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.
View Article and Find Full Text PDFSingle-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.
View Article and Find Full Text PDFAlzheimer'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.
View Article and Find Full Text PDFPlasticity 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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