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Molecular mechanisms underlying protective effects of quercetin against mitochondrial dysfunction and progressive dopaminergic neurodegeneration in cell culture and MitoPark transgenic mouse models of Parkinson's Disease
Molecular mechanisms underlying protective effects of quercetin against mitochondrial dysfunction and progressive dopaminergic neurodegeneration in cell culture and MitoPark transgenic mouse models of Parkinson's Disease
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Molecular mechanisms underlying protective effects of quercetin against mitochondrial dysfunction and progressive dopaminergic neurodegeneration in cell culture and MitoPark transgenic mouse models of Parkinson's Disease

Journal of neurochemistry, 2017-06, Vol.141 (5), p.766-782 [Peer Reviewed Journal]

2017 International Society for Neurochemistry ;2017 International Society for Neurochemistry. ;Copyright © 2017 International Society for Neurochemistry ;ISSN: 0022-3042 ;EISSN: 1471-4159 ;DOI: 10.1111/jnc.14033 ;PMID: 28376279

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Manganese-Induced Neurotoxicity: New Insights Into the Triad of Protein Misfolding, Mitochondrial Impairment, and Neuroinflammation
Manganese-Induced Neurotoxicity: New Insights Into the Triad of Protein Misfolding, Mitochondrial Impairment, and Neuroinflammation
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Manganese-Induced Neurotoxicity: New Insights Into the Triad of Protein Misfolding, Mitochondrial Impairment, and Neuroinflammation

Frontiers in neuroscience, 2019-06, Vol.13, p.654-654 [Peer Reviewed Journal]

2019. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;Copyright © 2019 Harischandra, Ghaisas, Zenitsky, Jin, Kanthasamy, Anantharam and Kanthasamy. 2019 Harischandra, Ghaisas, Zenitsky, Jin, Kanthasamy, Anantharam and Kanthasamy ;ISSN: 1662-4548 ;ISSN: 1662-453X ;EISSN: 1662-453X ;DOI: 10.3389/fnins.2019.00654 ;PMID: 31293375

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Organophosphate pesticide chlorpyrifos impairs STAT1 signaling to induce dopaminergic neurotoxicity: Implications for mitochondria mediated oxidative stress signaling events
Organophosphate pesticide chlorpyrifos impairs STAT1 signaling to induce dopaminergic neurotoxicity: Implications for mitochondria mediated oxidative stress signaling events
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Organophosphate pesticide chlorpyrifos impairs STAT1 signaling to induce dopaminergic neurotoxicity: Implications for mitochondria mediated oxidative stress signaling events

Neurobiology of disease, 2018-09, Vol.117, p.82-113 [Peer Reviewed Journal]

EISSN: 1095-953X ;DOI: 10.1016/j.nbd.2018.05.019

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4
Mechanistic Interplay Between Autophagy and Apoptotic Signaling in Endosulfan-Induced Dopaminergic Neurotoxicity: Relevance to the Adverse Outcome Pathway in Pesticide Neurotoxicity
Mechanistic Interplay Between Autophagy and Apoptotic Signaling in Endosulfan-Induced Dopaminergic Neurotoxicity: Relevance to the Adverse Outcome Pathway in Pesticide Neurotoxicity
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Mechanistic Interplay Between Autophagy and Apoptotic Signaling in Endosulfan-Induced Dopaminergic Neurotoxicity: Relevance to the Adverse Outcome Pathway in Pesticide Neurotoxicity

Toxicological sciences, 2019-06, Vol.169 (2), p.333-352 [Peer Reviewed Journal]

The Author(s) 2019. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com 2019 ;The Author(s) 2019. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com. ;ISSN: 1096-6080 ;EISSN: 1096-0929 ;DOI: 10.1093/toxsci/kfz049 ;PMID: 30796443

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5
Mito-Apocynin Prevents Mitochondrial Dysfunction, Microglial Activation, Oxidative Damage, and Progressive Neurodegeneration in MitoPark Transgenic Mice
Mito-Apocynin Prevents Mitochondrial Dysfunction, Microglial Activation, Oxidative Damage, and Progressive Neurodegeneration in MitoPark Transgenic Mice
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Mito-Apocynin Prevents Mitochondrial Dysfunction, Microglial Activation, Oxidative Damage, and Progressive Neurodegeneration in MitoPark Transgenic Mice

Antioxidants & redox signaling, 2017-11, Vol.27 (14), p.1048-1066 [Peer Reviewed Journal]

(©) Copyright 2017, Mary Ann Liebert, Inc. ;Copyright 2017, Mary Ann Liebert, Inc. 2017 ;ISSN: 1523-0864 ;EISSN: 1557-7716 ;DOI: 10.1089/ars.2016.6905 ;PMID: 28375739

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6
Modified CAR T cells targeting membrane-proximal epitope of mesothelin enhances the antitumor function against large solid tumor
Modified CAR T cells targeting membrane-proximal epitope of mesothelin enhances the antitumor function against large solid tumor
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Modified CAR T cells targeting membrane-proximal epitope of mesothelin enhances the antitumor function against large solid tumor

Cell death & disease, 2019-06, Vol.10 (7), p.476-476, Article 476 [Peer Reviewed Journal]

The Author(s) 2019. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2019 ;ISSN: 2041-4889 ;EISSN: 2041-4889 ;DOI: 10.1038/s41419-019-1711-1 ;PMID: 31209210

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7
Protein kinase Cδ upregulation in microglia drives neuroinflammatory responses and dopaminergic neurodegeneration in experimental models of Parkinson's disease
Protein kinase Cδ upregulation in microglia drives neuroinflammatory responses and dopaminergic neurodegeneration in experimental models of Parkinson's disease
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Protein kinase Cδ upregulation in microglia drives neuroinflammatory responses and dopaminergic neurodegeneration in experimental models of Parkinson's disease

Neurobiology of disease, 2016-09, Vol.93, p.96-114 [Peer Reviewed Journal]

EISSN: 1095-953X ;DOI: 10.1016/j.nbd.2016.04.008

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8
Prokineticin-2 upregulation during neuronal injury mediates a compensatory protective response against dopaminergic neuronal degeneration
Prokineticin-2 upregulation during neuronal injury mediates a compensatory protective response against dopaminergic neuronal degeneration
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Prokineticin-2 upregulation during neuronal injury mediates a compensatory protective response against dopaminergic neuronal degeneration

Nature communications, 2016-10, Vol.7 (1), p.12932-18, Article 12932 [Peer Reviewed Journal]

Copyright Nature Publishing Group Oct 2016 ;Copyright © 2016, The Author(s) 2016 The Author(s) ;ISSN: 2041-1723 ;EISSN: 2041-1723 ;DOI: 10.1038/ncomms12932 ;PMID: 27703142

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9
Impact of Environmental Risk Factors on Mitochondrial Dysfunction, Neuroinflammation, Protein Misfolding, and Oxidative Stress in the Etiopathogenesis of Parkinson’s Disease
Impact of Environmental Risk Factors on Mitochondrial Dysfunction, Neuroinflammation, Protein Misfolding, and Oxidative Stress in the Etiopathogenesis of Parkinson’s Disease
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Impact of Environmental Risk Factors on Mitochondrial Dysfunction, Neuroinflammation, Protein Misfolding, and Oxidative Stress in the Etiopathogenesis of Parkinson’s Disease

International journal of molecular sciences, 2022-09, Vol.23 (18), p.10808 [Peer Reviewed Journal]

2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;2022 by the authors. 2022 ;ISSN: 1422-0067 ;ISSN: 1661-6596 ;EISSN: 1422-0067 ;DOI: 10.3390/ijms231810808 ;PMID: 36142718

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10
Mechanistic Insights Into Gut Microbiome Dysbiosis-Mediated Neuroimmune Dysregulation and Protein Misfolding and Clearance in the Pathogenesis of Chronic Neurodegenerative Disorders
Mechanistic Insights Into Gut Microbiome Dysbiosis-Mediated Neuroimmune Dysregulation and Protein Misfolding and Clearance in the Pathogenesis of Chronic Neurodegenerative Disorders
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Mechanistic Insights Into Gut Microbiome Dysbiosis-Mediated Neuroimmune Dysregulation and Protein Misfolding and Clearance in the Pathogenesis of Chronic Neurodegenerative Disorders

Frontiers in neuroscience, 2022-02, Vol.16, p.836605-836605 [Peer Reviewed Journal]

Copyright © 2022 Padhi, Worth, Zenitsky, Jin, Sambamurti, Anantharam, Kanthasamy and Kanthasamy. ;Copyright © 2022 Padhi, Worth, Zenitsky, Jin, Sambamurti, Anantharam, Kanthasamy and Kanthasamy. 2022 Padhi, Worth, Zenitsky, Jin, Sambamurti, Anantharam, Kanthasamy and Kanthasamy ;ISSN: 1662-4548 ;ISSN: 1662-453X ;EISSN: 1662-453X ;DOI: 10.3389/fnins.2022.836605 ;PMID: 35281490

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11
Microglial immune regulation by epigenetic reprogramming through histone H3K27 acetylation in neuroinflammation
Microglial immune regulation by epigenetic reprogramming through histone H3K27 acetylation in neuroinflammation
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Microglial immune regulation by epigenetic reprogramming through histone H3K27 acetylation in neuroinflammation

Frontiers in immunology, 2023-03, Vol.14, p.1052925-1052925 [Peer Reviewed Journal]

Copyright © 2023 Huang, Malovic, Ealy, Jin, Anantharam, Kanthasamy and Kanthasamy. ;Copyright © 2023 Huang, Malovic, Ealy, Jin, Anantharam, Kanthasamy and Kanthasamy 2023 Huang, Malovic, Ealy, Jin, Anantharam, Kanthasamy and Kanthasamy ;ISSN: 1664-3224 ;EISSN: 1664-3224 ;DOI: 10.3389/fimmu.2023.1052925 ;PMID: 37033967

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12
Mito-metformin protects against mitochondrial dysfunction and dopaminergic neuronal degeneration by activating upstream PKD1 signaling in cell culture and MitoPark animal models of Parkinson's disease
Mito-metformin protects against mitochondrial dysfunction and dopaminergic neuronal degeneration by activating upstream PKD1 signaling in cell culture and MitoPark animal models of Parkinson's disease
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Mito-metformin protects against mitochondrial dysfunction and dopaminergic neuronal degeneration by activating upstream PKD1 signaling in cell culture and MitoPark animal models of Parkinson's disease

Frontiers in neuroscience, 2024, Vol.18, p.1356703-1356703 [Peer Reviewed Journal]

Copyright © 2024 Ay, Charli, Langley, Jang, Padhi, Jin, Anantharam, Kalyanaraman, Kanthasamy and Kanthasamy. ;Copyright © 2024 Ay, Charli, Langley, Jang, Padhi, Jin, Anantharam, Kalyanaraman, Kanthasamy and Kanthasamy. 2024 Ay, Charli, Langley, Jang, Padhi, Jin, Anantharam, Kalyanaraman, Kanthasamy and Kanthasamy ;ISSN: 1662-4548 ;EISSN: 1662-453X ;DOI: 10.3389/fnins.2024.1356703 ;PMID: 38449738

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13
PKC Delta Activation Promotes Endoplasmic Reticulum Stress (ERS) and NLR Family Pyrin Domain-Containing 3 (NLRP3) Inflammasome Activation Subsequent to Asynuclein-Induced Microglial Activation: Involvement of Thioredoxin-Interacting Protein (TXNIP)/Thioredoxin (Trx) Redoxisome Pathway
PKC Delta Activation Promotes Endoplasmic Reticulum Stress (ERS) and NLR Family Pyrin Domain-Containing 3 (NLRP3) Inflammasome Activation Subsequent to Asynuclein-Induced Microglial Activation: Involvement of Thioredoxin-Interacting Protein (TXNIP)/Thioredoxin (Trx) Redoxisome Pathway
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PKC Delta Activation Promotes Endoplasmic Reticulum Stress (ERS) and NLR Family Pyrin Domain-Containing 3 (NLRP3) Inflammasome Activation Subsequent to Asynuclein-Induced Microglial Activation: Involvement of Thioredoxin-Interacting Protein (TXNIP)/Thioredoxin (Trx) Redoxisome Pathway

Frontiers in aging neuroscience, 2021-07, Vol.13, p.661505-661505 [Peer Reviewed Journal]

Copyright © 2021 Samidurai, Palanisamy, Bargues-Carot, Hepker, Kondru, Manne, Zenitsky, Jin, Anantharam, Kanthasamy and Kanthasamy. ;2021. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;Copyright © 2021 Samidurai, Palanisamy, Bargues-Carot, Hepker, Kondru, Manne, Zenitsky, Jin, Anantharam, Kanthasamy and Kanthasamy. 2021 Samidurai, Palanisamy, Bargues-Carot, Hepker, Kondru, Manne, Zenitsky, Jin, Anantharam, Kanthasamy and Kanthasamy ;ISSN: 1663-4365 ;EISSN: 1663-4365 ;DOI: 10.3389/fnagi.2021.661505 ;PMID: 34276337

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14
Fyn Kinase-Mediated PKCδ Y311 Phosphorylation Induces Dopaminergic Degeneration in Cell Culture and Animal Models: Implications for the Identification of a New Pharmacological Target for Parkinson's Disease
Fyn Kinase-Mediated PKCδ Y311 Phosphorylation Induces Dopaminergic Degeneration in Cell Culture and Animal Models: Implications for the Identification of a New Pharmacological Target for Parkinson's Disease
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Fyn Kinase-Mediated PKCδ Y311 Phosphorylation Induces Dopaminergic Degeneration in Cell Culture and Animal Models: Implications for the Identification of a New Pharmacological Target for Parkinson's Disease

Frontiers in pharmacology, 2021-04, Vol.12, p.631375 [Peer Reviewed Journal]

Copyright © 2021 Saminathan, Ghosh, Zhang, Song, Jin, Anantharam, Kanthasamy and Kanthasamy. ;Copyright © 2021 Saminathan, Ghosh, Zhang, Song, Jin, Anantharam, Kanthasamy and Kanthasamy. 2021 Saminathan, Ghosh, Zhang, Song, Jin, Anantharam, Kanthasamy and Kanthasamy ;ISSN: 1663-9812 ;EISSN: 1663-9812 ;DOI: 10.3389/fphar.2021.631375 ;PMID: 33995031

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15
New protocol for kinetic assay seeding ability recovery "KASAR" from formalin-fixed paraffin-embedded tissues
New protocol for kinetic assay seeding ability recovery "KASAR" from formalin-fixed paraffin-embedded tissues
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New protocol for kinetic assay seeding ability recovery "KASAR" from formalin-fixed paraffin-embedded tissues

Frontiers in molecular biosciences, 2023-01, Vol.10, p.1087982-1087982 [Peer Reviewed Journal]

Copyright © 2023 Hepker, Clabaugh, Jin and Kanthasamy. ;Copyright © 2023 Hepker, Clabaugh, Jin and Kanthasamy. 2023 Hepker, Clabaugh, Jin and Kanthasamy ;ISSN: 2296-889X ;EISSN: 2296-889X ;DOI: 10.3389/fmolb.2023.1087982 ;PMID: 36793788

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16
Protein kinase D1 (PKD1) phosphorylation promotes dopaminergic neuronal survival during 6-OHDA-induced oxidative stress
Protein kinase D1 (PKD1) phosphorylation promotes dopaminergic neuronal survival during 6-OHDA-induced oxidative stress
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Protein kinase D1 (PKD1) phosphorylation promotes dopaminergic neuronal survival during 6-OHDA-induced oxidative stress

PloS one, 2014-05, Vol.9 (5), p.e96947 [Peer Reviewed Journal]

COPYRIGHT 2014 Public Library of Science ;COPYRIGHT 2014 Public Library of Science ;2014 Asaithambi et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;2014 Asaithambi et al 2014 Asaithambi et al ;ISSN: 1932-6203 ;EISSN: 1932-6203 ;DOI: 10.1371/journal.pone.0096947 ;PMID: 24806360

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17
Use of microRNA Let-7 to control the replication specificity of oncolytic adenovirus in hepatocellular carcinoma cells
Use of microRNA Let-7 to control the replication specificity of oncolytic adenovirus in hepatocellular carcinoma cells
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Use of microRNA Let-7 to control the replication specificity of oncolytic adenovirus in hepatocellular carcinoma cells

PloS one, 2011-07, Vol.6 (7), p.e21307-e21307 [Peer Reviewed Journal]

COPYRIGHT 2011 Public Library of Science ;COPYRIGHT 2011 Public Library of Science ;2011 Jin et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;Jin et al. 2011 ;ISSN: 1932-6203 ;EISSN: 1932-6203 ;DOI: 10.1371/journal.pone.0021307 ;PMID: 21814544

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18
Mitochondrial dysfunction-induced H3K27 hyperacetylation perturbs enhancers in Parkinson's disease
Mitochondrial dysfunction-induced H3K27 hyperacetylation perturbs enhancers in Parkinson's disease
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Mitochondrial dysfunction-induced H3K27 hyperacetylation perturbs enhancers in Parkinson's disease

JCI insight, 2021-09, Vol.6 (17) [Peer Reviewed Journal]

2021 Huang et al. 2021 Huang et al. ;ISSN: 2379-3708 ;EISSN: 2379-3708 ;DOI: 10.1172/jci.insight.138088 ;PMID: 34494552

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19
Correction: Modified CAR T cells targeting membrane-proximal epitope of mesothelin enhances the antitumor function against large solid tumor
Correction: Modified CAR T cells targeting membrane-proximal epitope of mesothelin enhances the antitumor function against large solid tumor
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Correction: Modified CAR T cells targeting membrane-proximal epitope of mesothelin enhances the antitumor function against large solid tumor

Cell death & disease, 2020-04, Vol.11 (4), p.235-235, Article 235 [Peer Reviewed Journal]

The Author(s) 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2020 ;ISSN: 2041-4889 ;EISSN: 2041-4889 ;DOI: 10.1038/s41419-020-2450-z ;PMID: 32300103

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20
Eradicating tumor in a recurrent cervical cancer patient with autologous tumor-infiltrating lymphocytes and a modified lymphodepleting regimen
Eradicating tumor in a recurrent cervical cancer patient with autologous tumor-infiltrating lymphocytes and a modified lymphodepleting regimen
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Eradicating tumor in a recurrent cervical cancer patient with autologous tumor-infiltrating lymphocytes and a modified lymphodepleting regimen

Journal for immunotherapy of cancer, 2022-02, Vol.10 (2), p.e003887 [Peer Reviewed Journal]

Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ. ;2022 Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ. http://creativecommons.org/licenses/by-nc/4.0/ This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See http://creativecommons.org/licenses/by-nc/4.0/ . Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ. 2022 ;ISSN: 2051-1426 ;EISSN: 2051-1426 ;DOI: 10.1136/jitc-2021-003887 ;PMID: 35177415

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