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Je něco špatně v tomto záznamu ?
Levels of 17β-hydroxysteroid dehydrogenase type 10 in CSF are not a valuable biomarker for multiple sclerosis
Z. Kristofikova, J. Ricny, D. Kaping, J. Klaschka, J. Kotoucova, A. Bartos,
Jazyk angličtina Země Anglie, Velká Británie
Typ dokumentu časopisecké články, práce podpořená grantem
NLK
PubMed Central
od 2015 do Před 1 rokem
ProQuest Central
od 2007-06-01 do 2021-01-31
Health & Medicine (ProQuest)
od 2007-06-01 do 2021-01-31
Public Health Database (ProQuest)
od 2007-06-01 do 2021-01-31
PubMed
30520659
DOI
10.2217/bmm-2018-0061
Knihovny.cz E-zdroje
- MeSH
- 3-hydroxyacyl-CoA-dehydrogenasy MeSH
- amyloidní beta-protein MeSH
- biologické markery MeSH
- dospělí MeSH
- lidé MeSH
- peptidové fragmenty MeSH
- roztroušená skleróza MeSH
- Check Tag
- dospělí MeSH
- lidé MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
AIM: We aimed to characterize the role of mitochondrial 17β-hydroxysteroid dehydrogenase type 10 (17β-HSD10) overexpression in multiple sclerosis (MS) and to evaluate its use as a biomarker. Materials & methods: We estimated levels of 17β-HSD10, amyloid β 1-42, cyclophilin D, 17β-HSD10-cyclophilin D complexes or 17β-HSD10-parkin complexes in cerebrospinal fluid (CSF) samples. RESULTS: The increase in 17β-HSD10 levels or in 17β-HSD10-parkin complexes and links to leukocytes were found only in relapsing-remitting MS. The sensitivity of the biomarker was 64%, the specificity equaled 60-63% compared with controls. CONCLUSION: Increased CSF levels of 17β-HSD10 in later stages of MS could be interpreted via its upregulation in demyelinated neuronal axons. CSF levels of 17β-HSD10 are not the valuable biomarker for the early diagnosis or for the progression of MS.
Institute of Computer Science Academy of Sciences 182 07 Prague Czech Republic
National Institute of Mental Health 250 67 Klecany Czech Republic
Citace poskytuje Crossref.org
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- $a AIM: We aimed to characterize the role of mitochondrial 17β-hydroxysteroid dehydrogenase type 10 (17β-HSD10) overexpression in multiple sclerosis (MS) and to evaluate its use as a biomarker. Materials & methods: We estimated levels of 17β-HSD10, amyloid β 1-42, cyclophilin D, 17β-HSD10-cyclophilin D complexes or 17β-HSD10-parkin complexes in cerebrospinal fluid (CSF) samples. RESULTS: The increase in 17β-HSD10 levels or in 17β-HSD10-parkin complexes and links to leukocytes were found only in relapsing-remitting MS. The sensitivity of the biomarker was 64%, the specificity equaled 60-63% compared with controls. CONCLUSION: Increased CSF levels of 17β-HSD10 in later stages of MS could be interpreted via its upregulation in demyelinated neuronal axons. CSF levels of 17β-HSD10 are not the valuable biomarker for the early diagnosis or for the progression of MS.
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