Objective To investigate the effects of hyperoxaluria on rat renal tubular epithelium intracellular calcium concentration ([Ca~(2+)]i) and cell apoptosis, and explore the protective effects of calcium antagonist-nifedipine. Methods Sixty male SD rats were randomly divided into six groups (n=10). Rats in water-drinking group were treated with deionized water, nifedipine group with deionized water and nifedipine 10 mg·kg~(-1)·d~(-1), calculi-induced group with deionized water containing 1% ethylene glycol, and three calculi-induced+nifedipine-intervening groups with deionized water containing 1% ethylene glycol plus nifedipine 3, 6 and 10 mg·kg~(-1)·d~(-1), respectively. Four weeks later, the 24 h oxaluria concentration was measured, the apoptosis index of renal tubular epithelial cells was detected with TUNEL method, and Ca~(2+) fluorescence intensity of cells of renal proximal tubules was determined by flow cytometry using Fluo-3/AM staining. Results The 24 h oxaluria concentrations in calculi-induced group and calculi-induced+nifedipine-intervening groups were higher than those in water-drinking group and nifedipine group (P＜0.01). The apoptosis index and Ca~(2+) fluorescence intensity were significantly higher in calculi-induced group than those in water-drinking group (P<0.01). The Ca~(2+) fluorescence intensity in calculi-induced+nifedipine (3, 6 and 10 mg·kg~(-1)·d~(-1))-intervening groups was 76.7%, 62.7% and 56.4% of calculi-induced group, respectively, with a significant dose-effect relationship (r=0.839, P<0.01). The apoptosis index of renal tubular epithelial cells was significantly correlated with Ca~(2+) fluorescence intensity (r=0.826, P<0.01). Conclusion Hyperoxaluria can increase apoptosis and [Ca~(2+)]i concentration of renal tubular epithelial cells in rats, and nifedipine can effectively protect renal tubular epithelial cells to resist hyperoxaluria.

BACKGROUND:Core decompression with bone implantation in treatment of early avascular necrosis of femoral head may provide insufficient support for subchondral bone and increase the risk of fracture and col apse. Tantalum rod implantation can not only provide good biological support, but also promote the revascularization at necrotic regions, thus repairing the necrosis of femoral head.
OBJECTIVE:To evaluate the efficacy of core decompression, core decompression with bone implantation and core decompression with tantalum rod implantation in treating early-stage avascular necrosis of femoral head. METHODS:A total of 24 cases (28 hips) who suffered from ARCO I/II avascular necrosis of femoral head were treated with core decompression with bone implantation, and 25 cases (29 hips) who suffered from ARCO I/II avascular necrosis of femoral head were treated with core decompression with tantalum rod implantation. Al the subjects were fol owed up for 24 months. The efficacy of two different surgical methods was evaluated before and after treatment by observing the changes in Harris scores.
RESULTS AND CONCLUSION:Al involved patients were fol owed up. Harris score of core decompression with bone implantation group were increased 4.93 points at 6 months after surgery;Harris score of core decompression with tantalum rod implantation group were increased 6.89 points at 6 months after surgery. There were significant differences between two groups before and after surgery (P<0.05). After 12 months, Harris scores in the two groups were both significantly increased and the scores of core decompression with tantalum rod implantation group was higher than that of core decompression with bone implantation group (P<0.05). The overal fine/excellent rate of core decompression with tantalum rod implantation group was 83%, which was better than core decompression with bone implantation group (75%). After 24 months, X-ray score of core decompression with tantalum rod implantation group was significantly higher than core decompression with bone implantation group (P<0.05). Comparing with core decompression with bone implantation, core decompression with tantalum rod implantation can better prevent femoral head col apse, improve hip function and delay the process of osteonecrosis of the femoral head.

[Objective]To study the relationship between the existence and types of mediopatellar plica versus the chondral injury of the medial femoral condyle.[Method]Data were collected retrospectively from the photographic recording of arthroscopies performed from January 2004 to July 2008.Seventy-six knees were found with mediopatellar plica as the study group.Modified Sakakibara classification and the chondral injury(using the Outerbridge classification) of medial femoral condyle were recorded.Eighty knees without mediopatellar plica were randomly collected as controls.The correlation of mediopatellar plica and the cartilage injury on the surface of the medial femoral condyle was investigated.[Result]Patients with mediopatellar plica had a significantly higher incidence rate(89.5%) of medial femoral condyle cartilage lesion,in comparison with patients without mediopatellar plica(61.3%)(P=0.001).In the study group,a 64.3% proportion of the group with Sakakibara A mediopatellar plica was found to have cartilage lesion in the medial femoral condyle.The proportion of the group with Sakakibara BCD mediopatellar plica was found to be 95.2%,significantly higher than that in first group(P=0.004).The severity of cartilage injury in the medial femoral condyle was positively correlated with patient age(r=0.271,P=0.019) and the severity of the pathologic change of the mediopatellar plica(r=0.611,P=0.000).[Conclusion]According to this observation,the cartilage injury in the medial femoral condyle is more commonly found in patients with mediopatellar plica knees.A shelf-like appearance of the medial plica can increase the incidence of the cartilage injury.The severity of cartilage injury was positively correlated with patient age and the severity of the pathologic change of the mediopatellar plica.

[Objective] To investigate the effects of pyrroloquinoline quinine (PQQ) on proliferation and expression of NF - kB of Schwann cells. [Methods] Schwann cells were cultured from sciatic nerves of SD rats in vitro. The Schwann cells were identified and purified by immunofluorescence of S-100 and Ara-C. Experimental group with was 100 nmol/L of PQQ and control group were set up. The expression of NF-kB in Schwann cells was determined by RT-PCR and Western blotting. [ Results] The expression of NF - kB were up - ragulated by PQQ in cultured Schwann cells (P<0.05).[Conclusion ] PQQ could promote the proliferation of Schwann cells and up-regulation of NF-rd3 play an important role in this process.

Objective To explore the effect of high-fat diet on IRS-1 and IRS-2 expressions of fatty liver in rat. Methods After the rats were fed a high-fat diet (n=7) and a standard chow(n=7) for 8 weeks, insulin sensitivity,lipid metabolism, TNF-α and hepatic mRNA and protein expressions of IRS-1 and IRS-2 were measured. Results Compared with the normal control, the high-fat diet group displayed the elevated levels of insulin resistance,FFA and TNF-α.Hepatic IRS-1 mRNA expression and IRS-1 protein content were reduced by 28% and 32%(P<0.01),respectively. Similarly, hepatic IRS-2 mRNA and IRS-2 protein content were also reduced by 30% and 27% (P<0.01), respectively. Conclusions High-fat diet results in a significant decrease in expressions of mRNA and protein of hepatic IRS-1 and IRS-2 in rats, which might be one of the molecular mechanisms of insulin resistance in liver steatosis induced by high-fat diet

Objective To explore the effect of high-fat diet on IRS-1 and IRS-2 expressions of fatty liver in rat. Methods After the rats were fed a high-fat diet (n=7) and a standard chow(n=7) for 8 weeks, insulin sensitivity,lipid metabolism, TNF-? and hepatic mRNA and protein expressions of IRS-1 and IRS-2 were measured. Results Compared with the normal control, the high-fat diet group displayed the elevated levels of insulin resistance,FFA and TNF-?.Hepatic IRS-1 mRNA expression and IRS-1 protein content were reduced by 28% and 32%(P

37 ℃, cell growth became poor, and clone formation decreased. At 39 ℃, cells could not adhere. Under incubator CO2 concentration between 3% and 8%, there was no significant difference in cell clone formation. CONCLUSION: The optimized culture condition of Schwann cells were 7.2 pH, 10% fetal bovine serum, 37 ℃ of temperature and 5% of CO2(v/v) of incubator.

BACKGROUND:Local injection with simvastatin can induce osteogenesis, significantly increase the bone mineral density and mechanical strength of femoral neck and femoral condyle of rats with osteoporosis and analyze effects of local injection of simvastatin on trabecular bone of the femoral condyle.
OBJECTIVE:To explore the effects of local injection of simvastatin on trabecular bone of the femoral condyle of osteoporotic rats and provide experimental basis for the application of simvastatin in clinical topical treatment of osteoporosis.
METHODS:Eighteen female Sprague-Dawley rats received bilateral ovariotomy at 3 months, and were used to produce rat models of osteoporosis. They were assigned into three groups. Experimental rats received 5 and 10 mg simvastatin by single injection into right femoral cavity. Control rats received blank vector. The rat models were sacrificed at 1 month after injection and specimens were col ected. Right femoral condyles were taken out for bone histomorphometric analysis by Micro-CT.
RESULTS AND CONCLUSION:One month post-injection, Micro-CT scanning results revealed that cortical bone thickness, trabecular bone density and connection rate were significantly better in the simvastatin group than those in the control group. Results indicated that single injection of smal-dose simvastatin obviously promoted rebuilding of trabecular bone of condyles of femur, improved microstructure of skeleton, strengthened local skeleton, prevented and treated osteoporosis, and provided a further basis for the prevention and treatment of osteoporosis, especial y for osteoporotic fractures.

Objective To investigate the effect of vitamin K3 decreasing the urine oxalate excretion in rats. Methods A total of 80 male Sprague-Dawley rats (body weight, 200-250g) were randomly divided into 8 groups, ie, control group, only vitamin K3 group, stone forming group, stone forming plus 4.0、3.0、2.0、0.8、0.4mg/d Vit K3 group. Each group is 10 rats respectively. The change of urine oxalate was observed. Results Vitamin K3 can reduce the 24h urine oxalate excretion in stone-forming group rats, but there were no effects in control group rats(P

Objective To determine the effect of nifedipine on the formation of nephrolithiasis in rat models and its mechanism of action. Methods A total of 60 male Sprague-Dawley rats (body weight, 200-250g) were randomly divided into 6 groups, ie, control group, only nifedipine group, stone forming group, stone forming plus 3, 6, 10 mg?kg-1?d-1 nifedipine group. Each group is 10 rats respectively. Hyperoxaluria and calcium oxalate crystals were produced in rats by ethylene glycol in drinking water. Four weeks later, all rats were sacrificed and the calcium oxalate crystallization in kidney, the renal free radical level, the renal cell apoptosis indexes and the blood and urine biochemical indexes were detected. Results The renal calcium oxalate crystallization in the rat with different dose nifedipine was less than the stone forming rats 37.0%, 55.6%, 66.7% significantly (P