ReviewRevista medica del Instituto Mexicano del Seguro Social2026
[Embryonic origin of temperament: notochord and early signaling].
Review in Revista medica del Instituto Mexicano del Seguro Social, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is proposed that the origin of temperament is rooted in events of the third week of gestation, when gastrulation and the notochord organize body axes and morphogenetic gradients, integrated through intracellular pathways with downstream effects on circuit architecture and locomotion. The aim of this article is to propose a theoretical mechanistic model that articulates how gastrulation, the notochord, and prenatal epigenetic programming could contribute—probabilistically rather than deterministically—to the origin of human temperament. A three-phase mechanistic flow is proposed: Phase 1, in which gastrulation and the notochord establish axes and gradients that could modulate the organization of ventral circuits and central pattern generators; Phase 2, in which prenatal epigenetic programming calibrates stress, immune, and affective axes; and Phase 3, in which these levels integrate into profiles of activity, exploration, reactivity, and inhibition, consistent with the distributed polygenic architecture described by personality genomics. The notochord emerges as a plausible morphogenetic axis of temperament. Upon this embryonic scaffold, prenatal epigenetic programming may calibrate allostasis, stress reactivity, and affectivity, contributing to long-term temperamental variation. The model formulates falsifiable hypotheses and suggests translational priorities in perinatal prevention, multimodal biomarkers, and personalized neurodevelopmental medicine, whose short-term clinical feasibility remains uncertain.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.