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datacite.yml

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+# Metadata for DOI registration according to DataCite Metadata Schema 4.1.
+# For detailed schema description see https://doi.org/10.5438/0014
+
+## Required fields
+
+# The main researchers involved. Include digital identifier (e.g., ORCID)
+# if possible, including the prefix to indicate its type.
+authors:
+  -
+    firstname: "Andrea"
+    lastname: "Pozo-Rodrigalvarez"
+    affiliation: "Laboratory of Regenerative Neuroimmunology, Center for Brain Repair, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden"
+ 
+  -
+    firstname: "Yixian"
+    lastname: "Li"
+    affiliation: "Laboratory of Regenerative Neuroimmunology, Center for Brain Repair, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden"
+
+  -
+    firstname: "Jingyun"
+    lastname: "Wu"
+    affiliation: "Laboratory of Regenerative Neuroimmunology, Center for Brain Repair, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden"
+
+  -
+    firstname: "Verena"
+    lastname: "Dehm"
+    affiliation: "Laboratory of Regenerative Neuroimmunology, Center for Brain Repair, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden"
+
+  -
+    firstname: "Anna"
+    lastname: "Stokowska"
+    affiliation: "Laboratory of Regenerative Neuroimmunology, Center for Brain Repair, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden"
+    id: "ORCID:0000-0001-5237-3341"
+  -
+    firstname: "Hanna"
+    lastname: "Sourkova"
+    affiliation: "Laboratory of Astrocyte Biology and CNS Regeneration, Center for Brain Repair, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden"
+
+  -
+    firstname: "Harry"
+    lastname: "Steinbusch"
+    affiliation: "Department of Neuroscience, Faculty of Health, Medicine and Life Sciences, Maastricht University, The Netherlands"
+
+   -
+    firstname: "Carina"
+    lastname: "Mallard"
+    affiliation: "Centre of Perinatal Medicine & Health, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden"
+
+  -
+    firstname: "Henrik"
+    lastname: "Hagberg"
+    affiliation: "Centre of Perinatal Medicine & Health, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden"
+
+  -
+    firstname: "Milos"
+    lastname: "Pekny"
+    affiliation: "Laboratory of Astrocyte Biology and CNS Regeneration, Center for Brain Repair, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden"
+    id: "ORCID:0000-0003-1607-8075"
+  -
+    firstname: "Marcela"
+    lastname: "Pekna"
+    affiliation: "Laboratory of Regenerative Neuroimmunology, Center for Brain Repair, Department of Clinical Neuroscience, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden"
+    id: "ORCID:0000-0003-2734-8237"
+    
+
+# A title to describe the published resource.
+title: "C3a receptor signaling inhibits neurodegeneration induced by neonatal hypoxic-ischemic brain injury"
+
+# Additional information about the resource, e.g., a brief abstract.
+description: |
+  Hypoxic-ischemic neonatal encephalopathy due to perinatal asphyxia is the leading cause of brain injury 
+  in newborns. Clinical data suggest that brain inflammation induced by perinatal insults can persist for 
+  years. We previously showed that signaling through the receptor for complement peptide C3a (C3aR) 
+  protects against cognitive impairment induced by experimental perinatal asphyxia. To investigate the 
+  long-term neuropathological effects of hypoxic-ischemic injury to the developing brain and the role 
+  of C3aR signaling therein, we subjected wildtype mice, C3aR deficient mice, and mice expressing 
+  biologically active C3a in the CNS to mild hypoxic-ischemic brain injury on postnatal day 9. 
+  We found that such injury triggers neurodegeneration and pronounced reactive gliosis in the ipsilesional 
+  hippocampus both of which persist long into adulthood. Transgenic expression of C3a in reactive astrocytes
+  reduced hippocampal neurodegeneration and reactive gliosis. In contrast, neurodegeneration and microglial 
+  cell density increased in mice lacking C3aR. Intranasal administration of C3a for 3 days starting 
+  1 h after induction of hypoxia-ischemia reduced neurodegeneration and reactive gliosis in the hippocampus
+  of wildtype mice. We conclude that neonatal hypoxic-ischemic brain injury leads to long-lasting 
+  neurodegeneration. This neurodegeneration is substantially reduced by treatment with C3aR agonists, 
+  conceivably through modulation of reactive gliosis.
+  
+# Lit of keywords the resource should be associated with.
+# Give as many keywords as possible, to make the resource findable.
+keywords:
+  - Neonatal encephalopathy
+  - Developing brain
+  - Nypoxia-ischemia
+  - Neurodegeneration
+  - Reactive gliosis
+
+# License information for this resource. Please provide the license name and/or a link to the license.
+# Please add also a corresponding LICENSE file to the repository.
+license:
+  name: "Creative Commons CC0 1.0 Public Domain Dedication"
+  url: "https://creativecommons.org/publicdomain/zero/1.0/"
+
+
+
+## Optional Fields
+
+# Funding information for this resource.
+# Separate funder name and grant number by comma.
+#funding:
+# 
+
+
+# Related publications. reftype might be: IsSupplementTo, IsDescribedBy, IsReferencedBy.
+# Please provide digital identifier (e.g., DOI) if possible.
+# Add a prefix to the ID, separated by a colon, to indicate the source.
+# Supported sources are: DOI, arXiv, PMID
+# In the citation field, please provide the full reference, including title, authors, journal etc.
+# references:
+# -
+#   id: "doi:10.xxx/zzzz"
+#   reftype: "IsSupplementTo"
+#   citation: "Citation1"
+
+
+
+# Resource type. Default is Dataset, other possible values are Software, DataPaper, Image, Text.
+resourcetype: Dataset
+
+# Do not edit or remove the following line
+templateversion: 1.2