Evidence map›Paper›PMID 24949445›Full record

ArticleBioMed research international2014

The analysis of genetic aberrations in children with inherited neurometabolic and neurodevelopmental disorders.

Krystyna Szymańska, Krzysztof Szczałuba, Agnieszka Lugowska, Ewa Obersztyn, Marek Radkowski, Beata A Nowakowska, Katarzyna Kuśmierska, Jolanta Tryfon, Urszula Demkow

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.9field-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

5 citing papers in PubMed, 11 citations in OpenAlex.

  1. CMaf-Inducing Protein Promotes LUAD Proliferation and Metastasis by Activating the MAPK/ERK Pathway.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  2. Article
  3. CMIP is oncogenic in human gastric cancer cells.Molecular medicine reports · 2017
    Article
  4. Review
  5. 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

9 authors at 2 institutions in 1 country.

Krystyna SzymańskaDepartment of Clinical and Experimental Neuropathology, Mossakowski Medical Research Centre, Polish Academy of Sciences, 02-106 Warsaw, Poland ; Department of Child Psychiatry, Medical University of Warsaw, 00-576 Warsaw, Poland.
Krzysztof SzczałubaGenCentrum (Regional Center for Clinical Genetics and Modern Technologies), 25-375 Kielce, Poland.ORCID 0000-0001-8803-646X
Agnieszka LugowskaDepartment of Genetics, Institute of Psychiatry and Neurology, 02-957 Warsaw, Poland.
Ewa ObersztynDepartment of Medical Genetics, Institute of Mother and Child, 01-211 Warsaw, Poland.
Marek RadkowskiDepartment of Immunopathology of Infectious Diseases, Medical University of Warsaw, 02-091 Warsaw, Poland.
Beata A NowakowskaDepartment of Medical Genetics, Institute of Mother and Child, 01-211 Warsaw, Poland.
Katarzyna KuśmierskaClinic of Child and Adolescent Neurology, Institute of Mother and Child, 01-211 Warsaw, Poland.
Jolanta TryfonDepartment of Laboratory Diagnostics and Clinical Immunology, Medical University of Warsaw, 00-576 Warsaw, Poland.
Urszula DemkowClinic of Child and Adolescent Neurology, Institute of Mother and Child, 01-211 Warsaw, Poland.
Institute of Psychiatry and Neurology · PLMedical University of Warsaw · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inherited encephalopathies include a broad spectrum of heterogeneous disorders. To provide a correct diagnosis, an integrated approach including genetic testing is warranted. We report seven patients with difficult to diagnose inborn paediatric encephalopathies. The diagnosis could not be attained only by means of clinical and laboratory investigations and MRI. Additional genetic testing was required. Cytogenetics, PCR based tests, and array-based comparative genome hybridization were performed. In 4 patients with impaired language abilities we found the presence of microduplication in the region 16q23.1 affecting two dose-sensitive genes: WWOX (OMIM 605131) and MAF (OMIM 177075) (1 case), an interstitial deletion of the 17p11.2 region (2 patients further diagnosed as Smith-Magenis syndrome), and deletion encompassing first three exons of Myocyte Enhancer Factor gene 2MEF2C (1 case). The two other cases represented progressing dystonia. Characteristic GAG deletion in DYT1 consistently with the diagnosis of torsion dystonia was confirmed in 1 case. Last enrolled patient presented with clinical picture consistent with Krabbe disease confirmed by finding of two pathogenic variants of GALC gene and the absence of mutations in PSAP. The integrated diagnostic approach including genetic testing in selected examples of complicated hereditary diseases of the brain is largely discussed in this paper.

Indexed as

Genetic TestingAdolescentBrain Diseases, MetabolicChildChild, PreschoolChromosomes, Human, Pair 16Comparative Genomic HybridizationCytodiagnosisFemaleGenes, DuplicateHumansMaleMutationSequence Deletion

Identifiers

PMID24949445
PMCPMC4052700
OpenAlexW2137257054

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Registered trials

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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.