Osteoporotic vertebral compression fracture (OVCF) can lead to lower back pain and may be even accompanied by scoliosis, neurological dysfunction and other complications, which will affect the daily activities and life quality of patients. Vertebral augmentation is an effective treatment method for OVCF, but it cannot correct unbalance of bone metabolism or improve the osteoporotic status, causing complications like lower back pain, limited spinal activities and vertebral refracture. The post-operative systematic and standardized rehabilitation treatments can improve curative effect and therapeutic efficacy of anti-osteoporosis, reduce risk of vertebral refracture, increase patient compliance and improve quality of life. Since there still lack relevant clinical treatment guidelines for postoperative rehabilitation treatments following vertebral augmentation for OVCF, the current treatments are varied with uneven therapeutic effect. In order to standardize the postoperative rehabilitation treatment, the Spine Trauma Group of the Orthopedic Branch of Chinese Medical Doctor Association organized relevant experts to refer to relevant literature and develop the "Guideline for postoperative rehabilitation treatment following vertebral augmentation for osteoporotic vertebral compression fracture (2022 version)" based on the clinical guidelines published by the American Academy of Orthopedic Surgeons (AAOS) as well as on the principles of scientificity, practicality and advancement. The guideline provided evidence-based recommendations on 10 important issues related to postoperative rehabilitation treatments of OVCF.

Newcastle disease virus-like particles (NDV VLPs) are composed of matrix protein (M) as the skeleton,with the insertion of hemagglutinin-neuraminidase and/or fusion protein.NDV VLPs are reported to be immunogenic and can induce specific humoral and cellular immune responses.However,its relationship with innate immunity remains elusive.Dendritic cells (DCs) are a group of specialized antigen presenting cells,which are crucial in connecting innate immunity and adaptive immunity.In this study,NDV VLPs and murine DCs were used to investigate the connection between NDV VLPs and innate immunity.The DC maturation induced by NDV VLPs (M+ HN) was evaluated.The results showed that NDV VLPs could be effectively taken up by DC and presented to naive T cells.NDV VLPs-induced DC significantly up-regulated the expression of MHC Ⅱ and costimulatory molecules on DC surface,and subsequently promoted the secretion of proinflammatory cytokines.This experiments also showed that different assembled NDV VLPs induced significant stimulating ability in cytokine levels.In summary,NDV VLPs can induce DC maturation,which gives insights to better understanding of VLPs-mediated innate immunity and provide information in selecting preferred NDV VLPs candidate.

Characteristic clinical manifestations of Newcastle disease include leukopenia and immunosuppression. Peripheral blood mononuclear cells (PBMCs) are the main targets of Newcastle disease virus (NDV) infection. To survey changes in proteomic expression in chicken PBMCs following NDV infection, PBMC proteins from 30 chickens were separated using two-dimensional electrophoresis (2-DE) and subjected to mass spectrometry analysis. Quantitative intensity analysis showed that the expression of 78 proteins increased more than two-fold. Thirty-five proteins exhibited consistent changes in expression and 13 were identified as unique proteins by matrix assisted laser desorption ionization-time of flight mass spectrometer/mass spectrometer including three that were down-regulated and 10 that were up-regulated. These proteins were sorted into five groups based on function: macromolecular biosynthesis, cytoskeleton organization, metabolism, stress responses, and signal transduction. Furthermore, Western blot analysis confirmed the down-regulation of integrin-linked kinase expression and up-regulation of lamin A production. These data provide insight into the in vivo response of target cells to NDV infection at the molecular level. Additionally, results from this study have helped elucidate the molecular pathogenesis of NDV and may facilitate the development of new antiviral therapies as well as innovative diagnostic methods.
Animals ; Avian Proteins/*genetics/metabolism ; *Chickens ; *Gene Expression Regulation ; Leukocytes, Mononuclear/enzymology/virology ; Newcastle Disease/*genetics/virology ; Newcastle disease virus/*physiology ; Poultry Diseases/*genetics/virology ; *Proteome ; Specific Pathogen-Free Organisms ; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization/veterinary ; Tandem Mass Spectrometry/veterinary

A plasmids of continuous expressing shRNAs targeting the NDV NA-1 Phosphoprotein (P) gene was designed.Virus titration,Real Time RT-PCR,CPE indicated that P-specific siRNA could inhibit virus replication at 36 h post-virus infection.In future studies,a combination of siRNAs targeting the NP and L gene may be used as a tool to study NDV replication and antiviral therapy.

Objective To evaluate the effects of inhaled nitric oxide in the early period after extracardiac total cavopulmonary connection (ETCPC). Methods 32 patients after ETCPC were evaluated,of them 16 patients (experimental group) were administered with inhaled nitric oxide in the early postoperative period. Another 16 patients were as control. The cardiac index (CI), pulmonary vascular resistance(PVR), respiratory index(RI), pulmonary-left atrium pressure gradient(PLG), duration of ventilation, intensive care time, hydrothorax drainage and hospital stay were recorded. Results In experimental group, after inhaled NO, RI decreased from 2.61?0.32 to 1.41?0.21 (t=2.35,P

Objective: To study blood distribution in extracardiac total cavopulmonary connection (ETCPC). Methods: To combine a bidirectional cavopulmonary anastomosis with a Gore-Tex extracardiac conduit interposition between the inferior vena cava and the main pulmonary artery, and to evaluate the changes of pulmonary blood distribution with SPECT in all surviving patients. Results: The cournts of pulmonary radionuclide was (313.7?40.1)?10 3 increased significantly after surgery (t=2.23, P

OBJECTIVETo study the changes of calcitonin gene-related peptide (CGRP) in patients who underwent total cavopulmonary connection (TCPC) and to assess the effects of non-pulsatile blood flow on the secretion function of the lung.

METHODSTwenty-six patients were divided into 2 groups: study group, 13 patients who underwent extracardiac TCPC, and control group, 13 patients who underwent definitive repair for ventricular septal or atrial septal defect. Blood samples for measurement of CGRP were obtained preoperatively, postoperatively or in the follow-up period. Cardiac index (CI) and pulmonary vascular resistance (PVR) were measured by cardiac catheter.

RESULTSThe plasma level of CGRP was significantly higher in the study group than in the control group. CGRP was negatively correlated with PVR (r = -0.99, t = 9.82, P < 0.05), and positively correlation with CI (r = 0.98, t = 6.95, P < 0.05).

CONCLUSIONSAfter total right heart bypass, the non-pulsatile blood flow in pulmonary circulation may stimulate the lung to secrete CGRP, leading to the decrease of PVR and improve early postoperative recovery.

Adolescent ; Adult ; Calcitonin Gene-Related Peptide ; secretion ; Child ; Child, Preschool ; Fontan Procedure ; Heart Defects, Congenital ; physiopathology ; surgery ; Humans ; Pulmonary Circulation ; Vascular Resistance

Objective　To investigate the mechanism for that insulin facilitates increase of glucose uptake. Methods　The expression of myocardial GLUT4 polypeptide was determined by semiquantitative immunoblotting. The expression of GLUT4 mRNA was determined by semiquantitative Northern blotting. Results　After infusing insulin for 8　hours，the　expression　of　GLUT4 mRNA and GLUT4 polypeptide was significantly higher in canine myocardium than in　those　found normal ones. The glucose uptake was upregulated at　the　same　time．Conclusions　Our findings suggest that insulin facilitates the expression of GLUT4 mRNA and GLUT4 polypeptide in canine hearts. Enhanced GLUT4 expression is one of the important molecular mechanism by which myocardial cells enhance glucose uptake by insulin stimulation.

AIM: To investigate the mechanism underlying insulin-stimulated increase in glucose uptake during low-flow myocardial ischemia. METHODS: The expression of myocardial GLUT1 polypeptide was determined by semiquantitative immunoblotting. The expression of GLUT1 mRNA was determined by semiquantitative Northern blotting. RESULTS: After infusing insulin during low- flow myocardial ischemia for 8 h，the expression of both GLUT1 mRNA and GLUT1 polypeptide was significantly higher in experimental myocardium than that in normal myocardium. The glucose uptake was upregulated at the same time in the exprimental myocardium. CONCLUSION: Insulin enhances the expression of GLUT1 mRNA and GLUT1 polypeptide in ischemic myocardial regions. GLUT1 expression may be an important mechanism by which myocardial cells enhance glucose uptake and metabolism during low-flow myocardial ischemia.

Objective: To investigate whether there is additi ve effects of hyperinsulinemia and ischemia on expression of canine myocardial G LUT4 gene in vivo. Methods: The expression of myocardial GLU T4 was determined by semiquantitative immunoblotting.The expression of GLUT4 mRN A was determined by semiquantitative Northern blotting. Results: Dramatic changes were seen in GLUT4 mRNA and GLUT4 expression in the ischemic hearts.After infusing insulin for 8 h,regional GLUT4 mRNA and GLUT4 levels in is chemic hearts were 2.5, 2.3-fold that of expression in normal hearts(P<0.01 ). Myocardial glucose uptake in ischemic hearts was increased by 4-fold when co mpared with normal hearts(P<0.01). Conclusion: There are not only additive effects of hyperinsulinemia and low-flow ischemia on canine myoc ardial GLUT4 mRNA and GLUT4 expression in vivo, but also increase of myocar dial glucose uptake. Enhanced GLUT4 expression may be an important protective m echanism by which myocardial cells enhance glucose uptake and metabolism during low-flow ischemia.