10.3969/j.issn.2095-4344.2013.24.019

Objective To establish a paraspinal neural pathway of quadriceps femoris by end-to-end anastomoses between the spinal ventral root after spinal cord injury(SCI) in rats. Methods Twenty-fourweek old SD rats, with the weight of 120 g to 150 g, were included. The left side was the experimental side, while the right side served as a control. Electrostimulating of L1-L5 ventral root was done respectively to decide the predominant nerve of quadriceps femoris. The lumbar 1 ventral root was reveal to little innervation of quadriceps femoris, and the lumbar 3 ventral root was predominant innervation. End-to-end anastomosis between the left L1 and L3 ventral root was done. After axona regeneration, the new paraspinal neural pathway of quadriceps femoris was established. At 6 months postoperatively, the early function of the new pathway was observed by electrophysiological examinations, hindlimb locomotion and BBB (basso, beattie and bresnahan)scale at 1,3,7, 14,21,28 d after SCI. Results Sixteen rats survived for 6 months after operation and only ten rats got good results because of tissue adhesion postoperatively. Single stimuli (2.5 mA,0.2 ms, 1 Hz) of the left anastomoses nerve resulted in action potential recorded from the left quadriceps femoris before and after the spinal cord hemisection horizontally between L2 segmental levels. The amplitudes of the action potentials were (7.63 ± 1.86) mV and (6.00 ± 1.92)mV, respectively, and there was no significant difference (P ＞ 0.05). The left quadriceps femoris contraction was initiated by single stimuli (2.5mA, 0.2 ms, 1 Hz) of the left anastomoses nerve. After paraplegia, when the right L3 ventral root was stimulated, the amplitude of the action potential was (15.87 ± 1.16) mV. Locomotion of the left hindlimb was partially restored after spinal cord hemisection while creeping and climbing. According to BBB scale, there was significant difference at 1, 3, 7 d, and little difference at 14, 21, 28 d after SCI. Conclusion Spinal ventral roots cross-ananstomosis to reconstruct the paraspinal pathway of quadriceps femoris after SCI is efficient reinnervation of hindlamb muscles in a rat model and may have potential in clinical application.

Forty-four patients suffering from hip pain after the hip and femoral head replacement were treated by revision for total hip arthroplasty in Spinal and Joint Surgery of Gaozhou People’s Hospital between August 2000 and August 2006. Forty-one patients were followed up. The surgeon, an associate chief physician, had been engaging in artificial joint field for 9 years, and performed artificial joint replacement for 620 patients. ①There were 26 patients with pain after artificial femoral head replacement, including 17 males and 9 females with an average age of 72.3 years (range, 67-79 years). Of the 26 patients, 12 had loosening of prosthesis stem, 8 acetabular wear, 3 dislocation of artificial femoral head, 2 ossification around the joints, and 1 periprosthetic fracture. ②Fifteen patients suffered with pain after total hip replacement, including 9 males and 6 females with an average age of 73.4 years (range, 66-80). Of them, there were 6 with loosening of prosthesis, 2 with loosening of acetabular prosthesis, 2 with wear of acetabular prosthesis, 2 with dislocation of artificial femoral head, 1 with infection of incision, 1 with delayed infection, and 1 with periprosthetic fracture. ③During follow up, 4 cases developed bone cement response symptoms such as acute hypotension, hypoxemia, and arrhythmia, but no rejection induced by artificial joint was found. X-ray films showed that no metal corrosion or acetabular polyethylene prosthesis degradation occurred. ④White blood count was generally elevated the day after revision of total hip arthroplasty, and mostly recovered 7 days after revision. Three patients had venous thrombosis of lower extremities. All 41 patients were followed up for 1-7 years, and odynolysis rate was 90.2%. The results indicate that the complications such as loosening of prosthesis, acetabular wear, dislocation of artificial femoral head, and ossification around the joints are main causes of hip pain after hip prosthesis replacement. Revision of total hip arthroplasty is an efficient method to relieve the pain.

Objective To explore the establishment of an new artificial bladder reflex arc for controlled micturition function in the conical spinal cord injury(SCI). Methods One conical SCI patients were included by lateral microanastomosis of the L6 ventral root to S2 ventral root. After several months of axonal regeneration, the function of bladder were examined clinically and urodynamically. Results Stimulation of the new artificial reflex are could inuduce controlled voiding, and could cause detrusor contraction when following 55 months of one patient. Conclusions Establishing of an new artificial reflex arc may effective for controlled micturition in conical SCI.

Objective To explore inhibition of nicotine on apoptosis of chondrocytes induced by monosodium iodoacetate ( MIA) .Methods Rat primary chondrocytes were isolated by enzyme digestion, and the cells were treated with 10 -8 , 10 -7 , 10 -6 , 10 -5 mol/L nicotine for 48 h.The cases were randomly divided into five groups, except for normal group, the other four groups were treated with 4μmol/L MIA 24 h, and three groups were treated 10 -8 , 10 -7 , 10 -6 mol/L nicotine.The viability of chondrocytes was detected by MTT assay.The apoptosis of chondrocytes was examed by Annexin V-FITC/PI flow dual-staining method.The activity of cysteinyl aspartate specific proteinase 3 ( Caspase 3 ) was measured by spectrophotography method.The activation of phosphatidylinositol 3 kinase ( PI3K)/protein kinase B ( AKT) and the expression of down-stream molecule Bax, Bcl-2 was assayed by western blot.Results 10 -7 , 10 -6 mol/L nicotine increased chondrocytes' viability (P<0.05), 10 -5mol/L nicotine reduced chondrocytes' viability (P<0.05), and 10 -8 mol/L nicotine didn't effect on chondrocytes' viability (P>0.05).10 -8, 10 -7, 10 -6 mol/L nicotine could increase MIA-induced chondrocytes' viability (P<0.05), suppress MIA-induced chondrocytes' apoptosis and the activity of MIA-induced Caspase 3 (P <0.05).Moreover, 10 -7, 10 -6 mol/L nicotine could increase the expression of PI3K and phosphorylation of AKT ( P<0.05) , down-regulate the expression of Bax and up-regulate the expression of Bcl-2 in MIA-induced rat chondrocytes ( P<0.05 ) .Conclusion These results suggested nicotine could exert anti-apoptosis in MIA-induced rat chondrocytes, which might be related to PI3K/AKT signal pathway.

Objective: Hypertrophy ligamentum flavum (LFH) is a common cause of lumbar spinal stenosis, resulting in significant disability and morbidity. Although long noncoding RNAs (lncRNAs) have been associated with various biological processes and disorders, their involvement in LFH remains not fully understood. Methods: Human ligamentum flavum samples were analyzed using lncRNA sequencing followed by validation through quantitative real-time polymerase chain reaction. To explore the potential biological functions of differentially expressed lncRNA-associated genes, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed. We also studied the impact of lncRNA PARD3-AS1 on the progression of LFH in vitro. Results: In the LFH tissues when compared to that in the nonhypertrophic ligamentum flavum (LFN) tissues, a total of 1,091 lncRNAs exhibited differential expression, with 645 upregulated and 446 downregulated. Based on GO analysis, the differentially expressed transcripts primarily participated in metabolic processes, organelles, nuclear lumen, cytoplasm, protein binding, nucleic acid binding, and transcription factor activity. Moreover, KEGG pathway analysis indicated that the differentially expressed lncRNAs were associated with the hippo signaling pathway, nucleotide excision repair, and nuclear factor-kappa B signaling pathway. The expression of PARD3-AS1, RP11-430G17.3, RP1-193H18.3, and H19 was confirmed to be consistent with the sequencing analysis. Inhibition of PARD3-AS1 resulted in the suppression of fibrosis in LFH cells, whereas the overexpression of PARD3-AS1 promoted fibrosis in LFH cells in vitro. Conclusion This study identified distinct expression patterns of lncRNAs that are linked to LFH, providing insights into its underlying mechanisms and potential prognostic and therapeutic interventions. Notably, PARD3-AS1 appears to play a significant role in the pathophysiology of LFH.

Objective: Hypertrophy ligamentum flavum (LFH) is a common cause of lumbar spinal stenosis, resulting in significant disability and morbidity. Although long noncoding RNAs (lncRNAs) have been associated with various biological processes and disorders, their involvement in LFH remains not fully understood. Methods: Human ligamentum flavum samples were analyzed using lncRNA sequencing followed by validation through quantitative real-time polymerase chain reaction. To explore the potential biological functions of differentially expressed lncRNA-associated genes, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were performed. We also studied the impact of lncRNA PARD3-AS1 on the progression of LFH in vitro. Results: In the LFH tissues when compared to that in the nonhypertrophic ligamentum flavum (LFN) tissues, a total of 1,091 lncRNAs exhibited differential expression, with 645 upregulated and 446 downregulated. Based on GO analysis, the differentially expressed transcripts primarily participated in metabolic processes, organelles, nuclear lumen, cytoplasm, protein binding, nucleic acid binding, and transcription factor activity. Moreover, KEGG pathway analysis indicated that the differentially expressed lncRNAs were associated with the hippo signaling pathway, nucleotide excision repair, and nuclear factor-kappa B signaling pathway. The expression of PARD3-AS1, RP11-430G17.3, RP1-193H18.3, and H19 was confirmed to be consistent with the sequencing analysis. Inhibition of PARD3-AS1 resulted in the suppression of fibrosis in LFH cells, whereas the overexpression of PARD3-AS1 promoted fibrosis in LFH cells in vitro. Conclusion This study identified distinct expression patterns of lncRNAs that are linked to LFH, providing insights into its underlying mechanisms and potential prognostic and therapeutic interventions. Notably, PARD3-AS1 appears to play a significant role in the pathophysiology of LFH.