The Influence of Metformin to the Transcriptional Activity of the mTOR and FOX3 Genes in Parapancreatic Adipose Tissue of Streptozotocin-Induced Diabetic Rats.
Identifieur interne : 000001 ( Main/Exploration ); précédent : 000000; suivant : 000002The Influence of Metformin to the Transcriptional Activity of the mTOR and FOX3 Genes in Parapancreatic Adipose Tissue of Streptozotocin-Induced Diabetic Rats.
Auteurs : Denis Anatolievich Putilin [Ukraine] ; Sergey Yuryevich Evchenko [Ukraine] ; Larisa Yaroslavivna Fedoniuk [Ukraine] ; Olexandr Stepanovich Tokarskyy [Ukraine] ; Oleksandr Mikhailovich Kamyshny [Ukraine] ; Liudmyla Mikhailivna Migenko [Ukraine] ; Serhiy Mikhailovich Andreychyn [Ukraine] ; Iryna Ihorivna Hanberher [Ukraine] ; Tetyana Oleksandrivna Bezruk [Ukraine]Source :
- Journal of medicine and life [ 1844-3117 ]
Descripteurs français
- KwdFr :
- ARN messager (génétique), ARN messager (métabolisme), Animaux (MeSH), Diabète expérimental (anatomopathologie), Diabète expérimental (génétique), Facteurs de transcription Forkhead (génétique), Facteurs de transcription Forkhead (métabolisme), Interleukine-1 bêta (génétique), Interleukine-1 bêta (métabolisme), Metformine (pharmacologie), Mâle (MeSH), Rat Wistar (MeSH), Streptozocine (MeSH), Sérine-thréonine kinases TOR (génétique), Sérine-thréonine kinases TOR (métabolisme), Tissu adipeux (anatomopathologie), Transcription génétique (effets des médicaments et des substances chimiques).
- MESH :
- anatomopathologie : Diabète expérimental, Tissu adipeux.
- effets des médicaments et des substances chimiques : Transcription génétique.
- génétique : ARN messager, Diabète expérimental, Facteurs de transcription Forkhead, Interleukine-1 bêta, Sérine-thréonine kinases TOR.
- métabolisme : ARN messager, Facteurs de transcription Forkhead, Interleukine-1 bêta, Sérine-thréonine kinases TOR.
- pharmacologie : Metformine.
- Animaux, Mâle, Rat Wistar, Streptozocine.
English descriptors
- KwdEn :
- Adipose Tissue (pathology), Animals (MeSH), Diabetes Mellitus, Experimental (genetics), Diabetes Mellitus, Experimental (pathology), Forkhead Transcription Factors (genetics), Forkhead Transcription Factors (metabolism), Interleukin-1beta (genetics), Interleukin-1beta (metabolism), Male (MeSH), Metformin (pharmacology), RNA, Messenger (genetics), RNA, Messenger (metabolism), Rats, Wistar (MeSH), Streptozocin (MeSH), TOR Serine-Threonine Kinases (genetics), TOR Serine-Threonine Kinases (metabolism), Transcription, Genetic (drug effects).
- MESH :
- chemical , genetics : Forkhead Transcription Factors, Interleukin-1beta, RNA, Messenger, TOR Serine-Threonine Kinases.
- drug effects : Transcription, Genetic.
- genetics : Diabetes Mellitus, Experimental.
- chemical , metabolism : Forkhead Transcription Factors, Interleukin-1beta, RNA, Messenger, TOR Serine-Threonine Kinases.
- pathology : Adipose Tissue, Diabetes Mellitus, Experimental.
- chemical , pharmacology : Metformin.
- Animals, Male, Rats, Wistar, Streptozocin.
Abstract
The mammalian target of rapamycin is not only a central regulator of lipid metabolism that controls the processes of adipogenesis and lipolysis but also a regulator of the immunometabolism of immune cells that infiltrate adipose tissue. In turn, the level of progression of diabetes is significantly influenced by the Treg subpopulation, the complexity and heterogeneity of which is confirmed by the detection of numerous tissue-specific Tregs, including the so-called VAT Tregs (visceral adipose tissue CD4+Foxp3+ regulatory T cells). Therefore, the purpose of the study was to determine the mRNA expression levels of mTOR, Foxp3, IL1β, and IL17A genes in rat parapancreatic adipose tissue with experimental streptozotocin-induced diabetes mellitus, with or without metformin administration. The experiments were performed on male Wistar rats with induced diabetes as a result of streptozotocin administration. Molecular genetic studies were performed using real-time reverse transcription-polymerase chain reaction. The development of diabetes caused transcriptional activation of the mammalian target of rapamycin protein kinase gene, as well as increased mRNA expression of the pro-inflammatory cytokines IL1β and IL17A, but did not affect Foxp3 mRNA expression. The intervention with metformin in diabetic rats inhibited the mammalian target of rapamycin mRNA expression and caused an increase in the transcriptional activity of the Foxp3 gene in parapancreatic adipose tissue.
DOI: 10.25122/jml-2020-0029
PubMed: 32341701
PubMed Central: PMC7175427
Affiliations:
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Horbachevsky Ternopil National Medical University, Ternopil</wicri:regionArea><wicri:noRegion>Ternopil</wicri:noRegion></affiliation></author><author><name sortKey="Hanberher, Iryna Ihorivna" sort="Hanberher, Iryna Ihorivna" uniqKey="Hanberher I" first="Iryna Ihorivna" last="Hanberher">Iryna Ihorivna Hanberher</name><affiliation wicri:level="1"><nlm:affiliation>Department of Propedeutics of Internal Medicine and Phthisiology, I. Horbachevsky Ternopil National Medical University, Ternopil, Ukraine.</nlm:affiliation><country xml:lang="fr">Ukraine</country><wicri:regionArea>Department of Propedeutics of Internal Medicine and Phthisiology, I. 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Horbachevsky Ternopil National Medical University, Ternopil, Ukraine.</nlm:affiliation><country xml:lang="fr">Ukraine</country><wicri:regionArea>Medical Biology Department, I. Horbachevsky Ternopil National Medical University, Ternopil</wicri:regionArea><wicri:noRegion>Ternopil</wicri:noRegion></affiliation></author><author><name sortKey="Tokarskyy, Olexandr Stepanovich" sort="Tokarskyy, Olexandr Stepanovich" uniqKey="Tokarskyy O" first="Olexandr Stepanovich" last="Tokarskyy">Olexandr Stepanovich Tokarskyy</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medical Biochemistry, I. Horbachevsky Ternopil National Medical University, Ternopil, Ukraine.</nlm:affiliation><country xml:lang="fr">Ukraine</country><wicri:regionArea>Department of Medical Biochemistry, I. Horbachevsky Ternopil National Medical University, Ternopil</wicri:regionArea><wicri:noRegion>Ternopil</wicri:noRegion></affiliation></author><author><name sortKey="Kamyshny, Oleksandr Mikhailovich" sort="Kamyshny, Oleksandr Mikhailovich" uniqKey="Kamyshny O" first="Oleksandr Mikhailovich" last="Kamyshny">Oleksandr Mikhailovich Kamyshny</name><affiliation wicri:level="1"><nlm:affiliation>Department of Microbiology, Virology and Immunology, Molecular Genetics Laboratory, Zaporizhzhia State Medical University, Zaporizhzhia, Ukraine.</nlm:affiliation><country xml:lang="fr">Ukraine</country><wicri:regionArea>Department of Microbiology, Virology and Immunology, Molecular Genetics Laboratory, Zaporizhzhia State Medical University, Zaporizhzhia</wicri:regionArea><wicri:noRegion>Zaporizhzhia</wicri:noRegion></affiliation></author><author><name sortKey="Migenko, Liudmyla Mikhailivna" sort="Migenko, Liudmyla Mikhailivna" uniqKey="Migenko L" first="Liudmyla Mikhailivna" last="Migenko">Liudmyla Mikhailivna Migenko</name><affiliation wicri:level="1"><nlm:affiliation>Second Department of Internal Medicine, I. Horbachevsky Ternopil National Medical University, Ternopil, Ukraine.</nlm:affiliation><country xml:lang="fr">Ukraine</country><wicri:regionArea>Second Department of Internal Medicine, I. Horbachevsky Ternopil National Medical University, Ternopil</wicri:regionArea><wicri:noRegion>Ternopil</wicri:noRegion></affiliation></author><author><name sortKey="Andreychyn, Serhiy Mikhailovich" sort="Andreychyn, Serhiy Mikhailovich" uniqKey="Andreychyn S" first="Serhiy Mikhailovich" last="Andreychyn">Serhiy Mikhailovich Andreychyn</name><affiliation wicri:level="1"><nlm:affiliation>Department of Propedeutics of Internal Medicine and Phthisiology, I. Horbachevsky Ternopil National Medical University, Ternopil, Ukraine.</nlm:affiliation><country xml:lang="fr">Ukraine</country><wicri:regionArea>Department of Propedeutics of Internal Medicine and Phthisiology, I. Horbachevsky Ternopil National Medical University, Ternopil</wicri:regionArea><wicri:noRegion>Ternopil</wicri:noRegion></affiliation></author><author><name sortKey="Hanberher, Iryna Ihorivna" sort="Hanberher, Iryna Ihorivna" uniqKey="Hanberher I" first="Iryna Ihorivna" last="Hanberher">Iryna Ihorivna Hanberher</name><affiliation wicri:level="1"><nlm:affiliation>Department of Propedeutics of Internal Medicine and Phthisiology, I. Horbachevsky Ternopil National Medical University, Ternopil, Ukraine.</nlm:affiliation><country xml:lang="fr">Ukraine</country><wicri:regionArea>Department of Propedeutics of Internal Medicine and Phthisiology, I. Horbachevsky Ternopil National Medical University, Ternopil</wicri:regionArea><wicri:noRegion>Ternopil</wicri:noRegion></affiliation></author><author><name sortKey="Bezruk, Tetyana Oleksandrivna" sort="Bezruk, Tetyana Oleksandrivna" uniqKey="Bezruk T" first="Tetyana Oleksandrivna" last="Bezruk">Tetyana Oleksandrivna Bezruk</name><affiliation wicri:level="1"><nlm:affiliation>Department of Internal Medicine and Infectious Diseases, Bukovinian State Medical University, Chernivtsi, Ukraine.</nlm:affiliation><country xml:lang="fr">Ukraine</country><wicri:regionArea>Department of Internal Medicine and Infectious Diseases, Bukovinian State Medical University, Chernivtsi</wicri:regionArea><wicri:noRegion>Chernivtsi</wicri:noRegion></affiliation></author></analytic><series><title level="j">Journal of medicine and life</title><idno type="eISSN">1844-3117</idno></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adipose Tissue (pathology)</term><term>Animals (MeSH)</term><term>Diabetes Mellitus, Experimental (genetics)</term><term>Diabetes Mellitus, Experimental (pathology)</term><term>Forkhead Transcription Factors (genetics)</term><term>Forkhead Transcription Factors (metabolism)</term><term>Interleukin-1beta (genetics)</term><term>Interleukin-1beta (metabolism)</term><term>Male (MeSH)</term><term>Metformin (pharmacology)</term><term>RNA, Messenger (genetics)</term><term>RNA, Messenger (metabolism)</term><term>Rats, Wistar (MeSH)</term><term>Streptozocin (MeSH)</term><term>TOR Serine-Threonine Kinases (genetics)</term><term>TOR Serine-Threonine Kinases (metabolism)</term><term>Transcription, Genetic (drug effects)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ARN messager (génétique)</term><term>ARN messager (métabolisme)</term><term>Animaux (MeSH)</term><term>Diabète expérimental (anatomopathologie)</term><term>Diabète expérimental (génétique)</term><term>Facteurs de transcription Forkhead (génétique)</term><term>Facteurs de transcription Forkhead (métabolisme)</term><term>Interleukine-1 bêta (génétique)</term><term>Interleukine-1 bêta (métabolisme)</term><term>Metformine (pharmacologie)</term><term>Mâle (MeSH)</term><term>Rat Wistar (MeSH)</term><term>Streptozocine (MeSH)</term><term>Sérine-thréonine kinases TOR (génétique)</term><term>Sérine-thréonine kinases TOR (métabolisme)</term><term>Tissu adipeux (anatomopathologie)</term><term>Transcription génétique (effets des médicaments et des substances chimiques)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Forkhead Transcription Factors</term><term>Interleukin-1beta</term><term>RNA, Messenger</term><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Diabète expérimental</term><term>Tissu adipeux</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Transcription, Genetic</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Transcription génétique</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Diabetes Mellitus, Experimental</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>ARN messager</term><term>Diabète expérimental</term><term>Facteurs de transcription Forkhead</term><term>Interleukine-1 bêta</term><term>Sérine-thréonine kinases TOR</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Forkhead Transcription Factors</term><term>Interleukin-1beta</term><term>RNA, Messenger</term><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ARN messager</term><term>Facteurs de transcription Forkhead</term><term>Interleukine-1 bêta</term><term>Sérine-thréonine kinases TOR</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Adipose Tissue</term><term>Diabetes Mellitus, Experimental</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Metformine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Metformin</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Male</term><term>Rats, Wistar</term><term>Streptozocin</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Mâle</term><term>Rat Wistar</term><term>Streptozocine</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The mammalian target of rapamycin is not only a central regulator of lipid metabolism that controls the processes of adipogenesis and lipolysis but also a regulator of the immunometabolism of immune cells that infiltrate adipose tissue. In turn, the level of progression of diabetes is significantly influenced by the Treg subpopulation, the complexity and heterogeneity of which is confirmed by the detection of numerous tissue-specific Tregs, including the so-called VAT Tregs (visceral adipose tissue CD4+Foxp3+ regulatory T cells). Therefore, the purpose of the study was to determine the mRNA expression levels of mTOR, Foxp3, IL1β, and IL17A genes in rat parapancreatic adipose tissue with experimental streptozotocin-induced diabetes mellitus, with or without metformin administration. The experiments were performed on male Wistar rats with induced diabetes as a result of streptozotocin administration. Molecular genetic studies were performed using real-time reverse transcription-polymerase chain reaction. The development of diabetes caused transcriptional activation of the mammalian target of rapamycin protein kinase gene, as well as increased mRNA expression of the pro-inflammatory cytokines IL1β and IL17A, but did not affect Foxp3 mRNA expression. The intervention with metformin in diabetic rats inhibited the mammalian target of rapamycin mRNA expression and caused an increase in the transcriptional activity of the Foxp3 gene in parapancreatic adipose tissue.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" IndexingMethod="Curated" Owner="NLM"><PMID Version="1">32341701</PMID><DateCompleted><Year>2020</Year><Month>06</Month><Day>26</Day></DateCompleted><DateRevised><Year>2020</Year><Month>06</Month><Day>26</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1844-3117</ISSN><JournalIssue CitedMedium="Internet"><Volume>13</Volume><Issue>1</Issue><PubDate><MedlineDate>2020 Jan-Mar</MedlineDate></PubDate></JournalIssue><Title>Journal of medicine and life</Title><ISOAbbreviation>J Med Life</ISOAbbreviation></Journal><ArticleTitle>The Influence of Metformin to the Transcriptional Activity of the mTOR and FOX3 Genes in Parapancreatic Adipose Tissue of Streptozotocin-Induced Diabetic Rats.</ArticleTitle><Pagination><MedlinePgn>50-55</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.25122/jml-2020-0029</ELocationID><Abstract><AbstractText>The mammalian target of rapamycin is not only a central regulator of lipid metabolism that controls the processes of adipogenesis and lipolysis but also a regulator of the immunometabolism of immune cells that infiltrate adipose tissue. In turn, the level of progression of diabetes is significantly influenced by the Treg subpopulation, the complexity and heterogeneity of which is confirmed by the detection of numerous tissue-specific Tregs, including the so-called VAT Tregs (visceral adipose tissue CD4+Foxp3+ regulatory T cells). Therefore, the purpose of the study was to determine the mRNA expression levels of mTOR, Foxp3, IL1β, and IL17A genes in rat parapancreatic adipose tissue with experimental streptozotocin-induced diabetes mellitus, with or without metformin administration. The experiments were performed on male Wistar rats with induced diabetes as a result of streptozotocin administration. Molecular genetic studies were performed using real-time reverse transcription-polymerase chain reaction. The development of diabetes caused transcriptional activation of the mammalian target of rapamycin protein kinase gene, as well as increased mRNA expression of the pro-inflammatory cytokines IL1β and IL17A, but did not affect Foxp3 mRNA expression. The intervention with metformin in diabetic rats inhibited the mammalian target of rapamycin mRNA expression and caused an increase in the transcriptional activity of the Foxp3 gene in parapancreatic adipose tissue.</AbstractText><CopyrightInformation>©Carol Davila University Press.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Putilin</LastName><ForeName>Denis Anatolievich</ForeName><Initials>DA</Initials><AffiliationInfo><Affiliation>Department of Normal Physiology, Zaporizhzhia State Medical University, Zaporizhzhia, Ukraine.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Evchenko</LastName><ForeName>Sergey Yuryevich</ForeName><Initials>SY</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Virology and Immunology, Zaporizhzhia State Medical University, Zaporizhzhia, Ukraine.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fedoniuk</LastName><ForeName>Larisa Yaroslavivna</ForeName><Initials>LY</Initials><AffiliationInfo><Affiliation>Medical Biology Department, I. Horbachevsky Ternopil National Medical University, Ternopil, Ukraine.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tokarskyy</LastName><ForeName>Olexandr Stepanovich</ForeName><Initials>OS</Initials><AffiliationInfo><Affiliation>Department of Medical Biochemistry, I. Horbachevsky Ternopil National Medical University, Ternopil, Ukraine.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kamyshny</LastName><ForeName>Oleksandr Mikhailovich</ForeName><Initials>OM</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Virology and Immunology, Molecular Genetics Laboratory, Zaporizhzhia State Medical University, Zaporizhzhia, Ukraine.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Migenko</LastName><ForeName>Liudmyla Mikhailivna</ForeName><Initials>LM</Initials><AffiliationInfo><Affiliation>Second Department of Internal Medicine, I. Horbachevsky Ternopil National Medical University, Ternopil, Ukraine.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Andreychyn</LastName><ForeName>Serhiy Mikhailovich</ForeName><Initials>SM</Initials><AffiliationInfo><Affiliation>Department of Propedeutics of Internal Medicine and Phthisiology, I. Horbachevsky Ternopil National Medical University, Ternopil, Ukraine.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hanberher</LastName><ForeName>Iryna Ihorivna</ForeName><Initials>II</Initials><AffiliationInfo><Affiliation>Department of Propedeutics of Internal Medicine and Phthisiology, I. Horbachevsky Ternopil National Medical University, Ternopil, Ukraine.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bezruk</LastName><ForeName>Tetyana Oleksandrivna</ForeName><Initials>TO</Initials><AffiliationInfo><Affiliation>Department of Internal Medicine and Infectious Diseases, Bukovinian State Medical University, Chernivtsi, Ukraine.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Romania</Country><MedlineTA>J Med Life</MedlineTA><NlmUniqueID>101477617</NlmUniqueID><ISSNLinking>1844-122X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051858">Forkhead Transcription Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C500522">Foxp3 protein, 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sortKey="Putilin, Denis Anatolievich" sort="Putilin, Denis Anatolievich" uniqKey="Putilin D" first="Denis Anatolievich" last="Putilin">Denis Anatolievich Putilin</name></noRegion><name sortKey="Andreychyn, Serhiy Mikhailovich" sort="Andreychyn, Serhiy Mikhailovich" uniqKey="Andreychyn S" first="Serhiy Mikhailovich" last="Andreychyn">Serhiy Mikhailovich Andreychyn</name><name sortKey="Bezruk, Tetyana Oleksandrivna" sort="Bezruk, Tetyana Oleksandrivna" uniqKey="Bezruk T" first="Tetyana Oleksandrivna" last="Bezruk">Tetyana Oleksandrivna Bezruk</name><name sortKey="Evchenko, Sergey Yuryevich" sort="Evchenko, Sergey Yuryevich" uniqKey="Evchenko S" first="Sergey Yuryevich" last="Evchenko">Sergey Yuryevich Evchenko</name><name sortKey="Fedoniuk, Larisa Yaroslavivna" sort="Fedoniuk, Larisa Yaroslavivna" uniqKey="Fedoniuk L" first="Larisa Yaroslavivna" last="Fedoniuk">Larisa Yaroslavivna Fedoniuk</name><name sortKey="Hanberher, Iryna Ihorivna" sort="Hanberher, Iryna Ihorivna" uniqKey="Hanberher I" first="Iryna Ihorivna" last="Hanberher">Iryna Ihorivna Hanberher</name><name sortKey="Kamyshny, Oleksandr Mikhailovich" sort="Kamyshny, Oleksandr Mikhailovich" uniqKey="Kamyshny O" first="Oleksandr Mikhailovich" last="Kamyshny">Oleksandr Mikhailovich Kamyshny</name><name sortKey="Migenko, Liudmyla Mikhailivna" sort="Migenko, Liudmyla Mikhailivna" uniqKey="Migenko L" first="Liudmyla Mikhailivna" last="Migenko">Liudmyla Mikhailivna Migenko</name><name sortKey="Tokarskyy, Olexandr Stepanovich" sort="Tokarskyy, Olexandr Stepanovich" uniqKey="Tokarskyy O" first="Olexandr Stepanovich" last="Tokarskyy">Olexandr Stepanovich Tokarskyy</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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