Publications by authors named "Y M Jiang"

Aim: We aim to assess association of DNA methylation (DNAm) at birth with total immunoglobulin E (IgE) trajectories from birth to late adolescence and whether such association is ethnicity-specific.

Methods: We examined the association of total IgE trajectories from birth to late adolescence with DNAm at birth in two independent birth cohorts, the Isle of wight birth cohort (IOWBC) in UK ( = 796; White) and the maternal and infant cohort study (MICS) in Taiwan ( = 60; Asian). Biological pathways and methylation quantitative trait loci (methQTL) for associated Cytosine-phosphate-Guanine sites were studied.

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Purpose: This work aims to raise a novel design for navigator-free multiband (MB) multishot uniform-density spiral (UDS) acquisition and reconstruction, and to demonstrate its utility for high-efficiency, high-resolution diffusion imaging.

Theory And Methods: Our design focuses on the acquisition and reconstruction of navigator-free MB multishot UDS diffusion imaging. For acquisition, radiofrequency-pulse encoding was used to achieve controlled aliasing in parallel imaging in MB imaging.

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Cholesterol plays a pivotal role in modulating the activity of mechanistic target of rapamycin complex 1 (mTOR1), thereby regulating cell growth and metabolic homeostasis. LYCHOS, a lysosome-localized G-protein-coupled receptor-like protein, emerges as a cholesterol sensor and is capable of transducing the cholesterol signal to affect the mTORC1 function. However, the precise mechanism by which LYCHOS recognizes cholesterol remains unknown.

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Hierarchy has been identified as a principle underlying the organization of human brain networks. However, it remains unclear how the network hierarchy is disrupted in Parkinson's disease (PD) motor symptoms and, how it is modulated by the underlying genetic architecture. The aim of this study was to explore alterations in the motor functional hierarchical organization of the cerebrum and their underlying genetic mechanism.

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Background: Skeletal fluorosis is a chronic metabolic bone disease caused by excessive accumulation of fluoride in the bones. Previous studies have found that when the intake of tea fluoride is similar, the prevalence of skeletal fluorosis varies greatly among different ethnic groups, which may be related to different genetic backgrounds. Single nucleotide polymorphisms (SNPs) of estrogen receptor 1 (ESR1) and collagen type 1 α1 (COL1A1) were strongly associated with bone metabolism as well as bone growth and development, but their association with the risk of skeletal fluorosis has not been reported.

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