Evidence map›Paper›PMID 22009353›Full record

ArticleResults and problems in cell differentiation2012

Exploring the zebra finch Taeniopygia guttata as a novel animal model for the speech-language deficit of fragile X syndrome.

Claudia Winograd, Stephanie Ceman

Abstract read
In one paragraph

Article in Results and problems in cell differentiation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
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

2 authors at 1 institution in 1 country.

Claudia WinogradUniversity of Illinois at Urbana-Champaign, Urbana, IL, USA. cwinogr2@illinois.edu
Stephanie Ceman
University of Illinois Urbana-Champaign · US

Funding

Role of phosphorylation on FMRP functionR01HD041591 · NICHD · UNIVERSITY OF ILLINOIS URBANA-CHAMPAIGN · PI CEMAN, STEPHANIE · 2002 to 2005
$958k
NICHD NIH HHS HD41591NICHD NIH HHS R01 HD041591
6 · The paper itself

Abstract

Fragile X syndrome (FXS) is the most common cause of inherited intellectual disability and presents with markedly atypical speech-language, likely due to impaired vocal learning. Although current models have been useful for studies of some aspects of FXS, zebra finch is the only tractable lab model for vocal learning. The neural circuits for vocal learning in the zebra finch have clear relationships to the pathways in the human brain that may be affected in FXS. Further, finch vocal learning may be quantified using software designed specifically for this purpose. Knockdown of the zebra finch FMR1 gene may ultimately enable novel tests of therapies that are modality-specific, using drugs or even social strategies, to ameliorate deficits in vocal development and function. In this chapter, we describe the utility of the zebra finch model and present a hypothesis for the role of FMRP in the developing neural circuitry for vocalization.

Indexed as

Disease Models, AnimalAnimalsFinchesFragile X Messenger Ribonucleoprotein 1Fragile X SyndromeGene Knockdown TechniquesHumansLanguage DisordersLearningPhenotypeSpeech DisordersVocalization, AnimalFragile X Messenger Ribonucleoprotein 1

Identifiers

PMID22009353
PMCPMC4340592
OpenAlexW16049638

What OpenQuestion holds

Textmetadata
LicenceTDM
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.