Objective To explore the differentia expression of long chain noncoding RNA (IncRNA) in peripheral blood mononuclear cells (PBMCs) of the patients with rheumatoid arthritis (RA) and normal human and to analyze to further clarify the pathogenesis of RA.Methods Twenty-two cases of RA in our hospital from January to April 2016 were selected as the observation group and 22 healthy persons served as the control group.The differential expression of IncRNA and mRNA in PBMCs of 5 RA cases and 5 healthy persons were determined by using Agilent human IncRNA chip;GO and Pathway were used to analyze the functional distribution of differentially expressed IncRNA,the co-expression pressionsnetwork was constructed and the Trans-and Cis -were adopted to predict the RA onset related IncRNA.Results There were 1623 differential expressions of IncRNA in PBMCs of RA patients and healthy persons and 851 differential expressions of mRNA.GO and Pathway analysis showed that the main function of differentially expressed mRNA was to participate in the binding and transcriptional regulation of protein kinase,nucleotide and metal ions,and also participate in the regulation of B cell receptor signaling pathway and TNF signaling pathway.After Cis-and Trans-analysis prediction and real-time PCR validation,the 3 IneRNA could be related with RA onset,which were NONHSAT 120696,uc.80+ and NONHSAT 031501.Conclusion IncRNA has differential expression in PBMCs of RA patients and healthy persons,three 031501 IncRNA of NONHSAT 120696,uc.80+,NONHSAT may be related to the pathogenesis of RA.

Objective:To detect expression level of miR-410 in patients with systemic lupus erythematosus (SLE),and to expose the role of miR-410 and its target genes by bioinformatics methods.Methods:Expression level of miR-410 were detected by quantitative RT-PCR in peripheral blood mononuclear cells of SLE patients,and miR-410 sequence,its target genes and Genecards database were analyzed,and analysis of GO enrichment and KEGG Pathway was further performed.Results:miR-410 expression was significantly reduced in SLE patients,and its nucleotide sequence was highly conserved among species.These genes that were predicted to be regulated by miR-410 and associated with LE pathogenesis,included FASLG,CSF2,IFNAR2,MAPK1,PLCG2,IL4 and other genes.Analysis of GO enrichment revealed that miR-410's target genes were involved in cell growth,proliferation,programmed cell death,cell differentiation,immune system development and other biological activities.Analysis of KEGG Pathway showed that the target genes of miR-410 were significantly enriched in a series of signaling pathways including pathways in cancer,cytokine-cytokine receptor interaction,glioma,melanoma,TGF-β and JAK-STAT signaling pathway.Conclusion:miR-410 maybe directly regulate its target molecules,mediate various signal pathway networks,thus participate in the occurrence and development of SLE.

Objective By using 18F-deoxyglucose (18F-FDG) positron emission computed tomography (PET-CT) to measure the brain glucose metabolism of patients with severe traumatic brain injury before and after hyperbaric oxygen (HBO) therapy,and to investigate the mechanisms of H BO treating patients with traumatic brain injury.Methods Twenty-six patients suffered form severe traumatic brain injury with stable vital signs within 2 weeks were randomly divided into the HBO group and the control group.The patients of both groups received routine clinical interventions (including neuroprotection,dehydration,reducing intracranial pressure,anti-infection and other symptomatic treatments).Patients of the HBO group received the basic treatment combined with HBO therapy one tine per day for 7 days per week.In early stage and 4 weeks after treatment,all patients were examined with PET-CT scanning and Glasgow coma scale (GCS),disability rating scale (DRS) at the same time.Results There was standard uptake value (SUV) of significant difference between affected and unaffected brain areas in two groups before treatment(P＜0.01),but no significant difference between two groups (P＞0.05).After 4-week of treatment,SUV of affected and unaffected brain areas of two groups improved,the damaged area of HBO group improved obviously and the SUV was much better than before treatment and the control group (P＜0.0l).The GCS and DRS scores of HBO group were also significantly better than that of control group (P＜0.05).Conclusion The 18F-FDG PET-CT examination showed that HBO therapy can significantly improve glucose metabolism function of the brain damaged area,promote the brain functional recovery and awakening,and improve the prognosis in patients with severe traumatic brain injury.

Objective To observe the effects of hyperbaric oxygen (HBO) on cerebral small vessel disease (CSVD) and on learning,memory and the expression of brain-derived neurotrophic factor (BDNF) and acetylcholine (Ach) in the cerebral cortex and hippocampus.Methods Sixty healthy,male Wistar rats were studied.Allograft thrombosis particles 48 to 74 μm in diameter were injected into the rats' external carotid arteries to create a CSVD model.The rats were then divided randomly into a hyperbaric oxygen group,a nimotop group and a control group.The hyperbaric oxygen group rats were given hyperbaric oxygen therapy 12 hours after the modeling.The nimotop group rats were given nimodipine by intragastric perfusion 12h after the modeling.The rats in the control group had no special intervention.At 7,14 and 28 days after the modeling,any changes in learning and memory were assessed with a Morris water maze test.Enzyme-linked immunosorbent assay (ELISA) was used to detect the expression of BDNF in the cerebral cortex and of Ach in the hippocampus at 28 days.Results At both 14 and 28 days the average escape latency of the rats in the hyperbaric oxygen group was significantly shorter than those of the nimotop and control groups.The average platform crossing time had increased significantly more than in the nimotop and control groups.At both 14 and 28 days the escape latency and platform crossing times of the nimotop group were significantly better than in the control group.Ach content and BDNF content were significantly higher in the HBO group than in the nimotop and control groups.Conclusions Hyperbaric oxygen treatment can promote BDNF release in CSVD,which is helpful to protect and repair neural mitochondria,to maintain the cortex and hippocampal neurotransmitters on a stable level,and to improve learning and memory.Its effect is better than that of nimotop.

OBJECTIVETo study the features of vascular smooth muscle cell (VSMC) proliferation induced by endothelin-1 (ET-1).

METHODSVSMCs of spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats were cultured and treated with ET-1. Basic fibroblast growth factor (bFGF) gene expression was measured using both Northern blot and an enzyme-linked immunoassay.

RESULTSET-1 resulted in an increase in bFGF transcripts at 8 - 24 h; bFGF levels were significantly higher in VSMCs treated with ET-1 than in those not treated. However, VSMCs growth responses in SHR and WKY were different. Smooth muscle cells of SHR were hyper-responsive to ET-1. Maximal bFGF mRNA levels were elevated 3.5-fold at 4 h of stimulation in WKY and 8-fold at 8h in SHR4. Moreover, the proliferation of VSMCs induced by ET-1 was inhibited by antisense phosphorothioate oligodeoxynucleotides (10 micromol/L AS-bFGF) but not sense bFGF oligomers at the same concentrations, being reduced by 80% in SHR and 40% in WKY vs control, respectively. Furthermore, the effect of AS-bFGF oligomers on SHR SMC proliferation is significantly greater than on WKY SMC proliferation.

CONCLUSIONET-1 may be required for exaggerated vascular growth responses in SHR and bFGF may be involved.

Animals ; Cell Division ; drug effects ; Cells, Cultured ; DNA, Antisense ; pharmacology ; Dose-Response Relationship, Drug ; Endothelin-1 ; pharmacology ; Fibroblast Growth Factor 2 ; genetics ; Gene Expression Regulation ; drug effects ; Muscle, Smooth, Vascular ; cytology ; drug effects ; metabolism ; Oligonucleotides ; pharmacology ; RNA, Messenger ; drug effects ; genetics ; metabolism ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Time Factors