Evidence map›Paper›PMID 28293529›Full record

ArticlePlastic and reconstructive surgery. Global open2016

Facial Nerve Recovery in KbDb and C1q Knockout Mice: A Role for Histocompatibility Complex 1.

Seden Akdagli, Ryan A Williams, Hyun J Kim, Yuling Yan, Mirna Mustapha, Sam P Most

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Plastic and reconstructive surgery. Global open, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed, 1 pooled it
–field-weighted citation impact, top 87% 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

1 citing paper in PubMed, 1 synthesis or guideline pooled it, 1 citations in OpenAlex.

  1. Pooled it
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.

Seden AkdagliDivision of Facial Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, Calif.; Department of Bioengineering, Santa Clara University, Santa Clara, Calif.; and Department of Otolaryngology-Head and Neck Surgery, Stanford University School of Medicine, Stanford, Calif.
Ryan A WilliamsDivision of Facial Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, Calif.; Department of Bioengineering, Santa Clara University, Santa Clara, Calif.; and Department of Otolaryngology-Head and Neck Surgery, Stanford University School of Medicine, Stanford, Calif.
Hyun J KimDivision of Facial Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, Calif.; Department of Bioengineering, Santa Clara University, Santa Clara, Calif.; and Department of Otolaryngology-Head and Neck Surgery, Stanford University School of Medicine, Stanford, Calif.
Yuling YanDivision of Facial Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, Calif.; Department of Bioengineering, Santa Clara University, Santa Clara, Calif.; and Department of Otolaryngology-Head and Neck Surgery, Stanford University School of Medicine, Stanford, Calif.
Mirna MustaphaDivision of Facial Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, Calif.; Department of Bioengineering, Santa Clara University, Santa Clara, Calif.; and Department of Otolaryngology-Head and Neck Surgery, Stanford University School of Medicine, Stanford, Calif.
Sam P MostDivision of Facial Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, Calif.; Department of Bioengineering, Santa Clara University, Santa Clara, Calif.; and Department of Otolaryngology-Head and Neck Surgery, Stanford University School of Medicine, Stanford, Calif.
Stanford University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundUnderstanding the mechanisms in nerve damage can lead to better outcomes for neuronal rehabilitation. The purpose of our study was to assess the effect of major histocompatibility complex I deficiency and inhibition of the classical complement pathway (C1q) on functional recovery and cell survival in the facial motor nucleus (FMN) after crush injury in adult and juvenile mice.

methodsA prospective blinded analysis of functional recovery and cell survival in the FMN after a unilateral facial nerve crush injury in juvenile and adult mice was undertaken between wild-type, C1q knockout (C1q-/-), and KbDb knockout (KbDb-/-) groups. Whisker function was quantified to assess functional recovery. Neuron counts were performed to determine neuron survival in the FMN after recovery.

resultsAfter facial nerve injury, all adult wild-type mice fully recovered. Juvenile mice recovered incompletely corresponding to a greater neuron loss in the FMN of juveniles compared with adults. The C1q-/- juvenile and adult groups did not differ from wild type. The KbDb-/- adults demonstrated 50% recovery of whisker movement and decreased cell survival in FMN. The KbDb-/- juvenile group did not demonstrate any difference from control group.

conclusionHistocompatibility complex I plays a role for neuroprotection and enhanced facial nerve recovery in adult mice. Inhibition of the classical complement pathway alone does not affect functional recovery or neuronal survival. The alternative and mannose binding pathways pose alternative means for activating the final components of the pathway that may lead to acute nerve damage.

Identifiers

PMID28293529
PMCPMC5222674
OpenAlexW2562747645

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.