Publications by authors named "Lianying Jiang"

Facial nerve schwannomas (FNS) represents one of the more difficult treatment paradigms in neurotology. The aim of this study is to investigate the molecular alterations of FNS, thus providing potential targets treatable in the tumour. We for the first time suggest that the deficiency of merlin (the product of tumour suppressor) is probably one of the key mechanisms underlying FNS tumourigenesis, although no disease-causing mutations were demonstrated in tumour samples.

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Article Synopsis
  • The study investigates the role of two ADAM10 gene polymorphisms (rs514049 and rs653765) in genetic susceptibility to Alzheimer's disease (AD) using a sample of 362 AD patients and 370 healthy controls from China.
  • No significant overall differences in gene variants were found between AD patients and controls, but an age-at-onset analysis indicated that the rs653765 CC genotype was linked to lower ADAM10 levels and faster cognitive decline in late-onset AD patients.
  • The meta-analysis revealed that the rs653765 and rs514049 polymorphisms were associated with AD risk, suggesting that the CC genotype may reduce ADAM10 expression and influence sRAGE levels, possibly affecting the progression of AD.
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Single-nucleotide polymorphisms (SNPs) located in the promoter region of the receptor for advanced glycation end products () gene have been linked to the activity of RAGE. However, contrary to our expectation, we previously detected no correlation between SNPs within the RAGE promoter and ulcerative colitis (UC) risk in a case-control study. Here, we investigated the methylation of the promoter and analyzed the collective contribution of methylation and SNPs to UC risk.

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Alzheimer's disease (AD) is an insidious and progressive neurodegenerative disease. The main pathological features of AD are the formation of amyloid-β deposits in the anterior cerebral cortex and hippocampus as well as the formation of intracellular neurofibrillary tangles. Thus far, accumulating evidence shows that glycation is closely related to AD.

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Plasticity changes of uninjured nerves can result in a novel neural circuit after spinal cord injury, which can restore sensory and motor functions to different degrees. Although processes of neural plasticity have been studied, the mechanism and treatment to effectively improve neural plasticity changes remain controversial. The present study reviewed studies regarding plasticity of the central nervous system and methods for promoting plasticity to improve repair of injured central nerves.

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