To review the outcome of the endovascular treatment of aortoiliac occlusive disease,the recent literature concerning endovascular treatment as well as aortoiliac occlusive disease was extensively reviewed,and the research and development were summarized.The results are:(1) In most cases,endovascular invention is better than surgery ; (2) Stent placement has a higher technical success rates and a better longterm outcome than percutaneous transluminal angioplasty,primary or selective stent placement,which is better,is controversial; (3)Covered stents perform better than bare stents in longer-term patency and clinical outcome ; (4)Endovascular treatment of complex AIOD provides excellent early and long-term results,similar to those obtained in the treatment of simple lesions.So,in general,endovascular treatment of aortoiliac occlusive disease provides excellent clinical results,further research is needed.

BACKGROUND: Studies have shown that chitosan can improve the proliferation and migration of fibroblasts, promote the synthesis of extracellular matrix, and create a favorable environment for defect healing.OBJECTIVE: To observe the effect of highly simulated chitosan scaffolds in repairing abdominal wall defects in rats.METHODS: Sixty adult Sprague-Dawley rats were used to make animal models of abdominal wall defects, and then model rats were randomly divided into two groups: experimental group and control group followed by implantation with the highly simulated chitosan scaffold and polypropylene mesh, respectively. At 2, 4 weeks after repair, gross, adhesion and histopathological observations of the repair part were performed.RESULTS AND CONCLUSION: Gross observation: in the control group, omental adhesion was found at 2 weeks after repair; and at 4 weeks after repair, the mesh was thickened and exhibited clear boundaries with the surrounding tissue, but common color and integration. In the experimental group, there was mild adhesion between the scaffold and the defect site at 2 weeks after repair, and the mesh was thickened, but the wound healed well with no prominence, swelling, and infection at 4 weeks after repair. Kadata adhesion score in the experimental group was lower than that the control group at 4 weeks after repair (P < 0.05). Pathological observation showed that at 4 weeks after repair, there were a large number of infiltrated inflammatory cells, capillary growth, and a large number of fibroblasts at the defect site in the control group; and meanwhile, a small amount of infiltrated inflammatory cell infiltration and a large number of collagen fibers and capillaries, with better granulation tissue maturity,were found in the experimental group. To conclude, the highly simulated chitosan scaffold can promote the repair of abdominal wall defects and reduce inflammatory reactions.

Objective To investigate the effects of selective cyclooxygenase-2(COX-2) inhibitor nimesulide on the proliferation of colon adenocarcinoma cells in vitro and the expression of matrix metalloproteinase-2(MMP-2).Methods The human colon cancer cell lines HT-29 and HCT-116 were employed in the study,grouped as nimesulide group,DMSO control group and blank control group.After treatment with nimesulide,the inhibitory effect of nimesulide on the proliferation of cancer cells was quantified by MTT assay,and the expression of MMP-2 in the cells was detected by quantitative zymography.Results Nimesulide inhibited the proliferation of HT-29 and HCT-116 cells in time and dose-dependent manners.The inhibitory effect on HT-29 cells was stronger than that on HCT-116 cells.Nimesulide down-regulated the MMP-2 expression in HT-29 cells,whereas the expression in HCT-116 cells remained unchanged.Conclusion Nimesulide can obviously inhibit the growth of colon cancer HT-29 cells with positive COX-2 protein,suggesting that nimesulide may down-regulate the expression of MMP-2 by inhibiting the activity of COX-2.

Objective: To explore the prevention and treatment of total flavonoids from Gleditsiae Spina (TFGS) on lung cancer and its mechanisms. Methods: Mouse Lewis lung cancer (LLC) and embryonic lung fibroblast (L929) cells were treated with different doses of TFGS for 48 h, cell proliferation and adhesion were examined by MTT assay, and gap junctional intercellual communication (GJIC) was measured through scrape loading and dye transfer. The mice were randomly divided into model, quercetin (100 mg/kg, positive control), high-and low-dose (100 and 30 mg/kg) TFGS groups. The mice were ip injected with urethane twice weekly for five weeks to induce lung carcinogenesis and treated once daily for 10 weeks following the first urethane injection. The prevention of TFGS on chemocarcinogenesis was evaluated and the expression of gap junctional protein connexin 43 (Cx43) in lung tissue with tumors was compared by immunohistochemistry. The LLC cells were injected into the lateral axilla and tail vein respectively to establish the LLC sc allograft and experimental lung metastasis. The tumor-inocubating mice were randomly divided into model, doxorubicin (5 mg/kg, positive control), high-and low-dose (same as above) TFGS groups. The mice received the treatment for three weeks following tumor inocubation, and the effects of TFGS on the tumor size, metastasis, and life span were evaluated. Results: TFGS inhibited LLC cell proliferation in a dose dependent manner but had no effect on L929 cell proliferation in vitro. TFGS with a little effect on cell proliferation decreased cell adhesion and promoted GJIC in a dose dependent manner in LLC cells but did not affect the L929 cell adhesion. TFGS was able to prevent carcinogenesis induced by urethane and enhance Cx43 staining in lung region with tumor in immunohistochemistry. Compared with untreated model mice, GJIC reduced the tumor size and metastasis and prolongated life span in a dose dependent manner. Conclusion: TFGS could promote GJIC to prevent and treat tumor and might be a potential antitumor agent.

OBJECTIVETo evaluate the clinical effects of arthroscopic reconstruction of anterior cruciate ligament (ACL) and minimally invasive reconstruction of posteromedial corner (PMC).

METHODSThere were 22 cases of ACL and PMC tear were performed with reconstruction from March 2012 to February 2014. The patients were 29.4 years old on average, including 8 males and 14 females. ACL reconstruction was performed under arthroscopy and PMC reconstruction was performed minimally invasively through the ACL incision. The stability of knee was assessed by anterior drawer test,Lachman test,vulgus stress test and Slocum test. The function of knee was assessed by Lysholm score and Tegner activity rating. MRI of knee was checked 12 months after operation.

RESULTSThe stability tests of all patients were negative at 2 and 6 months after operation, and there was one positive case in anterior drawer test and another positive case in vulgus stress test at 12 months after operation. Lysholm score of all patients 12 months after operation was 96.8 +/- 6.8, which was significantly better than 32.0 +/- 11.2 before operation. Tegner activity rating of all patients at 12 months postoperatively was 6.1 +/- 0.9, which was significantly better than 0.9 +/- 0.5 before operation. It showed the grafts were very well in the MRI 12 months postoperatively.

CONCLUSIONArthroscopic ACL reconstruction and minimally invasive PMC reconstruction can restore the stability of knee.

Adult ; Anterior Cruciate Ligament ; physiopathology ; surgery ; Anterior Cruciate Ligament Injuries ; Anterior Cruciate Ligament Reconstruction ; Female ; Humans ; Knee Injuries ; physiopathology ; surgery ; Knee Joint ; physiopathology ; surgery ; Male ; Middle Aged ; Minimally Invasive Surgical Procedures ; Treatment Outcome ; Young Adult

Objective To evaluate the potential roles of celecoxib on proliferation and cell cycle progression of colon adenocarcinoma cells and on the hepatic metastasis of nude mice. Methods The human colon cancer cells HT-29 and HCT-116 were employed in the study. After treatment with celecoxib, the inhibitory effects of celecoxib on the proliferation of cancer cells were quantified by MTT assay, and the cell cycle progression was detected by flow cytometry, tumor cells were inoculated in nude mice, and the hepatic metastasis was detected. Results ①Celecoxib inhibited the proliferation of the tumor cells in time and dose-dependent manners (P

Objective To investigate the effects of COX-2 antisense oligonucleotide (AsODN) on the proliferation and expression of COX-2 in human skin squamous cell carcinoma cell line Coio-16. Methods The COX-2 AsODN was synthesized artificially, and various concentrations (50, 100, 200, 400 nmol/L) of the AsODN were transfected into Colo-16 cells with lipofectin followed by additional culture for different durations. The transfection results were observed with fluorescence microscopy. Subsequently, MTT assay,Western blotting and reverse transcription PCR were used to detect the cell proliferation, protein and mRNA expression of COX-2 in Coio-16 cells, respectively. Restults Compared with untreated cells, the proliferation of Colo-16 cells was inhibited significantly at 24, 48, 72 and 96 hours after transfection with different concentrations of COX-2 AsODN (all P < 0.05), and the COX-2 AsODN of 400 nmol/L exerted the highest inhibition rate of 60.3% at 48 hour. The average gray scale was 0.763±0.070, 0.600±0.065, 0.430±0.074 and 0.251±0.045 for COX-2 protein, 0.778±0.025, 0.602±0.041, 0.417±0.031 and 0.297±0.051 for COX-2 mRNA in Colo-16 cells transfected with COX-2 AsODN of 50, 100, 200, and 400 nmol/L respectively,significantly lower than that in untreated Colo-16 cells (all P < 0.05); there was a significant difference in the expression of COX-2 protein and mRNA among the cells transfected with the four concentrations of COX-2 AsODN and untreated cells (F = 83.54, 132.48, respectively, both P < 0.05). Conehtsions COX-2 AsODN can inhibit the proliferation, as well as the expression of COX-2 protein and mRNA in Colo-16 cells, which suggests that COX-2 AsODN has a potential therapeutic effect on skin squamous cell carcinoma.

Objective To investigate the effects of rosiglitazone on the proliferation,connective tissue growth factor and Smad expression in cultured cardiac fibroblasts induced by advanced glycosylation end-products (AGEs).Methods After being treated with various amounts of rosiglitazone,the cultured neonatal rat cardiac fibroblasts were incubated with AGEs.The status of cardiac fibroblasts proliferation and cell cycle were detected by 3-(4,5-dimethyhhiazol-2-yl) -2,5-diphenyl tetrazolium bromide (MTI) assay and flow cytometry.Furthermore,ELISA technique was applied to identify the level of TGF-β1.The protein expressions of CTGF and Smad in cardiac fibroblasts of neonatal SD rats were detected with Western blotting.Results The exposure of cardiac fibroblasts to AGEs at doses of 0-200 mg/L induced a dose-dependent increase in cell proliferation.At the concentration of rosiglitazooe (0.1,1,and 10 μmol/L),the cell proliferation was reduced compared with 200 mg/L AGEs group by O.823±0.072,0.785±0.060,0.601±0.081 vs 0.981±0.049,respectively (P < 0.05).The increased levels of TGF-β1 in supematants of cultured cardiac fibroblasts stimulated by AGEs were inhibited by rosiglitazone at the concentrations of 0.1,1,10μmol/L by 257.77±9.09,230.29±6.56,200.84±10.26 vs 300.68±8.56,respectively (vs 200 mg/L AGEs,P<0.01).Western blot indicated that pretreatment with rosiglitazone (0.1,1,and 10 μmol/L) inhibited CTGF protein production in a dose-dependent by 0.769±0.108,0.590±0.095,0.534±0.115 vs 1.021±0.113,respectively (vs 200 mg/L AGEs,P<0.01).It was also demonstrated that pretreatment with rosiglitazone (1 and 10 μmol/L) inhibited Smad2 protein production by 0.424±0.059,0.396±O.080 vs 0.572±0.073,respectively (vs 200 mg/L AGEs,P < 0.05 or P < 0.01).Meanwhile pretreatment with rosiglitazone (1 and 10 μmol/L) inhibited Smad4 protein production by 0.580±0.063,0.556±0.051 vs 0.672±0.059,respectively (vs 200 mg/L AGEs,P < 0.05 or P < 0.01).Conclusions The findings suggest that AGEs promote the proliferation of cardiac fibroblasts and stimulate the protein production of Smad and CTGF of cardiac fibroblasts.Rosiglitazone inhibits the above reaction.These results indicate that CTGF/Smad pathway may play an important role in the protective effect of rosiglitazone on myocardial fibrosis.

Hypertensive renal damage is based on the extent and duration of hypertension, renal damage caused by varying severity. Hypertensive renal damage due to various causes imbalance of vascular active substances, renal arteriosclerosis, so that the abnormal renal hemodynamic, renal ischemia, low specific gravity of urine, low osmotic pressure and urine. The rapidly increasing incidence of hypertensive renal damage has become one of the most important reasons of end stage renal disease (ESRD). Effective treatment of hypertension is limited by poor compliance and significant adverse reaction of antihypertensive drugs. Therefore, some patients have turned to Chinese medicine (CM), hoping that such treatments might improve the efficiency. The author reviews relevant theory and the latest researches, on the basis of combining diseases and syndrome, discusses state and achievement of hypertensive renal damage with Chinese herbal medicines from fundamental and clinical research and action mechanism from standpoints of Chinese herbal compound and herbal effective chemical composition to take future research for important reference.
Antihypertensive Agents ; therapeutic use ; Disease Progression ; Drugs, Chinese Herbal ; therapeutic use ; Humans ; Hypertension, Renal ; diagnosis ; drug therapy ; Kidney ; drug effects ; Medicine, Chinese Traditional ; methods

The intracellular signal transduction pathways play an important role in the occurrence and development of thyroid cancer.Mitogen activated protein kinase (MAPK) signal transduction pathway,phosphatidylinositol 3-kinase (PI3K)-AKT pathway,NF-κB pathway and RASSF1-MST1-FOXO3 pathway affect the occurrence and development of thyroid cancer by modulating the activity and expression of specifical proteins,and determine the growth and apoptosis of thyroid cancer cells.