Evidence map›Paper›PMID 25985271›Full record

ArticleThe Journal of clinical investigation2015

Fertility and fragrance: another cause of Kallmann syndrome.

Shlomo Melmed

Open access · bronzeAbstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2015. 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
0.8field-weighted citation impact, top 20% 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, 8 citations in OpenAlex.

  1. Article
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author.

Shlomo Melmed

Funding

Treatment of pituitary Cushing disease with a selective CDK inhibitor, R-roscovitR21DK103198 · NIDDK · CEDARS-SINAI MEDICAL CENTER · PI MELMED, SHLOMO · 2014 to 2015
$445k
NIDDK NIH HHS DK 103198NIDDK NIH HHS R21 DK103198
6 · The paper itself

Abstract

Kallmann syndrome is an inherited deficiency of gonadotropin-releasing hormone (GnRH) that is characterized by hypogonadism with delayed or absent puberty and dysfunctional olfaction. While Kallmann syndrome-associated mutations have been identified in some sets of patients, for many of these individuals, the underlying cause remains unknown. In this issue of the JCI, Cariboni and colleagues identify mutations in semaphorin 3E (SEMA3E) in two brothers with Kallmann syndrome. In animal models, loss of SEMA3E signaling recapitulated phenotypes of the probands and resulted in enhanced GnRH neuron death during development. The results of this study offer important insight into the development of Kallmann syndrome and provide tools for elucidating mutations that underlie complex hormonal phenotypes.

Indexed as

MutationAnimalsGlycoproteinsGonadotropin-Releasing HormoneHumansKallmann SyndromeMaleMembrane ProteinsNeuronsSemaphorinsGlycoproteinsGonadotropin-Releasing HormoneMembrane ProteinsSemaphorins

Identifiers

PMID25985271
PMCPMC4497770
OpenAlexW1524754491

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.