15 results on '"Manotheepan, Ravinea"'
Search Results
2. High circulating levels of the homeostatic chemokines CCL19 and CCL21 predict mortality and disease severity in Covid-19
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Tveita, Anders, Murphy, Sarah Louise, Holter, Jan Cato, Kildal, Anders Benjamin, Michelsen, Annika E, Lerum, Tøri Vigeland, Kaarbø, Mari, Heggelund, Lars, Holten, Aleksander Rygh, Finbråten, Ane-Kristine, Müller, Karl Erik, Mathiessen, Alexander, Bøe, Simen, Fevang, Børre, Granerud, Beathe Kiland, Tonby, Kristian, Lind, Andreas, Dudman, Susanne Gjeruldsen, Henriksen, Katerina Nezvalova, Müller, Fredrik, Skjønsberg, Ole Henning, Trøseid, Marius, Barratt-Due, Andreas, Dyrhol-Riise, Anne Ma, Aukrust, Pål, Halvorsen, Bente, Dahl, Tuva Børresdatter, Ueland, Thor, Austad, Cathrine, Bogen, Mette, Hermann, Anne, Opsand, Hanne, Steinsvik, Trude, Woll, Bjørn Martin, Christensen, Erik Egeland, Eftestøl, Kristin, Hesstvedt, Liv, Jenum, Synne, Jørgensen, Marthe Jøntvedt, Landaas, Elisabeth Toverud, Nur, Sarah, Ormaasen, Vidar, Pettersen, Frank Olav, Quist-Paulsen, Else, Reikvam, Dag Henrik, Røstad, Kjerstin, Skeie, Linda, Steffensen, Anne Katrine, Stiksrud, Birgitte, Gravrok, Berit, Skogen, Vegard, Tylden, Garth Daryl, Andersen, Jan Terje, Kolderup, Anette, Kåsine, Trine, Lund-Johansen, Fridtjof, Olsen, Inge Christoffer, Skåra, Karoline Hansen, Tran, Trung, Fladeby, Cathrine, Holberg-Petersen, Mona, Johal, Simreen Kaur, Vaage, Eline Brenno, Aballi, Saad, Brynhildsen, Jorunn, Ghanima, Waleed, Halstensen, Anne Marie, Berg, Åse, Blomberg, Bjørn, Kvåle, Reidar, Langeland, Nina, Mohn, Kristin Greve Isdahl, Dalgard, Olav, Eiken, Ragnhild, Molvik, Richard Alexander, Ystrøm, Carl Magnus, Ernst, Gernot, Thoresen, Lars, Gustad, Lise Tuset, Saxhaug, Lars Mølgaard, Skei, Nina Vibeche, Hannula, Raisa, Haugli, Mette, Olsen, Roy Bjørkholt, Hoel, Hedda, Hoff, Dag Arne Lihaug, Johannessen, Asgeir, Åsheim-Hansen, Bjørn, Kittang, Bård Reikvam, Le, Lan Ai Kieu, Manotheepan, Ravinea, Nordberg, Lena Bugge, Rasmussen, Hans Schmidt, Stenvik, Grethe-Elisabeth, Thorkildsen, Ruth Foseide, Vinge, Leif Erik, Mielnik, Pawel, Skudal, Hilde, and Tholin, Birgitte
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Inflammation ,Receptors, CCR7 ,Infectious Diseases ,Chemokine CCL21 ,SARS-CoV-2 ,Patient Acuity ,Humans ,Chemokine CCL19 ,COVID-19 ,Immunology and Allergy ,Chemokines - Abstract
Background Immune dysregulation is a major factor in the development of severe coronavirus disease 2019 (COVID-19). The homeostatic chemokines CCL19 and CCL21 have been implicated as mediators of tissue inflammation, but data on their regulation in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is limited. We thus investigated the levels of these chemokines in COVID-19 patients. Methods Serial blood samples were obtained from patients hospitalized with COVID-19 (n = 414). Circulating CCL19 and CCL21 levels during hospitalization and 3-month follow-up were analyzed. In vitro assays and analysis of RNAseq data from public repositories were performed to further explore possible regulatory mechanisms. Results A consistent increase in circulating levels of CCL19 and CCL21 was observed, with high levels correlating with disease severity measures, including respiratory failure, need for intensive care, and 60-day all-cause mortality. High levels of CCL21 at admission were associated with persisting impairment of pulmonary function at the 3-month follow-up. Conclusions Our findings highlight CCL19 and CCL21 as markers of immune dysregulation in COVID-19. This may reflect aberrant regulation triggered by tissue inflammation, as observed in other chronic inflammatory and autoimmune conditions. Determination of the source and regulation of these chemokines and their effects on lung tissue is warranted to further clarify their role in COVID-19. Clinical Trials Registration NCT04321616 and NCT04381819.
- Published
- 2022
3. Respiratory dysfunction three months after severe COVID-19 is associated with gut microbiota alterations
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Vestad, Beate, Ueland, Thor, Lerum, Tøri Vigeland, Dahl, Tuva Børresdatter, Holm, Kristian, Barratt-Due, Andreas, Kåsine, Trine, Dyrhol-Riise, Anne Ma, Stiksrud, Birgitte, Tonby, Kristian, Hoel, Hedda, Olsen, Inge Christoffer, Henriksen, Katerina N., Tveita, Anders Aune, Manotheepan, Ravinea, Haugli, Mette, Eiken, Ragnhild, Berg, Åse, Halvorsen, Bente, Lekva, Tove, Ranheim, Trine, Michelsen, Annika Elisabeth, Kildal, Anders Benjamin, Johannessen, Asgeir, Thoresen, Lars, Skudal, Hilde Kristin, Kittang, Bård Reiakvam, Olsen, Roy Bjørkholt, Ystrøm, Carl Magnus, Skei, Nina Vibeche, Hannula, Raisa, Aballi, Saad, Kvåle, Reidar, Skjønsberg, Ole Henning, Aukrust, Pål, Hov, Johannes Espolin Roksund, and Trøseid, Marius
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Inflammation ,Clinical Trials as Topic ,SARS-CoV-2 ,Post-Acute COVID-19 Syndrome ,RNA, Ribosomal, 16S ,Internal Medicine ,COVID-19 ,Humans ,microbiome ,Gastrointestinal Microbiome ,pulmonary function - Abstract
Background - Although coronavirus disease 2019 (COVID-19) is primarily a respiratory infection, mounting evidence suggests that the gastrointestinal tract is involved in the disease, with gut barrier dysfunction and gut microbiota alterations being related to disease severity. Whether these alterations persist and are related to long-term respiratory dysfunction remains unknown. Methods - Plasma was collected during hospital admission and after 3 months from the NOR-Solidarity trial (n = 181) and analyzed for markers of gut barrier dysfunction and inflammation. At the 3-month follow-up, pulmonary function was assessed by measuring the diffusing capacity of the lungs for carbon monoxide (DLCO). Rectal swabs for gut microbiota analyses were collected (n = 97) and analyzed by sequencing the 16S rRNA gene. Results - Gut microbiota diversity was reduced in COVID-19 patients with respiratory dysfunction, defined as DLCO below the lower limit of normal 3 months after hospitalization. These patients also had an altered global gut microbiota composition, with reduced relative abundance of 20 bacterial taxa and increased abundance of five taxa, including Veillonella, potentially linked to fibrosis. During hospitalization, increased plasma levels of lipopolysaccharide-binding protein (LBP) were strongly associated with respiratory failure, defined as pO2/fiO2 (P/F ratio)
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- 2022
4. The oxidation‐resistant CaMKII‐MM281/282VV mutation does not prevent arrhythmias in CPVT1
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Sadredini, Mani, primary, Manotheepan, Ravinea, additional, Lehnart, Stephan E., additional, Anderson, Mark E., additional, Sjaastad, Ivar, additional, and Stokke, Mathis K., additional
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- 2021
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5. Gut microbiota alterations in patients with persistent respiratory dysfunction three months after severe COVID-19
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Vestad, Beate, primary, Ueland, Thor, additional, Lerum, Tøri Vigeland, additional, Børresdatter Dahl, Tuva, additional, Holm, Kristian, additional, Barratt-Due, Andreas, additional, Kåsine, Trine, additional, Dyrhol-Riise, Anne Ma, additional, Stiksrud, Birgitte, additional, Tonby, Kristian, additional, Hoel, Hedda, additional, Olsen, Inge Christoffer, additional, Henriksen, Katerina Nezvalova, additional, Tveita, Anders, additional, Manotheepan, Ravinea, additional, Haugli, Mette, additional, Eiken, Ragnhild, additional, Berg, Åse, additional, Halvorsen, Bente, additional, Lekva, Tove, additional, Ranheim, Trine, additional, Michelsen, Annika Elisabeth, additional, Kildal, Anders Benjamin, additional, Johannessen, Asgeir, additional, Thoresen, Lars, additional, Skudal, Hilde, additional, Kittang, Bård Reiakvam, additional, Bjørkholt Olsen, Roy, additional, Ystrøm, Carl Magnus, additional, Skei, Nina Vibeche, additional, Hannula, Raisa, additional, Aballi, Saad, additional, Kvåle, Reidar, additional, Skjønsberg, Ole Henning, additional, Aukrust, Pål, additional, Hov, Johannes Roksund, additional, and Trøseid, Marius, additional
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- 2021
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6. Exercise Training Stabilizes RyR2-Dependent Ca2+ Release in Post-infarction Heart Failure
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Danielsen, Tore Kristian, primary, Sadredini, Mani, additional, Manotheepan, Ravinea, additional, Aronsen, Jan Magnus, additional, Frisk, Michael, additional, Hansen, Marie Haugsten, additional, Andressen, Kjetil Wessel, additional, Hougen, Karina, additional, Levy, Finn Olav, additional, Louch, William E., additional, Sejersted, Ole Mathias, additional, Sjaastad, Ivar, additional, and Stokke, Mathis Korseberg, additional
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- 2021
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7. Arrhythmia-preventive effects of exercise training in catecholaminergic polymorphic ventricular tachycardia type 1. From experimental models to patients
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Manotheepan, Ravinea
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cardiovascular system ,cardiovascular diseases - Abstract
Catecholaminergic polymorphic ventricular tachycardia type 1 (CPVT1) is a rare disease caused by inherited mutations in the cardiac ryanodine receptor (RyR2) that lead to ventricular tachycardia (VT) triggered by acute physical or psychological stress. The work in this thesis has explored the mechanisms underlying arrhythmias in CPVT1, and whether the chronic effects of exercise could stabilize RyR2 and prevent arrhythmias. Our data indicate a beneficial effect of individualized exercise training at a safe level for patients with CPVT1. This is supported by experimental data that also suggest a mechanistic explanation for this effect. These results should motivate further research on the acute and chronic effects of exercise training on RyR-function in CPVT1 and other cardiac diseases.
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- 2018
8. Arrhythmia initiation in catecholaminergic polymorphic ventricular tachycardia type 1 depends on both heart rate and sympathetic stimulation
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Danielsen, Tore K., primary, Manotheepan, Ravinea, additional, Sadredini, Mani, additional, Leren, Ida S., additional, Edwards, Andrew G., additional, Vincent, Kevin P., additional, Lehnart, Stephan E., additional, Sejersted, Ole M., additional, Sjaastad, Ivar, additional, Haugaa, Kristina H., additional, and Stokke, Mathis K., additional
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- 2018
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9. Exercise training prevents ventricular tachycardia in CPVT1 due to reduced CaMKII-dependent arrhythmogenic Ca2+release
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Manotheepan, Ravinea, primary, Danielsen, Tore K., additional, Sadredini, Mani, additional, Anderson, Mark E., additional, Carlson, Cathrine R., additional, Lehnart, Stephan E., additional, Sjaastad, Ivar, additional, and Stokke, Mathis K., additional
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- 2016
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10. Beta-Adrenoceptor Stimulation Reveals Ca2+ Waves and Sarcoplasmic Reticulum Ca2+ Depletion in Left Ventricular Cardiomyocytes from Post-Infarction Rats with and without Heart Failure
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Sadredini, Mani, primary, Danielsen, Tore Kristian, additional, Aronsen, Jan Magnus, additional, Manotheepan, Ravinea, additional, Hougen, Karina, additional, Sjaastad, Ivar, additional, and Stokke, Mathis Korseberg, additional
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- 2016
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11. Exercise training prevents ventricular tachycardia in CPVT1 due to reduced Ca2+ dependent arrhythmogenic Ca21 release.
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Manotheepan, Ravinea, Danielsen, Tore K., Sadredini, Mani, Anderson, Mark E., Carlson, Cathrine R., Lehnart, Stephan E., Sjaastad, Ivar, and Stokke, Mathis K.
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EXERCISE , *VENTRICULAR tachycardia , *CATECHOLAMINES , *RYANODINE receptors , *ARRHYTHMIA , *PREVENTION - Abstract
Aims: Catecholaminergic polymorphic ventricular tachycardia type 1 (CPVT1) is caused by mutations in the cardiac ryanodine receptor (RyR2) that lead to disrupted Ca2+ handling in cardiomyocytes and ventricular tachycardia. The aim of this study was to test whether exercise training could reduce the propensity for arrhythmias in mice with the CPVT1-causative missense mutation Ryr2-R2474S by restoring normal Ca2+ handling. Methods and results:Ryr2-R2474S mice (RyR-RS) performed a 2 week interval treadmill exercise training protocol. Each exercise session comprised five 8 min intervals at 80-90% of the running speed at maximal oxygen uptake (VO2max) and 2 min active rest periods at 60%. VO2max increased by 10±2% in exercise trained RyR-RS (ET), while no changes were found in sedentary controls (SED). RyR-RS ET showed fewer episodes of ventricular tachycardia compared with RyR-RS SED, coinciding with fewer Ca2+ sparks and waves, less diastolic Ca2+ leak from the sarcoplasmic reticulum, and lower phosphorylation levels at RyR2 sites associated with Ca2+-calmodulin-dependent kinase type II (CaMKII) compared with RyR-RS SED. The CaMKII inhibitor autocamtide-2-related inhibitory peptide and also the antioxidant N-acetyl-L-cysteine reduced Ca2+ wave frequency in RyR-RS equally to exercise training. Protein analysis as well as functional data indicated a mechanism depending on reduced levels of oxidized CaMKII after exercise training. Two weeks of detraining reversed the beneficial effects of the interval treadmill exercise training protocol in RyR-RS ET. Conclusion: Long-term effects of interval treadmill exercise training reduce ventricular tachycardia episodes in mice with a CPVT1- causative Ryr2 mutation through lower CaMKII-dependent phosphorylation of RyR2. [ABSTRACT FROM AUTHOR]
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- 2016
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12. Beta-Adrenoceptor Stimulation Reveals Ca2+ Waves and Sarcoplasmic Reticulum Ca2+ Depletion in Left Ventricular Cardiomyocytes from Post-Infarction Rats with and without Heart Failure.
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Sadredini, Mani, Danielsen, Tore Kristian, Aronsen, Jan Magnus, Manotheepan, Ravinea, Hougen, Karina, Sjaastad, Ivar, and Stokke, Mathis Korseberg
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BETA adrenoceptors ,SARCOPLASMIC reticulum ,LEFT heart ventricle ,HEART physiology ,HEART cells ,HEART failure ,LABORATORY rats ,PHYSIOLOGY - Abstract
Abnormal cellular Ca
2+ handling contributes to both contractile dysfunction and arrhythmias in heart failure. Reduced Ca2+ transient amplitude due to decreased sarcoplasmic reticulum Ca2+ content is a common finding in heart failure models. However, heart failure models also show increased propensity for diastolic Ca2+ release events which occur when sarcoplasmic reticulum Ca2+ content exceeds a certain threshold level. Such Ca2+ release events can initiate arrhythmias. In this study we aimed to investigate if both of these aspects of altered Ca2+ homeostasis could be found in left ventricular cardiomyocytes from rats with different states of cardiac function six weeks after myocardial infarction when compared to sham-operated controls. Video edge-detection, whole-cell Ca2+ imaging and confocal line-scan imaging were used to investigate cardiomyocyte contractile properties, Ca2+ transients and Ca2+ waves. In baseline conditions, i.e. without beta-adrenoceptor stimulation, cardiomyocytes from rats with large myocardial infarction, but without heart failure, did not differ from sham-operated animals in any of these aspects of cellular function. However, when exposed to beta-adrenoceptor stimulation, cardiomyocytes from both non-failing and failing rat hearts showed decreased sarcoplasmic reticulum Ca2+ content, decreased Ca2+ transient amplitude, and increased frequency of Ca2+ waves. These results are in line with a decreased threshold for diastolic Ca2+ release established by other studies. In the present study, factors that might contribute to a lower threshold for diastolic Ca2+ release were increased THR286 phosphorylation of Ca2+ /calmodulin-dependent protein kinase II and increased protein phosphatase 1 abundance. In conclusion, this study demonstrates both decreased sarcoplasmic reticulum Ca2+ content and increased propensity for diastolic Ca2+ release events in ventricular cardiomyocytes from rats with heart failure after myocardial infarction, and that these phenomena are also found in rats with large myocardial infarctions without heart failure development. Importantly, beta-adrenoceptor stimulation is necessary to reveal these perturbations in Ca2+ handling after a myocardial infarction. [ABSTRACT FROM AUTHOR]- Published
- 2016
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13. Beneficial effects on Aerobic Capacity and Threshold Heart Rate for Arrhythmias from Exercise Training in Patients with Catecholaminergic Polymorphic Ventricular Tachycardia
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Manotheepan, Ravinea, Saberniak, Jorg, Danielsen, Tore K., Thor Edvardsen, Sjaastad, Ivar, Haugaa, Kristina H., and Stokke, Mathis K.
14. Respiratory dysfunction three months after severe COVID-19 is associated with gut microbiota alterations.
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Vestad B, Ueland T, Lerum TV, Dahl TB, Holm K, Barratt-Due A, Kåsine T, Dyrhol-Riise AM, Stiksrud B, Tonby K, Hoel H, Olsen IC, Henriksen KN, Tveita A, Manotheepan R, Haugli M, Eiken R, Berg Å, Halvorsen B, Lekva T, Ranheim T, Michelsen AE, Kildal AB, Johannessen A, Thoresen L, Skudal H, Kittang BR, Olsen RB, Ystrøm CM, Skei NV, Hannula R, Aballi S, Kvåle R, Skjønsberg OH, Aukrust P, Hov JR, and Trøseid M
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- Clinical Trials as Topic, Humans, Inflammation, RNA, Ribosomal, 16S genetics, SARS-CoV-2, Post-Acute COVID-19 Syndrome, COVID-19 complications, Gastrointestinal Microbiome
- Abstract
Background: Although coronavirus disease 2019 (COVID-19) is primarily a respiratory infection, mounting evidence suggests that the gastrointestinal tract is involved in the disease, with gut barrier dysfunction and gut microbiota alterations being related to disease severity. Whether these alterations persist and are related to long-term respiratory dysfunction remains unknown., Methods: Plasma was collected during hospital admission and after 3 months from the NOR-Solidarity trial (n = 181) and analyzed for markers of gut barrier dysfunction and inflammation. At the 3-month follow-up, pulmonary function was assessed by measuring the diffusing capacity of the lungs for carbon monoxide (DL
CO ). Rectal swabs for gut microbiota analyses were collected (n = 97) and analyzed by sequencing the 16S rRNA gene., Results: Gut microbiota diversity was reduced in COVID-19 patients with respiratory dysfunction, defined as DLCO below the lower limit of normal 3 months after hospitalization. These patients also had an altered global gut microbiota composition, with reduced relative abundance of 20 bacterial taxa and increased abundance of five taxa, including Veillonella, potentially linked to fibrosis. During hospitalization, increased plasma levels of lipopolysaccharide-binding protein (LBP) were strongly associated with respiratory failure, defined as pO2 /fiO2 (P/F ratio) <26.6 kPa. LBP levels remained elevated during and after hospitalization and were associated with low-grade inflammation and respiratory dysfunction after 3 months., Conclusion: Respiratory dysfunction after COVID-19 is associated with altered gut microbiota and persistently elevated LBP levels. Our results should be regarded as hypothesis generating, pointing to a potential gut-lung axis that should be further investigated in relation to long-term pulmonary dysfunction and long COVID., (© 2022 The Association for the Publication of the Journal of Internal Medicine.)- Published
- 2022
- Full Text
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15. Exercise Training Stabilizes RyR2-Dependent Ca 2+ Release in Post-infarction Heart Failure.
- Author
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Danielsen TK, Sadredini M, Manotheepan R, Aronsen JM, Frisk M, Hansen MH, Andressen KW, Hougen K, Levy FO, Louch WE, Sejersted OM, Sjaastad I, and Stokke MK
- Abstract
Aim: Dysfunction of the cardiac ryanodine receptor (RyR2) is an almost ubiquitous finding in animal models of heart failure (HF) and results in abnormal Ca
2+ release in cardiomyocytes that contributes to contractile impairment and arrhythmias. We tested whether exercise training (ET), as recommended by current guidelines, had the potential to stabilize RyR2-dependent Ca2+ release in rats with post-myocardial infarction HF. Materials and Methods: We subjected male Wistar rats to left coronary artery ligation or sham operations. After 1 week, animals were characterized by echocardiography and randomized to high-intensity interval ET on treadmills or to sedentary behavior (SED). Running speed was adjusted based on a weekly VO2max test. We repeated echocardiography after 5 weeks of ET and harvested left ventricular cardiomyocytes for analysis of RyR2-dependent systolic and spontaneous Ca2+ release. Phosphoproteins were analyzed by Western blotting, and beta-adrenoceptor density was quantified by radioligand binding. Results: ET increased VO2max in HF-ET rats to 127% of HF-SED ( P < 0.05). This coincided with attenuated spontaneous SR Ca2+ release in left ventricular cardiomyocytes from HF-ET but also reduced Ca2+ transient amplitude and slowed Ca2+ reuptake during adrenoceptor activation. However, ventricular diameter and fractional shortening were unaffected by ET. Analysis of Ca2+ homeostasis and major proteins involved in the regulation of SR Ca2+ release and reuptake could not explain the attenuated spontaneous SR Ca2+ release or reduced Ca2+ transient amplitude. Importantly, measurements of beta-adrenoceptors showed a normalization of beta1 -adrenoceptor density and beta1 :beta2 -adrenoceptor ratio in HF-ET. Conclusion: ET increased aerobic capacity in post-myocardial infarction HF rats and stabilized RyR2-dependent Ca2+ release. Our data show that these effects of ET can be gained without major alterations in SR Ca2+ regulatory proteins and indicate that future studies should include upstream parts of the sympathetic signaling pathway., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Danielsen, Sadredini, Manotheepan, Aronsen, Frisk, Hansen, Andressen, Hougen, Levy, Louch, Sejersted, Sjaastad and Stokke.)- Published
- 2021
- Full Text
- View/download PDF
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