In order to identify whether the regeneration of costal cartilage is the basis of post-surgical repair of pectus excavatum and thoracic cage remodeling, 151 cases were followed up for 0.25 to 14 years. The main procedures in treatment were 3 steps: To curve the mental strut as a bow, to repair the perichondrium as a tube, and to persist in post-operative therapy. The results showed that regeneration of the costal cartilages appeared 3 months postoperatively in the cases treated by this method. It was concluded that a satisfactory thoracic cage could be remodeled by improving the technique of repairing pectus excavatum and persisting in postoperative therapy according to the regeneration regularity.
Objective To evaluate the left ventricular remodeling after valve replacement for valvular heart disease with giant left ventricle. Methods The clinical material of 92 patients with valvular heart disease and giant left ventricle after valve replacement was retrospectively reviewed. The results of ultrosonic cardial gram（UCG） and the changes of cardiac function before and after operation were compared. Results There was no operative death. The value of left ventricular end-diastolic dimension （LVEDD）, left ventricular end-systolic dimension （LVESD）, left atrial dimension （LAD）, left ventricular ejection fraction （LVEF）, left ventricular fractional shortening （LVFS）, stroke volume （SV） and cardiothoracic ratio in 2 weeks and 2 months after operation were more decreased than those before operation（P〈0. 05）. The value of LVEDD and LAD in 2 months after operation were much more decreased than those in 2 weeks after operation （P〈0. 05）. The cardiac function in early stage after operation was more decreased than that before operation,but the cases of cardiac functional class Ⅱ （38 cases, 41.3% ） in 2 months after operation was significantly more than those before operation （5 cases, 5.4 % ）. Conclusions The early effect of left ventricular remodeling is significant for valvular heart disease with giant left ventricle after valve replacement. The diameter of left ventricle and left atrial are significantly decreased after operation. The protection for cardiac function should be carefully taken in order to prevent the occurrence of complication after operation.
ObjectiveTo study the local vascular remodeling, inflammatory response, and their correlations following acute spinal cord injury (SCI) with different grades, and to assess the histological changes in SCI rats.MethodsOne hundred and sixteen adult female Sprague Dawley rats were randomly divided into 4 groups (n=29). The rats in sham group were received laminectomy only. A standard MASCIS spinal cord compactor was applied with drop height of 12.5, 25.0, or 50.0 mm to establish the mild, moderate, or severe SCI model, respectively. Quantitative rat endothelial cell antigen 1 (RECA1) and CD68 positive areas and the correlations were studied by double immunofluorescent (DIF) staining at 12 hours, 24 hours, 3 days, 7 days, and 28 days following SCI. Moreover, qualitative neurofilament-H (NF-H) and glial fibrillary acidic protein (GFAP) positive glial cells were studied by DIF staining at 28 days. ELISA was used to detect the levels of tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), and IL-6 in spinal cord homogenates at 12 hours, 24 hours, and 3 days, and the correlations between TNF-α, IL-1β, or IL-6 levels and microvascular density (RECA1) were accordingly studied. Moreover, the neural tissue integrity and neuron damage were assessed by HE staining at 12 hours, 24 hours, 3 days, 7 days, and 28 days, and Nissl’s staining at 28 days following SCI, respectively.ResultsDIF staining revealed that the ratio of RECA1 positive area was the highest in moderate group, higher in mild and severe groups, and the lowest in sham group with significant differences between groups (P<0.05). The ratio of CD68 positive area was the highest in severe group, higher in moderate and mild groups, and the lowest in sham group with significant differences between groups (P<0.05), except the comparisons between mild and moderate groups at 24 hours and 28 days after SCI (P>0.05). There was no significant correlation between the RECA1 and CD68 expressions in sham group at different time points (P>0.05). At 12 and 24 hours after SCI, the RECA1 and CD68 expressions in mild and moderate groups showed significant positive correlations (P<0.05), while no significant correlation was found in severe group (P>0.05). No significant correlations between the RECA1 and CD68 expressions was shown in all SCI groups at 3 days and in severe group at 7 days (P>0.05), while the negative correlations were shown in mild and moderate groups at 7 days, and in all SCI groups at 28 days (P<0.05). In mild, moderate, and severe groups, the axons became disrupted, shorter and thicker rods-like, or even merged blocks with increased injury, while the astrocytes decreased in number, unorganized and condensed in appearance. ELISA studies showed that TNF-α, IL-1β, and IL-6 levels in sham group were significantly lower than those in other 3 groups at different time points (P>0.05). The differences in TNF-α, IL-1β, and IL-6 levels between SCI groups at different time points were sinificant (P<0.05), except IL-1β levels between the mild and moderate groups at 12 hours (P>0.05). Three inflammatory factors were all significantly correlated with the microvascular density grades (P<0.05). Histological analysis indicated that the damage to spinal cord tissue structure correlated with the extent of SCI. In severe group, local hemorrhage, edema, and infiltration of inflammatory cells were found the most drastic, the grey/white matter boundary was disappeared concurrently with the formation of cavity and shortage of normal neurons.ConclusionIn the acute stage following mild or moderate SCI, progressively aggravated injury result in higher microvessel density and increased inflammation. However, at the SCI region, the relation between microvessel density and inflammation inverse with time in the different grades of SCI. Accordingly, the destruction of neural structures positively relate to the grades of SCI and severity of inflammation.
【Abstract】 Objective To discuss the role of leukocyte activation and inflammatory processes in the disease of chronic venous insufficiency （CVI）. Methods The relevant literatures about the role of leukocyte activation and inflammatory reaction in CVI were reviewed. Results The role of inflammatory reaction in occurrence and development of venous diseases has been studied a lot in recent years. It was found that the leukocyte activation and inflammatory reaction are involved in the structural remodeling of venous valves and walls, leading to valvular incompetence and formation of varicose veins. Conclusion Leukocyte activation and inflammatory processes take important roles in the occurrence and progression of CVI.
The stiffness of an ideal fracture internal fixation implant should have a time-varying performance, so that the fracture can generate reasonable mechanical stimulation at different healing stages, and biodegradable materials meet this performance. A topology optimization design method for composite structures of fracture internal fixation implants with time-varying stiffness is proposed, considering the time-dependent degradation process of materials. Using relative density and degradation residual rate to describe the distribution and degradation state of two materials with different degradation rates and elastic modulus, a coupled mathematical model of degradation simulation mechanical analysis was established. Biomaterial composite structures were designed based on variable density method to exhibit time-varying stiffness characteristics. Taking the bone plate used for the treatment of tibial fractures as an example, a composite structure bone plate with time-varying stiffness characteristics was designed using the proposed method. The optimization results showed that material 1 with high stiffness formed a columnar support structure, while material 2 with low stiffness was distributed at the degradation boundary and inside. Using a bone remodeling simulation model, the optimized bone plates were evaluated. After 11 months of remodeling, the average elastic modulus of callus using degradable time-varying stiffness plates, titanium alloy plates, and stainless steel plates were 8 634 MPa, 8 521 MPa, and 8 412 MPa, respectively, indicating that the use of degradable time-varying stiffness plates would result in better remodeling effects on the callus.
ObjectiveTo review the role and mechanism of protein factors in bone remodeling, and provides theoretical basis for further elucidating the pathogenesis and clinical treatment of bone-related diseases. MethodsThe relevant research results at home and abroad in recent years were extensively consulted, analyzed, and summarized. ResultsBone remodeling is an important physiological process to maintain bone homeostasis. Protein, as an important stimulator in bone remodeling, regulates the balance between bone resorption and bone formation. ConclusionAt present, the research on the mechanism of protein in bone remodeling is insufficient. Therefore, it is necessary to further study the specific time, process, and interaction network of protein in bone remodeling, and to confirm its mechanism in bone remodeling, so as to reveal and treat the pathogenesis of bone-related diseases.
Objective To investigate the effects of smoking intensity, duration and cessation on mRNA and protein expressions of matrix metalloproteinase-9 ( MMP-9) in tracheal epitheliumof rats, and the relationship between smoking or smoking cessation and airway remodeling in chronic obstructive pulmonary disease ( COPD) . Methods Forty Wistar rats were randomly divided into 5 groups, ie. a normal control group, a long termheavy smoking group, a short termheavy smoking group, a long termlight smoking group,and a smoking cessation group which was exposed to room air for 10 weeks after long term heavy smoking.The expressions of MMP-9 mRNA and protein in tracheal epithelium of rats were detected by in situ hybridization and munohistochemistry respectively. Results ( 1) The pathological changes of emphysema were observed in the lung tissue of every smoking rat, and were most sever in the long term heavy smoking group. ( 2) Compared with the normal control group [ ( 0. 88 ±0. 88) PU, ( 2. 80 ±1. 66) PU] , the expressions of MMP-9 mRNA and proteins in tracheal epithelium were remarkable elevated in the long term heavy smoking group [ ( 22. 01 ±2. 86) PU, ( 20. 81 ±2. 46) PU] , the short term heavy smoking group [ ( 14. 94 ±3. 46) PU, ( 13. 68 ±2. 00) PU] , the long term light smoking group [ ( 6. 92 ±2. 71) PU,( 8. 84 ±1. 80) PU] and the smoking cessation group [ ( 19. 00 ±3. 36) PU, ( 14. 82 ±1. 74) PU] ( P lt;0. 01) . Compared with the long term heavy smoking group, the expressions of MMP-9 in tracheal epithelium were decreased in other three smoking groups ( P lt; 0. 05) . Conclusions Smoking could increase the expression of MMP-9 in tracheal epithelium and cause trachea damage and remodeling with intensity and duration in rats. Smoking cessation could decrease the MMP-9 expression and alleviate trachea remodeling,suggesting its role in the prevention of COPD.
Objective To investigate surgical treatment and evaluate the curative effect in patients with moderate to severe ischemic mitral regurgitation (IMR). Methods The clinical data of the patients with coronary heart disease complicated with moderate to severe IMR who agreed to receive surgical treatment from June 2014 to June 2019 in our hospital were analyzed retrospectively. The patients were divided into two groups: a coronary artery bypass grafting (CABG) group and a CABG+mitral valve surgery (MVS) group. The preoperative and postoperative clinical data between the two groups were compared. Results Finally 105 patients were collected, including 75 males and 30 females, aged 40-79 (62.70±7.90) years. There were 34 patients in the CABG group, and 71 patients in the CABG+MVS group including 2 patients of mitral valvuloplasty and 29 patients of mitral valve replacement. Among the 105 patients, 5 died during the perioperative period and 2 died in 3 months after operation, all of whom were from the CABG+MVS group. There was no statistical difference in perioperative and postoperative 3-month mortality rate between the two groups (P=0.14). Eighty-seven patients were followed up in the medium and long term. There was no statistical difference in the degree of preoperative mitral insufficiency (MI) (P=0.59) and left atrium diameter (P=0.51) between the two groups, but the degree of postoperative MI in the CABG group was significantly higher than that in the CABG+MVS group (P<0.01). However, the left atrium diameter in the CABG group was significantly smaller than that in the CABG+MVS group (P<0.01). Paired analysis showed that systolic pulmonary artery pressure, left ventricular end-diastolic diameter, left ventricular end-systolic diameter, left ventricular ejection fraction and MI were significantly improved after operation (P<0.01); left atrium diameter was significantly improved after operation in the CABG group (P<0.01), but there was no statistical difference before and after operation in the CABG+MVS group (P=0.10). Conclusion For patients with moderate to severe IMR, CABG with mitral valve treatment can improve left ventricular remodeling, but can not significantly improve left atrial remodeling. Whether performing mitral valve treatment during CABG should be cautious. CABG alone is a safe and effective scheme for elderly patients with poor physical condition and low life expectancy.
The occurrence and development of myopia is closely related to scleral remodeling. Therefore, in order to effectively prevent and cure myopia, it is very important to clarify the mechanism of scleral remodeling. In recent years, Chinese scholars have found that endoplasmic reticulum stress can regulate the expression of apoptotic proteins through the inositol demand protein-1/X box binding protein-1 pathway in the unfolded protein response, thus it is involved in regulating the state of scleral fibroblasts under hypoxia and regulating the occurrence and development of scleral remodeling. At the same time, some studies have found that inhibiting and knocking out protein kinase RNA-like endoplasmic reticulum kinase and activated transcription factor 6 in endoplasmic reticulum stress can effectively inhibit the growth of ocular axis. This proves that endoplasmic reticulum stress plays an important role in the occurrence and development of scleral remodeling. However, the comprehensive analysis of endoplasmic reticulum stress and scleral remodeling has not been reported at home and abroad. In-depth analysis of the relationship between endoplasmic reticulum and scleral remodeling is of great significance for the follow-up analysis and study of the mechanism of scleral remodeling.
Abstract: Objective To observe the changes in morphology, structure, and ventricular function of infarct heart after bone marrow mononuclear cells (BMMNC) implantation. Methods Twenty-four dogs were divided into four groups with random number table, acute myocardial infarction (AM I) control group , AM I-BMMNC group , old myocardial infarct ion (OMI) control group and OM I-BMMNC group , 6 dogs each group. Autologous BMMNC were injected into infarct and peri-infarct myocardium fo r transplantation in AM I-BMMNC group and OM I-BMMNC group. The same volume of no-cells phosphate buffered solution (PBS) was injected into the myocardium in AM Icontrol group and OM I-control group. Before and at six weeks of cell t ransplantation, ult rasonic cardiography (UCG) were performed to observe the change of heart morphology and function, then the heart was harvested for morphological and histological study. Results U CG showed that left ventricular end diastolic dimension (LV EDD) , left ventricular end diastolic volume (LVEDV ) , the thickness of left ventricular postwall (LVPW ) in AM I-BMMNC group were significantly less than those in AM I-control group (32. 5±5. 1mm vs. 36. 6±3. 4mm , 46. 7±12. 1m l vs. 57. 5±10. 1m l, 6. 2±0. 6mm vs. 6. 9±0. 9mm; P lt; 0. 05). LVEDD, LVEDV , LVPW in OM I-BMMNC group were significantly less than those in OM I-control group (32. 8±4. 2 mm vs. 36. 8±4. 4mm , 48. 2±12. 9m l vs. 60.6±16.5m l, 7. 0±0. 4mm vs. 7. 3±0. 5mm; P lt; 0. 05). The value of eject fraction (EF) in OM I-BMMNC group were significantly higher than that in OM I-control group (53. 3% ±10. 3% vs. 44. 7%±10. 1% ). Compared with their control group in morphological measurement, the increase of infarct region thickness (7. 0 ± 1. 9mm vs. 5. 0 ±2.0mm , 6.0±0. 6mm vs. 4. 0±0. 5mm; P lt; 0. 05) and the reduction of infarct region length (25. 5±5. 2mm vs. 32. 1±612mm , 33. 6±5. 5mm vs. 39. 0±3. 2mm , P lt; 0. 05) were observed after transplantation in AM I-BMMNC group and OM I-BMMNC group, no ventricular aneurysm was found in AM I-BMMNC group, and the ratio between long axis and minor axis circumference of left ventricle increased in OM I-BMMNC group (0. 581±0. 013 vs. 0. 566±0.015; P lt; 0. 05). Both in AM I-BMMNC group and OM I-BMMNC group, fluorescence expressed in transplantation region was observed, the morphology of most nuclei with fluorescencew as irregular, and the differentiated cardiocyte with fluorescence was not found in myocardium after transplantation. The histological examination showed more neovascularization after transp lantation both in AMI and in OM I, and significant lymphocyte infiltration in AM I-BMMNC group. Conclusion BMMNC implantation into infarct myocardium both in AMI and OMI have a beneficial effect, which can attenuate deleterious ventricular remodeling in morphology and st ructure, and improve neovascularization in histology, and improve the heart function.