Evidence map›Paper›PMID 30019623›Full record

ArticleJournal of neurotrauma2019

Traumatic Injury Leads to Inflammation and Altered Tryptophan Metabolism in the Juvenile Rabbit Brain.

Zhi Zhang, Lindsey Rasmussen, Manda Saraswati, Raymond C Koehler, Courtney Robertson, Sujatha Kannan

Open access · greenAbstract read
In one paragraph

Article in Journal of neurotrauma, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.0field-weighted citation impact, top 13% of its field
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.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 47 citations in OpenAlex.

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4 · The record

Corrections and comments

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 at 1 institution in 1 country.

Zhi ZhangDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University School f Medicine, Baltimore, Maryland.
Lindsey RasmussenDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University School f Medicine, Baltimore, Maryland.
Manda SaraswatiDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University School f Medicine, Baltimore, Maryland.
Raymond C KoehlerDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University School f Medicine, Baltimore, Maryland.
Courtney RobertsonDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University School f Medicine, Baltimore, Maryland.
Sujatha KannanDepartment of Anesthesiology and Critical Care Medicine, Johns Hopkins University School f Medicine, Baltimore, Maryland.
Johns Hopkins University · US

Funding

Targeting glutamate carboxypeptidase in perinatal brain injuryR01NS093416 · NINDS · JOHNS HOPKINS UNIVERSITY · PI Sujatha Kannan, Kannan Rangaramanujam · 2016 to 2026
$4.8M
Role of 20-HETE in Pediatric Traumatic Brain InjuryR01NS092747 · NINDS · JOHNS HOPKINS UNIVERSITY · PI ROBERTSON, COURTNEY L · 2016 to 2020
$1.8M
NINDS NIH HHS R01 NS092747NINDS NIH HHS R01 NS093416
6 · The paper itself

Abstract

Neuroinflammation after traumatic brain injury (TBI) contributes to widespread cell death and tissue loss. Here, we evaluated sequential inflammatory response in the brain, as well as inflammation-induced changes in brain tryptophan metabolism over time, in a rabbit pediatric TBI model. On post-natal days 5-7 (P5-P7), New Zealand white rabbit littermates were randomized into three groups: naïve (no injury), sham (craniotomy alone), and TBI (controlled cortical impact). Animals were sacrificed at 6 h and 1, 3, 7, and 21 days post-injury for evaluating levels of pro- and anti-inflammatory cytokines, as well as the major components in the tryptophan-kynurenine pathway. We found that 1) pro- and anti-inflammatory cytokine levels in the brain injury area were differentially regulated in a time-dependent manner post-injury; 2) indoleamine 2,3 dioxygeenase 1 (IDO1) was upregulated around the injury area in TBI kits that persisted at 21 days post-injury; 3) mean length of serotonin-staining fibers was significantly reduced in the injured brain region in TBI kits for at least 21 days post-injury; and 4) kynurenine level significantly increased at 7 days post-injury. A significant decrease in serotonin/tryptophan ratio and melatonin/tryptophan ratio at 21 days post-injury was noted, suggesting that tryptophan metabolism is altered after TBI. A better understanding of the temporal evolution of immune responses and tryptophan metabolism during injury and repair after TBI is crucial for the development of novel therapeutic strategies targeting these pathways.

Indexed as

IDOinflammationmicrogliaserotoninTBI

Identifiers

PMID30019623
PMCPMC12430859
OpenAlexW2883351178

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 OpenQuestion graph.