The cortexes were obtained from new-born rats and dissociated to single cells by triturating. The cells were cultured in neural stem cell (NSC) culture medium (DMEM supplemented with bFGF, EGF and B27) and formed primary neurospheres after 7 days. Single cells dissociated from neurosphere were cultured in 96-well plates and formed single-cell cloning neurosphere 7 days later. The primary and single-cell cloning neurospheres were both positive for the immunofluorescent staining of nestin and were identified as NSC. It was proved that NSC can be expanded in vitro and provide seed cells for neural tissue engineering.
Animals, Newborn ; Cell Separation ; Cells, Cultured ; Cerebral Cortex/*cytology ; Culture Media ; Neurons/*cytology ; Rats, Sprague-Dawley ; Stem Cells/*cytology ; Tissue Engineering

Objective To systematically evaluate the influence of acupuncture-moxibustion on the peroneal nerve conduction velocity in type 2 diabetic peripheral neuropathy (DPN), and to provide clinical references for acupuncture-moxibustion treatment for DPN.Method By searching the CBM, CNKI, VIP, Wanfang, Pubmed, Springer and Medline databases, randomized controlled trials (RCT) of acupuncture-moxibustion for the type 2 DPN published from January 2000 to January 2014 were retrieved and the relevant data of the peroneal nerve conduction velocity were collected for methodological evaluation. RevMan 5.1 software was adopted to conduct the meta-analysis.Result Totally 10 RCTs were recruited with 685 cases involved, including 355 cases in the treatment group and 330 cases in the control group. The meta-analysis results indicated that acupuncture-moxibustion can produce a better effect in improving the motor nerve conduction velocity (MNCV) and sensory nerve conduction velocity (SNCV) of peroneal nerve in type 2 DPN than the treatments used in the control group, and the differences were statistically significant between the two groups [MD=3.55, 95%CI (0.79, 6.31); MD=4.10, 95%CI (0.22, 7.99)].Conclusion Acupuncture-moxibustion can improve the peroneal nerve conduction velocity in type 2 DPN, and thus is worth application in clinic. Due to the limitation of the included studies, such as small sample size and low quality of the articles and high probability of bias, RCTs of large sample size and high quality are required to confirm the above conclusions.

Objective To study the expression of hypoxia inducible factor-1alpha (HIF-1α) mRNA in re-nal tissue after renal ischemia-reperfusion injury (IRI), and to investigate the effect of hyperbaric oxygen (HBO) on renal IRI and its mechanism. Methods Forty-two Wistar rats were randomly divided into a normal control group(n =6), a renal IRI group (n=18) and an HBO treatment group (n=18). Renal IRI models were established in all the rats. The plasma levels of Cr in the experimental groups were then measured after 1, 3 and 5 hours. The expres-sion of HIF-1α mRNA was also detected using real-time PCR and immunohistochemistry. Kidney tissue sections were preserved for ultrastructure examination. Results (1) The average levels of plasma Cr in the renal IRI group were significantly higher than those in the control group. Compared with the renal IRI group, plasma Cr was significantly lower in the HBO treatment group. (2) The average expression of HIF-1α mRNA was significantly lower an hour after reperfusion, but significantly higher after 3 hours than in the control group. There was no significant difference by the 5th hour after reperfusion. In the HBO treatment group, HIF-1α mRNA was up-regulated significantly at the 1st and 3rd hour after reperfusion compared with the renal IRI group, but it was reduced significantly by the 5th hour after reperfusion. (3) The severity of the kidney injury increased gradually with time in the renal IRI group. After HBO treatment, however, the damage to the renal tissues decreased significantly. Conclusions HIF-1α mRNA plays an important role in the development of renal IRI. The damage to renal tissues and renal function improves significantly after reperfusion and HBO treatment through earlier priming and up-regulating of HIF-1α mRNA expression. HBO should be applied early to help prevent renal IRI.

Objective: To assess the mid-term effecitveness of femoroacetabular impingement (FAI) treated by surgical hip dislocation. Methods: Between April 2014 and August 2015, 15 patients (16 hips) with FAI were enrolled in the study and treated with surgical hip dislocation. There were 12 males and 3 females with an average age of 36.6 years (range, 22-59 years). Among them, 14 cases involved in unilateral hip and 1 in bilateral hips. The mean disease duration was 28 months (range, 4-120 months). Preoperative visual analogue scale (VAS) score and Harris hip score were 7.9±1.0 and 44.1±9.3, respectively. Results: All incisions healed by first intention. There was no main complication, such as vessel and nerve injuries and infection. All 15 patients were followed up 30-46 months (mean, 39.5 months). The VAS score was 2.5±1.6 at 3 months and 0.5±0.7 at last follow-up. The Harris score was 85.5±4.4 at 3 months and 95.6±3.9 at last follow-up. There were significant differences in two scores between pre- and post-operation and between 3 months and last follow-up ( P<0.05). The satisfaction rate of hip function was 93.8% (15/16) at last follow-up. X-ray examination showed that there was no sign of impingment at the femoral head and neck and acetabulum forming site of the affected hip joint, and no complication such as loosening of internal fixator, nonunion of osteotomy, avascular necrosis of femoral head, and heterotopic ossification occurred during follow-up. Conclusion: The surgical hip dislocation is a safe and effective way to treat FAI in the mid-term follow-up, which can repair torn labrum and trim acetabulum and femoral neck.

Objective: To assess the mid-term effectiveness of arthroscopic surgery in treatment of femoroacetabular impingement (FAI).

The cortexes were obtained from new-born rats and dissociated to single cells by triturating. The cells were cultured in neural stem cell (NSC) culture medium (DMEM supplemented with bFGF, EGF and B27) and formed primary neurospheres after 7 days. Single cells dissociated from neurosphere were cultured in 96-well plates and formed single-cell cloning neurosphere 7 days later. The primary and single-cell cloning neurospheres were both positive for the immunofluorescent staining of nestin and were identified as NSC. It was proved that NSC can be expanded in vitro and provide seed cells for neural tissue engineering.
Animals ; Animals, Newborn ; Cell Separation ; Cells, Cultured ; Cerebral Cortex ; cytology ; Culture Media ; Neurons ; cytology ; Rats ; Rats, Sprague-Dawley ; Stem Cells ; cytology ; Tissue Engineering

Gap junctions mediate direct communication between cells; however, toxicological cascade triggered by nonessential metals can abrogate cellular signaling mediated by gap junctions. Although cadmium (Cd) is known to induce apoptosis in organs and tissues, the mechanisms that underlie gap junction activity in Cd-induced apoptosis in BRL 3A rat liver cells has yet to be established. In this study, we showed that Cd treatment decreased the cell index (a measure of cellular electrical impedance) in BRL 3A cells. Mechanistically, we found that Cd exposure decreased expression of connexin 43 (Cx43), increased expression of p-Cx43 and elevated intracellular free Ca2+ concentration, corresponding to a decrease in gap junctional intercellular communication. Gap junction blockage pretreatment with 18β-glycyrrhizic acid (GA) promoted Cd-induced apoptosis, involving changes in expression of Bax, Bcl-2, caspase-3 and the mitochondrial transmembrane electrical potential (Δψm). Additionally, GA was found to enhance ERK and p38 activation during Cd-induced activation of mitogen-activated protein kinases, but had no significant effect on JNK activation. Our results indicated the apoptosis-related proteins and the ERK and p38 signaling pathways may participate in gap junction blockage promoting Cd-induced apoptosis in BRL 3A cells.
Animals ; Apoptosis/*drug effects ; Cadmium/*toxicity ; Calcium/metabolism ; Cell Communication/drug effects ; Connexin 43/genetics ; Enzyme Activation/drug effects ; Gap Junctions/*drug effects ; Gene Expression Regulation/drug effects ; Hepatocytes/cytology/*drug effects ; Rats ; Signal Transduction/drug effects