ObjectiveTo investigate the feasibility of establishing intervertebral disc degeneration (IDD) model by using minimally invasive acupuncture and rotary-cutting. MethodsForty New Zealand white rabbits [male or female, (2.9±0.3) kg in weight] were randomly divided into control group (n=20) and experimental group (n=20). No treatment was done in the control group; percutaneous puncture was performed on L4, 5 and L5, 6 intervertebral disc by using 18G needle under C-arm X-ray monitoring for rotary-cutting of nucleus pulposus to promote degeneration of the disc in the experimental group. At 4, 8, 12, and 16 weeks after operation, general observation and MRI observation were done, and intervertebral disc degeneration was accessed based on Pfirrmann grade; the specimens were harvested for Masson staining and Safranine O staining. ResultsThe nucleus pulposus showed dark colors and reduced elasticity in the experimental group when compared with the control group. T2-weighted MRI images indicated that the disc signal intensity of control group had no obvious change at early stage, and weakened slightly at late stage; disc signal intensity of the experimental group decreased with time. According to Pfirrmann grade for disc degeneration, disc degeneration degree was significantly aggravated with time in 2 groups (P < 0.05); degeneration was significantly more severe in the experimental group than the control group at the other time points (P < 0.05) except 4 weeks (P > 0.05). Masson staining results showed that irregular arrangement of annulus with integrate structure was observed in the control group with time; the annulus of the experimental group arranged in disorder, or even disc fibrous circle rupture appeared with time. Safranin O staining showed that the nucleus pulposus cells reduced significantly in the experimental group, but did not in the control group. ConclusionMinimally invasive acupuncture and rotary-cutting could successfully establish the IDD model in rabbits.
Objective To analyze the clinical effect of partial aortic root remodeling for root reconstruction on Stanford type A aortic dissection. Methods From January 2010 to December 2015, 30 patients (25 males, 5 females) underwent partial aortic root remodeling for root reconstruction on Stanford type A aortic dissection with involvement of aortic root. The range of age was from 27 to 72 years, and the mean age was 51.2±8.0 years. The proximal aortic dissection received partial aortic root remodeling, and the operation procedures included partial aortic root remodeling+ascending aortic replacement in 9 patients, partial aortic root remodeling+ascending aortic replacement+hemi-arch replacement in 6 patients, partial aortic root remodeling+ascending aortic replacement+Sun's procedure in 15 patients. The patients were followed up for 10 to 60 months with a mean of 37.9±3.2 months. Preoperative and postoperative degrees of aortic regurgitation were compared. Results All patients survived from the operation, and one patient died from severe pulmonary infection 15 days after operation. The overall survival rate was 96.7% (29/30). One patient died during the follow-up. Two patients underwent aortic valve replacement in the 12th and 15th postoperative month respectively because of severe aortic regurgitation (AI). Up to the last follow-up, trivial or no aortic regurgitation was demonstrated in 24 patients, but mild aortic regurgitation occurred in 2 patients. Conclusion The surgical treatment for aortic root pathology due to Stanford type A aortic dissection is challenging, and partial aortic root remodeling operations could restore valve durability and function, and obtains the early- and mid-term results.
Objective To evaluate the effects of oxidative stress in the airway inflammation and remodeling of high-fat diet induced obese mice with asthma. Methods Sixty female C57 /6J mice were randomly divided into four groups, ie. an asthma group, an obese group, an obese asthma group, and a control group. The mice in the asthma group were sensitized and challenged with ovalbumin ( OVA) and fed with normal diets. The mice in the obese group were fed with high-fat diets. The mice in the obese asthma group were sensitized and challenged as the asthma group, and fed as the obese group. The mice in the control group were sensitized and challenged with normal saline and fed with normal diets. After 12 weeks, bronchoalveolar lavage fluid ( BALF) were collected for total and differential cell count. IL-6 and 8-iso-prostaglandin F2α ( 8-iso-PGF2α) in lung tissue homognate were detected by ELISA. The pathological changes were observed under light microscope by HE staining. Meanwhile the remodeling indices including total bronchial wall area ( WAt) , smooth muscle area ( WAm) , and bronchial basement membrane perimeter ( Pbm) were measured. Results In comparison with the obese group and the asthma group, the leukocytes and eosinophils in BALF, WAt/ Pbm, and IL-6 in lung tissue increased significantly in the obese asthma group ( P lt; 0. 05) . 8-iso-PGF2αin lung tissue increased in sequence of the control group, the obese group, the asthma group, and the obese asthma group significantly. Pearson correlation analysis showed that leukocyte in BALF, WAt/ Pbm, and IL-6 were in positive correlation with 8-iso-PGF2α( r =0. 828, 0. 863, 0. 891, respectively, P lt;0. 01) . Conclusion Oxidative stress is involved in the airway inflammation and remodeling of obese asthma mice with high-fat diets.
Objective Engineer heart tissue (EHT) was constructed with mesenchymal stem cells (MSCs) and poly lacticacidCOglycolic acid (PLGA), and grafted onto the surface of myocardial infarction rats. We hypothesized that great omentum wrapping would increase EHT blood supply and ameliorate EHT microenvironment which is in favor of cardiac collagen remodling and heart function. We hope that omentun wrapped EHT could provide a valuable strategy for surgically myocardial infarction therapy. Methods MSCs were isolated from SD rats.Eight weeks after SD rats were subjected to left anterior descending (LAD) ligation, 18 rats were enrolled and divided into three groups, group A(n=6): great omentum wrapped MSCsPLGA EHT implantation; group B (n=6):MSCsPLGA EHT implantation; control group (n=6): the myocardial infarction; the sham group (n=6): only opened and closed chest, underwent LAD ligation, but no EHT implantation. Four weeks after transplantation, the following variables were evaluated: specimen stained with picrosirius red, left ventricle function evaluated by echocardiography, infarction ventricular wall motion by color kinesis (CK). Results Hearts of group A showed significantly less fibrosis than group B and control group (Plt;0.05). Infarction ventricular wall motion assessed by CK indicated significantly improvement in group A compared with group B and control group (Plt;0.05). Four weeks after transplantation, cardiac echocardiography showed left ventricle ejection fraction was lower in control group and group B compared with group A (Plt;0.05). Conclusion Transplantation of MSCsPLGA EHT with great omentum wrapping ameliorated infarction ventricular collagen remodeling, ameliorated infarction ventricular wall motion and preserved left ventricular function.
Objective To investigate the change of vasa vasorum in vessel wall of varicose vein of the lower extre-mity. Methods Thirty-two patients with varicose vein of the lower extremity were collected， in which of 12 patients with simple varicose veins （varicose group）， 9 patients with recurrent varicose veins （recurrent group）， 11 patients withthrombophlebitis of varicose vein （thrombophlebitis group）， 9 patients with normal venous tissue as control group. HE staining was performed to observe the distribution of vasa vasorum and detect the vasa vasorum density. Results The increasing vasa vasorums were observed in the adventitia and media， but few was observed in the intima in the varicose， recurrent， and thrombophlebitis groups. The distribution of vasa vasorum was in the adventitia in the control group. The vasa vasorum densities （/mm2） in the varicose， recurrent， and thrombophlebitis groups （5.65±1.45，6.20±1.73， and 5.94±1.63， respectively） were greater than those in the control group （2.87±0.54）， the difference wasstatistically significant （P＜0.05）， but there was no significant difference of the vasa vasorum density among the varicosevein， recurrent， and thrombophlebitis groups （P＞0.05）. Conclusion Change of vasa vasorum is an important pathol-gical change with the nosogenis of varicose vein of the lower extremity.
As a representative part of the oral system and masticatory robot system, the modeling method of the dental model is an important factor influencing the accuracy of the multi-body dynamic model. Taking the right first molars of the masticatory robot as the research object, an equivalent model, point-contact higher kinematic pair composed of v-shaped surface and sphere surface, was proposed. Firstly, the finite element method was used to analyze the occlusal dynamics of the original model in three static contact cases (intrusive contact, centric occlusion, and extrusive contact) and one dynamic chewing case, and the expected bite force was obtained. Secondly, the Hertz contact model was adopted to establish the analytical expression of the bite force of the equivalent model in three static contact cases. The normal vectors and contact stiffness in the expression were designed according to the expected bite force. Finally, the bite force performance of the equivalent model in three static contact cases and one dynamic chewing case was evaluated. The results showed that the equivalent model could achieve the equivalent bite force of 8 expected items in the static contact cases. Meanwhile, the bite force in the early and late stages of the dynamic chewing case coincides well with the original model. In the middle stage, a certain degree of impact is introduced, but it can be weakened by subsequent trajectory planning. The equivalent modeling scheme of the dental model proposed in this paper further improves the accuracy of the dynamic model of the multi-body system. It provides a new idea for the dynamic modeling of other complex human contacts.
ObjectiveTo investigate the expression of extracellular signalregulated kinase (ERK) and p38 mitogenactivated protein kinase （p38 MAPK） in autogenous vein grafts during vascular remodeling.MethodsAn autogenous vein graft model was established by transplanting the right jugular vein to infrarenal abdominal aorta in 80 Wistar rats. Vein graft samples were harvested 6 hours, 24 hours, 3 days, 7 days, 2 weeks, 4 weeks, 6 weeks and 8 weeks after surgery. Gene expression of ERK and p38 MAPK was measured by reverse transcriptionPCR. Western blot was used to detect the expression of protein products and phosphorylation protein products of ERK and p38 MAPK. Apoptosis of vascular smooth muscle cells (VSMCs) was determined by TUNEL. Proliferating cell nuclear antigen(PCNA) of VSMCs also was studied.ResultsThe expression of ERK1 mRNA and p38 MAPK mRNA increased considerably after surgery. ERK1 mRNA reached the peak on the 7th day 〔（33.2±14.2）%, P＜0.01〕, but p38 MAPK mRNA reached the peak on the second week after surgery 〔(58.8±26.2）%, P＜0.01〕. The expression of ERK1/2 detected by western blot reached the peak during 1 to 2 weeks and decreased gradually to normal level 6 weeks after surgery. The expression of p38 MAPK reached the peak during 2 to 4 weeks and decreased to 1/4 to 1/2fold 8 weeks after surgery. There was a positive relationship between ERK1 and PCNA(r=0.759 6，P＜0.01) and a positive relationship between p38 MAPK and apoptosis(r=0.892 2，P＜0.01). ConclusionActivation of MAPK system exists in autogenous vein grafts and it may become a new target for the therapy of stenosis after vein grafts.
Objective To evaluate the effect of smooth muscle cell transplantation on myocardial interstitial reconstruction shortly after myocardial infarction. Methods A total of 48 female Wister rats were randomly divided into two groups with the random number table, the control group (n=24) and the smooth muscle cell transplantation group (n=24). The left coronary artery was ligated to set up the myocardial infarction animal model. An amount of 05 ml phosphate buffered saline(PBS) containing 1×106 smooth muscle cells or 0.5 ml PBS without cells was injected into the injured myocardium immediately. By immunoblot and reverse transcriptionolymerase china reaction (RT-PCR), we observed the amount of protein and mRNA of matrix metalloproteinase2(MMP-2), matrix metalloproteinase-9(MMP-9) and tissue inhibitor of metalloprotease-3 (TIMP-3) in the myocardium of the rats. Results The transplanted smooth muscle cells survived well. Compared with the control group, myocardial TIMP3 mRNA (1.06±0.22 vs. 0.81±0.19, t=－2.358, P=0.033) and protein content (3.33±0.53 vs. 1.63±0.47, t=－6.802, Plt;0.001) were significantly increased in the transplantation group. Myocardial MMP-2, MMP-9 mRNA (0.49±0.12 vs. 1.16±0.18, t=8.453, Plt;0.001; 0.45±0.12 vs. 0.80±0.11, t=5.884, Plt;0.001) and protein content (3.98±1.08 vs. 6.05±0.91, t=4.139, P=0.001; 0.39±0.14 vs. 0.57±0.17, t=2.409, P=0.031) [CM(1585mm]were significantly reduced in the transplantation group compared with the control group. Conclusion transplanted smooth muscle cells can survive well in the infarction myocardium and can increase the amount of myocardial TIMP-3 mRNA and protein content and reduce myocardial MMP-2, MMP-9 mRNA and protein content, which is an effective way to prevent harmful cardiac remodeling.
ObjectiveTo explore the possibility that GREM1, a bone morphogenetic protein (BMP) antagonist, is a mechanical explanation for BMP signal suppression in congenital heart disease associated pulmonary arterial hypertension (CHD/PAH) patients.MethodsSystemic-to-pulmonary shunt induced PAH was surgically established in rats. At the postoperative 12th week, right heart catheterization and echocardiography evaluation were performed to evaluate hemodynamic indexes and morphology of right heart system. Right heart hypotrophy index and pulmonary vascular remodeling were evaluated. Changes of BMP signal pathway related proteins and GREM1 in lungs and plasma GREM1 concentration were detected. The effect of GREM1 on the proliferation and apoptosis of pulmonary arterial endothelial cells (PAECs) was also explored.ResultsThe hypertensive status was successfully reproduced in rats with systemic-to-pulmonary shunt model. BMP signal pathway was suppressed but GREM1 was up-regulated with no change in hypoxia inducible factor-1 in lungs exposed to systemic-to-pulmonary shunt, while this trend was reversed by systemic-to-pulmonary shunt correction (P<0.05). Immunohistochemical staining demonstrated enhanced staining of GREM1 in remodeled pulmonary arteries. In vitro experiments found that BMP signal was down-regulated but GREM1 expression and secretion were up-regulated in proliferative PAECs (P<0.05). Furthermore, BMP2 significantly inhibited PAECs proliferation and promoted PAECs apoptosis (P<0.05), which could be antagonized by GREM1. In addition, plasma level of GREM1 in rats with systemic-to-pulmonary shunt was also increased and positively correlated with pulmonary hemodynamic indexes.ConclusionSystemic-to-pulmonary shunt induces the up-regulation of GREM1 in lungs, which promotes pulmonary vascular remodeling via antagonizing BMP cascade. These results present a new mechanical explanation for BMP pathway suppression in lungs of CHD/PAH patients.
Atrial fibrillation(AF) is the most common disorder of cardiac rhythm. It has a high morbidity, mortality and disability, and serious impact on quality of life of patients. It is demonstrated that atrial remodeling which includes atrial electrical remodeling and structural remodeling,are the central contributors to the development and selfperpetuating of AF. However, The mechanisms that underlie the atrial remodeling process in AF have not yet been completely elucidated. New strategies for the prevention and termination of AF should build on our knowledge of the mechanisms of atrial remodeling. Medication for the reversal of atrial remodeling may be the new target for the treatment of AF. At present, drugs that target atrial remodeling have already obtained fruitful results in the experimental and clinical investigations. Now some recent advancements of this area is reviewed in this article.