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.
Aortic aneurysm and dissection are critical cardiovascular diseases that threaten human life and health seriously. No pharmacological treatment can effectively prevent disease progression. The imbalance of aortic wall cells and non-cellular components leads to structural or functional degeneration of the aorta, which is a prerequisite for disease occurrence. As the important non-cellular component, extracellular matrix (ECM) is crucial to maintain the aortic structure, function, and homeostasis. Abnormal production of elastin and collagen, destruction of cross-linking between elastic fibers and collagen fibers, and the imbalance of metalloproteinase and inhibitors leads to excessive degradation of ECM proteins, all of which have destroyed the structure and function of aorta. It will provide more ideas for disease prevention and treatment by learning ECM proteins and their metabolic mechanism. Here, we focus on the ECM proteins that have been reported to be involved in aortic aneurysm and dissection, and discuss the regulatory mechanism of metalloproteinase and inhibitors.
Astronauts who are exposed to weightless environment in long-term spaceflight might encounter bone density and mass loss for the mechanical stimulus is smaller than normal value. This study built a three dimensional model of human femur to simulate the remodeling process of human femur during bed rest experiment based on finite element analysis (FEA). The remodeling parameters of this finite element model was validated after comparing experimental and numerical results. Then, the remodeling process of human femur in weightless environment was simulated, and the remodeling function of time was derived. The loading magnitude and loading cycle on human femur during weightless environment were increased to simulate the exercise against bone loss. Simulation results showed that increasing loading magnitude is more effective in diminishing bone loss than increasing loading cycles, which demonstrated that exercise of certain intensity could help resist bone loss during long-term spaceflight. At the end, this study simulated the bone recovery process after spaceflight. It was found that the bone absorption rate is larger than bone formation rate. We advise that astronauts should take exercise during spaceflight to resist bone loss.
Objective To assess the clinical efficacy of endovascular treatment in the second stage for patients with progression to local or full-length dissection-like changes at the distal aorta following initial surgery for aortic intramural hematoma. Methods Between July 2020 and December 2022, patients with aortic intramural hematoma were treated initially for proximal lesions. During follow-up, if the distal aortic hematoma was not resorbed and entry tears were identified with progression to local or full-length dissection-like changes and possible focal contrast enhancement, and the patients undergoing a second-stage stent intervention were retrospectively collected. Initial surgeries included total aortic arch replacement or thoracic endovascular aortic repair (TEVAR) targeting the proximal entry tear. In the secondary stage, stents were strategically placed in three delineated regions of the distal aorta to seal the entry tears, promote hematoma resorption, and induce thrombosis of the false lumen. Results A total of 18 patients were collected, including 15 males and 3 females with a mean age of 53.5±10.6 years, ranging from 39 to 76 years. All patients achieved procedural success, yielding a technical success rate of 100%. Intraoperative and postoperative imaging confirmed effective sealing of the distal entry tears without stent leakage, visceral branch stenosis, or occlusion, and there were no serious complications such as perioperative cerebral infarction, paraplegia, or organ ischemia. Follow-up assessments showed complete thrombosis and disappearance of the false lumen in all patients. Conclusion In patients with unresolved entry tears and dissection-like changes post-initial surgery for aortic intramural hematoma, secondary stent placement effectively seals these tears, promotes thrombosis and resorption of the hematoma, and improves endovascular remodeling of the aorta, demonstrating favorable short- to medium-term outcomes.
ObjectiveTo investigate the effect of distal tears on postoperative aortic remodeling after Thoracic Endovascular Aortic Repair (TEVAR) for the patients with subacute stage of Stanford type B aortic dissection.MethodsForty three cases with Stanford type B aortic dissection, admitted in Anhui Provincial Hospital from July 2011 to April 2015, who underwent TEVAR to repair the proximal aortic entrance tear, after which the blood reflex from distal tears were still observed were analyzed retrospectively. According to the number of heart volume required to fill the two groups, group A (≤2 heart rate) group B （>2 heart rate）, We then assessed the changes of the true and false lumen area and analyzed the effects of direction of blood flow and the number of heart rate to fill the false lumen on formation of false lumen thrombosis in the period of 3–24 months.ResultsAll the stents were successful implanted. There was a statistically significant difference in lumen area between the two groups before and after surgery, and univariate analysis showed that the direction of distal rupture of blood flow into the false lumen had no effect on postoperative aortic remodeling (P<0.05), but postoperative hypertension (≥140/90 mmHg) slows down the formation of false lumen thrombosis.ConclusionPatients had entrance tear in the distal of aortic, still broken and faster flow after TEVAR stent-graft implantation in the proximal closed entrance tear. Blood pressure should be strictly controlled and close follow-up also needed, meanwhile, the distal entrances can be closed the same period if there is a faster flow from them.
Survivors from myocardial infarction (MI) eventually develop heart failure due to the post-infarct ventricular remodeling which could not be suppressed by existing treatments. Currently, coronary heart disease has become the major cause of heart failure instead of rheumatic heart disease in China. For this reason, seeking effective treatment to prevent post-infarct ventricular remodeling is urgent. Intramyocardial injection of hydrogels as a new strategy for MI treatment has made great progress recently. This review discusses the principle, present status, mechanisms and prospects of injectable hydrogel therapies for MI.
This study demonstrates that nerve growth factor (NGF) plays a protective role in myocardial infarction and early reperfusion by reducing the myocardial cell apoptosis and by improving ventricular remodeling and seeks to assess the effects and mechanisms of NGF on late reperfusion after myocardial infarction. The models of late reperfusion were established by ligating the left main coronary artery and then cutting the suture 2 hours after coronary artery ligation. The rats in NGF treatment group were injected 10μL Ad-NGF (by constructing the adenovirus vector Ad-NGF containing NGF gene) at four locations around infarction. The rats in adenoviral vector (Adv) group were injected 10μL adenoviral cector as the NGF group. The late reperfusion group and the sham group were given normal saline as above, and the sham group underwent thracotomy without coronary ligation. On the 3rd, 7th, 14th and 28th day after operation, we investigated the role of NGF on late reperfusion by recording cardiac structure and function with echocardiography, by examining the expression of NGF andⅧfactor with immunohistochemical method, and by evaluating the myocardial cell apoptosis with terminal dUTP nick end-labeling method (TUNEL). We found that the NGF group had higher expression of NGF protein (P < 0.01) and lower apoptosis index (AI) (P < 0.01 or P < 0.05) compared to the late reperfusion group and Adv group on all time points. The NGF group had remarkably higher level of neovascularization compared to the late reperfusion group on the 14th day (P < 0.01) and the 28th day (P < 0.05). The NGF group also had higher LVEF and FS levels compared to the late reperfusion group on the 14th day (P=0.006, P=0.006) and on the 28th day (P=0.000, P=0.000). Whereas the NGF group had lower LVEDD, LVESD (P=0.038, P=0.000) and lower LVEDV, LVESV (P=0.001, P=0.000) on the 28th day compared to late reperfusion group. In this experiment, the NGF gene carried by adenovirus vector had been trans-fected and obviously increased the expression of NGF protein in NGF group. NGF may help postpone the myocardial remodeling and improve the heart function by promoting the myocardial neovascularization and inhibiting myocardial apoptosis.
Bone remodeling requires an intimate cross-talk between osteoclasts and osteoblasts and is tightly coordinated with regulatory proteins that interact through complex autocrine/paracrine processes. Osteocytes, bone lining cells, osteomacs and vascular endothelial cells also regulate bone remodeling in the basic multicellular unit (BMU) via cell signaling networks of ligand-receptor complexes. In addition, through secreted and membrane-bound factors in the bone microenvironment, T and B lymphocytes mediate bone homeostasis for osteoimmunology. Osteoporosis and other bone diseases occur because multicellular communication within the BMU is disrupted. This review focuses on the roles of the cells in the BMU and the interaction between these cells and the factors involved in regulating bone remodeling at the cellular level. Understanding the process of bone remodeling and related genes could help us to lay the foundation for drug development against bone diseases.
ObjectiveTo investigate the effects of icariin (ICA) on serum bone turnover markers expressions and histological changes of cartilage and subchondral bone in mouse osteoarthritis (OA) model.MethodsEighty 8-week-old male C57BL/6J mouse were randomly divided into 8 groups (n=10). The OA model was established by anterior cruciate ligament transaction (ACLT). Group A: sham operation/early-stage normal saline administration; group B: sham operation/early-stage ICA administration; group C: ACLT/early-stage normal saline administration; group D: ACLT/early-stage ICA administration; group E: sham operation/late-stage normal saline administration; group F: sham operation/late-stage ICA administration; group G: ACLT/late-stage normal saline administration; group H: ACLT/late-stage ICA administration. Each animal received either ACLT or simply opening joint capsule, respectively. For groups B and D, ICA was given by gavage [10 mg/(kg·day)] on the first day after ACLT. For groups F and H, ICA was given with the same volume at 4 weeks after operation. The blood serum of the mouse was collected and prepared at 8 weeks after operation. Serum bone turnover markers and cytokines, including C-telopeptide of type I collagen (CTX), osteocalcin (OC), interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), and IL-1β, were measured by ELISA. Tissue samples from the knee were stained by alcian blue/hematoxylin & orange G (AB/H&OG). Histological changes of cartilage and subchondral bone were observed and evaluated by Osteoarthritis Research Society International (OARSI) scoring system.ResultsComparison between each group with early-stage administration (groups A, B, C, and D): Compared with groups A and B, the levels of CTX and OC in group C were significantly reduced (P<0.05); the levels of IL-6, TNF-α, and IL-1β and OARSI score was significantly increased (P<0.05). Compared with group C, the levels of CTX and OC in group D were significantly increased (P<0.05); the level of IL-6 was significantly reduced (P<0.05); the levels of TNF-α and IL-1β were not changed (P>0.05), and OARSI score was significantly reduced (P<0.05). Histological observation showed that the tibial cartilage loss was significantly improved. Comparison between each group with late-stage administration (groups E, F, G, and H): Compared with groups E and F, the levels of CTX and OC in group G were significantly reduced (P<0.05); the levels of IL-6, TNF-α, and IL-1β and OARSI score were significantly increased (P<0.05). Compared with group G, the level of CTX in group H were increased (P<0.05); the levels of OC, IL-6, TNF-α, and IL-1β and OARSI score were not changed (P>0.05). Histological observation showed that the tibial cartilage loss had no changes after late-stage ICA administration.ConclusionICA plays protective effects on subchondral bone, hyaline, and calcified cartilage. Meanwhile, ICA can improve bone remodeling in subchondral bone of OA to some extent. The consistent changes of serum bone markers and pathological morphology suggest that early intervention of ICA on OA is more effective.
ObjectiveTo observe the effect of metformin on airway remodeling in asthma and its possible mechanism.MethodsTwenty-eight B/N rats were randomly divided into control group, asthma group, metformin intervention group and rapamycin intervention group. After that, the asthma model was established and intervened with metformin and rapamycin. The airway resistance and airway reactivity were measured 48 hours after the last challenge, and then the lung tissue samples were collected. Histopathological examination was used to observe airway inflammatory cell infiltration, goblet cell proliferation, airway wall fibrosis and remodeling, as well as airway smooth muscle proliferation. The expression of AMPK/mTOR pathway related proteins was detected by Western blot.ResultsCompared with the asthma group, metformin and rapamycin significantly reduced the airway responsiveness induced by high concentration of acetylcholine (P<0.05), reduced the infiltration of inflammatory cells in lung tissue and the changes of airway wall structure (P<0.05), reduced goblet cell proliferation in airway epithelium, collagen fiber deposition in lung tissue and bronchial smooth muscle hyperplasia (P<0.05). Further studies showed that the effects of metformin and rapamycin were related to AMPK/mTOR pathway. Compared with the asthma group, metformin and rapamycin could significantly reduce the expression of p-mTOR, p-p70s6k1 and SKP2, while p21 protein expression was significantly increased (P<0.05). In addition, metformin and rapamycin had similar effects (P>0.05).ConclusionMetformin can alleviate airway hyperresponsiveness and airway remodeling by activating AMPK and then inhibiting mTOR pathway, which may be a potential drug for treating asthma and preventing airway remodeling.