[Objective]To observe the effect of cross-finger-like micro-weave suture plus sodium hyaluronate technology in the treatment of extensor tendon injury by the animal experiments.[Method]Twenty-eight Leghorn chickens were randomly divided into four groups,double-cross stitching was used in group A in the treatment of extensor tendon injury,double-cross stitching plus sodium hyaluronate in group B,cross-finger-like micro-braided suture in group C,cross-finger-like micro-braided suture plug sodium hyaluronate surgery in group D.Six weeks after surgery,morphological observation,histological observation and biomechanical determination were done by using the naked eye and microscope,as well as the results of the experiments were statistically analyzed.[Result]In the group of the cross-finger-like micro-weave suture plus sodium hyaluronate,tendon grew in good shape without nodules after surgery,pseudome was formed around tendon,tendon cells mostly arranged regularly in bunches,maximum load was (70.9 ? 5.68) N on average,it was significantly larger than those in other groups and there was a significant difference by the analysis of variance (P

Objective:To establish a trace chromogenic substrate method for the determination of anti-FIIαactivity in compound heparin sodium cream .Methods: The anti-FIIαactivity in compound heparin sodium cream was determined by a trace chromogenic substrate method according to the completely random design of experiment based on the amount reaction principle of 4*4 parallel lines in the biological test statistics method .Results:The calibration curve was linear within the range of 0.005 04 IU· ml-1-0.021 IU· ml-1(r=0.992).The average recovery was 101.6% with RSD of 2.76% (n=9).Conclusion: The method is accurate, reliable and reproducible , and can be used for evaluating the quality of compound heparin sodium cream .

ObjectiveToestablisharatmodelofincreasedbloodflow-inducedpulmonaryarterialhypertension generatedbyanastomosisoftheleftcommoncarotidarterytoleftexternaljugularvein.Methods 45maleSDratswere divided into three groups:the shunt group , the ligation group and the sham group .At twelve weeks after the procedure , the general status of the rats was observed . Heart conditions , cardiac output and shunt patency were measured by echocardiography .Right ventricular systolic pressure ( RVSP ) and Qp/Qs were checked by catheterization . Right ventricular hypertrophy index ( RVHI) was calculated and lung tissues were examined by pathology using hematoxylin -eosin and elastin Van Gieson staining .All data were analyzed statistically by one-way ANOVA test using SPSS 16.0.Results There was no significant difference in body weight gains between the groups .The patency rate of shunt was 84.6%.The heart was enlarged in the group shunt .Cardiac output increased significantly in the shunt group than that in the other two groups [(309.8 ±33.1) mL/min?kg vs.(245.6 ±31.9) mL/min?kg, (240.8 ±30.9)mL/min?kg, respectively, P<0.05].In the shunt group Qp/Qs was 2.16 ±0.38 and RVSP increased to (35.8 ±4.9) mmHg, RVHI was 0.3263 ± 0.0342, significantly higher than that of the other groups .The pulmonary arteriolar wall was evidently thickened in contrast to that in the sham group [ ( 22.3 ±1.7 )% vs.( 10.6 ±1.7 )%, P <0.05 ) .Conclusions Anastomosis of the left common carotid artery to left external jugular vein can successfully establish pulmonary arterial hypertension model induced by high blood flow in rats .

Objective To explore an effective method of isolating and culturing the vascular endothelial cells of rat thoracic aorta.MethodThe thoracic aorta was harvested under aseptic condition from the thorax of a Wistar rat.The peripheral connective tissue and fat of the thoracic aorta were stripped and disposed,and then the thoracic aorta was turned inside out to expose the intima.The thoracic aorta was ligated with silk and cauterized on both ends with heated forceps.Then the thoracic aorta was cultured in medium DMEM/F12 containing 20% newborn calf serum in a 50 ml culture bottle which was already blanketed with rat tail collagen.The thoracic aorta was discarded and the new culture medium was added into the culture bottle six days later.The migrating cells were differentially digested by 0.125% pancreatic enzyme for serial subcultivation.The cells were identified by immunohistochemical method with anti-Ⅷ factor antibody.ResultA small amount of cells were seen to migrate from the aorta and adhered to the bottom of culture bottle 6 days after cultivation;the migrating cells spread to cover most part of the bottom of culture bottle 12-14 days later.About 70% of the migrated cells were in a confluent monolayer.The confluent cells grew rapidly after being digested with pancreatic enzyme,and they showed a typical cobblestone appearance.The cells were identified as endothelial cells with 100% expression of Ⅷ factor,which was regarded as the marker of endothelial cells.ConclusionThe method established in the present study is simple and easy to handle,it does not need collagen enzyme and endothelial cell growth promoting substrate,and it is economical and applicable.It is especially suitable for isolation and cultivation of vascular endothelial cells of vessels of small caliber.

Objective To investigate the effects of anti-adhesion treatment and high-strength suture technique on the treatment of extensor tendon rupture by animal experiments and clinical application.Methods Twenty-eight leg-born chickens were randomly divided into four groups(7 each).Double cross suture was applied in group A,while double cross suture combined with sodium hyaluronate spraying in group B,cross-finger-like micro-braided suture in group C,and cross-finger-like micro-braided suture combined with sodium hyaluronate spraying in group D.The animals were sacrificed 6 weeks after operation,morphological,histological and biomechanics were observed and compared among the groups.One hundred and sixteen patients were treated with the surgical method in group D(89 males,27 females,aged 20-55 with an average of 36 years;73 with extensor tendon rupture,38 with strain/chalasis,5 with firearm injuries;56 on back of hand,48 on central slip,12 on lateral fixing chorda;82 with one-stage operation,and 34 with second-stage operation),and then followed-up for 2-5 years to observe the therapeutic effects.Results The repaired tendons in group D was in good contour,most tendon cells arranged regularly in bunches.The maximum load was significantly higher in group D(70.9?5.7N) than in group A(48.4?5.7N),Group B(51.3?3.2N) and Group C(68.3?2.8N,P

OBJECTIVETo observe the protective effect of tectorigenin on the vascular endothelial cells(VEC) injured by oxidant low density lipoprotein-cholesterol and the expression of MCP-1 and ICAM-1 mRNA, and explore the mechanism of anti-atherosclerosis.

METHODThe VEC of rat was cultured in vitro and the 100 mg x L(-1) ox-LDL inducing oxidant injured model was used in this study. Different dosage tectorigenin was added into VEC and the activity of VEC was observed by MTT colorimetry. The expression of MCP-1 and ICAM-1 mRNA in VEC was detected by RT-PCR.

RESULTTectorigenin had significantly protective effect on the VEC injured by ox-LDL and obviously inhibited the excessive expression of MCP-1 and ICAM-1 mRNA in VEC.

CONCLUSIONIt was the critical mechanism of anti-atherosclerosis that tectorigenin prevented the VEC oxidant injured and inhibited the excessive expression of MCP-1 and ICAM-1.

Animals ; Atherosclerosis ; drug therapy ; genetics ; metabolism ; Cells, Cultured ; Chemokine CCL2 ; genetics ; metabolism ; Disease Models, Animal ; Endothelial Cells ; drug effects ; metabolism ; Gene Expression ; drug effects ; Humans ; Intercellular Adhesion Molecule-1 ; genetics ; metabolism ; Isoflavones ; pharmacology ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Wistar

Objective To develop a new type of blast injury simulator to establish a mouse model of brain blast injury and study its damage mechanism. Methods Thirty healthy Kunming mice were randomly(random number) divided into the normal control group and brain blast injury model (TBI) group. A mouse model of traumatic brain injury was prepared by a self-developed explosive injury simulator. Morris water maze, Evans blue experiment and HE staining were used to observe the effects of shockwave exposure on spatial memory, blood-brain barrier, and pathological changes of brain tissues. T test was used for statistical analysis. Western blot method was used for detecting expression of brain injury markers Tau, S100β, Choline, inflammatory factors IL-1β, IL-4, IL-6, IL-10, NF-κB, apoptosis factors Bcl-2, Bax, Caspase3, and oxide protein stress-related factors IREα, MDA5, COX2 SOD1, and SOD2. Results Compared with the normal control group, (11.2±2.1) s, the time of searching platform in the TBI group was (54.6±8.4) s, was significantly longer (t=-19.330, P<0.05), and the EB exudation in the TBI group was 3.22 times (t=-13.903, P<0.05). Pathological staining revealed neuronal damage in the hippocampus, and TBI induced brain injury markers Tau(0.26±0.03 vs 0.46±0.04,t=-9.788, P<0.05), S100β(0.54±0.03 vs 0.74±0.02,t=-12.433, P<0.05) and Choline(0.54±0.05 vs 0.80±0.04, t=-7.970, P<0.05), inflammatory cytokines IL-1β(0.22±0.04 vs 0.31±0.05,t=-3.431, P<0.05), IL-4(0.65±0.02 vs 0.97±0.03, t=-18.927, P<0.05), IL-6(0.88±0.05 vs 1.07±0.08, t=-9.488, P<0.05) and NF-κB(0.80±0.06 vs 1.03±0.07,t=-4.507, P<0.05), and pro-apoptotic cytokines Bax(0.66±0.04 vs 0.78±0.04, t=-13.007, P<0.05) and Caspase3(0.44±0.03 vs 0.60±0.05, t=-4.472, P<0.05), oxidative stress-related factor pro IREα(0.72±0.06 vs 1.07±0.04, t=-9.665, P<0.05), MDA5(0.47±0.02 vs 0.77±0.02, t=-23.678, P<0.05) and expression of COX2(0.70±0.07 vs 0.86±0.02, t=-6.421, P<0.05), inhibition of inflammation inhibitory factor IL-10(1.14±0.06 vs 0.74±0.07, t=13.729, P<0.05), inhibition of apoptosis factors Bcl-2(0.72±0.05 vs 0.46±0.02, t=11.491, P<0.05) and inhibition of oxidative stress factors SOD1(1.17±0.05 vs 0.99±0.01, t=7.731, P<0.05) and SOD2(0.81±0.05 vs 0.61±0.04, t=10.257, P<0.05) expression. Conclusions The brain injury induced by blast exposure can induce spatial learning and memory loss, blood brain barrier disruption, neuronal damage hippocampus in mice, and promote the expression of brain injury markers, induce inflammation, oxidative stress and apoptosis. The self-developed explosive shock simulator successfully establishes a mouse brain blast injury model.