumab induces a selective and substantial increase in plasma IP-10 and MIP-1β in non-ST-elevation myocardial infarction

Author

Kleveland, Ola, Ueland, Thor, Kunszt, Gabor, Bratlie, Marte, Yndestad, Arne, Broch, Kaspar, Holte, Espen, Ryan, Liv, Amundsen, Brage H., Bendz, Bjørn, Aakhus, Svend, Espevik, Terje, Halvorsen, Bente, Mollnes, Tom E., Wiseth, Rune, Gullestad, Lars, Aukrust, Pål, and Damås, Jan Kristian

Published
2018
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43. Circulating markers of extracellular matrix remodelling in severe COVID‐19 patients.

Author

Murphy, Sarah Louise, Halvorsen, Bente, Holter, Jan Cato, Huse, Camilla, Tveita, Anders, Trøseid, Marius, Hoel, Hedda, Kildal, Anders Benjamin, Holten, Aleksander Rygh, Lerum, Tøri Vigeland, Skjønsberg, Ole Henning, Michelsen, Annika E, Aaløkken, Trond M, Tonby, Kristian, Lind, Andreas, Dudman, Susanne, Granerud, Beathe Kiland, Heggelund, Lars, Bøe, Simen, and Dyrholt‐Riise, Anne Ma

Subjects
*COVID-19, *EXTRACELLULAR matrix, *CALCIUM-binding proteins, *MATRIX metalloproteinases, *INTENSIVE care units, *PULMONARY fibrosis
Abstract

Background: Abnormal remodelling of the extracellular matrix (ECM) has generally been linked to pulmonary inflammation and fibrosis and may also play a role in the pathogenesis of severe COVID‐19. To further elucidate the role of ECM remodelling and excessive fibrogenesis in severe COVID‐19, we examined circulating levels of mediators involved in various aspects of these processes in COVID‐19 patients. Methods: Serial blood samples were obtained from two cohorts of hospitalised COVID‐19 patients (n = 414). Circulating levels of ECM remodelling mediators were quantified by enzyme immunoassays in samples collected during hospitalisation and at 3‐month follow‐up. Samples were related to disease severity (respiratory failure and/or treatment at the intensive care unit), 60‐day total mortality and pulmonary pathology after 3‐months. We also evaluated the direct effect of inactivated SARS‐CoV‐2 on the release of the different ECM mediators in relevant cell lines. Results: Several of the measured markers were associated with adverse outcomes, notably osteopontin (OPN), S100 calcium‐binding protein A12 and YKL‐40 were associated with disease severity and mortality. High levels of ECM mediators during hospitalisation were associated with computed tomography thorax pathology after 3‐months. Some markers (i.e. growth differential factor 15, galectin 3 and matrix metalloproteinase 9) were released from various relevant cell lines (i.e. macrophages and lung cell lines) in vitro after exposure to inactivated SARS‐CoV‐2 suggesting a direct link between these mediators and the causal agent of COVID‐19. Conclusion: Our findings highlight changes to ECM remodelling and particularly a possible role of OPN, S100A12 and YKL‐40 in the pathogenesis of severe COVID‐19. [ABSTRACT FROM AUTHOR]

Published
2023
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44. Increased plasma levels of non-sugar sweeteners in patients with symptomatic carotid atherosclerosis.

Author

Stø, Kristine, Skagen, Karolina R., Valeur, Jørgen, Yang, Kuan, Bjerkeli, Vigdis, Aukrust, Pål, Skjelland, Mona, and Halvorsen, Bente

Abstract

Purpose. The non-sugar sweeteners acesulfame K and saccharin are considered safe, but there is conflicting evidence on their effects on cardiovascular health. Materialsandmethods. In this explorative pilot study, we measured plasma levels of acesulfame K and saccharin in 15 patients with symptomatic carotid atherosclerosis, 18 asymptomatic patients and 15 control subjects. Fecal microbiota and short-chain fatty acids were analyzed. Dietary and medical history was assessed. Results. Symptomatic patients had higher levels of acesulfame K and saccharin compared to controls. Acesulfame K was associated with increased leukocyte count. Saccharin was associated with more severe carotid stenosis, as well as lower fecal butyric acid. [ABSTRACT FROM AUTHOR]

Published
2023
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45. Cytokine pattern in patients with ST-elevation myocardial infarction treated with the interleukin-6 receptor antagonist tocilizumab

Author

Woxholt, Sindre, primary, Ueland, T, additional, Aukrust, Pål, additional, Anstensrud, Anne Kristine, additional, Broch, Kaspar, additional, Tøllefsen, Ingvild Maria, additional, Ryan, Liv, additional, Bendz, Bjørn, additional, Hopp, Einar, additional, Kløw, Nils-Einar, additional, Seljeflot, Ingebjørg, additional, Halvorsen, Bente, additional, Dahl, Tuva B, additional, Huse, Camilla, additional, Andersen, Geir Øystein, additional, Gullestad, Lars, additional, Wiseth, Rune, additional, Amundsen, Brage H, additional, Damas, Jan Kristian, additional, and Kleveland, Ola, additional

Published
2023
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47. Intestinal fatty acid binding protein is associated with cardiac function and gut dysbiosis in chronic heart failure

Author

Nendl, Andraž, primary, Raju, Sajan C., additional, Broch, Kaspar, additional, Mayerhofer, Cristiane C. K., additional, Holm, Kristian, additional, Halvorsen, Bente, additional, Lappegård, Knut Tore, additional, Moscavitch, Samuel, additional, Hov, Johannes Roksund, additional, Seljeflot, Ingebjørg, additional, Trøseid, Marius, additional, and Awoyemi, Ayodeji, additional

Published
2023
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48. YKL-40 (Chitinase-3-Like Protein 1) Serum Levels in Aortic Stenosis

Author

Arain, Fizza, Abraityte, Aurelija, Bogdanova, Mariia, Solberg, Ole G., Michelsen, Annika E., Lekva, Tove, Aakhus, Svend, Holm, Sverre, Halvorsen, Bente, Finsen, Alexandra V., Vinge, Leif-Erik, Nymo, Ståle, Espeland, Torvald, Ranheim, Trine, Aukrust, Pål, Vaage, Ingvar Jarle, Auensen, Andreas, Gullestad, Lars, and Ueland, Thor

Published
2020
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