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The mechanisms underlying this disorder are unknown.
To date, on the basis of clinical observations and experimental studies, several theories have been proposed for the mechanisms underlying this disorder.
In the present article, we review rehabilitation strategies for spatial neglect in relation to certain damaged psychobiological processes underlying this disorder.
The fundamental pathogenetic mechanisms underlying this disorder include pulmonary vasoconstriction, in situ thrombosis, medial hypertrophy, and intimal proliferation, leading to occlusion of the small to mid-sized pulmonary arterioles and the formation of plexiform lesions.
The objective of this article is to provide a scientific review of the biology underlying this disorder and a critical review of the state-of-the-art investigational preventive strategies in order to stimulate further research in this exciting area.
The cellular and molecular mechanisms underlying this disorder are largely unknown.
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Given the relationship of CRS to other airway disorders with well-characterized genetic components (eg, asthma), study of the genetics of CRS deserves increased attention and investment, including the organization of large, detailed, and collaborative studies to advance knowledge of the mechanisms that underlie this disorder.
A phase delay in the melatonin rhythm is thought to partially underlie this disorder (reviewed in [ 4]).
This report broadens the spectra of phenotype and genetic mutations underlying this rare disorder.
Alterations in brain insulin metabolism have been suggested as one pathophysiological factor underlying this neurodegenerative disorder [ 6– 8].
In general, genes identified from GWAS and genetic typing have confirmed the idea that there might be an autoimmune etiology underlying this sleep disorder.
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