BACKGROUND:Many scholars researched the biomechanics of middle clavicle fracture plate fixation, but little researched the plate position. OBJECTIVE:To observe the biomechanical characteristics ofanterior and superior plates for clavicle fracture with three-dimensional finite element models. METHODS:Three-dimensional finite element models of clavicle fracture with anterior and superior plates were established. The stress after anterior and superior plate fixation was analyzed. The maximum stress and displacement of plate fixation for clavicular fracture were observed under compression, torsion and three-point bending. RESULTS AND CONCLUSION:(1) In the compressed condition, the maximum stressand maximum fracture displacement were similar between the superior and anterior plate fixation (P> 0.05). (2) Under clockwise twist condition, the maximum stress and maximum fracture displacement were smaler in the superior plate fixation group than inthe anterior plate fixation group (P< 0.05). (3) Under counterclockwise twist condition, the maximum stress and maximum fracture displacement were similar between the anterior and superior plate fixation groups (P> 0.05). (4) Under three-point bending condition, the maximum stress was similar between the superior and anterior plate fixation groups (P> 0.05). The maximum fracture displacement was bigger in the superior plate fixation group than in the anterior plate fixation group (P< 0.05). (5) These findings suggest that superior fixation of clavicle fracture reconstruction plate has more advantages than the anterior plate fixation.

Objective To assess the safety of intrathecal administration of betamethasone.MethodsTwenty-four adult white rabbits of both sexes were randomly divided into four groups with 6 rabbits in each group.Group Ⅰ (blank control group)in which nothing was injected intrathecally;group Ⅱ(NS control group)in whichnormal saline(NS)0.2ml was injected into the subarachnoid space through great occipital foramen once a weekand the animals were killed at the end of the 3rd week;in group Ⅲ and Ⅳ betamethasone 200 ?g or 400 ?g in 0.2ml was injected intrathecally once a week instead of NS.The animals were anesthetized and killed by intra-aorticinjection of NS and 2% glutaraldehyde.The cervical section of the spinal cord(C_(1-6))was immediately removedand fixed with 2% glutaraldehyde for microscopic examination.Results No neural histo-pathologic changes shownby microscopic examination were observed in group Ⅰ and Ⅱ.In group Ⅲ and Ⅳ microscopic examination showeddifferent degrees of swelling and demyelination of the nerve fibers and edema and vacuolization ofmitochondria.Conclusion Intrathecal betamethasone can damage the spinal cord.

Objective To investigate the expressions of cancerous inhibitor of protein phosphatase 2A (CIP2A) and vascular endothelial growth factor (VEGF) in hepatocellular carcinomas and their clinical significance.Methods The expressions of CIP2A and VEGF proteins were tested with immunohistochemistry in 60 cases of hepatocellular carcinomas and adjacent paracancerous tissues.Results The positive rate of CIP2A in hepatocellular carcinomas was significantly higher than adjacent paracancerous tissues (83.3％ vs 9.5％,P ＜ 0.05).Significant differences were also observed in the expression rate of VEGF between the patients with hepatocellular carcinomas and paracancerous tissues (75.0％ vs 14.3％,P ＜0.05).The expression of CIP2A in hepatocellular carcinomas was significantly positively correlated with its pathological grading,differentiation,and tumor node metastasis (TNM) stage (P ＜ 0.05).The expression of VEGF in hepatocellular carcinomas was significantly positively correlated with its pathological grading,differentiation,and TNM stage (P ＜ 0.05).Significantly positive correlation was found between expressions of CIP2A and VEGF with Spearman correlation analysis (rs =0.465,P ＜ 0.01).Conclusions The abnormal expressions of CIP2A and VEGF gene may promote tumor angiogenesis and progression of a hepatocellular carcinoma.The study supports positive regulation between expressions of CIP2A and VEGF in a hepatocellular carcinoma.

Objective To investigate the expressions of receptor for advanced glycation endproducts (RAGE) and nuclear factor κB(NF-κB) in brain hippocampus of rat with chronic fluorosis,and to reveal the mechanism of brain damage resulted from chronic fluorosis.Methods Sixty clean grade SD rats were randomly divided to three groups(20 rats in each group,10 female and 10 male) fed with different contents of fluoride,control group with normal tap-water(＜ 0.5 mg/L fluoride),small dosage of fluoride exposure group(10 mg/L fluoride in tap-water) and large dosage of fluoride exposure group(50 mg/L fluoride) for six months.Then the rats were killed by femoral artery bleeding and hippocampus was removed.Protein and mRNA levels of RAGE and NF-κB in the hippocampus were determined by Western blotting and quantitative real time PCR,respectively.Results As compared to the control groups[(100.00 ± 2.60)％,(100.00 ± 7.80)％],the expressions of RAGE and NF-κB at protein level in the hippocampus were significantly increased in the small dosage of fluoride exposure groups [(205.00 ± 15.30)％,(156.00 ± 12.20)％] and the large dosage of fluoride exposure groups[(232.00 ± 10.90)％,(162.00 ± 9.80)％,all P ＜ 0.05]; for the mRNA level of RAGE and NF-κB,the expressions were higher in the small dosage of fluoride exposure groups(1.27 ± 0.09,0.83 ± 0.15) and the large dosage of fluoride exposure groups (2.60 ± 0.19,1.27 ± 0.19) than those of the control groups(0.66 ± 0.18,0.32 ± 0.08,all P＜ 0.05).Conclusions The increased expressions of RAGE and NF-κB in the hippocampus of rat brain are caused by chronic fluorosis,and these changes may be associated with the mechanism of nerve injury.

Objective Aim of the study is to investigate the expression of syndecan-4 and nuclear factor κB(NF-κB) in the kidney of rat with chronic fluorosis,and to reveal the mechanism of kidney damage resulted from the toxicity of excessive amount of fluoride.Methods According to body mass and sex,sixty SD rats were randomly divided to three groups according to body mass and fed with different contents of fluoride:control group with normal tap-water(＜ 0.5 mg/L fluoride),small dosage of fluoride exposure group (adding 10 mg/L fluoride in tap-water) and large dosage of fluoride exposure group (50 mg/L fluoride) for six months.The protein level of syndecan-4 and NF-κB in the kidney was detected by Western blotting and syndecan-4 mRNA level by quantitative real time PCR.Results As compared to the control group[(100.0 + 8.1)％],the expression of syndecan-4 at protein level in the kidney of rat was significantly increased in the small dosage of fluoride exposure group [(198.5 + 5.6)％,P ＜ 0.05] and large dosage of fluoride exposure group [(209.2 + 13.0)％,P ＜ 0.05]; the protein levels of NF-κB in the small dosage of fluoride exposure group[(284.4 + 11.1)％,P ＜ 0.05] and in the large dosage of fluoride exposure group[(343.2 + 2.9)％,P ＜ 0.05] were significantly increased than that of the control group[(100.0 ± 10.7)％].The mRNA levels of syndecan-4 in the kidney in the small dosage of fluoride exposure group and large dosage of fluoride exposure group(0.431 + 0.058 and 0.453 ± 0.065,both P ＜ 0.05,respectively) were significantly increased than that of the control(0.128 + 0.026).Conclusions The increased expression of NF-κB in the kidney is induced by increased expression of syndecan-4,which may be involved in kidney damage of chronic fluorosis.

Objective To study effects of yinlingⅠon cell viability and oxidative injury of lead-exposed cell.Methods After lead exposure Vero cell was treated with yinlingⅠof different concentrations.The cell viablitity was measured by methyl thiaxiolyl tetrazolium(MTT) method and the superoxide dismutase(SOD)and malondialdehyde(MDA) activity in cell suspensions were measured.Results When Vero cell lived in 125 ?mol/L lead acetate surrounding,the MDA concentration increased,but the viability of cell and the SOD content in the Vero cell suspension decreased.YinlingⅠcould increase the viability of lead-exposed cell during a certain extent;in the most non-toxicity concentration yinlingⅠcould elevate the SOD content in the Vero cell suspension,reduced the MDA concentration and resisting lead toxication in vitro.Conclusion YinlingⅠhas the protective effects on the cell viability and oxidative injury of lead-exposed cell.

[Abstratc] Objective The function of cIAP1 in the progression of ovarian cancer has not been clarified . This study is to explore the involvement of cIAP 1 in regulating biological behaviors of ovarian cancer cells by u-sing RNA interference(RNAi)technology.Mte hods The short hairpin RNA plasmid targeting cIAP1 was con-structed and transfected into Skov 3 cells.The levels of cIAP1 mRNA and protein were investigated by RT -PCR and Western Blot respectively .MTT assay and flow cytometry were used to evaluate cell proliferation and apopto-sis.R esults The rate of cIAP1 transfection was 74.7%performed by flow cytometric analysis .cIAP1 expression was significantly down -regulated at both mRNA and protein levels ,which resulted in a decrease of cell prolifera-tion and invasion capability in vitro .Conclusion This study implies that cIAP 1 might play an important role in the progression of ovarian cancer ,and it could be a potential target for therapeutic anti -cancer drugs .

AIM: To determine the effects of NF-?B on the development of rat pancreatic fibrosis mediated by angiotensin II. METHODS: Spraque-Dawley rats (200-300g) were randomly divided into normal group, control group and losartan-treatment group. Pancreatic fibrosis was induced by injection of 2% TNBS into biliopancreatic duct. Rats in losartan-treatment group and control group were respectively treated with losartan (10 mg?kg~(-1)?d~(-1)) by gavage and the same volume of saline vehicle. The expression, distribution, and activation of NF-?B were studied by Western blot, immunohistochemistry and TransAM~(TM). Toluidine blue staining and transmission electron microscopy were also used to observe the number, distribution and degranulation of mast cells. In addition, RT-PCR was performed to detect the intrapancreatic ICAM-1 mRNA expression. RESULTS: The expression and activity of intrapancreatic NF-?B p65 protein were significantly increased on day 3 after operation, reaching peak on day 7 [(0.406?0.086) mg/g total protein]. Mast cell activation was observed and ICAM-1 mRNA levels on day 3 and 7 were up-regulated in control group. Losartan treatment inhibited NF-?B expression and activation, reduced mast cell infiltration and degranulation and decreased ICAM-1 mRNA expression compared with control rats. CONCLUSION: It might be associated with the expression and activation of NF-?B that angiotensin II mediates inflammation and fibrosis in the early stage of pancreatic fibrosis. [

AIM: To examine the effects of PPAR? activation on the growth of human pancreatic carcinoma in vitro and to explore the role of NF-?B and activator protein-1 (AP-1) in this process. METHODS: SW-1990 pancreatic cancer cells were treated with ligand of RXR?, 9-cis-RA, ligand of PPAR?, 15d-PGJ_2, and both. Antiproliferative effect was evaluated by using MTT assay; the expression of NF-?B p65 active protein was assayed by using TransAM~TM technique. Expression of c-jun and c-fos by SW1990 cells, which were treated with 15d-PGJ_2, 9-cis-RA and both at varying concentrations, were detected by RT-PCR. RESULTS: MTT assay demonstrated that 15d-PGJ_2, 9-cis-RA and the combination of both had a potent inhibitory effect on the growth of SW1990 cells in a dose-dependent manner. 9-cis-RA had a synergic action with 15d-PGJ_2 on the growth inhibition of pancreatic carcinoma. TransAM~TM showed a down-regulation trend of P65 active protein in SW1990 cells treated with 15d-PGJ_2, 9-cis-RA and both. RT-PCR demonstrated that the expression of c-jun mRNA in 15d-PGJ_2, 9-cis-RA and the combination of both-treated cells were firstly increased and then decreased, the expression of c-fos was decreased in 15d-PGJ_2 or 9-cis-RA treated SW1990 cells, but increased in cells treated with both 15d-PGJ_2 and 9-cis-RA. CONCLUSION: Activation of PPAR? exerts a negative regulatory effect on the growth of pancreatic carcinoma in vitro. Activation of RXR? has a synergic action with PPAR? agonist. The mechanism is probably associated with down-regulating the expression of NF-?B and AP-1. [

Objective To investigate the expressions of phosphatidylinositol 3-kinase (PI3K), Akt and E-cadherin and their clinical significance in thyroid papillary carcinomas.Methods Expressions of PI3K, Akt, and E-cadherin were detected in 62 cases of thyroid papillary carcinomas,30 cases of thyroid goiter and 30 cases of normal thyroid by immunohistochemistry (EnVison),and simultaneously compared with age, sex, tumor size, clinical tumor node metastasis( TNM) stages, and lymph node metastasis in thy-roid papillary carcinomas.Results The expression rate of PI3K, Akt, and E-cadherin was 74.2%(46/62), 66.1%(41/62), 16.1%(10/62),respectively.Expressions of three proteins in thyroid papillary carcinomas were significantly different from those in thyroid goiter and normal thyroid tissues ( P <0.05). The lower positive rates of PI3K and Akt proteins were obtained in the group of stageⅠ~Ⅱthan that in the group of stageⅢ~Ⅳ(χ2 =4.976, P =0.026;χ2 =6.233, P =0.013).Higher positive rates of PI3K and Akt proteins were obtained in the group of lymph-node metastasis than that in group of non-lymph-node metastasis (χ2 =6.675, P =0.010;χ2 =7.511, P =0.006).Higher positive rate of E-cadherin protein was obtained in the group of stage Ⅰ~Ⅱ than that in the group of stage Ⅲ ~Ⅳ (χ2 =6.558, P =0.010 ) .Higher positive rate of E-cadherin proteins was obtained in the group of non-lymph-node metastasis than that in the group of lymph node metastasis(χ2 =5.678, P =0.017).There was significant positive correlation between expressions of PI3K and Akt through Spearman correlation analysis ( r =0.423, P <0.05).PI3K was negatively correlated with E-cadherin with Spearman correlation analysis ( r =-0.527, P <0.05).Akt was also negatively correlated with E-cadherin ( r =-0.417, P <0.05).Conclusions PI3K/Akt pathway might regulate thyroid papillary carcinoma cells proliferation, invasion and metastasis.