Publications by authors named "Jiakai Wei"

Currently, artificial meniscus prostheses are mostly homogenous, low strength, and difficult to mimic the distribution of internal fibers in the native meniscus. To promote the overall mechanical performance of meniscus prostheses, this paper designed a new artificial braided meniscus model and conducted finite element analysis. Firstly, we designed the spatial fiber interweaving structure of meniscus model to mimic the internal fiber distribution of the native meniscus.

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Infectious diseases pose a fatal risk to neonates. Timely and accurate pathogen detection is crucial for proper clinical diagnosis and therapeutic strategies. Limited sample volumes from neonatal patients seriously hindered the accurate detection of pathogens.

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Objective: To analyze the clinical features, biochemical characteristics and molecular pathogenesis of a girl with isovaleric acidemia.

Methods: Clinical features, blood spot amino acid profiles and urinary organic acid profiles of the patient were analyzed. Targeted capture, next generation sequencing and Sanger sequencing were carried out to detect potential variant of the IVD gene.

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Objective: Early postnatal life is considered as a critical time window for the determination of long-term metabolic states and organ functions. Extrauterine growth restriction (EUGR) causes the development of adult-onset chronic diseases, including pulmonary hypertension. However, the effects of nutritional disadvantages during the early postnatal period on pulmonary vascular consequences in later life are not fully understood.

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Chronic hypoxia pulmonary hypertension (CH-PHT) in adulthood is likely to be of fetal origin following intrauterine growth retardation (IUGR). Oxygen (O₂)-sensitive voltage-gated potassium channels (Kv channels) in resistance pulmonary artery smooth muscle cells (PASMCs) play an important role in scaling pulmonary artery (PA) pressure. Expression and functional changes of Kv channels are determined, in part, by embryonic development.

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Background: Accumulating evidence reveals that intrauterine growth retardation (IUGR) can cause varying degrees of pulmonary arterial hypertension (PAH) later in life. Moreover, epigenetics plays an important role in the fetal origin of adult disease. The goal of this study was to investigate the role of epigenetics in the development of PAH following IUGR.

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