Exact(1)
While our data provide genetic evidence for the shared ancestry of the Fijian R. samoensis and American Rhizophoras, there remains unanswered questions about how this species crossed more than 8,000km of the southern Pacific Ocean, especially where many islands in between have apparently suitable habitat, and yet unoccupied.
Similar(59)
Here, we review the current evidence for this shared genetic architecture and, based on these data, outline models for shared pathways, the underlying hypotheses for them, how these models can be tested and validated.
The clustering of autoimmune disorders within families and/or individuals also provided supportive evidence for these shared genetic factors [ 29].
These findings are important because they provide additional evidence for the sharing of antigenically similar components across phylogenetically distant fungal species.
Evidence for the sharing of these elements was first provided by cross-reactivity studies (1 4).
Finally, while our sampling of breeds was small, we found little evidence for the sharing of sweeps among phylogenetically closely related breeds.
Bipolar and genetically related spectrum disorders such as unipolar affective disorders have a heritability of 89% with environmental effects limited to the specific or unique environment with no evidence for effects from the shared family environment [McGuffin et al., 2003].
The evidence for both shared and specific genetic influences on the resting EEG is compelling.
61 Initial evidence for a shared role for the IFG in musical processing, particularly processing harmonic syntax, came from event-related potential (ERP) and magnetoencephalography (MEG) studies.
Subsequent immunofluorescence analysis of cortical neurons further supported these findings, thus providing the first evidence for a shared molecular mechanism behind neuronal degeneration in the different forms of NCL.
The strongest evidence for a shared genetic etiology between FTLD and ALS came from multiple linkage and genome-wide association (GWA) studies that established a shared disease locus on chromosome 9p (120–131).
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