{"entity": "researcher", "timestamp": "2026-08-20T20:37:36.882Z", "family": "Thelin", "given": "Eric P", "initials": "EP", "orcid": "0000-0002-2338-4364", "affiliations": ["Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.", "Department of Neurology, Karolinska University Hospital, Stockholm, Sweden."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/4c369b6006c44f47a2f8801632b05c55.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/4c369b6006c44f47a2f8801632b05c55"}}, "publications": [{"entity": "publication", "iuid": "d8403987609040cebaa5bbccc48f0983", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/d8403987609040cebaa5bbccc48f0983.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/d8403987609040cebaa5bbccc48f0983"}}, "title": "Inflammatory Mediators Related to Vascular Dysfunction are Linked to ICP, PRx, and CPP Following Human Severe Traumatic Brain Injury.", "authors": [{"family": "Smith", "given": "Claudia Ann", "initials": "CA", "orcid": "0000-0003-3643-6191", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/00caa1ee179346f8960c6ff3a1a3f496.json"}}, {"family": "Lindblad", "given": "Caroline", "initials": "C", "orcid": "0000-0003-4952-8597", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/b3fe10d5ae0a4812a87c1d416201d408.json"}}, {"family": "Needham", "given": "Edward", "initials": "E", "orcid": "0000-0001-7042-7462", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/8ee0e6f48b4d40bd8301eec6401979bf.json"}}, {"family": "Beqiri", "given": "Erta", "initials": "E"}, {"family": "Bergstr\u00f6m", "given": "Sofia", "initials": "S"}, {"family": "Smielewski", "given": "Peter", "initials": "P"}, {"family": "Nilsson", "given": "Peter", "initials": "P"}, {"family": "Thelin", "given": "Eric", "initials": "E", "orcid": "0000-0002-2338-4364", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/4c369b6006c44f47a2f8801632b05c55.json"}}, {"family": "Helmy", "given": "Adel", "initials": "A"}], "type": "journal article", "published": "2025-11-00", "journal": {"title": "J. Neurotrauma", "issn": "1557-9042", "volume": "42", "issue": "21-22", "pages": "1974-1984", "issn-l": "0897-7151"}, "abstract": "Disturbed cerebral autoregulation (represented by a positive pressure reactivity index [PRx]), elevated intracranial pressure (ICP), and decreased cerebral perfusion pressure (CPP) are key treatment targets following severe traumatic brain injury (sTBI). This study investigated neuroinflammation as a potential mechanism underlying these intracranial disturbances. Plasma samples from 11 sTBI patients (from a prior Phase II drug trial) were analyzed for 174 proteins using an antibody-based suspension bead array, with intervention effects accounted for where possible. Dimensionality reduction techniques, including principal component analysis (PCA) and supervised methods, were applied to protein data, informed by physiological variables (ICP, CPP, and PRx). PCA revealed distinct protein clustering patterns related to ICP >20 mmHg and PRx > 0, with PC1 linked to patient ID, time from injury, and intervention, and PC2/PC3 significantly associated with PRx dose (p < 0.001). Markers relating to inflammation of the vascular system comprised 20% of the top 50 proteins influencing PC2, implicating complement inflammation in these processes. Notably, MASP-2 (p = 0.027) and complement factor I (p = 0.039) were significantly associated with PRx dose in a mixed-effects model. These findings suggest that vascular inflammation, particularly complement activation, may contribute to intracranial physiological disturbances in sTBI, highlighting the complement pathway as a potential target for further investigation.", "doi": "10.1177/08977151251363979", "pmid": "40763090", "labels": [], "xrefs": [], "notes": [], "created": "2026-08-20T12:17:09.342Z", "modified": "2026-08-20T12:17:09.537Z"}, {"entity": "publication", "iuid": "9a3af6680beb45adbfd6b8c2d57bc505", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/9a3af6680beb45adbfd6b8c2d57bc505.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/9a3af6680beb45adbfd6b8c2d57bc505"}}, "title": "Proteomic profiles in cerebrospinal fluid predicted death and disability in term infants with perinatal asphyxia: A pilot study.", "authors": [{"family": "Leifsdottir", "given": "Kristin", "initials": "K", "orcid": "0000-0003-0491-7302", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/a894ec05a780449fabd8e85f353134fb.json"}}, {"family": "Thelin", "given": "Eric P", "initials": "EP", "orcid": "0000-0002-2338-4364", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/4c369b6006c44f47a2f8801632b05c55.json"}}, {"family": "Lassar\u00e9n", "given": "Philipp", "initials": "P", "orcid": "0000-0003-0833-1093", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/540036b27ee849e2842ce548d79cf112.json"}}, {"family": "Siljehav", "given": "Veronica", "initials": "V"}, {"family": "Nilsson", "given": "Peter", "initials": "P", "orcid": "0000-0002-4657-8532", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/3db33fa3edb94febb8be7927a16838d0.json"}}, {"family": "Eksborg", "given": "Staffan", "initials": "S", "orcid": "0000-0001-7326-9471", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/2f2dbdced2e94babb5e11b0c118b5550.json"}}, {"family": "Herlenius", "given": "Eric", "initials": "E", "orcid": "0000-0002-6859-0620", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/efcfd309d5db4aa384d96ed35d40fbfe.json"}}], "type": "journal article", "published": "2022-05-00", "journal": {"title": "Acta Paediatr", "issn": "1651-2227", "volume": "111", "issue": "5", "pages": "961-970", "issn-l": null}, "abstract": "Perinatal asphyxia, resulting in hypoxic-ischaemic encephalopathy (HIE), has been associated with high mortality rates and severe lifelong neurodevelopmental disabilities. Our aim was to study the association between the proteomic profile in cerebrospinal fluid (CSF) and the degree of HIE and long-term outcomes.\n\nWe prospectively enrolled 18-term born infants with HIE and 10-term born controls between 2000 and 2004 from the Karolinska University Hospital. An antibody suspension bead array and FlexMap3D analysis was used to characterise 178 unique brain-derived and inflammation associated proteins in their CSF.\n\nIncreased CSF concentrations of several brain-specific proteins were observed in the proteome of HIE patients compared with the controls. An upregulation of neuroinflammatory pathways was also noted and this was confirmed by pathway analysis. Principal component analysis revealed a gradient from favourable to unfavourable HIE grades and outcomes. The proteins that provided strong predictors were structural proteins, including myelin basic protein and alpha-II spectrin. The functional proteins included energy-related proteins like neuron-specific enolase and synaptic regulatory proteins. Increased CSF levels of 51 proteins correlated with adverse outcomes in infants with HIE.\n\nBrain-specific proteins and neuroinflammatory mediators in CSF may predict HIE degrees and outcomes after perinatal asphyxia.", "doi": "10.1111/apa.16277", "pmid": "35106835", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC9305740"}], "notes": [], "created": "2026-08-20T11:17:17.875Z", "modified": "2026-08-20T11:17:18.156Z"}]}