Objective To investigate the effects of low-to-moderate intensity treadmill exercise on pain and anxiety-like behaviors in rats with chronic constriction injury of the sciatic nerve(CCI),and to explore the neural mechanism of the exercise-related brain-derived neurotrophic factor(BDNF)/tropomyosin receptor kinase B(TrkB)-cAMP-response element binding protein(CREB)pathway in relieving pain and anxiety behaviors in CCI rats.Methods Thirty-two D rats were divided randomly into four groups:sham group,CCI group,sham+exercise(Sham+Exe)group,and CCI+exercise(CCI+Exe)group.Rats in the exercise groups underwent treadmill training for 4 weeks.The paw withdrawal threshold(PWT)and paw withdrawal latency(PWL)were measured before and at different time points after the operation.The elevated plus maze(EPM)and open field test(OFT)were used to evaluate anxiety-like behaviors in the rats.mRNA and protein expression levels of BDNF,TrkB,and CREB in the hippocampus were detected by real-time quantitative reverse transcription PCR and Western Blot,respectively.Results(1)The PWT and PWL on the operative side of the rats were significantly lower in the CCI compared with the sham group at 7,14,21,28,and 35 days after the operation(P＜0.001).The PWT on the ipsilateral side was significantly increased in the CCI+Exe group after 21 days compared with the CCI group(P＜0.05),and the PWL on the ipsilateral side increased significantly after 14 days(P＜0.05).(2)The EPM result showed that rats in the CCI group spent a significantly lower proportion of time in the open arms(P＜0.001)and significantly more time in the closed arms compared with the sham group(P＜0.01).Rats in the CCI+Exe group spent significantly more time in the open arms than the CCI group(P＜0.05).(3)The OFT result showed that rats in the CCI group spent a significantly lower proportion of time in the central area of the open field compared with the sham group(P＜0.001),while the percentage of time was significantly increased in the CCI+Exe group compared with the CCI group(P＜0.05).(4)BDNF,TrkB,and CREB mRNA and protein levels in the hippocampus were significantly lower in the CCI group compared with the sham group(P＜0.05,P＜0.01).Four-week treadmill exercise increased the mRNA and protein expression levels of BDNF,TrkB,and CREB in the hippocampus of CCI rats(P＜0.05).Conclusions Four weeks of treadmill exercise alleviates mechanical and thermal hyperalgesia and anxiety induced by chronic pain in CCI rats.Up-regulation of the BDNF/TrkB-CREB pathway may be one of the mechanisms by which exercise relieves chronic pain and improves anxiety.

There are few clinical reports on the diagnosis and treatment of upper urinary tract stones secondary to urinary diversion. This study included 30 patients with upper urinary tract stones secondary to urinary diversion, and all of which were successfully managed. The individualized treatment with the ureteroscopy and/or percutaneous nephrolithotripsy with antegrade, retrograde, or a combination of antegrade and retrograde is safe and feasible.

Objective:To investigate the expression of microRNA (miR) -26a in human skin fibroblasts during photoaging induced by ultraviolet A (UVA) , and to evaluate the effect of up-or down-regulation of miR-26a expression on the methylation level of the whole genome, the target gene enhancer of zeste homolog 2 (EZH2) and cell aging.Methods:Some human skin fibroblasts were irradiated with 10 J/cm 2 UVA once a day for 7 consecutive days, RNA was extracted on days 0, 3 and 7, and real-time quantitative reverse PCR (RT-PCR) was performed to determine the expression of miR-26a; miR-26a mimics and inhibitors were transfected into fibroblasts to up-or down-regulate the expression of miR-26a respectively, and fluorescence microscopy and RT-PCR were performed to determine the expression of miR-26a and evaluate the transfection efficiency. Some human skin fibroblasts were divided into 6 groups: blank control group receiving no treatment, UVA group treated with UVA irradiation according to the above method, miR-26a mimic group transfected with miR-26a-mimics, UVA+miR-26a mimic group transfected with miR-26a-mimics followed by UVA irradiation, miR-26a inhibitor group transfected with miR-26a inhibitors, UVA+miR-26a inhibitor group transfected with miR-26a inhibitors followed by UVA irradiation. On day 7, cells in each group were collected after the end of UVA irradiation. Then, flow cytometry was performed to detect cell cycle, DNA methylation quantitative detection kit was used to detect the methylation level of whole genome, RT-PCR was conducted to determine the mRNA expression of EZH2 (a histone-lysine N-methyltransferase enzyme) , DNA methyltransferase 1 (DNMT1) and miR-26a, and Western blot analysis was performed to determine the protein expression of EZH2 and DNMT1. Statistical analysis was carried out by using one-way analysis of variance and least significant difference- t test. Results:Compared with the unirradiated control group, the expression of miR-26a gradually increased in the UVA irradiation group over time during the culture, and there was a significant difference in the expression of miR-26a between the two groups after 7 days of UVA irradiation ( t=5.295, P < 0.05) . Strong fluorescence signals were observed in the miR-26a mimic-or miR-26a inhibitor-transfected fibroblasts, suggesting a high transfection efficiency. Flow cytometry showed that the proportion of cells at G1 phase significantly differed among the blank control group, UVA group, miR-26a mimic group, UVA+miR-26a mimic group, miR-26a inhibitor group, and UVA+miR-26a inhibitor group (52.82% ± 2.56%, 78.56% ± 4.34%, 53.63% ± 3.13%, 89.52% ± 4.17%, 54.39% ± 3.86%, 65.34% ± 4.78%, respectively; F=46.728, P < 0.01) , and significantly higher in the UVA group than in the blank control group ( t=8.848, P < 0.01) , higher in the UVA+miR-26a mimic group than in the miR-26a mimic group and UVA group ( t=11.922, 3.154, P < 0.01, < 0.05, respectively) , and higher in the UVA+miR-26a inhibitor group than in the miR-26a-inhibitor group ( t=3.087, P < 0.05) , but significantly lower in the UVA+miR-26a inhibitor group than in the UVA group ( t=3.547, P < 0.05) . Detection of the genome-wide methylation level showed that the methylation level ( A450 value) significantly differed among the above groups (0.676 ± 0.024, 0.323 ± 0.043, 0.506 ± 0.035, 0.169 ± 0.024, 0.602 ± 0.036, 0.422 ± 0.029, respectively, F=97.402, P < 0.01) , and significantly lower in the UVA group than in the blank control group ( P < 0.01) , lower in the UVA+miR-26a mimic group than in the miR-26a mimic group and UVA group (both P < 0.01) , and lower in the UVA+miR-26a inhibitor group than in the miR-26a inhibitor group ( P < 0.01) , but significantly higher in the UVA+miR-26a inhibitor group than in the UVA group ( P < 0.05) . RT-PCR and Western blot analysis showed significant differences in the mRNA and protein expression of EZH2 and DNMT1 respectively among the 6 groups (both P < 0.05) , which were significantly lower in the UVA group than in the blank control group ( P < 0.05) , lower in the UVA+miR-26a mimic group than in the miR-26a mimic group and UVA group (both P < 0.05) , and lower in the UVA+miR-26a inhibitor group than in the miR-26a inhibitor group ( P < 0.05) , but significantly higher in the UVA+miR-26a inhibitor group than in the UVA group ( P < 0.05) . Conclusion:In the UVA irradiation-induced photoaging of skin fibroblasts, miR-26a expression was up-regulated, cellular proliferative activity and genome-wide methylation level decreased; up-regulation of miR-26a expression could down-regulate the expression of its target gene EZH2 and methylation-related gene DNM1, and promote cell photoaging, while down-regulation of miR-26a expression could up-regulate the expression of EZH2 and DNMT1, and inhibit cell photoaging.

Objective To observe capillary vessel changes in rabbits with hormone-induced avascular necrosis of femoral head and the possible mechanism involved in the treatment of the disorder with hyperbaric oxygen (HBO).Methods Forty-eight adult Japanese white rabbits were randomly divided into 2 groups:the experimental model group (n =36) and the control group (n =12).The animals in the experimental model group were injected with prednisolone acetate (10 mg/kg),twice a week and the animals in the control group were injected with physiological saline (2 ml) also twice a week for 6 weeks.Then,rabbits in experimental group were randomized into the HBO group (n =18) and the control group (n =18).The HBO group received HBO treatment for 6 weeks,while the control group was treated with normobaric air.Hemorrheology paramcters,vascular endothelial growth factor (VEGF),changes in tissue pathology,as well as changes in radiographic imaging were detected at week 2,4,6,8,10 and 12 following experiment.Results Features of hemorrheology for the model group deteriorated at weeks 2,4 and 6.Endangium in the femoral head capillary vessel of the experimental group was disrupted,and there were thrombosis and osteoporosis in the femoral head.Optical microscopy revealed that the number of empty bone lacunae and fat cells increased,and some bone trabeculae were disrupted.Electron microscopy indicated that cell volume of the femoral head decreased and nuclei shrank,more osteocytes after necrosis occurred were dissolved into fragments.For the HBO treatment group,features of hemorrheology improved,and positive expressions of VEGF in large amounts could be detected in osteogenic cells and blood vessels on thc surface of bone trabeculae in the femoral head,with the positive site being mainly located in endangium.Under optical microscope,repair of necrotic osteocytes could be found,and nascent osteocytes could be detected by transmission microscopy.Conclusions Large dosage of hormones could induce damage to endangium of capillary vessels,which might be an important reason for the necrosis of the femoral head in rabbits.HBO could promote the secretion of such cytokines as VEGF,accelerate revascularization and ossification,which might be an important theoretical evidence for the treatment of hormone-induced avascular necrosis of the femoral head by HBO.

Objective To observe capillary vessel changes in rabbits with hormone-induced avascular necrosis of femoral head and the possible mechanism involved in the treatment of the disorder with hyperbaric oxygen (HBO).Methods Forty-eight adult Japanese white rabbits were randomly divided into 2 groups:the experimental model group (n =36) and the control group (n =12).The animals in the experimental model group were injected with prednisolone acetate (10 mg/kg),twice a week and the animals in the control group were injected with physiological saline (2 ml) also twice a week for 6 weeks.Then,rabbits in experimental group were randomized into the HBO group (n =18) and the control group (n =18).The HBO group received HBO treatment for 6 weeks,while the control group was treated with normobaric air.Hemorrheology paramcters,vascular endothelial growth factor (VEGF),changes in tissue pathology,as well as changes in radiographic imaging were detected at week 2,4,6,8,10 and 12 following experiment.Results Features of hemorrheology for the model group deteriorated at weeks 2,4 and 6.Endangium in the femoral head capillary vessel of the experimental group was disrupted,and there were thrombosis and osteoporosis in the femoral head.Optical microscopy revealed that the number of empty bone lacunae and fat cells increased,and some bone trabeculae were disrupted.Electron microscopy indicated that cell volume of the femoral head decreased and nuclei shrank,more osteocytes after necrosis occurred were dissolved into fragments.For the HBO treatment group,features of hemorrheology improved,and positive expressions of VEGF in large amounts could be detected in osteogenic cells and blood vessels on thc surface of bone trabeculae in the femoral head,with the positive site being mainly located in endangium.Under optical microscope,repair of necrotic osteocytes could be found,and nascent osteocytes could be detected by transmission microscopy.Conclusions Large dosage of hormones could induce damage to endangium of capillary vessels,which might be an important reason for the necrosis of the femoral head in rabbits.HBO could promote the secretion of such cytokines as VEGF,accelerate revascularization and ossification,which might be an important theoretical evidence for the treatment of hormone-induced avascular necrosis of the femoral head by HBO.

Objective To observe microvascular changes in hormone-induced bone necrosis and also to study the mechanism of hyperbaric oxygen (HBO) in the treatment of femoral head bone necrosis.Methods Forty-eight adult Japanese white rabbits were randomly divided into 2 groups:the experiment group (n =36) and the control group (n =12).The animals in the model group (or the experimental group) were injected with 10mg/kg of prednisone acetate,twice a week for a duration of 6 weeks,while the animals in the control group were injected with 2 ml of normal saline,also twice a week for a duration of 6 weeks.Then,the rabbits in the experimental group were randomly divided into the HBO group (n =17) and the control group (n =17).The HBO group received HBO treatment,for 6 successive weeks,while the control group breathed normal fresh air.At the end of 2,4,6,8,10 and 12 weeks after experiment,blood rheology,vascular endothelial growth factor (VEGF),pathological changes in the tissue involved and radiological imaging changes were observed closely.Results At the end of the 2nd week,4th week and 6th week after experiment,features of hemorheology in the model group deteriorated.The animals of the model group developed endangium,thrombosis,osteoporosis of the femoral head,increased numbers of empty bone lacunae and fat cells,rupture of certain bone trabecula,volume reduction of bone cells of the femoral head and quite a few bone cells were seen to be dead and dissolved into fragments under the electron microscope.In the HBO treatment group,hemorheologic features tended to be better,positive expressions of VEGF could be seen in the osteoblasts on the bone trabecula surface and blood vessels as well,and positive expressions were mainly detected in endangium.Repair of necrostic bone cells to some extent could be seen under the light microscope,and neogenetic bone cells could also be seen under the transmission electron microscope.Conclusions Large dosage of hormone could induce damage to endangium,which might be the main cause of avascular necrosis of the femoral head.HBO could accelerate the processes of vascular regeneration and bone ossification through the expressions of VEGF and other cytokines and promote bone repair,which might provide an important theoretical evidence for the treatment of hormone-induced bone necrosis of femoral head.

Objective To observe microvascular changes in hormone-induced bone necrosis and also to study the mechanism of hyperbaric oxygen (HBO) in the treatment of femoral head bone necrosis.Methods Forty-eight adult Japanese white rabbits were randomly divided into 2 groups:the experiment group (n =36) and the control group (n =12).The animals in the model group (or the experimental group) were injected with 10mg/kg of prednisone acetate,twice a week for a duration of 6 weeks,while the animals in the control group were injected with 2 ml of normal saline,also twice a week for a duration of 6 weeks.Then,the rabbits in the experimental group were randomly divided into the HBO group (n =17) and the control group (n =17).The HBO group received HBO treatment,for 6 successive weeks,while the control group breathed normal fresh air.At the end of 2,4,6,8,10 and 12 weeks after experiment,blood rheology,vascular endothelial growth factor (VEGF),pathological changes in the tissue involved and radiological imaging changes were observed closely.Results At the end of the 2nd week,4th week and 6th week after experiment,features of hemorheology in the model group deteriorated.The animals of the model group developed endangium,thrombosis,osteoporosis of the femoral head,increased numbers of empty bone lacunae and fat cells,rupture of certain bone trabecula,volume reduction of bone cells of the femoral head and quite a few bone cells were seen to be dead and dissolved into fragments under the electron microscope.In the HBO treatment group,hemorheologic features tended to be better,positive expressions of VEGF could be seen in the osteoblasts on the bone trabecula surface and blood vessels as well,and positive expressions were mainly detected in endangium.Repair of necrostic bone cells to some extent could be seen under the light microscope,and neogenetic bone cells could also be seen under the transmission electron microscope.Conclusions Large dosage of hormone could induce damage to endangium,which might be the main cause of avascular necrosis of the femoral head.HBO could accelerate the processes of vascular regeneration and bone ossification through the expressions of VEGF and other cytokines and promote bone repair,which might provide an important theoretical evidence for the treatment of hormone-induced bone necrosis of femoral head.