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  1. Article: Epigenetic Alterations in Alzheimer's Disease: Impact on Insulin Signaling and Advanced Drug Delivery Systems.

    Greeny, Alosh / Nair, Ayushi / Sadanandan, Prashant / Satarker, Sairaj / Famurewa, Ademola C / Nampoothiri, Madhavan

    Biology

    2024  Volume 13, Issue 3

    Abstract: Alzheimer's disease (AD) is a neurodegenerative condition that predominantly affects the hippocampus and the entorhinal complex, leading to memory lapse and cognitive impairment. This can have a negative impact on an individual's behavior, speech, and ... ...

    Abstract Alzheimer's disease (AD) is a neurodegenerative condition that predominantly affects the hippocampus and the entorhinal complex, leading to memory lapse and cognitive impairment. This can have a negative impact on an individual's behavior, speech, and ability to navigate their surroundings. AD is one of the principal causes of dementia. One of the most accepted theories in AD, the amyloid β (Aβ) hypothesis, assumes that the buildup of the peptide Aβ is the root cause of AD. Impaired insulin signaling in the periphery and central nervous system has been considered to have an effect on the pathophysiology of AD. Further, researchers have shifted their focus to epigenetic mechanisms that are responsible for dysregulating major biochemical pathways and intracellular signaling processes responsible for directly or indirectly causing AD. The prime epigenetic mechanisms encompass DNA methylation, histone modifications, and non-coding RNA, and are majorly responsible for impairing insulin signaling both centrally and peripherally, thus leading to AD. In this review, we provide insights into the major epigenetic mechanisms involved in causing AD, such as DNA methylation and histone deacetylation. We decipher how the mechanisms alter peripheral insulin signaling and brain insulin signaling, leading to AD pathophysiology. In addition, this review also discusses the need for newer drug delivery systems for the targeted delivery of epigenetic drugs and explores targeted drug delivery systems such as nanoparticles, vesicular systems, networks, and other nano formulations in AD. Further, this review also sheds light on the future approaches used for epigenetic drug delivery.
    Language English
    Publishing date 2024-02-28
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2661517-4
    ISSN 2079-7737
    ISSN 2079-7737
    DOI 10.3390/biology13030157
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  2. Article ; Online: Involvement of the nervous system in COVID-19: The bell should toll in the brain.

    Satarker, Sairaj / Nampoothiri, Madhavan

    Life sciences

    2020  Volume 262, Page(s) 118568

    Abstract: The world is fuming at SARS-CoV-2 for being the culprit for causing the devastating COVID-19, claiming millions of lives across the globe in the form of respiratory disorders. But lesser known are its effects on the CNS that are slowly surfacing in the ... ...

    Abstract The world is fuming at SARS-CoV-2 for being the culprit for causing the devastating COVID-19, claiming millions of lives across the globe in the form of respiratory disorders. But lesser known are its effects on the CNS that are slowly surfacing in the worldwide population. Our review illustrates findings that claim SARS-CoV-2's arrival onto the ACE2 receptors of neuronal and glial cells mainly via CSF, olfactory nerve, trigeminal nerve, neuronal dissemination, and hematogenous pathways. The role of SARS-CoV-2 structural proteins in its smooth viral infectivity of the host cannot be ignored, especially the spike proteins that mediate spike attachment and host membrane fusion. Worth mentioning the nucleocapsid, envelope, and membrane proteins make the proliferation of SARS-CoV-2 much simpler than expected in spreading infection. This has led to catastrophic conditions like seizures, Guillain-Barré syndrome, viral encephalitis, meningoencephalitis, acute cerebrovascular disease, and respiratory failures. Placing a magnifying lens on the lesser-explored CNS consequences of COVID-19, we attempt to shift the focus of our readers onto the new supporting threats to which further studies are needed.
    MeSH term(s) Brain/physiopathology ; COVID-19/complications ; COVID-19/physiopathology ; Central Nervous System Diseases/complications ; Central Nervous System Diseases/physiopathology ; Humans ; Pandemics ; SARS-CoV-2/physiology
    Keywords covid19
    Language English
    Publishing date 2020-10-06
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 3378-9
    ISSN 1879-0631 ; 0024-3205
    ISSN (online) 1879-0631
    ISSN 0024-3205
    DOI 10.1016/j.lfs.2020.118568
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  3. Article ; Online: Structural Proteins in Severe Acute Respiratory Syndrome Coronavirus-2.

    Satarker, Sairaj / Nampoothiri, Madhavan

    Archives of medical research

    2020  Volume 51, Issue 6, Page(s) 482–491

    Abstract: What began with a sign of pneumonia-related respiratory disorders in China has now become a pandemic named by WHO as Covid-19 known to be caused by Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2). The SARS-CoV-2 are newly emerged β ... ...

    Abstract What began with a sign of pneumonia-related respiratory disorders in China has now become a pandemic named by WHO as Covid-19 known to be caused by Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2). The SARS-CoV-2 are newly emerged β coronaviruses belonging to the Coronaviridae family. SARS-CoV-2 has a positive viral RNA genome expressing open reading frames that code for structural and non-structural proteins. The structural proteins include spike (S), nucleocapsid (N), membrane (M), and envelope (E) proteins. The S1 subunit of S protein facilitates ACE2 mediated virus attachment while S2 subunit promotes membrane fusion. The presence of glutamine, asparagine, leucine, phenylalanine and serine amino acids in SARS-CoV-2 enhances ACE2 binding. The N protein is composed of a serine-rich linker region sandwiched between N Terminal Domain (NTD) and C Terminal Domain (CTD). These terminals play a role in viral entry and its processing post entry. The NTD forms orthorhombic crystals and binds to the viral genome. The linker region contains phosphorylation sites that regulate its functioning. The CTD promotes nucleocapsid formation. The E protein contains a NTD, hydrophobic domain and CTD which form viroporins needed for viral assembly. The M protein possesses hydrophilic C terminal and amphipathic N terminal. Its long-form promotes spike incorporations and the interaction with E facilitates virion production. As each protein is essential in viral functioning, this review describes the insights of SARS-CoV-2 structural proteins that would help in developing therapeutic strategies by targeting each protein to curb the rapidly growing pandemic.
    MeSH term(s) Betacoronavirus/chemistry ; COVID-19 ; Capsid/chemistry ; Coronavirus Infections/virology ; Genome, Viral ; Humans ; Lung/virology ; Open Reading Frames ; Pandemics ; Phosphorylation ; Pneumonia, Viral/virology ; Protein Binding ; Protein Domains ; RNA, Viral/genetics ; SARS-CoV-2 ; Spike Glycoprotein, Coronavirus/chemistry ; Viral Envelope Proteins/chemistry
    Chemical Substances RNA, Viral ; Spike Glycoprotein, Coronavirus ; Viral Envelope Proteins ; spike protein, SARS-CoV-2
    Keywords covid19
    Language English
    Publishing date 2020-05-25
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1156844-6
    ISSN 1873-5487 ; 0188-4409 ; 0188-0128
    ISSN (online) 1873-5487
    ISSN 0188-4409 ; 0188-0128
    DOI 10.1016/j.arcmed.2020.05.012
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  4. Article ; Online: Repressor Element-1 Binding Transcription Factor (REST) as a Possible Epigenetic Regulator of Neurodegeneration and MicroRNA-Based Therapeutic Strategies.

    Nassar, Ajmal / Satarker, Sairaj / Gurram, Prasada Chowdari / Upadhya, Dinesh / Fayaz, S M / Nampoothiri, Madhavan

    Molecular neurobiology

    2023  Volume 60, Issue 10, Page(s) 5557–5577

    Abstract: Neurodegenerative disorders (NDD) have grabbed significant scientific consideration due to their fast increase in prevalence worldwide. The specific pathophysiology of the disease and the amazing changes in the brain that take place as it advances are ... ...

    Abstract Neurodegenerative disorders (NDD) have grabbed significant scientific consideration due to their fast increase in prevalence worldwide. The specific pathophysiology of the disease and the amazing changes in the brain that take place as it advances are still the top issues of contemporary research. Transcription factors play a decisive role in integrating various signal transduction pathways to ensure homeostasis. Disruptions in the regulation of transcription can result in various pathologies, including NDD. Numerous microRNAs and epigenetic transcription factors have emerged as candidates for determining the precise etiology of NDD. Consequently, understanding by what means transcription factors are regulated and how the deregulation of transcription factors contributes to neurological dysfunction is important to the therapeutic targeting of pathways that they modulate. RE1-silencing transcription factor (REST) also named neuron-restrictive silencer factor (NRSF) has been studied in the pathophysiology of NDD. REST was realized to be a part of a neuroprotective element with the ability to be tuned and influenced by numerous microRNAs, such as microRNAs 124, 132, and 9 implicated in NDD. This article looks at the role of REST and the influence of various microRNAs in controlling REST function in the progression of Alzheimer's disease (AD), Parkinson's disease (PD), and Huntington's disease (HD) disease. Furthermore, to therapeutically exploit the possibility of targeting various microRNAs, we bring forth an overview of drug-delivery systems to modulate the microRNAs regulating REST in NDD.
    MeSH term(s) Humans ; Transcription Factors/metabolism ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; MicroRNAs/genetics ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/therapy ; Epigenesis, Genetic
    Chemical Substances Transcription Factors ; RE1-silencing transcription factor ; Repressor Proteins ; MicroRNAs
    Language English
    Publishing date 2023-06-16
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 645020-9
    ISSN 1559-1182 ; 0893-7648
    ISSN (online) 1559-1182
    ISSN 0893-7648
    DOI 10.1007/s12035-023-03437-1
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    Zs.A 2411: Show issues Location:
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  5. Article ; Online: Astrocytic transcription factors REST, YY1, and putative microRNAs in Parkinson's disease and advanced therapeutic strategies.

    Nassar, Ajmal / Kodi, Triveni / Satarker, Sairaj / Gurram, Prasada Chowdari / Fayaz, S M / Nampoothiri, Madhavan

    Gene

    2023  Volume 892, Page(s) 147898

    Abstract: Transcription factors (TF) and microRNAs are regulatory factors in astrocytes and are linked to several Parkinson's disease (PD) progression causes, such as disruption of glutamine transporters in astrocytes and concomitant disrupted glutamine uptake and ...

    Abstract Transcription factors (TF) and microRNAs are regulatory factors in astrocytes and are linked to several Parkinson's disease (PD) progression causes, such as disruption of glutamine transporters in astrocytes and concomitant disrupted glutamine uptake and inflammation. REST, a crucial TF, has been documented as an epigenetic repressor that limits the expression of neuronal genes in non-neural cells. REST activity is significantly linked to its corepressors in astrocytes, specifically histone deacetylases (HDACs), CoREST, and MECP2. Another REST-regulating TF, YY1, has been studied in astrocytes, and its interaction with REST has been investigated. In this review, the molecular processes that support the astrocytic control of REST and YY1 in terms of the regulation of glutamate transporter EAAT2 were addressed in a more detailed and comprehensive manner. Both TFs' function in astrocytes and how astrocyte abnormalities cause PD is still a mystery. Moreover, microRNAs (short non-coding RNAs) are key regulators that have been correlated to the expression and regulation of numerous genes linked to PD. The identification of numerous miRs that are engaged in astrocyte dysfunction that triggers PD has been shown. The term "Gut-brain axis" refers to the two systems' mutual communication. Gut microbial dysbiosis, which mediates an imbalance of the gut-brain axis, might contribute to neurodegenerative illnesses through altered astrocytic regulation. New treatment approaches to modify the gut-brain axis and prevent astrocytic repercussions have also been investigated in this review.
    MeSH term(s) Humans ; Transcription Factors/metabolism ; Astrocytes/metabolism ; Parkinson Disease/genetics ; Parkinson Disease/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Glutamine/metabolism ; YY1 Transcription Factor/genetics ; YY1 Transcription Factor/metabolism
    Chemical Substances Transcription Factors ; MicroRNAs ; Glutamine (0RH81L854J) ; YY1 protein, human ; YY1 Transcription Factor
    Language English
    Publishing date 2023-10-11
    Publishing country Netherlands
    Document type Review ; Journal Article
    ZDB-ID 391792-7
    ISSN 1879-0038 ; 0378-1119
    ISSN (online) 1879-0038
    ISSN 0378-1119
    DOI 10.1016/j.gene.2023.147898
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  6. Article: Involvement of the nervous system in COVID-19: The bell should toll in the brain

    Satarker, Sairaj / Nampoothiri, Madhavan

    Life sciences. 2020 Dec. 01, v. 262

    2020  

    Abstract: The world is fuming at SARS-CoV-2 for being the culprit for causing the devastating COVID-19, claiming millions of lives across the globe in the form of respiratory disorders. But lesser known are its effects on the CNS that are slowly surfacing in the ... ...

    Abstract The world is fuming at SARS-CoV-2 for being the culprit for causing the devastating COVID-19, claiming millions of lives across the globe in the form of respiratory disorders. But lesser known are its effects on the CNS that are slowly surfacing in the worldwide population. Our review illustrates findings that claim SARS-CoV-2's arrival onto the ACE2 receptors of neuronal and glial cells mainly via CSF, olfactory nerve, trigeminal nerve, neuronal dissemination, and hematogenous pathways. The role of SARS-CoV-2 structural proteins in its smooth viral infectivity of the host cannot be ignored, especially the spike proteins that mediate spike attachment and host membrane fusion. Worth mentioning the nucleocapsid, envelope, and membrane proteins make the proliferation of SARS-CoV-2 much simpler than expected in spreading infection. This has led to catastrophic conditions like seizures, Guillain-Barré syndrome, viral encephalitis, meningoencephalitis, acute cerebrovascular disease, and respiratory failures. Placing a magnifying lens on the lesser-explored CNS consequences of COVID-19, we attempt to shift the focus of our readers onto the new supporting threats to which further studies are needed.
    Keywords COVID-19 infection ; Severe acute respiratory syndrome coronavirus 2 ; brain ; cerebrovascular disorders ; membrane fusion ; meningoencephalitis ; nerve tissue ; neurons ; nucleocapsid ; pathogenicity ; viral encephalitis
    Language English
    Dates of publication 2020-1201
    Publishing place Elsevier Inc.
    Document type Article
    Note NAL-light
    ZDB-ID 3378-9
    ISSN 1879-0631 ; 0024-3205
    ISSN (online) 1879-0631
    ISSN 0024-3205
    DOI 10.1016/j.lfs.2020.118568
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  7. Article ; Online: In silico screening of neurokinin receptor antagonists as a therapeutic strategy for neuroinflammation in Alzheimer's disease.

    Satarker, Sairaj / Maity, Swastika / Mudgal, Jayesh / Nampoothiri, Madhavan

    Molecular diversity

    2021  Volume 26, Issue 1, Page(s) 443–466

    Abstract: Neuroinflammation is one of the detrimental factors leading to neurodegeneration in Alzheimer's disease (AD) and other neurodegenerative disorders. The activation of microglial neurokinin 1 receptor (NK1R) by substance P (SP) enhances neuroinflammation ... ...

    Abstract Neuroinflammation is one of the detrimental factors leading to neurodegeneration in Alzheimer's disease (AD) and other neurodegenerative disorders. The activation of microglial neurokinin 1 receptor (NK1R) by substance P (SP) enhances neuroinflammation which is mediated through pro-inflammatory pathways involving NFkB, ERK1/2, and P38 and thus projects the scope and importance of NK1R inhibitors. Emphasizing the inhibitory role of N Acetyl L Tryptophan (L-NAT) on NK1R, this is the first in silico screening of L-NAT mediated NK1R antagonism. In addition, FDA- approved ligands were screened for their potential NK1R antagonism. The L-NAT was docked in XP (Extra Precision) mode while FDA-approved ligands were screened in HTVS (High Throughput Virtual Screening), SP (Standard Precision), and XP mode onto NK1R (PDB:6HLO). The L-NAT and top 3 compounds FDA-approved ligands were subjected to molecular dynamics (MD) studies of 100 ns simulation time. The XP docking of L-NAT, indacaterol, modafinil and alosetron showed good docking scores. Their 100 ns MD showed brief protein-ligand interactions with an acceptable root mean square deviation. The protein-ligand contacts depicted pi-pi stacking, pi-cation, hydrogen bonds, and water bridges with the amino acids necessary for NK1R inhibition. The variable colour band intensities on the protein-ligand contact map indicated their binding strength with amino acids. The molecular mechanics/generalized born surface area (MM-GBSA) scores suggested favourable binding free energy of the complexes. Thus, our study predicted the ability of L-NAT, indacaterol, modafinil, and alosetron as capable NK1R inhibitors that can aid to curb neuroinflammation in conditions of AD which could be further ascertained in subsequent studies.
    MeSH term(s) Alzheimer Disease/drug therapy ; Humans ; Ligands ; Molecular Docking Simulation ; Molecular Dynamics Simulation ; Neuroinflammatory Diseases
    Chemical Substances Ligands
    Language English
    Publishing date 2021-07-31
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 1376507-3
    ISSN 1573-501X ; 1381-1991
    ISSN (online) 1573-501X
    ISSN 1381-1991
    DOI 10.1007/s11030-021-10276-6
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  8. Article ; Online: Involvement of the nervous system in COVID-19

    Satarker, Sairaj / Nampoothiri, Madhavan

    Life Sciences

    The bell should toll in the brain

    2020  Volume 262, Page(s) 118568

    Keywords General Pharmacology, Toxicology and Pharmaceutics ; General Biochemistry, Genetics and Molecular Biology ; General Medicine ; covid19
    Language English
    Publisher Elsevier BV
    Publishing country us
    Document type Article ; Online
    ZDB-ID 3378-9
    ISSN 1879-0631 ; 0024-3205
    ISSN (online) 1879-0631
    ISSN 0024-3205
    DOI 10.1016/j.lfs.2020.118568
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  9. Article ; Online: Dialogue between Neuroinflammation and Neurodegenerative Diseases in COVID-19.

    Chowdhury, Bisruta / Sharma, Apoorva / Satarker, Sairaj / Mudgal, Jayesh / Nampoothiri, Madhavan

    Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer

    2021  Volume 40, Issue 3, Page(s) 37–49

    Abstract: It has now been almost a year since the emergence of the deadly SARS-CoV-2 with millions of people losing their lives due to resultant COVID-19. Apart from the well-known consequences of respiratory illnesses, it has even effortlessly mapped itself into ... ...

    Abstract It has now been almost a year since the emergence of the deadly SARS-CoV-2 with millions of people losing their lives due to resultant COVID-19. Apart from the well-known consequences of respiratory illnesses, it has even effortlessly mapped itself into the nervous system through routes like blood, CSF, neurons, and olfactory cells. Interestingly, the interaction of SARS-CoV-2 with the nervous system cells like neurons, microglia, and astrocytes has been a factor to worsen COVID-19 through its neuroinflammatory actions. The release of cytokines due to astrocyte and microglial activation could progress towards the most anticipated cytokine storm proving to be detrimental in the management of COVID-19. Such hyper-inflammatory conditions could make the BBB vulnerable, encouraging excessive viral particles into the CNS, leading to further neurodegenerative pathologies like Alzheimer's disease, Parkinson's disease, Creutzfeldt-Jakob disease, and Multiple Sclerosis. Excessive neuroinflammation and neurodegeneration being the anticipated root causes of these multiple conditions, it is also essential to look into other factors that synergistically enhance the worsening of these diseases in COVID-19 patients for which additional studies are essential.
    MeSH term(s) COVID-19/etiology ; Cytokines/metabolism ; Host-Pathogen Interactions ; Humans ; Inflammation/pathology ; Inflammation/virology ; Microglia/pathology ; Microglia/virology ; Multiple Sclerosis/pathology ; Multiple Sclerosis/virology ; Neurodegenerative Diseases/pathology ; Neurodegenerative Diseases/virology ; Neurons/pathology ; Neurons/virology ; SARS-CoV-2/pathogenicity
    Chemical Substances Cytokines
    Language English
    Publishing date 2021-09-29
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 441790-2
    ISSN 2162-6537 ; 0731-8898 ; 0146-4779
    ISSN (online) 2162-6537
    ISSN 0731-8898 ; 0146-4779
    DOI 10.1615/JEnvironPatholToxicolOncol.2021038365
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  10. Article ; Online: Astrocytic Glutamatergic Transmission and Its Implications in Neurodegenerative Disorders.

    Satarker, Sairaj / Bojja, Sree Lalitha / Gurram, Prasada Chowdari / Mudgal, Jayesh / Arora, Devinder / Nampoothiri, Madhavan

    Cells

    2022  Volume 11, Issue 7

    Abstract: Several neurodegenerative disorders involve impaired neurotransmission, and glutamatergic neurotransmission sets a prototypical example. Glutamate is a predominant excitatory neurotransmitter where the astrocytes play a pivotal role in maintaining the ... ...

    Abstract Several neurodegenerative disorders involve impaired neurotransmission, and glutamatergic neurotransmission sets a prototypical example. Glutamate is a predominant excitatory neurotransmitter where the astrocytes play a pivotal role in maintaining the extracellular levels through release and uptake mechanisms. Astrocytes modulate calcium-mediated excitability and release several neurotransmitters and neuromodulators, including glutamate, and significantly modulate neurotransmission. Accumulating evidence supports the concept of excitotoxicity caused by astrocytic glutamatergic release in pathological conditions. Thus, the current review highlights different vesicular and non-vesicular mechanisms of astrocytic glutamate release and their implication in neurodegenerative diseases. As in presynaptic neurons, the vesicular release of astrocytic glutamate is also primarily meditated by calcium-mediated exocytosis. V-ATPase is crucial in the acidification and maintenance of the gradient that facilitates the vesicular storage of glutamate. Along with these, several other components, such as cystine/glutamate antiporter, hemichannels, BEST-1, TREK-1, purinergic receptors and so forth, also contribute to glutamate release under physiological and pathological conditions. Events of hampered glutamate uptake could promote inflamed astrocytes to trigger repetitive release of glutamate. This could be favorable towards the development and worsening of neurodegenerative diseases. Therefore, across neurodegenerative diseases, we review the relations between defective glutamatergic signaling and astrocytic vesicular and non-vesicular events in glutamate homeostasis. The optimum regulation of astrocytic glutamatergic transmission could pave the way for the management of these diseases and add to their therapeutic value.
    MeSH term(s) Astrocytes/physiology ; Calcium ; Glutamic Acid ; Humans ; Neurodegenerative Diseases ; Neurotransmitter Agents ; Synaptic Transmission/physiology
    Chemical Substances Neurotransmitter Agents ; Glutamic Acid (3KX376GY7L) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2022-03-28
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells11071139
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