ArticleTherapeutic hypothermia and temperature management2013
Effects of Mild Hypothermia Treatment on Rat Hippocampal β-Amyloid Expression Following Traumatic Brain Injury.
Article in Therapeutic hypothermia and temperature management, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Novel therapies for combating chronic neuropathological sequelae of TBI.Neuropharmacology · 2019Review
- iTRAQ-Based Quantitative Proteomics Reveals the New Evidence Base for Traumatic Brain Injury Treated with Targeted Temperature Management.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2018Article
- Neuroprotective effects of bloodletting at Jing points combined with mild induced hypothermia in acute severe traumatic brain injury.Neural regeneration research · 2016Article
- Impairment of Rat Spatial Learning and Memory in a New Model of Cold Water-Induced Chronic Hypothermia: Implication for Alzheimer's Disease.Neurotoxicity research · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have reported that mild induced hypothermia (MIH) treatment has positive effects on traumatic brain injury (TBI) outcomes, which have recently been linked to β-amyloid (Aβ)-induced secondary brain injury (SBI) extent in hippocampal tissues. We therefore investigate the relationship between MIH treatment and expression of Aβ and related proteins following TBI. Adult Sprague-Dawley rats were randomly divided into three equal groups (S: sham-operated, N: normothermia, and H: mild hypothermia). After TBI induced by fluid percussion, group N remained at normal temperature, and group H underwent MIH (32°C) for 6 hours. Behavioral scale scores were then assessed. All rats were sacrificed 24 hours and hippocampal tissues were harvested, stained with hematoxylin and eosin. mRNA and protein expressions of Aβ, β-amyloid protein precursor (APP), and β-secretase (BACE) were analyzed. Our results revealed significantly improved behavioral scale scores and the surviving neuron numbers were observed in group H compared to group N (
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Registered trials
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