11 results on '"Post-Acute COVID-19 Syndrome pathology"'
Search Results
2. Cohort profile: EFTER-COVID - a Danish nationwide cohort for assessing the long-term health effects of the COVID-19 pandemic.
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Sørensen AIV, Bager P, Nielsen NM, Koch A, Spiliopoulos L, Hviid A, and Ethelberg S
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- Humans, Middle Aged, COVID-19 Testing, Denmark, Cohort Studies, Male, Female, Adolescent, Young Adult, Adult, Aged, 80 and over, COVID-19 diagnosis, COVID-19 epidemiology, COVID-19 pathology, Surveys and Questionnaires, Post-Acute COVID-19 Syndrome epidemiology, Post-Acute COVID-19 Syndrome pathology
- Abstract
Purpose: To follow SARS-CoV-2-infected persons up to 18 months after a positive test in order to assess the burden and nature of post acute symptoms and health problems., Participants: Persons in Denmark above 15 years of age, who were tested positive for SARS-CoV-2 during 1 September 2020 to 21 February 2023 using a RT-PCR test. As a reference group, three test-negative individuals were selected for every two test-positive individuals by matching on test date., Findings to Date: In total, 2 427 913 invitations to baseline questionnaires have been sent out and 839 528 baseline questionnaires (34.5%) have been completed. Females, the age group 50-69 years, Danish-born and persons, who had received at least one SARS-CoV-2 vaccination booster dose were more likely to participate. Follow-up questionnaires were sent at 2, 4, 6, 9, 12 and 18 months after the test, with response rates at 42%-54%., Future Plans: New participants have been recruited on a daily basis from 1 August 2021 to 23 March 2023. Data collection will continue until the last follow-up questionnaires (at 18 months after test) have been distributed in August 2024., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)
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- 2024
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3. Herpesvirus Infection of Endothelial Cells as a Systemic Pathological Axis in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.
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Nunes JM, Kell DB, and Pretorius E
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- Humans, Herpesviridae physiology, Virus Latency, Post-Acute COVID-19 Syndrome pathology, Post-Acute COVID-19 Syndrome physiopathology, Endothelial Cells virology, Fatigue Syndrome, Chronic virology, Fatigue Syndrome, Chronic physiopathology, Herpesviridae Infections virology
- Abstract
Understanding the pathophysiology of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is critical for advancing treatment options. This review explores the novel hypothesis that a herpesvirus infection of endothelial cells (ECs) may underlie ME/CFS symptomatology. We review evidence linking herpesviruses to persistent EC infection and the implications for endothelial dysfunction, encompassing blood flow regulation, coagulation, and cognitive impairment-symptoms consistent with ME/CFS and Long COVID. This paper provides a synthesis of current research on herpesvirus latency and reactivation, detailing the impact on ECs and subsequent systemic complications, including latent modulation and long-term maladaptation. We suggest that the chronicity of ME/CFS symptoms and the multisystemic nature of the disease may be partly attributable to herpesvirus-induced endothelial maladaptation. Our conclusions underscore the necessity for further investigation into the prevalence and load of herpesvirus infection within the ECs of ME/CFS patients. This review offers conceptual advances by proposing an endothelial infection model as a systemic mechanism contributing to ME/CFS, steering future research toward potentially unexplored avenues in understanding and treating this complex syndrome.
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- 2024
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4. Developing effective strategies to optimize physical activity and cardiorespiratory fitness in the long Covid population- The need for caution and objective assessment.
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Faghy MA, Duncan R, Hume E, Gough L, Roscoe C, Laddu D, Arena R, Asthon REM, and Dalton C
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- Humans, COVID-19 complications, Quality of Life, Cardiorespiratory Fitness, Exercise, Post-Acute COVID-19 Syndrome diagnosis, Post-Acute COVID-19 Syndrome pathology, Post-Acute COVID-19 Syndrome therapy
- Abstract
The Post Covid-19 Condition (commonly known as Long Covid) has been defined by the World Health Organisation as occurring in individuals with a history of probable or confirmed SARS CoV 2 infection, usually within 3 months from the onset of acute Covid-19 infection with symptoms that last for at least two months which cannot be explained by an alternative diagnosis. Long Covid is associated with over two hundred recognised symptoms and affects tens of millions of people worldwide. Widely reported reductions in quality of life(QoL) and functional status are caused by extremely sensitive and cyclical symptom profiles that are augmented following exposure to physical, emotional, orthostatic, and cognitive stimuli. This manifestation prevents millions of people from engaging in routine activities of daily living (ADLs) and has important health and well-being, social and economic impacts. Post-exertional symptom exacerbation (PESE) (also known as post-exertional malaise) is an exacerbation in the severity of fatigue and other symptoms following physical, emotional, orthostatic and cognitive tasks. Typically, this will occur 24-72 h after "over-exertion" and can persist for several days and even weeks. It is a hallmark symptom of Long Covid with a reported prevalence of 86%. The debilitating nature of PESE prevents patients from engaging in physical activity which impacts functional status and QoL. In this review, the authors present an update to the literature relating to PESE in Long Covid and make the case for evidence-based guidelines that support the design and implementation of safe rehabilitation approaches for people with Long Covid. This review also considers the role of objective monitoring to quantify a patient's response to external stimuli which can be used to support the safe management of Long Covid and inform decisions relating to engagement with any stimuli that could prompt an exacerbation of symptoms., Competing Interests: Declaration of competing interest None., (Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.)
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- 2024
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5. Serotonin reduction in post-acute sequelae of viral infection.
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Wong AC, Devason AS, Umana IC, Cox TO, Dohnalová L, Litichevskiy L, Perla J, Lundgren P, Etwebi Z, Izzo LT, Kim J, Tetlak M, Descamps HC, Park SL, Wisser S, McKnight AD, Pardy RD, Kim J, Blank N, Patel S, Thum K, Mason S, Beltra JC, Michieletto MF, Ngiow SF, Miller BM, Liou MJ, Madhu B, Dmitrieva-Posocco O, Huber AS, Hewins P, Petucci C, Chu CP, Baraniecki-Zwil G, Giron LB, Baxter AE, Greenplate AR, Kearns C, Montone K, Litzky LA, Feldman M, Henao-Mejia J, Striepen B, Ramage H, Jurado KA, Wellen KE, O'Doherty U, Abdel-Mohsen M, Landay AL, Keshavarzian A, Henrich TJ, Deeks SG, Peluso MJ, Meyer NJ, Wherry EJ, Abramoff BA, Cherry S, Thaiss CA, and Levy M
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- Humans, COVID-19 complications, Disease Progression, Inflammation, Virus Diseases, Post-Acute COVID-19 Syndrome blood, Post-Acute COVID-19 Syndrome pathology, Serotonin blood
- Abstract
Post-acute sequelae of COVID-19 (PASC, "Long COVID") pose a significant global health challenge. The pathophysiology is unknown, and no effective treatments have been found to date. Several hypotheses have been formulated to explain the etiology of PASC, including viral persistence, chronic inflammation, hypercoagulability, and autonomic dysfunction. Here, we propose a mechanism that links all four hypotheses in a single pathway and provides actionable insights for therapeutic interventions. We find that PASC are associated with serotonin reduction. Viral infection and type I interferon-driven inflammation reduce serotonin through three mechanisms: diminished intestinal absorption of the serotonin precursor tryptophan; platelet hyperactivation and thrombocytopenia, which impacts serotonin storage; and enhanced MAO-mediated serotonin turnover. Peripheral serotonin reduction, in turn, impedes the activity of the vagus nerve and thereby impairs hippocampal responses and memory. These findings provide a possible explanation for neurocognitive symptoms associated with viral persistence in Long COVID, which may extend to other post-viral syndromes., Competing Interests: Declaration of interests E.J.W. is an advisor for Danger Bio, Janssen, New Limit, Marengo, Pluto Immunotherapeutics Related Sciences, Rubius Therapeutics, Santa Ana Bio, Synthekine, and Surface Oncology. E.J.W. is a founder of and holds stock in Surface Oncology, Danger Bio, and Arsenal Biosciences. N.J.M. reports consulting fees from Endpoint Health Inc and AstraZeneca and receives funding from Quantum Leap Healthcare Collaborative outside of the published work., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)
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- 2023
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6. Exploring the mechanisms of long COVID: Insights from computational analysis of SARS-CoV-2 gene expression and symptom associations.
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Das S and Kumar S
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- Humans, Female, Child, Precision Medicine, Receptors, G-Protein-Coupled, Biomarkers analysis, Male, Post-Acute COVID-19 Syndrome drug therapy, Post-Acute COVID-19 Syndrome genetics, Post-Acute COVID-19 Syndrome pathology, Gene Expression Profiling
- Abstract
Long coronavirus disease (COVID) has emerged as a global health issue, affecting a substantial number of people worldwide. However, the underlying mechanisms that contribute to the persistence of symptoms in long COVID remain obscure, impeding the development of effective diagnostic and therapeutic interventions. In this study, we utilized computational methods to examine the gene expression profiles of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and their associations with the wide range of symptoms observed in long COVID patients. Using a comprehensive data set comprising over 255 symptoms affecting multiple organ systems, we identified differentially expressed genes and investigated their functional similarity, leading to the identification of key genes with the potential to serve as biomarkers for long COVID. We identified the participation of hub genes associated with G-protein-coupled receptors (GPCRs), which are essential regulators of T-cell immunity and viral infection responses. Among the identified common genes were CTLA4, PTPN22, KIT, KRAS, NF1, RET, and CTNNB1, which play a crucial role in modulating T-cell immunity via GPCR and contribute to a variety of symptoms, including autoimmunity, cardiovascular disorders, dermatological manifestations, gastrointestinal complications, pulmonary impairments, reproductive and genitourinary dysfunctions, and endocrine abnormalities. GPCRs and associated genes are pivotal in immune regulation and cellular functions, and their dysregulation may contribute to the persistent immune responses, chronic inflammation, and tissue abnormalities observed in long COVID. Targeting GPCRs and their associated pathways could offer promising therapeutic strategies to manage symptoms and improve outcomes for those experiencing long COVID. However, the complex mechanisms underlying the condition require continued study to develop effective treatments. Our study has significant implications for understanding the molecular mechanisms underlying long COVID and for identifying potential therapeutic targets. In addition, we have developed a comprehensive website (https://longcovid.omicstutorials.com/) that provides a curated list of biomarker-identified genes and treatment recommendations for each specific disease, thereby facilitating informed clinical decision-making and improved patient management. Our study contributes to the understanding of this debilitating disease, paving the way for improved diagnostic precision, and individualized therapeutic interventions., (© 2023 Wiley Periodicals LLC.)
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- 2023
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7. Long COVID-19: A Systematic Review.
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Karuturi S
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- Humans, COVID-19 epidemiology, SARS-CoV-2, Post-Acute COVID-19 Syndrome epidemiology, Post-Acute COVID-19 Syndrome pathology, Post-Acute COVID-19 Syndrome therapy
- Abstract
Coronavirus disease 2019's (COVID-19's) wide dissemination casts long-term health jeopardy for millions. Long COVID-19, a lingering multisystem malady, weaves a complex array of symptoms. Understanding its full impact requires extensive research over months or years. The pace of recovery remains uncertain, challenging healthcare systems. An evidence-based symphony of medical care and support is urgently needed for long haulers. Understanding long COVID's genesis and advocating for patients is vital. Our comprehension remains limited, prompting a systematic scoping study to explore the existing knowledge and pave the way for future research, illuminating the enigma of "long COVID" and guiding the path towards understanding this relentless condition. How to cite this article: Karuturi S. Long COVID-19: A Systematic Review. J Assoc Physicians India 2023;71(9):82-94., (© Journal of the Association of Physicians of India 2023.)
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- 2023
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8. Haunting innate immune memories of COVID-19.
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Sawitzki B
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- Humans, Epigenomics, Hematopoietic Stem Cells, SARS-CoV-2, Trained Immunity, Inflammation pathology, COVID-19 genetics, COVID-19 immunology, COVID-19 pathology, Post-Acute COVID-19 Syndrome immunology, Post-Acute COVID-19 Syndrome pathology
- Abstract
In addition to acute hyperinflammatory responses, SARS-CoV-2 infections can have long-term effects on our immune system leading to, for example, post-acute sequelae of COVID-19 (PASC). In this issue of Cell, Cheong et al. show that severe infections via IL-6 induce persistent epigenetic signatures in hemopoietic stem cells and their myeloid progenitors associated with increased inflammatory potential., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2023 Elsevier Inc. All rights reserved.)
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- 2023
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9. Epigenetic memory of coronavirus infection in innate immune cells and their progenitors.
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Cheong JG, Ravishankar A, Sharma S, Parkhurst CN, Grassmann SA, Wingert CK, Laurent P, Ma S, Paddock L, Miranda IC, Karakaslar EO, Nehar-Belaid D, Thibodeau A, Bale MJ, Kartha VK, Yee JK, Mays MY, Jiang C, Daman AW, Martinez de Paz A, Ahimovic D, Ramos V, Lercher A, Nielsen E, Alvarez-Mulett S, Zheng L, Earl A, Yallowitz A, Robbins L, LaFond E, Weidman KL, Racine-Brzostek S, Yang HS, Price DR, Leyre L, Rendeiro AF, Ravichandran H, Kim J, Borczuk AC, Rice CM, Jones RB, Schenck EJ, Kaner RJ, Chadburn A, Zhao Z, Pascual V, Elemento O, Schwartz RE, Buenrostro JD, Niec RE, Barrat FJ, Lief L, Sun JC, Ucar D, and Josefowicz SZ
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- Animals, Humans, Mice, Cell Differentiation, Disease Models, Animal, Hematopoietic Stem Cells, Inflammation genetics, Trained Immunity, Monocytes immunology, COVID-19 immunology, Epigenetic Memory, Post-Acute COVID-19 Syndrome genetics, Post-Acute COVID-19 Syndrome immunology, Post-Acute COVID-19 Syndrome pathology
- Abstract
Inflammation can trigger lasting phenotypes in immune and non-immune cells. Whether and how human infections and associated inflammation can form innate immune memory in hematopoietic stem and progenitor cells (HSPC) has remained unclear. We found that circulating HSPC, enriched from peripheral blood, captured the diversity of bone marrow HSPC, enabling investigation of their epigenomic reprogramming following coronavirus disease 2019 (COVID-19). Alterations in innate immune phenotypes and epigenetic programs of HSPC persisted for months to 1 year following severe COVID-19 and were associated with distinct transcription factor (TF) activities, altered regulation of inflammatory programs, and durable increases in myelopoiesis. HSPC epigenomic alterations were conveyed, through differentiation, to progeny innate immune cells. Early activity of IL-6 contributed to these persistent phenotypes in human COVID-19 and a mouse coronavirus infection model. Epigenetic reprogramming of HSPC may underlie altered immune function following infection and be broadly relevant, especially for millions of COVID-19 survivors., Competing Interests: Declaration of interests J.D.B. holds patents related to ATAC-seq and scATAC-seq and serves on the Scientific Advisory Board of CAMP4 Therapeutics, seqWell, and CelSee. S.Z.J. and F.J.B. declare a related patent application: 10203-02-PC; EFS ID: 44924864 Enrichment and Characterization of Rare Circulating Cells, including Progenitor Cells from Peripheral Blood and Uses Thereof. F.J.B. is a co-founder and scientific advisor of IpiNovyx Bio. E.J.S. reports personal fees from NIAID through Axle Informatics for the subject matter expert program for the COVID-19 vaccine clinical trials. R.E.S. is on the scientific advisory board of Miromatrix Inc. and Lime Therapeutics and is a paid consultant and speaker for Alnylam Inc., (Copyright © 2023 Elsevier Inc. All rights reserved.)
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- 2023
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10. Receptor-binding domain of SARS-CoV-2 is a functional αv-integrin agonist.
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Norris EG, Pan XS, and Hocking DC
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- Animals, Humans, Mice, Cell Adhesion physiology, Fibroblasts metabolism, Fibronectins metabolism, Integrin alpha5beta1 genetics, Integrin alpha5beta1 metabolism, Oligopeptides, Post-Acute COVID-19 Syndrome pathology, SARS-CoV-2 metabolism, COVID-19 complications, COVID-19 pathology, Integrin alphaV metabolism
- Abstract
Among the novel mutations distinguishing SARS-CoV-2 from similar coronaviruses is a K403R substitution in the receptor-binding domain (RBD) of the viral spike (S) protein within its S1 region. This amino acid substitution occurs near the angiotensin-converting enzyme 2-binding interface and gives rise to a canonical RGD adhesion motif that is often found in native extracellular matrix proteins, including fibronectin. Here, the ability of recombinant S1-RBD to bind to cell surface integrins and trigger downstream signaling pathways was assessed and compared with RGD-containing, integrin-binding fragments of fibronectin. We determined that S1-RBD supported adhesion of fibronectin-null mouse embryonic fibroblasts as well as primary human small airway epithelial cells, while RBD-coated microparticles attached to epithelial monolayers in a cation-dependent manner. Cell adhesion to S1-RBD was RGD dependent and inhibited by blocking antibodies against α
v and β3 but not α5 or β1 integrins. Similarly, we observed direct binding of S1-RBD to recombinant human αv β3 and αv β6 integrins, but not α5 β1 integrins, using surface plasmon resonance. S1-RBD adhesion initiated cell spreading, focal adhesion formation, and actin stress fiber organization to a similar extent as fibronectin. Moreover, S1-RBD stimulated tyrosine phosphorylation of the adhesion mediators FAK, Src, and paxillin; triggered Akt activation; and supported cell proliferation. Thus, the RGD sequence of S1-RBD can function as an αv -selective integrin agonist. This study provides evidence that cell surface αv -containing integrins can respond functionally to spike protein and raises the possibility that S1-mediated dysregulation of extracellular matrix dynamics may contribute to the pathogenesis and/or post-acute sequelae of SARS-CoV-2 infection., Competing Interests: Conflict of interest The authors declare that they have no conflicts of interest with the contents of this article., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)- Published
- 2023
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11. A systematic review and meta-analysis of long term physical and mental sequelae of COVID-19 pandemic: call for research priority and action.
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Zeng N, Zhao YM, Yan W, Li C, Lu QD, Liu L, Ni SY, Mei H, Yuan K, Shi L, Li P, Fan TT, Yuan JL, Vitiello MV, Kosten T, Kondratiuk AL, Sun HQ, Tang XD, Liu MY, Lalvani A, Shi J, Bao YP, and Lu L
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- Female, Humans, Male, Anxiety, Pandemics, Post-Acute COVID-19 Syndrome pathology, Lung pathology, Risk Factors, COVID-19 complications, COVID-19 epidemiology, COVID-19 psychology
- Abstract
The long-term physical and mental sequelae of COVID-19 are a growing public health concern, yet there is considerable uncertainty about their prevalence, persistence and predictors. We conducted a comprehensive, up-to-date meta-analysis of survivors' health consequences and sequelae for COVID-19. PubMed, Embase and the Cochrane Library were searched through Sep 30th, 2021. Observational studies that reported the prevalence of sequelae of COVID-19 were included. Two reviewers independently undertook the data extraction and quality assessment. Of the 36,625 records identified, a total of 151 studies were included involving 1,285,407 participants from thirty-two countries. At least one sequelae symptom occurred in 50.1% (95% CI 45.4-54.8) of COVID-19 survivors for up to 12 months after infection. The most common investigation findings included abnormalities on lung CT (56.9%, 95% CI 46.2-67.3) and abnormal pulmonary function tests (45.6%, 95% CI 36.3-55.0), followed by generalized symptoms, such as fatigue (28.7%, 95% CI 21.0-37.0), psychiatric symptoms (19.7%, 95% CI 16.1-23.6) mainly depression (18.3%, 95% CI 13.3-23.8) and PTSD (17.9%, 95% CI 11.6-25.3), and neurological symptoms (18.7%, 95% CI 16.2-21.4), such as cognitive deficits (19.7%, 95% CI 8.8-33.4) and memory impairment (17.5%, 95% CI 8.1-29.6). Subgroup analysis showed that participants with a higher risk of long-term sequelae were older, mostly male, living in a high-income country, with more severe status at acute infection. Individuals with severe infection suffered more from PTSD, sleep disturbance, cognitive deficits, concentration impairment, and gustatory dysfunction. Survivors with mild infection had high burden of anxiety and memory impairment after recovery. Our findings suggest that after recovery from acute COVID-19, half of survivors still have a high burden of either physical or mental sequelae up to at least 12 months. It is important to provide urgent and appropriate prevention and intervention management to preclude persistent or emerging long-term sequelae and to promote the physical and psychiatric wellbeing of COVID-19 survivors., (© 2022. The Author(s), under exclusive licence to Springer Nature Limited.)
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- 2023
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