WFRF:(Simister R.)
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| Fältnamn | Indikatorer | Metadata |
|---|---|---|
| 000 | 04360naa a2200793 4500 | |
| 001 | oai:gup.ub.gu.se/233995 | |
| 003 | SwePub | |
| 008 | 240528s2016 | |||||||||||000 ||eng| | |
| 024 | 7 | a https://gup.ub.gu.se/publication/2339952 URI |
| 024 | 7 | a https://doi.org/10.1159/0004422982 DOI |
| 040 | a (SwePub)gu | |
| 041 | a eng | |
| 042 | 9 SwePub | |
| 072 | 7 | a ref2 swepub-contenttype |
| 072 | 7 | a art2 swepub-publicationtype |
| 100 | 1 | a Bersano, A.4 aut |
| 245 | 1 0 | a Research Progresses in Understanding the Pathophysiology of Moyamoya Disease |
| 264 | c 2016-01-12 | |
| 264 | 1 | b S. Karger AG,c 2016 |
| 520 | a Background: The pathogenesis of moyamoya disease (MMD) is still unknown. The detection of inflammatory molecules such as cytokines, chemokines and growth factors in MMD patients' biological fluids supports the hypothesis that an abnormal angiogenesis is implicated in MMD pathogenesis. However, it is unclear whether these anomalies are the consequences of the disease or rather causal factors as well as these mechanisms remain insufficient to explain the pathophysiology of MMD. The presence of a family history in about 9-15% of Asian patients, the highly variable incidence rate between different ethnic and sex groups and the age of onset support the role of genetic factors in MMD pathogenesis. However, although some genetic loci have been associated with MMD, few of them have been replicated in independent series. Recently, RNF213 gene was shown to be strongly associated with MMD occurrence with a founder effect in East Asian patients. However, the mechanisms leading from RNF213 mutations to MMD clinical features are still unknown. Summary: The research on pathogenic mechanism of MMD is in its infancy. MMD is probably a complex and heterogeneous disorder, including different phenotypes and genotypes, in which more than a single factor is implicated. Key Message: Since the diagnosis of MMD is rapidly increasing worldwide, the development of more efficient stratifying risk systems, including both clinical but also biological drivers became imperative to improve our ability of predict prognosis and to develop mechanism-tailored interventions. | |
| 650 | 7 | a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicin0 (SwePub)3022 hsv//swe |
| 650 | 7 | a MEDICAL AND HEALTH SCIENCESx Clinical Medicine0 (SwePub)3022 hsv//eng |
| 653 | a Moyamoya disease | |
| 653 | a Pathophysiology | |
| 653 | a Angiogenesis | |
| 653 | a Endothelial progenitor cells | |
| 653 | a Genetics | |
| 653 | a endothelial progenitor cells | |
| 653 | a human-leukocyte antigen | |
| 653 | a rnf213 r4810k | |
| 653 | a rs112735431 | |
| 653 | a spontaneous occlusion | |
| 653 | a clinical-features | |
| 653 | a c.14576g-greater-than-a variant | |
| 653 | a angiogenic factors | |
| 653 | a surgical-treatment | |
| 653 | a cerebral-artery | |
| 653 | a adult patients | |
| 653 | a Neurosciences & Neurology | |
| 653 | a Cardiovascular System & Cardiology | |
| 700 | 1 | a Guey, S.4 aut |
| 700 | 1 | a Bedini, G.4 aut |
| 700 | 1 | a Nava, S.4 aut |
| 700 | 1 | a Herve, D.4 aut |
| 700 | 1 | a Vajkoczy, P.4 aut |
| 700 | 1 | a Tatlisumak, Turgutu Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology4 aut0 (Swepub:gu)xtatlt |
| 700 | 1 | a Sareela, M.4 aut |
| 700 | 1 | a van der Zwan, A.4 aut |
| 700 | 1 | a Klijn, C. J. M.4 aut |
| 700 | 1 | a Braun, K. P. J.4 aut |
| 700 | 1 | a Kronenburg, A.4 aut |
| 700 | 1 | a Acerbi, F.4 aut |
| 700 | 1 | a Brown, M. M.4 aut |
| 700 | 1 | a Calviere, L.4 aut |
| 700 | 1 | a Cordonnier, C.4 aut |
| 700 | 1 | a Henon, H.4 aut |
| 700 | 1 | a Thines, L.4 aut |
| 700 | 1 | a Khan, N.4 aut |
| 700 | 1 | a Czabanka, M.4 aut |
| 700 | 1 | a Kraemer, M.4 aut |
| 700 | 1 | a Simister, R.4 aut |
| 700 | 1 | a Prontera, P.4 aut |
| 700 | 1 | a Tournier-Lasserve, E.4 aut |
| 700 | 1 | a Parati, E.4 aut |
| 710 | 2 | a Göteborgs universitetb Institutionen för neurovetenskap och fysiologi4 org |
| 773 | 0 | t Cerebrovascular Diseasesd : S. Karger AGg 41:3-4, s. 105-118q 41:3-4<105-118x 1015-9770x 1421-9786 |
| 856 | 4 | u https://helda.helsinki.fi/bitstream/10138/161066/1/442298.pdf |
| 856 | 4 8 | u https://gup.ub.gu.se/publication/233995 |
| 856 | 4 8 | u https://doi.org/10.1159/000442298 |
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