Article in Proteoglycan research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
6 authors.
Larry S ShermanDivision of Neuroscience, Oregon National Primate Research Center, Oregon Health & Science University, Beaverton, Oregon, USA.ORCID 0000-0001-6098-6551
Barbara A SorgProgram in Neuroscience, Washington State University, Vancouver, Washington, USA.
Steven MatsumotoDivision of Neuroscience, Oregon National Primate Research Center, Oregon Health & Science University, Beaverton, Oregon, USA.
Weiping SuDivision of Neuroscience, Oregon National Primate Research Center, Oregon Health & Science University, Beaverton, Oregon, USA.
Fatima BanineDivision of Neuroscience, Oregon National Primate Research Center, Oregon Health & Science University, Beaverton, Oregon, USA.
Stephen A BackDepartment of Neurology, Oregon Health & Science University, Portland, Oregon, USA.
Funding
Upgrade of confocal microscopy at the Oregon National Primate Research CenterP51OD011092 · OD · OREGON HEALTH & SCIENCE UNIVERSITY · PI Bonnie J. Nagel · 2012 to 2026
$203.9M
Translational measures of risk for excessive alcohol consumptionP60AA010760 · NIAAA · OREGON HEALTH & SCIENCE UNIVERSITY · PI Christopher D Kroenke · 2006 to 2026
$34.5M
THERMAL AND METABOLIC DYSFUNCTION DURING WITHDRAWALP50AA010760 · NIAAA · OREGON HEALTH AND SCIENCE UNIVERSITY · PI CRABBE, JOHN C. · 1996 to 2005
$10.7M
Role of Extracellular Matrix in Hypoxic-Ischemic Perinatal White Matter InjuryR01NS054044 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI BACK, STEPHEN ARTHUR · 2006 to 2021
$4.8M
Oligodendrocyte Progenitors and Mechanisms of Human Vascular White Matter InjuryR01NS105984 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI BACK, STEPHEN ARTHUR · 2019 to 2023
$3.7M
Oligodendrocyte Progenitors and Hyaluronan-mediated Mechanisms of Human Vascular White Matter InjuryRF1AG065406 · NIA · OREGON HEALTH & SCIENCE UNIVERSITY · PI BACK, STEPHEN ARTHUR · 2020 to 2020
$2.9M
Cocaine, Parvalbumin, and Perineuronal NetsR01DA055645 · NIDA · LEGACY EMANUEL HOSPITAL AND HEALTH CENTER · PI SUE A AICHER, Travis Eugene Brown · 2023 to 2026
$2.9M
Regulation of diurnal rhythms in parvalbumin and perineuronal net functionR01NS131645 · NINDS · LEGACY EMANUEL HOSPITAL AND HEALTH CENTER · PI SOREN IMPEY, Barbara A Sorg · 2024 to 2026
$1.9M
Oligodendrocyte Progenitors and Hyaluronan-mediated Mechanisms of Human Vascular White Matter InjuryR01AG065406 · NIA · OREGON HEALTH & SCIENCE UNIVERSITY · PI BACK, STEPHEN ARTHUR · 2024 to 2024
Hyaluronan (HA) is a glycosaminoglycan synthesized at the cell membrane that can exist in numerous states in the extracellular matrix, including in ternary complexes with proteoglycans such as aggrecan and neurocan. HA synthesis is elevated following a wide variety of insults to the central nervous system (CNS) including neuroinflammatory disease, ischemia, and various forms of dementia. Recent studies have demonstrated that, in conjunction with increased HA synthesis, the expression and activities of hyaluronidases that digest HA are also elevated in the injured CNS. While high molecular weight forms of HA have their own functions that can be disrupted by hyaluronidases, digestion products of HA generated by these hyaluronidases have their own, distinct biological activities that can impact recovery from CNS damage. Here, we review some of the conditions and diseases in which hyaluronidase activity can play a role in preventing CNS repair and discuss the potential ways that hyaluronidase inhibitors could be used as therapeutic agents.
Indexed as
alcohol use disorderbrain injuryCEMIPhyaluronidasemultiple sclerosisstroke
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.
Hyaluronidases as Targets for the Treatment of Neurological Diseases. · full record | Socratic