The present study aimed to investigate differentially expressed genes (DEGs) in whole blood (WB) obtained from patients with lumbar disc prolapse (LDP) and healthy volunteers. A total of 8 patients with LDP and 8 healthy volunteers were recruited. An Agilent SurePrint G3 human gene expression microarray 8×60 K was used to perform the microarray analyses. R was employed to identify DEGs, which were then subjected to bioinformatics analysis, including a Gene Ontology (GO) analysis, Kyoto Encyclopaedia of Genes and Genomes (KEGG) pathway analysis and protein-protein interaction (PPI) network analysis. DEGs in the degenerative annulus fibrosis (AF) and nucleus pulposus (NP) compared with non-degenerative tissues were also identified based on microarray data and the intersections of the three were assessed. Furthermore, reverse transcription-quantitative (RT-q)PCR was performed to confirm the aberrant expression levels of selected DEGs in the WB of all subjects. A total of 161 DEGs between LDP patients and the healthy controls were identified (128 upregulated and 33 downregulated). These DEGs were enriched in 293 biological process, 36 cellular component and 21 molecular function GO terms, as well as in 24 KEGG pathways. The PPI network contained 4 submodules, and Toll-like receptor 4 had the highest degree centrality. A total of 22 DEGs were common to the three groups of DEGs. The RT-qPCR assay confirmed that the expression levels of cytochrome P450 family 27 subfamily A member 1, superoxide dismutase 2, protein disulfide isomerase family A member 4, FKBP prolyl isomerase 11 and ectonucleotide pyrophosphatase/phosphodiesterase 4 were significantly different between the patient group and the volunteer group. In conclusion, several genes were identified as potential biomarkers in WB that should be further explored in future studies to determine their potential application in the clinical treatment and diagnosis of LDP, and the present bioinformatics analysis revealed several GO terms, KEGG pathways and submodules of the PPI network that may be involved in LDP, although the exact mechanisms remain elusive.

Background Although the pathology of sciatica has been studied extensively, the transcriptional changes in the peripheral blood caused by sciatica have not been characterized. This study aimed to characterize the peripheral blood transcriptomic signature for sciatica. Methods We used a microarray to identify differentially expressed genes in the peripheral blood of patients with sciatica compared with that of healthy controls, performed a functional analysis to reveal the peripheral blood transcriptomic signature for sciatica, and conducted a network analysis to identify key genes that contribute to the observed transcriptional changes. The expression levels of these key genes were assessed by qRT-PCR. Results We found that 153 genes were differentially expressed in the peripheral blood of patients with sciatica compared with that of healthy controls, and 131 and 22 of these were upregulated and downregulated, respectively. A functional analysis revealed that these differentially expressed genes (DEGs) were strongly enriched for the inflammatory response or immunity. The network analysis revealed that a group of genes, most of which are related to the inflammatory response, played a key role in the dysregulation of these DEGs. These key genes are Toll-like receptor 4, matrix metallopeptidase 9, myeloperoxidase, cathelicidin antimicrobial peptide, resistin and Toll-like receptor 5, and a qRT-PCR analysis validated the higher transcript levels of these key genes in the peripheral blood of patients with sciatica than in that of healthy controls. Conclusion We revealed inflammatory characteristics that serve as a peripheral blood transcriptomic signature for sciatica and identified genes that are essential for mRNA dysregulation in the peripheral blood of patients with sciatica.

Objective. This systematic review aimed to assess the effectiveness and safety of acupuncture for lateral epicondylitis (LE). Methods. Seven databases and the WHO International Clinical Trials Registry Platform Search Portal were searched to identify relevant studies. The data were extracted and assessed by two independent authors, and Review Manager Software (V.5.3) was used for data synthesis with effect estimate presented as standard mean difference (SMD) and mean difference (MD) with a 95% confidence interval. The Grading of Recommendations Assessment, Development, and Evaluation (GRADE) was used to assess the level of evidence. Results. Four RCTs with 309 participants were included with poor methodological quality. Participants who received acupuncture and acupuncture plus moxibustion with material insulation were likely to have an improvement in elbow functional status and/or myodynamia. The overall quality rated by GRADE was from very low to low. Two studies reported that the needle pain would be the main reason for the dropout. Conclusion. For the small number of included studies with poor methodological quality, no firm conclusion can be drawn regarding the effect of acupuncture of elbow functional status and myodynamia for LE. This trial is registered with CRD42015016199.

Background Although the regression of symptomatic lumbar disc herniation (SLDH) has been widely reported, little data exist regarding the generalized incidence of regression (IR). We aimed to review the varying IRs and to synthesize the pooled IR of non-surgically-treated SLDH. Methods Four electronic databases were searched for relevant studies pertaining to the regression of SLDH after non-surgical treatment and for potential studies that may have reported morphological changes in lumbar disc herniation in the follow-up results of SLDH patients treated non-surgically. The main outcome was the regression of SLDH. A random effects model was used to determine the pooled IR of SLDH. Results We identified 13,672 articles, 38 of which were eligible for analysis. Our analysis included 2219 non-surgically treated SLDH patients, 1425 of whom presented regression. The pooled IR was 63% (95% CI 0.49–0.77). In subgroup analyses, studies that quantitatively measured the regression of SLDH yielded statistically higher pooled IRs than those that used qualitative methods. The pooled IRs gradually increased in randomized controlled trials and prospective and retrospective studies. The pooled IR varied from 62 to 66% after the sequential omission of any single study. Meta-regression showed that study types, herniation levels and regression measurements caused heterogeneity. Conclusions We report an overall IR of 63% among non-surgically treated SLDH patients, thus providing clinical decision makers with quantitative evidence of IR. Based on our systematic review, we suggest a follow-up timeline with time points 4 and 10.5 months after onset when deciding whether to perform surgery for SLDH.

Degeneration of the intervertebral disc (IVD), which consists of the annulus fibrosus (AF) and nucleus pulposus (NP), is a multifactorial physiological process associated with lower back pain. Despite decades of research, the knowledge of the underlying molecular mechanisms of IVD degeneration (IDD) has remained limited. The present study aimed to reveal the differential gene expression patterns in AF and NP during the process of IDD and to identify key biomarkers contributing to these differences. The microarray dataset GSE70362 containing 24 AF and 24 NP samples was retrieved from the Gene Expression Omnibus database. Of these, 8 healthy samples were discarded. GeneSpring11.5 software was employed to identify differentially expressed genes (DEGs). Metascape online tools were used to perform enrichment analyses. Finally, the DEGs were mapped with the Search Tool for the Retrieval of Interacting Genes, and a protein-protein interaction (PPI) network was constructed in Cytoscape software. A total of 87 DEGs were identified. Gene ontology enrichment revealed that these DEGs were mainly involved in the inflammatory response, the extracellular matrix and RNA polymerase II transcription factor activity. Pathway enrichment revealed that the DEGs were mainly involved in the transforming growth factor (TGF-β) and estrogen signaling pathways. Matrix metalloproteinase (MMP)1 and interleukin (IL)6 were included in the genes enriched in rheumatoid arthritis, whereas bone morphogenetic protein (BMP)2 and thrombospondin 1 (THBS1) were among the genes enriched in the TGF-β signaling pathway. In the PPI network, IL6 was identified as the central gene. In conclusion, as MMP1 has been demonstrated degrade collagen III at higher rates compared with other types of collagen (which is at a higher quantity in AF than NP), collagen types may be in different distribution patterns, which may contribute to the upregulation of MMP1 in AF. Differences in the expression of BMP2, ESR1 and THBS1 may explain for the pathological differences between AF and NP. IL6 may have a key role in different degeneration processes in AF and NP.