Hongguang Xu

The role of preoperative pulmonary function tests in the surgical treatment of scoliosis.

Study Design. A retrospective study on the correlation between preoperative pulmonary function tests, preoperative pulmonary symptoms, and postoperative pulmonary complications. Objective. To evaluate the incidence of immediate postoperative pulmonary complications and their correlation to pulmonary function tests, preoperative pulmonary symptoms, and surgical approaches. Summary of Background Data. The pulmonary function of patients with scoliosis is likely to be abnormal, whereas surgical procedures may lead to further deterioration and postoperative pulmonary complications. Evaluation of the pulmonary symptoms and pulmonary function before surgery is helpful to predict and avoid postoperative pulmonary complications by selecting the appropriate surgical approach. Methods. This study reviewed 298 scoliosis patients (107 male, 191 female) who underwent anterior and/or posterior operation. The mean age of the patients was 16.4 years (range 6–62 years). The average coronal Cobb angle was 73.26° (range 45–141°). Preoperative pulmonary function tests of 115 cases were normal, whereas the other 183 cases were abnormal. Seventeen cases had preoperative pulmonary symptoms and 3 of them had normal preoperative pulmonary function tests. Seventy-nine cases received transthoracic surgery, and 19 cases had postoperative pulmonary complications, including postoperative ventilation support in 6 cases, atelectasis in 4 cases, hydrothorax in 2 cases, pneumothorax in 3 cases, pneumonia in 3 cases, and hypoxemia in 1 case. Of these 19 patients, 12 patients received anterior transthoracic procedure. When the patients with abnormal pulmonary function tests were divided into 3 groups: 1) 60% ≤ forced vital capacity ratio < 80%; 2) 40% ≤ forced vital capacity ratio < 60%; and 3) forced vital capacity ratio < 40%, the incidence of postoperative pulmonary complications were 2.72% (3 out of 110), 7.40% (4 out of 54) and 31.60% (6 out of 19), respectively. Results. There was significant correlation between abnormal preoperative pulmonary function tests and preoperative pulmonary symptoms (P = 0.0086). No significant correlation was found between preoperative pulmonary symptoms and postoperative pulmonary complications (P = 0.5164). There was a trend that the postoperative complications increased with the deterioration of pulmonary function. The correlation between postoperative pulmonary complications and the surgical approach was statistically significant (P = 0.0000); the incidence of postoperative pulmonary complication of transthoracic procedure was 18 times as that of posterior approach. No significant difference was noted regarding ages, preoperative coronal Cobb angles, and preoperative pulmonary function between these 2 groups. There was no significant correlation between preoperative pulmonary symptoms and postoperative complications. Conclusions. The incidence of postoperative pulmonary complications increased with the deterioration of pulmonary function tests. The posterior procedure had a very low incidence of postoperative pulmonary complications, but a transthoracic procedure increased the complications significantly. Preoperative pulmonary symptoms usually predicted abnormal results of pulmonary function tests but had no correlation with postoperative pulmonary complication.

Apoptotic effects of curcumin on human osteosarcoma U2OS cells

Objective:  Curcumin, an active ingredient derived from the rhizome of the plant, Curcuma longa, has antioxidant, anti‐inflammatory and anti‐cancer activities. The aims of this study were to examine whether curcumin can induce apoptosis in an osteosarcoma cell line.

Intermittent Cyclic Mechanical Tension-Induced Calcification and Downregulation of ankh Gene Expression of End Plate Chondrocytes

Study Design. Intermittent Cyclic Mechanical Tension (ICMT) was applied to end plate chondrocytes by using an FX-4000T Flexercell Tension Plus unit (Flexcell International Corporation, Hillsborough, NC). Changes of end plate chondrocytes were observed after ICMT stimulation. Objective. To investigate the relationship between mechanical stimulation and calcification of end plate chondrocytes. Summary of Background Data. Previous study showed that end plate calcification was related to mechanical stress, but there was no clear evidence to indicate whether or not mechanical stimulation could induce calcification of end plate chondrocytes in vitro. Methods. Rat end plate chondrocytes were cultured and ICMT (strain at 0.5 Hz sinusoidal curve at 10% elongation) was applied for 25 days, 4 hours a day and continued to culture for 5 days. End plate chondrocytes were incubated for 12 hours in the presence or absence of 10 ng/mL of transforming growth factor-&bgr;1 (TGF-&bgr;1) (prepared from a stock solution at 10 &mgr;g/mL in 2 mM citric acid containing 2 mg/mL bovine serum albumin) in MEM/F-12 containing a final concentration of 1% FCS. End plate chondrocytes calcification was stained by alizarin red S (AR-S). End plate chondrocytes viability was examined by LIVE/DEAD viability/cytotoxicity kit (Invitrogen, Carlsbad, CA). Related gene expression was examined by reverse transcription-polymerase chain reaction and Western blot. Results. LIVE/DEAD assay verified that the nonloading (NC) group and the ICMT group end plate chondrocytes remained adherent, with no change in viability after the application of ICMT. Alizarin red staining showed that ICMT induced the calcification of end plate chondrocytes. Real-time reverse transcription-polymerase chain reaction showed that mRNA expression of endogenous TGF-&bgr;1 decreased and mRNA expression of type I, type X, osteocalcin and osteopontin increased after ICMT. The ankh gene expression of both mRNA and protein levels decreased in the ICMT stimulation. The ankh gene expression of both mRNA and protein levels increased in TGF-&bgr;1 stimulation. Compared with NC group, the alkaline phosphatase activities significantly increased in ICMT group. Conclusion. Our results directly showed that ICMT induced the calcification and downregulation of ankh gene expression of end plate chondrocytes, which may be caused by the endogenous TGF-&bgr;1.

Continuous cyclic mechanical tension increases ank expression in endplate chondrocytes through the TGF-β1 and p38 pathway.

The normal ANK protein has a strong influence on anti-calcification. It is known that TGF-β1 is also able to induce extracellular inorganic pyrophosphate (ePPi) elaboration via the TGF-β1-induced ank gene expression and the mitogen-activated protein kinase (MAPK) signaling acts as a downstream effector of TGF-β1. We hypothesized that the expression of the ank gene is regulated by mechanics through TGF-β1-p38 pathway. In this study, we investigated the mechanism of short-time mechanical tension-induced ank gene expression. We found that the continuous cyclic mechanical tension (CCMT) increased the ank gene expression in the endplate chondrocytes, and there was an increase in the TGF-β1 expression after CCMT stimulation. The ank gene expression significantly increased when treated by TGF-β1 in a dose-dependent manner and decreased when treated by SB431542 (ALK inhibitor) in a dose-dependent manner. Our study results indicate that CCMT-induced ank gene expressions may be regulated by TGF-β1 and p38 MAPK pathway.

Intermittent Cyclic Mechanical Tension-induced Down-regulation of Ectonucleotide Pyrophosphatase Phosphodiesterase 1 Gene Expression is Mainly Dependent on TGF-β1 in End-plate Chondrocytes

To investigate the relationship between ectonucleotide pyrophosphatase phosphodiesterase‐1(ENPP‐1) expression and transforming growth factor beta 1 (TGF‐β1) of end‐plate chondrocytes after stimulation with intermittent cyclic mechanical tension (ICMT) by using an FX‐4000T Flexercell Tension Plus unit.

Intermittent cyclic mechanical tension promotes endplate cartilage degeneration via canonical Wnt signaling pathway and E-cadherin/β-catenin complex cross-talk

OBJECTIVE This study aimed to investigate the role of the Wnt/β-catenin signaling pathway and E-cadherin/β-catenin complex in intermittent cyclic mechanical tension (ICMT)-induced endplate cartilage degeneration. DESIGN β-Catenin expression was measured in disc samples obtained from patients with disc degeneration and those with cervical vertebrae fracture or dislocation. Histological staining was performed to examine the disc tissue morphology and extracellular matrix after application of ICMT in vitro and in vivo. Multiple strategies were employed to examine activation of Wnt/β-catenin signaling after ICMT application in vivo and in vitro. Co-immunoprecipitation was performed to examine the interaction between E-cadherin and β-catenin. Pathway-specific inhibitors and an E-cadherin expression plasmid were used to regulate Wnt/β-catenin signaling and E-cadherin expression. RESULTS β-Catenin protein expression was elevated significantly, whereas cartilaginous genes were down-regulated in endplate cartilage samples obtained from patients with disc degeneration. ICMT loading led to Wnt/β-catenin signaling activation and the loss of the chondrogenic phenotype of endplate chondrocytes in both an in vivo rabbit model and in vitro endplate chondrocyte culture system. Inhibition of Wnt/β-catenin signaling suppressed the decrease in ICMT-induced cartilaginous gene expression. Furthermore, E-cadherin expression was inhibited by ICMT stimulation, resulting in a decrease in the interaction between E-cadherin and β-catenin proteins. Over-expression of E-cadherin rescued the cartilaginous gene expression by enhancing the interaction between E-cadherin and β-catenin proteins. CONCLUSIONS ICMT promotes endplate cartilage degeneration via activation of Wnt/β-catenin signaling and suppression of physical protein-protein interactions between E-cadherin and β-catenin.

Investigating conversion of endplate chondrocytes induced by intermittent cyclic mechanical unconfined compression in three-dimensional cultures.

Mechanical stimulation is known to regulate the calcification of endplate chondrocytes. The Ank protein has a strong influence on anti-calcification by transports intracellular inorganic pyrophosphate (PPi) to the extracellular matrix. It is known that TGF-β1 is able to induce Ank gene expression and protect chondrocyte calcification. Intermittent cyclic mechanical tension (ICMT) could induce calcification of endplate chondrocytes by decrease the expression of Ank gene. In this study, we investigated the relation of intermittent cyclic mechanical unconfined compression (ICMC) and Ank gene expression. We found that ICMC decreased the Ank gene expression in the endplate chondrocytes, and there was an decreased in the TGF-β1 expression after ICMC stimulation. The Ank gene expression significantly increased when treated by transforming growth factor alpha 1 (TGF-β1) in a dose-dependent manner and decreased when treated by SB431542 (ALK inhibitor) in a dose-dependent manner. Our results implicate that ICMC-induced downregulation of Ank gene expression may be regulated by TGF-β1 in end-plate chondrocytes.

Modified unilateral transpedicular percutaneous vertebroplasty for treatment of osteoporotic vertebral compression fractures

Objective:  To comparatively assess the clinical outcome of modified unilateral percutaneous vertebroplasty for the treatment of osteoporotic vertebral compression fractures.

Imaging study of wedge changes in the vertebral bodies and intervertebral discs in adolescent idiopathic scoliosis

Objective:  To observe wedge changes in the vertebral bodies and intervertebral discs in progressive adolescent idiopathic scoliosis before and after conservative treatment with braces, and to explore the correlation between wedge changes in the vertebral bodies or intervertebral discs and scoliosis curves.

P120‐catenin mediates intermittent cyclic mechanical tension‐induced inflammation in chondrocytes

To study the role of the nuclear factor (NF)‐κB signaling pathway and P120‐catenin in the inflammatory effects of intermittent cyclic mechanical tension (ICMT) on endplate chondrocytes. Inflammatory reactions of endplate chondrocyte were measured by real‐time reverse transcription‐polymerase chain reaction, enzyme‐linked immunosorbent assays, a dual‐luciferase reporter assay system, immunofluorescence, and Western blot analysis. ICMT loading led to inflammatory reactions of endplate chondrocytes in both the rabbit endplate cartilage model and rat endplate chondrocytes in vitro. Inhibition of NF‐κB signaling significantly ameliorated the inflammation induced by ICMT in endplate chondrocytes. Moreover, the expression of P120‐catenin was decreased by ICMT. However, over‐expression of P120‐catenin suppressed NF‐κB signaling and reversed the inflammatory effects. P120‐catenin prevents endplate chondrocytes from undergoing ICMT‐mediated inflammation by suppressing the expression of NF‐κB. J. Cell. Biochem. 118: 4508–4516, 2017.