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  4. Atypical Hemolytic Uremic Syndrome

Atypical Hemolytic Uremic Syndrome

Name
Atypical Hemolytic Uremic Syndrome
Namespace Keyword
MeSHDisease
Namespace
MeSH
Namespace Version
20170511
Namespace URL
https://arty.scai.fraunhofer.de/artifactory/bel/annotation/mesh-diseases/mesh-diseases-20170511.belanno

Sample Annotated Edges 5

a(CHEBI:heme) increases path(MESH:"Thrombotic Microangiopathies") View Subject | View Object

Heme may be implicated and contribute to the development of (i) bp(MESH: PubMed:26875449

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Serum
MeSH
Atypical Hemolytic Uremic Syndrome
Text Location
Review

path(HM:"endothelial lesions") increases path(MESH:Hemolysis) View Subject | View Object

From hemolytic uremic syndrome (HUS), we know that damage to the endothelium (endothelial lesions) might be the primary cause of hemolysis. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Atypical Hemolytic Uremic Syndrome
Text Location
Review

path(HM:"endothelial lesions") increases path(MESH:Hemolysis) View Subject | View Object

During HUS, endothelial lesions cause a complement dependent activation of immune response and local thrombus formation—attachment of fibrin and platelets to the endothelial lesions and consequently disseminated intravascular coagulation (DIC)—and further mechanical destruction of the red blood cells in the fibrin mesh resulting in hemolysis [82]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Atypical Hemolytic Uremic Syndrome
Text Location
Review

path(HM:"endothelial lesions") increases path(MESH:Thrombosis) View Subject | View Object

During HUS, endothelial lesions cause a complement dependent activation of immune response and local thrombus formation—attachment of fibrin and platelets to the endothelial lesions and consequently disseminated intravascular coagulation (DIC)—and further mechanical destruction of the red blood cells in the fibrin mesh resulting in hemolysis [82]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Atypical Hemolytic Uremic Syndrome
Text Location
Review

path(HM:"endothelial lesions") increases path(MESH:"Disseminated Intravascular Coagulation") View Subject | View Object

During HUS, endothelial lesions cause a complement dependent activation of immune response and local thrombus formation—attachment of fibrin and platelets to the endothelial lesions and consequently disseminated intravascular coagulation (DIC)—and further mechanical destruction of the red blood cells in the fibrin mesh resulting in hemolysis [82]. PubMed:29956069

Appears in Networks:
Annotations
Cell Ontology (CL)
erythrocyte
MeSH
Liver
MeSH
Atypical Hemolytic Uremic Syndrome
Text Location
Review

Showing 5 of 5 edges

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.