Pub Date : 2025-03-01Epub Date: 2025-02-15DOI: 10.1016/j.ceca.2025.103002
Barbara A. Niemeyer , David I. Yule
{"title":"Changing of the guards while steering a familiar course","authors":"Barbara A. Niemeyer , David I. Yule","doi":"10.1016/j.ceca.2025.103002","DOIUrl":"10.1016/j.ceca.2025.103002","url":null,"abstract":"","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"126 ","pages":"Article 103002"},"PeriodicalIF":4.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143436889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-01Epub Date: 2025-01-21DOI: 10.1016/j.ceca.2025.102998
Johann Böhm
{"title":"Commentary to An Orai1 gain-of-function tubular aggregate myopathy mouse model phenocopies key features of the human disease (Zhao et al., EMBO Journal 2024) and A gain-of-function mutation in the Ca2+ channel ORAI1 causes Stormorken syndrome with tubular aggregates in mice (Pérez-Guàrdia et al., Cells 2024)","authors":"Johann Böhm","doi":"10.1016/j.ceca.2025.102998","DOIUrl":"10.1016/j.ceca.2025.102998","url":null,"abstract":"","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"126 ","pages":"Article 102998"},"PeriodicalIF":4.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143058318","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-01Epub Date: 2025-02-01DOI: 10.1016/j.ceca.2025.103001
Boris Lavanderos , Maria Paz Saldias , Scott Earley
Brain capillaries contribute to neurovascular coupling (NVC) by sensing neural activity and coordinating upstream arteriole dilation. However, the mechanisms underlying conducted vasodilation remain incompletely understood. Recent findings (PNAS, 2024) identify a novel process, “electrocalcium coupling,” in which hyperpolarizing signals from K+ channels drive long-range Ca²⁺ signaling in capillaries, revealing new insights into the integration of vasodilatory signals in the brain.
{"title":"Shocking insights for neurovascular coupling: Electrical signals ignite calcium dynamics in brain capillaries","authors":"Boris Lavanderos , Maria Paz Saldias , Scott Earley","doi":"10.1016/j.ceca.2025.103001","DOIUrl":"10.1016/j.ceca.2025.103001","url":null,"abstract":"<div><div>Brain capillaries contribute to neurovascular coupling (NVC) by sensing neural activity and coordinating upstream arteriole dilation. However, the mechanisms underlying conducted vasodilation remain incompletely understood. Recent findings (<em>PNAS</em>, 2024) identify a novel process, “electrocalcium coupling,” in which hyperpolarizing signals from K<sup>+</sup> channels drive long-range Ca²⁺ signaling in capillaries, revealing new insights into the integration of vasodilatory signals in the brain.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"126 ","pages":"Article 103001"},"PeriodicalIF":4.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143363765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-01Epub Date: 2025-01-22DOI: 10.1016/j.ceca.2025.102999
Tamas Balla, Gergo Gulyas
Membrane contact sites (MCS) are specialized compartments found in all eukaryotic cells that are formed between membranes of different organelles that are in close proximity. MCS have important functions as they are sites of efficient transfer of molecules between neighboring organelles. Two recent articles have used the splitFAST system to mark and follow the dynamics of membrane contact sites and used the method to highlight the importance of MCS between the endoplasmic reticulum (ER) and lipid droplets in metabolic adaptation and MCS between the ER and mitochondria in Ca2+ signal propagation.
{"title":"You better keep an eye on your contacts","authors":"Tamas Balla, Gergo Gulyas","doi":"10.1016/j.ceca.2025.102999","DOIUrl":"10.1016/j.ceca.2025.102999","url":null,"abstract":"<div><div>Membrane contact sites (MCS) are specialized compartments found in all eukaryotic cells that are formed between membranes of different organelles that are in close proximity. MCS have important functions as they are sites of efficient transfer of molecules between neighboring organelles. Two recent articles have used the splitFAST system to mark and follow the dynamics of membrane contact sites and used the method to highlight the importance of MCS between the endoplasmic reticulum (ER) and lipid droplets in metabolic adaptation and MCS between the ER and mitochondria in Ca<sup>2+</sup> signal propagation.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"126 ","pages":"Article 102999"},"PeriodicalIF":4.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143037305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-03-01Epub Date: 2025-02-07DOI: 10.1016/j.ceca.2025.103000
Jacob D. Cunningham, Taylor A. Phillips, Jaroslava Seflova, Ellen E. Cho, Seth L. Robia
To determine how regulation of the sarco(endo)plasmic reticulum calcium ATPase (SERCA) affects the Ca2+ content of the endoplasmic reticulum (ER), we developed a ratiometric ER-localized Ca2+ indicator to rapidly quantify Ca2+ stores and assess SERCA function in live cells. This assay enables screening of membrane micropeptides and small molecules that modulate SERCA and Na+/K+-ATPase activity and may facilitate development of therapies that target cellular Ca2+ handling. Of the micropeptides tested, phospholamban (PLB) had the greatest degree of inhibition of SERCA, as measured by a decrease in ER Ca2+ content compared to control. Sarcolipin (SLN), endoregulin (ELN), and another-regulin (ALN) also decreased ER Ca2+ content, though less potently than PLB. We also investigated micropeptides that have been shown to have a positive effect on ER Ca2+ uptake. Dwarf open reading frame (DWORF), a positive modulator of SERCA activity, and phospholemman (PLM), an inhibitor of the Na+/K+-ATPase, both increased ER Ca2+ content compared to control. A superinhibitory variant of PLM, R70C, further increased ER Ca2+ load compared to wild type PLM. Overall, our findings indicate that the inhibitory potency of micropeptides is governed by their relative binding affinities to SERCA. This allows for finely tuned modulation of Ca2+ handling in different tissues based on differential expressions of micropeptide species. Understanding the contribution of each micropeptide to SERCA regulation may reveal novel strategies for therapeutic intervention in conditions where calcium dysregulation plays a role, such as heart disease, vascular disease, or neurodegenerative disorders.
{"title":"Rapid quantification of intracellular calcium stores reveals effects of membrane micropeptides on SERCA function","authors":"Jacob D. Cunningham, Taylor A. Phillips, Jaroslava Seflova, Ellen E. Cho, Seth L. Robia","doi":"10.1016/j.ceca.2025.103000","DOIUrl":"10.1016/j.ceca.2025.103000","url":null,"abstract":"<div><div>To determine how regulation of the sarco(endo)plasmic reticulum calcium ATPase (SERCA) affects the Ca<sup>2+</sup> content of the endoplasmic reticulum (ER), we developed a ratiometric ER-localized Ca<sup>2+</sup> indicator to rapidly quantify Ca<sup>2+</sup> stores and assess SERCA function in live cells. This assay enables screening of membrane micropeptides and small molecules that modulate SERCA and Na<sup>+</sup>/K<sup>+</sup>-ATPase activity and may facilitate development of therapies that target cellular Ca<sup>2+</sup> handling. Of the micropeptides tested, phospholamban (PLB) had the greatest degree of inhibition of SERCA, as measured by a decrease in ER Ca<sup>2+</sup> content compared to control. Sarcolipin (SLN), endoregulin (ELN), and another-regulin (ALN) also decreased ER Ca<sup>2+</sup> content, though less potently than PLB. We also investigated micropeptides that have been shown to have a positive effect on ER Ca<sup>2+</sup> uptake. Dwarf open reading frame (DWORF), a positive modulator of SERCA activity, and phospholemman (PLM), an inhibitor of the Na<sup>+</sup>/K<sup>+</sup>-ATPase, both increased ER Ca<sup>2+</sup> content compared to control. A superinhibitory variant of PLM, R70C, further increased ER Ca<sup>2+</sup> load compared to wild type PLM. Overall, our findings indicate that the inhibitory potency of micropeptides is governed by their relative binding affinities to SERCA. This allows for finely tuned modulation of Ca<sup>2+</sup> handling in different tissues based on differential expressions of micropeptide species. Understanding the contribution of each micropeptide to SERCA regulation may reveal novel strategies for therapeutic intervention in conditions where calcium dysregulation plays a role, such as heart disease, vascular disease, or neurodegenerative disorders.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"126 ","pages":"Article 103000"},"PeriodicalIF":4.3,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143367809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01Epub Date: 2024-12-07DOI: 10.1016/j.ceca.2024.102984
Verena Untiet , Chritsine R. Rose , Maiken Nedergaard , Alexei Verkhratsky
{"title":"Ionic signalling (beyond calcium) in the nervous system: Physiology and pathophysiology","authors":"Verena Untiet , Chritsine R. Rose , Maiken Nedergaard , Alexei Verkhratsky","doi":"10.1016/j.ceca.2024.102984","DOIUrl":"10.1016/j.ceca.2024.102984","url":null,"abstract":"","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"125 ","pages":"Article 102984"},"PeriodicalIF":4.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142821956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01Epub Date: 2024-11-29DOI: 10.1016/j.ceca.2024.102980
Maria Livia Sassano , Robbe Van Gorp , Geert Bultynck , Patrizia Agostinis
The endoplasmic reticulum (ER) controls intracellular Ca2+ dynamics. Depletion of ER Ca2+ stores results in short-term activation of store-operated Ca2+ entry (SOCE) via STIM1/Orai1 at ER-plasma membrane (ER-PM) contact sites (MCSs) and the long-term activation of the unfolded protein response (UPR), securing ER proteostasis. Recent work by Carreras-Sureda and colleagues describes a bidirectional control between IRE1 and STIM1 within the ER lumen that regulates ER-PM contact assembly and SOCE to sustain T-cell activation and myoblast differentiation.
{"title":"STIMulating IRE1: How store-operated Ca2+ entry intersects with ER proteostasis","authors":"Maria Livia Sassano , Robbe Van Gorp , Geert Bultynck , Patrizia Agostinis","doi":"10.1016/j.ceca.2024.102980","DOIUrl":"10.1016/j.ceca.2024.102980","url":null,"abstract":"<div><div>The endoplasmic reticulum (ER) controls intracellular Ca<sup>2+</sup> dynamics. Depletion of ER Ca<sup>2+</sup> stores results in short-term activation of store-operated Ca<sup>2+</sup> entry (SOCE) via STIM1/Orai1 at ER-plasma membrane (ER-PM) contact sites (MCSs) and the long-term activation of the unfolded protein response (UPR), securing ER proteostasis. Recent work by Carreras-Sureda and colleagues describes a bidirectional control between IRE1 and STIM1 within the ER lumen that regulates ER-PM contact assembly and SOCE to sustain T-cell activation and myoblast differentiation.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"125 ","pages":"Article 102980"},"PeriodicalIF":4.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01Epub Date: 2024-12-13DOI: 10.1016/j.ceca.2024.102986
Leandro C. Clementino , Andrew P. Thomas , Emily M. Rocha , Sabine Hilfiker
Elevated free fatty acids and oxidative stress may function as pathogenic factors in endothelial dysfunction that is associated with various cardiovascular complications. In recent work, Feng and colleagues report that activation of a lysosomal Ca2+ channel may be a viable option to alleviate oxidative damage by boosting lysosome biogenesis and mitophagy.
{"title":"A role for lysosomal calcium channels in mitigating mitochondrial damage and oxidative stress","authors":"Leandro C. Clementino , Andrew P. Thomas , Emily M. Rocha , Sabine Hilfiker","doi":"10.1016/j.ceca.2024.102986","DOIUrl":"10.1016/j.ceca.2024.102986","url":null,"abstract":"<div><div>Elevated free fatty acids and oxidative stress may function as pathogenic factors in endothelial dysfunction that is associated with various cardiovascular complications. In recent work, Feng and colleagues report that activation of a lysosomal Ca<sup>2+</sup> channel may be a viable option to alleviate oxidative damage by boosting lysosome biogenesis and mitophagy.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"125 ","pages":"Article 102986"},"PeriodicalIF":4.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142853110","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01Epub Date: 2024-12-26DOI: 10.1016/j.ceca.2024.102989
M. Raza Zaidi , Jonathan Soboloff
Recent findings by Abrahamian et al. (2024) provides new insights into the relationship between Two Pore Channel 2 (TPC2) activity and the development and progression of melanoma. Melanocyte inducing transcription factor (MITF) is a critical regulator of both melanocyte and melanoma behavior. Abrahamian et al. (2024) show that MITF-high melanoma requires BOTH Rab7a and TPC2 for proliferation, invasion and metastasis. They further identify Wnt signaling as the mediator of this phenomenon; Rab7a induces TPC2 activity in lysosomes and melanosomes, which regulates GSK-3β stability, thereby determining whether β-catenin escapes degradation and translocates to the nucleus to transcribe the MITF gene. These observations provide new insights into the relationship between ion channel function, lysosomal/melanosomal activity and control for oncogenesis and disease progression in melanoma.
{"title":"TPC2 controls MITF expression and metastasis in melanoma","authors":"M. Raza Zaidi , Jonathan Soboloff","doi":"10.1016/j.ceca.2024.102989","DOIUrl":"10.1016/j.ceca.2024.102989","url":null,"abstract":"<div><div>Recent findings by Abrahamian et al. (2024) provides new insights into the relationship between Two Pore Channel 2 (TPC2) activity and the development and progression of melanoma. Melanocyte inducing transcription factor (MITF) is a critical regulator of both melanocyte and melanoma behavior. Abrahamian et al. (2024) show that MITF-high melanoma requires BOTH Rab7a and TPC2 for proliferation, invasion and metastasis. They further identify Wnt signaling as the mediator of this phenomenon; Rab7a induces TPC2 activity in lysosomes and melanosomes, which regulates GSK-3β stability, thereby determining whether β-catenin escapes degradation and translocates to the nucleus to transcribe the <em>MITF</em> gene. These observations provide new insights into the relationship between ion channel function, lysosomal/melanosomal activity and control for oncogenesis and disease progression in melanoma.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"125 ","pages":"Article 102989"},"PeriodicalIF":4.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142909490","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2025-01-01Epub Date: 2024-12-28DOI: 10.1016/j.ceca.2024.102990
Salah A. Baker , Manushri Karwa , Ji Yeon Lee , Sarah Riar , Bernard T. Drumm , Kenton M. Sanders
Interstitial cells of Cajal in the plane of the myenteric plexus (ICC-MY) serve as electrical pacemakers in the stomach and small intestine. A similar population of cells is found in the colon, but these cells do not appear to generate regular slow wave potentials, as characteristic in more proximal gut regions. Ca2+ handling mechanisms in ICC-MY of the mouse proximal colon were studied using confocal imaging of muscles from animals expressing GCaMP6f exclusively in ICC. ICC-MY displayed stochastic, localized Ca2+ transients that seldom propagated between cells. Colonic ICC express ANO1 channels, so Ca2+ transients likely couple to activation of spontaneous transient inward currents (STICs) in these cells. The Ca2+ transients were due to Ca2+ release and blocked by cyclopiazonic acid (CPA), thapsigargin and caffeine, but unaffected by tetracaine. Antagonists of L- and T-type Ca2+ channels and reduction in extracellular Ca2+ had minimal effects on Ca2+ transients. We reasoned that STICs may not activate regenerative Ca2+ waves in ICC-MY because voltage-dependent Ca2+ conductances are largely inactivated at the relatively depolarized potentials of colonic muscles. We tested the effects of hyperpolarization with pinacidil, a KATP agonist. Ca2+ waves were initiated in some ICC-MY networks when muscles were hyperpolarized, and these events were blocked by a T-type Ca2+ channel antagonist, NNC 55–0396. Ca2+ waves activated by excitatory nerve stimulation were significantly enhanced by hyperpolarization. Our data suggest that colonic ICC-MY are conditional pacemaker cells that depend upon preparative hyperpolarization, produced physiologically by inputs from enteric inhibitory neurons and necessary for regenerative pacemaker activity.
{"title":"Ca²⁺ signaling in myenteric interstitial cells of Cajal (ICC-MY) and their role as conditional pacemakers in the colon","authors":"Salah A. Baker , Manushri Karwa , Ji Yeon Lee , Sarah Riar , Bernard T. Drumm , Kenton M. Sanders","doi":"10.1016/j.ceca.2024.102990","DOIUrl":"10.1016/j.ceca.2024.102990","url":null,"abstract":"<div><div>Interstitial cells of Cajal in the plane of the myenteric plexus (ICC-MY) serve as electrical pacemakers in the stomach and small intestine. A similar population of cells is found in the colon, but these cells do not appear to generate regular slow wave potentials, as characteristic in more proximal gut regions. Ca<sup>2+</sup> handling mechanisms in ICC-MY of the mouse proximal colon were studied using confocal imaging of muscles from animals expressing GCaMP6f exclusively in ICC. ICC-MY displayed stochastic, localized Ca<sup>2+</sup> transients that seldom propagated between cells. Colonic ICC express ANO1 channels, so Ca<sup>2+</sup> transients likely couple to activation of spontaneous transient inward currents (STICs) in these cells. The Ca<sup>2+</sup> transients were due to Ca<sup>2+</sup> release and blocked by cyclopiazonic acid (CPA), thapsigargin and caffeine, but unaffected by tetracaine. Antagonists of L- and T-type Ca<sup>2+</sup> channels and reduction in extracellular Ca<sup>2+</sup> had minimal effects on Ca<sup>2+</sup> transients. We reasoned that STICs may not activate regenerative Ca<sup>2+</sup> waves in ICC-MY because voltage-dependent Ca<sup>2+</sup> conductances are largely inactivated at the relatively depolarized potentials of colonic muscles. We tested the effects of hyperpolarization with pinacidil, a K<sub>ATP</sub> agonist. Ca<sup>2+</sup> waves were initiated in some ICC-MY networks when muscles were hyperpolarized, and these events were blocked by a T-type Ca<sup>2+</sup> channel antagonist, NNC 55–0396. Ca<sup>2+</sup> waves activated by excitatory nerve stimulation were significantly enhanced by hyperpolarization. Our data suggest that colonic ICC-MY are conditional pacemaker cells that depend upon preparative hyperpolarization, produced physiologically by inputs from enteric inhibitory neurons and necessary for regenerative pacemaker activity.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"125 ","pages":"Article 102990"},"PeriodicalIF":4.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11737426/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142926791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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