BACKGROUND:Carbon-fiber-reinforced polymer energy-storing transtibial prostheses are mature and ideal substitutes for professional disable athletes to increase performance.
OBJECTIVE:By discussing the update application and study of the carbon-fiber-reinforced polymer energy-storing transtibial prosthesis and understanding the characteristics of applying transtibial prostheses in different sports program, to provide a useful reference for the design of athletes prostheses.
METHODS:A computer-based search of PubMed and VIP databases was performed for articles related to carbon-fiber-reinforced polymer energy-storing transtibial prostheses published from January 1985 to December 2012. The keywords were“CFRP, energy-storing prosthesis, between-knee (transtibial) prosthesis, disable athletes”in English and Chinese, respectively.
RESULTS AND CONCLUSION:Currently, we focus on the gait analysis, energy cost and stiffness analysis of athletes who wear carbon-fiber-reinforced polymer energy-storing transtibial prostheses. Studies have demonstrated that carbon-fiber-reinforced polymer energy-storing transtibial prostheses have more advantages over traditional prostheses, but have predominantly disadvantages over able-bodied persons. Thus, there are many difficulties in the clinical application of building carbon-fiber-reinforced polymer energy-storing transtibial prostheses based on the characteristics of athletes’ body status and sports programs.

Objective To evaluate the role of albumin and the involvement of mitogenactivated protein kinases(MAPKs) in rat tubular cells apoptosis. Methods Rat tubular cells (NRK-52E) were incubated with various concentrations (10, 20, 30 mg/ml) of delipidated, endotoxin-free bovine serum albumin(BSA) for 6, 12, 18 and 24 h, respectively. The process of apoptosis was evaluated by fluorescence microscope, transmission electron microscope, scanning electron microscope, confocal laser scanning microscope (CLSM) and flow cytometry. To assess the roles of p38, and the activities of JNK and ERK in albumin-induced apoptosis, SB202190 (20 ?mol/L, p38 inhibitor), SP600125 (10 ?mol/L, JNK inhibitor) or PD98059 (20?mol/L, ERK inhibitor) were added to the NRK-52E cells separately in the presence of albumin for 24 hours. Activities of p38, JNK and ERK were assessed by Western blot analyses. Results The albumin induced tubular cell apoptosis in a doseand time-dependent manner. Albumin stimulated the expression of p38 and JNK, whereas it inhibited the expression of ERK. SB202190 and SP600125 ameliorated tubular cells apoptosis but PD980S9 treatment enhanced their apoptosis. Conclusions Albumin induces tabular cell apoptosis in a time- and dose-dependent manner in vitro, transducted through activation of p38 and JNK, and inhibition of ERK.

Objective To investigate the effect of p38MAPK on the RANTES expression after unilateral ureteral obstruction.Methods Twenty-two rats were randomly assigned to shame operation group (normal group) and operation group after unilateral ureteral obstruction.Renal tissues were examined by light microscopy at 8 h、24 h and 72 h after operation,Immunhistochemistry was applied to measure the expression of RANTES,RT-PCR,Western blot was performed to determine mRNA,protein,respectively.Results Compared with shame opeartion group,the mRNA and protein levels of RANTES in renal interstitum of operation group remarkly increased (P＜0.05),and also stimulated the phosphorylation of p38MAPK.Conclusion The overexpression of RANTES in UUO rats by p38MAPK signal transduction pathway.

Objective To investigate the effect of lectin like oxidized low density lipoprotein receptor 1 ( LOX-1 ) in NRK52E intaking lipid induced by oxidized low density lipoprotein ( ox-LDL). Methods NRK-52E was incubated with ox-LDL (0,25,50, and 100 g/ml ) for 24 hours or pre-treated with the chemical blocker of LOX-1 receptor- polyI or carrageenan, and then exposed to 50 μg/ml of ox-LDL. LOX-Ⅰ mRNA was examined by real-time PGR. LOX-1 protein was assessed by Western blot analysis. Lipid deposit was examined by oil red O. Results LOX-1 mRNA expression in 25,50,100 μg/ml ox-LDL group was 2. 13, 10. 14, 20. 81 times of that in 0 g/ml ox-LDL group ( P <0. 05 ,respectively). LOX-1 protein expression in 25,50,100 μg/ml ox-LDL group was 2. 53,12. 18,21.45 times of that in 0 μg/ml ox-LDL group( P <0. 05 ,respectively). Following the increased LOX-1, lipid intake increased. Pre-treatment with Poly Ⅰ or carrageenan, LOX-1 mRNA expression deceased by 48% or 47%, LOX-1 protein deceased by 72% or 65%, lipid intake induced by 41% or 49% ( P <0.05 ,respectively). Lipid had a close relationship with LOX-1 ( r = 0. 87, P < 0. 05). Conclusion Ox-LDL induced NRK52E to express LOX-1 and promoted NRK52E to intake lipid, and this effect could be partly blocked by LOX-1 blocker.

Eleven elderly patients undergoing maintenance hemodialysis without ARB or ACEI within 4 weeks were enrolled. Anti-hypertensive agents were replaced by telmisartan gradually to maintain stable blood pressure. Before and after 6 or 12 weeks of treatment, blood biochemical profiles, fasting blood glucose, fasting plasma insulin, insulin resistance index(HOMA-IR), blood pressure, and body weight were recorded. Our results showed that telmisartan did not affect body weight, high-density lipoprotein (HDL), triglyceride (TG), SCr, BUN, Alb, K+ , and PTH, although led to a significant decrease in TC and low-density lipoprotein (LDL). Following telmisartan treatment, FPG did not change significantly, but fasting insulin decreased from 13.9±3.6 mU/ml to 9.9±2.7 or 9.1±2.3 mU/ml at 6 and 12 week (P<0.01), and HOMA-IR decreased from 3.5±1.4 to 2.4±0.8 or 2.2±0.8 at 6 and 12 week (P<0.05). These results suggest that insulin resistance in elderly patients with MHD may be improved by telmisartan.

0. 20) after D test of normality. The normal range of GEMP was 63. 11-72. 94 ?mol fructose/L (P= 95%). When clinical cardiovasculopathy, nephropathy, retinopathy,peripheral neuropathy and auditus reduction in the aged were compared between two groups of diabetic patients, one with normal and another with abnormal values of GEMP, the clinical indices, excepting cardiovasculopathy, were significantly different between the groups.

BACKGROUND:Stem cel s have the potential to differentiate into various organs and tissues. In recent years, stem cel s have been proved to differentiate into hair fol icles under certain conditions. OBJECTIVE:To review the research progress and prospect of stem cel s differentiating to hair fol icles, thereby providing a reliable basis for clinical treatment of serious hair fol icle injury. METHODS:A computer-based search of PubMed, EMBASE, WanFang, CNKI databases was performed for related articles published between 2013 and 2015, using the keywords of“cel hair, fol icle stem, medicine regenerative, differentiation”in English and Chinese. A total of 207 articles were retrieved, and final y 34 articles were included in result analysis. RESULTS AND CONCLUSION:Stem cel s from different sources al have the ability to differentiate into hair fol icles under certain inductions. However, it is important to seek more scientific and rational methods for the differentiation of stem cel s into hair fol icles based on overcoming their own shortcomings. A great progress has been made in animal experiments and subclinical trials, and even a great breakthrough in some aspects. Further studies on combining the advantages and overcoming the shortcomings of various stem cel s during differentiation are required for the clinical treatment of serious hair fol icle injury.

Objective To investigate the effect of artorvastatin on macrophage accumulation in tubulointerstitium of unilateral ureteral obstructive (UUO) nephropathy and its possible mechanism.Methods Twenty-one rats were randomly divided into three groups: sham-operatipn, UUO, UUO+ artorvastatin. Immunohistochemistry staining of CD68 and M-CSF was used to define the macrophage accumulation and expression of interstitial M-CSF. Lipid profile in these groups was also determined. Results CD68 + cells and M-CSF expression were significantly increased at day 10 after UUO operation, this kind of CD68 + cell accumulation and M-CSF expression up-regulation were ameliorated by artorvastatin treatment. In UUO and atorvastatin treated groups, the number of macrophage was positively correlated with tubulointerstitial M-CSF expression. There was no significant difference about serum lipid among the three groups. Conclusion Atorvastatin can reduce interstitial macrophage accumulation in UUO nephropathy. This therapeutic effect might relate to down-regulation of tubulointerstitial M-CSF expression.

Objective To investigate the regulation of cyclooxygenase-2 expression and mechanism of selective cyclooxygenase-2 inhibitor Celecoxib suppressing tubulointerstitial fibrosis of rats with unilateral ureteral obstruction(UUO) model. Methods The UUO models were induced by ligating the left ureter. Rats were randomly divided into bulofen group (group B), Celecoxib group (group R), model group (group C) and sham operation group (group S). Rats in group B were given bulofen 300mg?Kg~ -1?d~ -1, and in group R were given Celecoxib 10mg?Kg~ -1?d~ -1 by gastric gavage from 24 h before the obstruction to 14 days after the induction. Rats were sacrificed at 3d, 6d and 14d in batch after the UUO models were induced. The mRNA expressions of cyclooxygenase-1(COX-1), cyclooxygenase-2(COX-2), transforming growth factor-beta 1 (TGF-?1), and connective tissue growth factor (CTGF) were detected by RT-PCR. The protein expressions of TGF-?1, CTGF and ?-SMA were detected using immunohistochemistry and the content of cAMP was determined by radioimmuno-assay. Results Compared with group S, the mRNA expressions of COX-2, TGF-?1 and CTGF in group C increased markedly after UUO treatment, and the content of cAMP decreased. It showed no significant difference in the mRNA expressions of TGF-?1, CTGF and the content of cAMP for the Bulofen treatment in the UUO model. With the Celecoxib treatment, there was no significant difference on the mRNA expression of TGF-?1, but the content of cAMP increased and the expression of CTGF decreased. Conclusion The COX-2 plays an important role in lesion of tubulointerstitial. Selective cyclooxygenase-2 inhibitor can partially up-regulate the content of cAMP and down-regulate the expression of CTGF, the downstream factor of TGF-?1, which may postpone the renal interstitial fibrosis.

Objective To investigate whether the signaling pathway of PI3K-AKT is involved in Ang II-induced apoptosis in rat renal tubular epithelial cells (NRK-52E).Methods Cultured cells were incubated in media containing either buffer (control) or different concentrations of Ang II (10-9 to 10-6 mol/L) for 24 h. Cells were stained by Annexin V-F1TC/PI Kit and apoptosis was evaluated by flow cytometer. Western blotting was performed to assess the levels of PI3K, total- and phosphor-AKT. Results Ang II induced tubular epithelial cell apoplosis in a dose dependent manner. Ang II significantly inhibited the phosphorylation of AKT. The level of AKT phosphorylation was negatively correlated with apoptosis in Ang II-stimulated cells(r=-0.90 ,P