Publications by authors named "Xian-Ming Wu"

Objectives: To observe the effect of moxibustion on pathological structure and ultrastructural changes of thoracic aorta, the expression of silent information regulator 1 (SIRT1) and endothelial nitric oxide synthase (eNOS) in ApoE atherosclerosis (AS) mice, so as to explore its possible mechanism in preventing and treating AS.

Methods: Ten C57BL/6J mice were fed a normal diet as the control group, and 30 ApoE mice were fed a high-fat diet to establish the AS model, which were randomly divided into the model group, moxibustion group, and moxibustion+EX527 group, with 10 mice in each group. Mice in the moxibustion group received mild moxibustion treatment at "Danzhong"(CV17), "Shenque"(CV8), "Neiguan"(PC6, bilateral), and "Xuehai" (SP10, bilateral) for 30 min, the mice in the moxibustion+EX527 group were given intraperitoneal injection of EX527 (10 mg/kg) 30 min before moxibustion, with both treatments given once daily, 5 times a week, with a total intervention period of 12 weeks.

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Objectives: To observe the effects of moxibustion on blood lipid metabolism, pathological morphology of thoracic aorta, and the expression of silent information regulator 1 (SIRT1) and forkhead box transcription factor O3a (FOXO3a) in ApoE atherosclerosis (AS) mice, so as to explore the potential mechanism of moxibustion in preventing and treating AS.

Methods: Ten C57BL/6J mice were fed a normal diet as the control group, and 30 ApoE mice were fed a high-fat diet to establish the AS model, which were randomly divided into the model group, simvastatin group, and moxibustion group, with 10 mice in each group. From the first day of modeling, mice in the moxibustion group received mild moxibustion treatment at "Shenque"(CV8), "Yinlingquan"(SP9), bilateral "Neiguan"(PC6) and "Xuehai"(SP10) for 30 min per time;the mice in the simvastatin group were given simvastatin orally (2.

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Objective: To observe the effect of mild moxibustion on blood lipid, histopathological structure of the aortic arch, thoracic aortic silent information regulator 1 (SIRT1)/nuclear factor κB (NF-κB) signaling pathway in atherosclerosis (AS) rabbits, so as to explore its underlying mechanisms in improving AS.

Methods: Sixty male rabbits were randomly divided into control group (=12), model group(=11), mild moxibustion group (=11), mild moxibustion + blocker (blocker) group (=12). The AS model was established by feeding the rabbits with high-fat forage for 8 weeks, followed by immune response damage.

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Background: LncRNA AK044604 (regulator of insulin sensitivity and autophagy, Risa) and autophagy-related factors Sirt1 and GSK3β play important roles in diabetic nephropathy (DN). In this study, we sought to explore the effect of Risa on Sirt1/GSK3β-induced podocyte injury.

Methods: Diabetic db/db mice received Risa-inhibition adeno-associated virus (AAV) via tail vein injection, and intraperitoneal injection of lithium chloride (LiCl).

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Atherosclerosis is the main pathological basis of cardiovascular disease and involves damage to vascular endothelial cells (ECs) that results in endothelial dysfunction (ED). The vascular endothelium is the key to maintaining blood vessel health and homeostasis. ED is a complex pathological process involving inflammation, shear stress, vascular tone, adhesion of leukocytes to ECs, and platelet aggregation.

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Aims: Neural stem cells (NSCs) in the adult mammalian spinal cord are activated in response to spinal cord injury (SCI); however, mechanisms modulating this process are not clear. Here, we noticed SCI elevated expression of vascular endothelial growth factor (VEGF) and we aimed to validate the roles of VEGF in NSCs activation after SCI and investigated the related signals during the process.

Methods: In vitro we detected whether VEGF promoted spinal cord NSCs proliferation and investigated the involved signals; In vivo, we injected VEGF into rat spinal cord to check the NSCs activation.

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Where in genes do pathogenic mutations tend to occur and does this provide clues as to the possible underlying mechanisms by which single nucleotide polymorphisms (SNPs) cause disease? As splice-disrupting mutations tend to occur predominantly at exon ends, known also to be hot spots of cis-exonic splice control elements, we examine the relationship between the relative density of such exonic cis-motifs and pathogenic SNPs. In particular, we focus on the intragene distribution of exonic splicing enhancers (ESE) and the covariance between them and disease-associated SNPs. In addition to showing that disease-causing genes tend to be genes with a high intron density, consistent with missplicing, five factors established as trends in ESE usage, are considered: relative position in exons, relative position in genes, flanking intron size, splice sites usage, and phase.

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The nearly neutral theory predicts that small effective population size provides the conditions for weakened selection. This is postulated to explain why our genome is more "bloated" than that of, for example, yeast, ours having large introns and large intergene spacer. If a bloated genome is also an error prone genome might it, however, be the case that selection for error-mitigating properties is stronger in our genome? We examine this notion using splicing as an exemplar, not least because large introns can predispose to noisy splicing.

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We conducted a comprehensive analysis of codon usage bias (CUB) based on the available non-redundant full-length cDNA (nrFLcDNA) and expressed sequence tags (ESTs) data of cultivar Micro-Tom and evaluated the associations of observed CUB and measurements of transcriptional and translational effectiveness. The analysis presented in our study suggests a correlation, which is negative but highly correlated between Axis 1 and GC3s (r=-0.827, P<0.

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Codon bias refers to the nonrandom usage of synonymous codons for encoding amino acids in organisms. As it is related to the carrier molecular of genetic information (DNA) and functional molecular (protein) of life, this phenomenon implicates important biological sense. In this review, we summarize the basic theories and analysis methods about codon bias; and present the softwares and websites which are usually used for codon usage analysis.

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