[Therapeutic mechanism of basic fibroblast growth factor on spinal cord injury in rats based on the Notch/signal transducer and activator of transcription 3 signaling pathway].

Objective: To explore the therapeutic effect of basic fibroblast growth factor (bFGF) on spinal cord injury (SCI) in rats and the influence of Notch/signal transducer and activator of transcription 3 (STAT3) signaling pathway. Methods: A total of 40 10-week-old male Sprague Dawley (SD) rats were selected to establish T 10-segment SCI model by a free falling object. Among them, 32 successful models were randomly divided into model group and bFGF group, with 16 in each group. Another 16 SD rats were selected as sham-operation group, with only T 10 processes, dura mater, and spinal cord exposed. After modeling, the rats in bFGF group were intraperitoneally injected with 100 µg/kg bFGF (once a day for 28 days), and the rats in model group and sham-operation group were injected with normal saline in the same way. The survival of rats in each group were observed after modeling. Basso-Beattie-Bresnahan (BBB) scores were performed before modeling and at immediate, 14 days, and 28 days after modeling to evaluate the functional recovery of hind limbs. Then, the spinal cord tissue at the site of injury was taken at 28 days and stained with HE, Nissl, and propidium iodide (PI) to observe the pathological changes, neuronal survival (number of Nissl bodies) and apoptosis (number of PI red stained cells) of the spinal cord tissue; immunohistochemical staining and ELISA were used to detect the levels of astrocyte activation markers [glial fibrillary acidic protein (GFAP)] and inflammatory factors [interleukin 1ß (IL-1ß), tumor necrosis factor α (TNF-α), interferon γ (IFN-γ)] in tissues, respectively. Western blot was used to detect the expressions of Notch/STAT3 signaling pathway related proteins [Notch, STAT3, phosphoryl-STAT3 (p-STAT3), bone morphogenetic protein 2 (BMP-2)] in tissues. Results: All rats survived until the experiment was completed. At immediate after modeling, the BBB scores in model group and bFGF group significantly decreased when compared to sham-operation group ( P<0.05). At 14 and 28 days after modeling, the BBB scores in model group significantly decreased when compared to sham-operation group ( P<0.05); the bFGF group showed an increase compared to model group ( P<0.05). Compared with before modeling, the BBB scores of model group and bFGF group decreased at immediate after modeling, and gradually increased at 14 and 28 days, the differences between different time points were significant ( P<0.05). The structure of spinal cord tissue in sham-operation group was normal; in model group, there were more necrotic lesions in the spinal cord tissue and fewer Nissl bodies with normal structures; the number of necrotic lesions in the spinal cord tissue of the bFGF group significantly reduced compared to the model group, and some normally structured Nissl bodies were visible. Compared with sham-operation group, the number of Nissl bodies in spinal cord tissue significantly decreased, the number of PI red stained cells, GFAP, IL-1ß, TNF-α, IFN-γ, Notch, p-STAT3 /STAT3, BMP-2 protein expression levels significantly increased in model group ( P<0.05). The above indexes in bFGF group significantly improved when compared with model group ( P<0.05). Conclusion: bFGF can improve motor function and pathological injury repair of spinal cord tissue in SCI rats, improve neuronal survival, and inhibit neuronal apoptosis, excessive activation of astrocytes in spinal cord tissue and inflammatory response, the mechanism of which may be related to the decreased activity of Notch/STAT3 signaling pathway.

Mild Hypothermia Protects Brain Injury After Intracerebral Hemorrhage in Mice Via Enhancing the Nrdp1/MyD88 Signaling Pathway.

BACKGROUND: Mild hypothermia has been identified to reduce brain injury following intracerebral hemorrhage (ICH) by protecting neuron cells through several pathways. However, the role of hypothermia in brain function following ICH and the related mechanisms have not been well identified. Ubiquitination-mediated inflammation plays important roles in the pathogenesis of immune diseases. The experiment analyzed anti-inflammatory effects of mild hypothermia following ICH. METHODS: The model of ICH was induced by injecting autologous blood. Neuregulin receptor degradation protein-1 (Nrdp1) and downstream molecule were analyzed. In addition, brain inflammatory response, brain edema, and neurological functions of ICH mice were also assessed. RESULTS: We found that mild hypothermia attenuated proinflammatory factors production after ICH. Mild hypothermia significantly inhibited BBB injury, water content, and neurological damage following ICH in vivo. Moreover, mild hypothermia also increased Nrdp1/MyD88 levels and thus affect neuronal apoptosis and inflammation. CONCLUSIONS: Taken together, these results suggest that mild hypothermia can attenuate the neuroinflammatory response and neuronal apoptosis after ICH through the regulation of the Nrdp1 levels.

Canonical Wnt signaling works downstream of iron overload to prevent ferroptosis from damaging osteoblast differentiation.

Excessive iron has emerged in a large population of patients suffering from degenerative or hematological diseases with a common outcome, osteoporosis. However, its underlying mechanism remains to be clarified in order to formulate effective prevention and intervention against the loss of bone-forming osteoblasts. We show herein that increased intracellular iron by ferric ammonium citrate (FAC) mimicking the so-called non-transferrin bound iron concentrations leads to ferroptosis and impaired osteoblast differentiation. FAC upregulates the expression of Trfr and DMT1 genes to increase iron uptake, accumulating intracellular labile ferrous iron for iron overload status. Then, the excessive ferrous iron generates reactive oxygen species (ROS) and lipid peroxidation products (LPO), causing ferroptosis with its typical mitochondrial morphological changes, such as shrinkaged and condensed membrane with diminution and loss of crista and outer membrane rupture. We further examined that ferroptosis is the main cause responsible for FAC-disrupted osteoblast differentiation, although apoptosis and senescence are concurrently induced as well. Mechanistically, we revealed that iron dose-dependently down-regulates the expression of Wnt target genes and inhibits the transcription of Wnt reporter TopFlash construct, so as to inhibit the canonical Wnt signaling. Wnt agonist, ferroptosis inhibitor, or antioxidant melatonin reverses iron-inhibited canonical Wnt signaling to restore osteoblast differentiation by reducing ROS and LPO production to prevent ferroptosis notably without reducing iron overload. This study proposes a working model against excessive iron-induced osteoporosis: iron chelator deferoxamine or the above three drugs prevent ferroptosis, restore traditional Wnt signaling to maintain osteoblast differentiation no matter whether iron overload is removed or not. Additionally, iron chelator should be used to a suitable extent because iron itself is necessary for osteogenic differentiation.

Unicondylar knee replacement versus total knee replacement for the treatment of medial knee osteoarthritis: a systematic review and meta-analysis.

BACKGROUND: Since the optimal surgery for isolated medial knee osteoarthritis (OA) is unclear, this study aimed at comparing the effectiveness of unicondylar knee replacement (UKR) with total knee replacement (TKR) for simple medial knee OA. METHODS: Literature searches of PubMed, Embase, Web of Science, and the Cochrane Library were searched up to 1th April 2020. Only studies comparing UKR with TKR for isolated medial knee OA were included. Data collection and extraction, quality assessment, and data analyses were performed according to the Cochrane standards. RESULTS: A total of 13 articles with 1888 patients were included, among which, 944 and 944 underwent UKR and TKR, respectively. The analyzed postoperative outcomes were mostly within 5 years of follow-up. The meta-analysis showed that UKR improved knee general function (P < 0.00001) and health (P = 0.02), moreover, reduced post-operative pain (P = 0.01) and complications (P < 0.05) more than TKR. There were no significant differences in postoperative revision (P = 0.252), high-activity arthroplasty score (HAAS) (P = 0.307) and Oxford knee score (OKS) (P = 0.15) between the two techniques. CONCLUSIONS: The patients of UKR could achieve better clinical results than that of TKR, moreover, there were negligible differences between the two techniques in postoperative revision in the early and mid-term follow-up and surgeons should be aware of the important reasons for revision of UKR. Thus, UKR instead of TKR should be performed in patients with late-stage isolated medial knee OA.

MiRNA-494 enhances M1 macrophage polarization via Nrdp1 in ICH mice model.

BACKGROUND: Ubiquitination-mediated M1/M2 macrophage polarization plays important roles in the pathogenesis of immune disease. However, the regulatory mechanism of ubiquitination during M1/M2 macrophage polarization following intracerebral hemorrhage (ICH) has not been well studied. METHODS: In the experiment, macrophages were administered with erythrocyte lysates, and then miR-494-, Nrdp1-, and M1/M2-related markers were analyzed. Brain inflammatory response, brain edema, and neurological functions of ICH mice were also assessed. RESULTS: We found that miR-494 levels increased while Nrdp1 levels decreased in macrophages after ICH. We also demonstrated that miR-494 inhibited Nrdp1 expression by directly binding its 3'-untranslated region. MiR-494 attenuated C/EBP-ß activation and downstream proinflammatory factor production. Upregulation of Nrdp1 in macrophages significantly promoted M2 macrophage polarization via ubiquitinating and activating C/EBP-ß. Moreover, the results indicated that miR-494 could enhance M1 macrophage polarization, promote brain edema, and impair neurological functions in ICH mice. CONCLUSIONS: Taken together, our results demonstrated that Nrdp1 contributed to M1/M2 macrophage polarization and neuroinflammation via ubiquitination and activation of C/EBP-ß in ICH. miR-494 may provide a promising therapeutic clue for ICH.

Prediction and identification of novel HLA-A*0201-restricted cytotoxic T lymphocyte epitopes from endocan.

BACKGROUND: Prediction and identification of cytotoxic T lymphocyte (CTL) epitopes from tumor associated antigens is a crucial step for the development of tumor immunotherapy strategy. Endocan has been identified as antigen overexpressed in various tumors. METHODS: In this experiment, we predicted and identified HLA-A2-restricted CTL epitopes from endocan by using the following procedures. Firstly, we predicted the epitopes from the amino acid sequence of endocan by computer-based methods; Secondly, we determined the affinity of the predicted peptide with HLA-A2.1 molecule by peptide-binding assay; Thirdly, we elicited the primary T cell response against the predicted peptides in vitro; Lastly, we tested the specific CTLs toward endocan and HLA-A2.1 positive target cells. RESULTS: These data demonstrated that peptides of endocan containing residues 4-12 and 9-17 could elicit specific CTLs producing interferon-γ and cytotoxicity. CONCLUSIONS: Therefore, our findings suggested that the predicted peptides were novel HLA-A2.1-restricted CTL epitopes, and might provide promising target for tumor immunotherapy.

Dendritic cells transduced with glioma-expressed antigen 2 recombinant adenovirus induces specific cytotoxic lymphocyte response and anti-tumor effect in mice.

INTRODUCTION: Glioma is an aggressive common cancer with high mortality worldwide. Up to date, the effective medical therapeutical strategy is limited. Numerous previous studies have indicated that glioma-expressed antigen 2 (GLEA2) might be an attractive prognostic glioma biomarker. METHODS: In this experiment, dendritic cells (DCs) transduced with GLEA2 recombinant adenovirus were utilized to generate cytotoxic lymphocytes (CTLs) in vitro. Additionally, trimera mice were immunized with the transduced DCs to generate CTLs in vivo. RESULTS: The data demonstrated that GLEA2 transduced DCs could effectively generate specific CTL response against glioma without lysing autologous lymphocytes. Moreover, GLEA2 transduced DCs significantly attenuated the tumor growth and prolonged the life span of tumor bearing mice. CONCLUSIONS: These findings suggested that DCs transduced with GLEA2 recombinant adenovirus could generate effective CTL mediated anti-tumor response, and might represent insight in glioma therapy.

miR­186 functions as a tumor suppressor in osteosarcoma cells by suppressing the malignant phenotype and aerobic glycolysis.

Osteosarcoma (OS) is the most common primary bone malignancy among children and adolescents. Deregulation of microRNAs has been well documented in OS, while the putative effects of miR­186 have not been identified yet. In the present study, we assessed the expression of miR­186 in a cohort of 40 OS tissues and explored its effects on OS cells. As expected, miR­186 was suppressed in OS tissues compared with relative normal tissues. Overexpression of miR­186 inhibited cell proliferation, arrested the cell cycle progression and suppressed the cell invasion of the HOS and U2 OS cell lines. These results indicated the tumor­suppressive role of miR­186 in OS. Among the target genes of miR­186, we found that pituitary tumor transforming gene 1 (PTTG1) may be a target gene of miR­186 in OS and that the overexpression of PTTG1 could partially abolish miR­186­mediated suppressive effects on OS cells. Aerobic glycolysis is the major way of energy supply and is one of the characteristic phenotypes of tumor cells. In addition, we found that overexpression of miR­186 significantly suppressed the expression of hypoxia­inducible factor 1 (HIF­1) and inhibited the glucose uptake and lactate production of OS cells. Collectively, our findings demonstrated that miR­186 functions as a tumor suppressor in OS cells partially by targeting PTTG1 and that HIF­1­mediated suppression of aerobic glycolysis may be also involved in its suppressive effects.

MicroRNA-23b attenuates the H2O2-induced injury of microglial cells via TAB3/NF-κB signaling pathway.

Apoptosis of microglia is one of the most important pathophysiologic changes after spinal cord injury (SCI). Recently, microRNAs (miRNAs) have been reported to play a crucial role in the regulation of neuronal apoptosis. However, the exact role and underlying mechanisms of miRNAs in the regulation of microglial apoptosis remain unclear. We first performed miRNA microarray to analyze the miRNA expression patterns in a rat SCI model. The expression of microRNA-23b (miR-23b) in spinal cord after contusion SCI was determined by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). BV-2 cells were exposed to H2O2 conditions to establish an in vitro model of SCI. Then, the effects of miR-23b on the apoptosis were investigated through both gain- and loss-of-function studies in this cellular model of SCI. Also, the expression of the main proteins in NF-κB signaling was assessed by Western Blot. Furthermore, bioinformatics analysis was used to predict the target of miR-23b in BV-2 cells, which was validated with a dual-luciferase reporter assay, qRT-PCR, and Western blot analysis. The expression of TGF-ß-activated kinase 1 binding protein 3 (TAB3) in cells was overexpressed by transfection with pcDNA-TAB3, and the effects of TAB3 overexpression on miR-23b-mediated apoptosis were detected. Here, we demonstrated that miR-23b was significantly down-regulated in SCI rat model. We also found that the expression level of phosphorylated p65 (p-p65) protein was increased in the SCI rat model. Subsequently, treatment of BV-2 cells with H2O2 decreased the levels of miR-23b and activated NF-κB pathway in a dose dependent manner. Furthermore, overexpression of miR-23b inhibited the BV-2 apoptosis and NF-κB activation, while miR-23b inhibition enhanced the apoptosis and NF-κB activation induced by H2O2. Moreover, our data showed TAB3, an upstream positive regulator of the NF-κB pathway, was proven to be a target of miR-23b in BV-2 cells. Most importantly, we demonstrated that overexpression of miR-23b attenuated the apoptosis by inhibiting the expression of TAB3. These findings suggested that miR-23b protected BV-2 cells from apoptosis by modulating the NF-κB pathway and could serve as a new strategy for the treatment of SCI.

MicroRNA-638 inhibits cell growth and tubule formation by suppressing VEGFA expression in human Ewing sarcoma cells.

Ewing sarcoma (EWS) is a kind of aggressive tumor of bone and soft tissues, which most occurring in children and adolescents. MicroRNAs (miRNAs) perform essential function in the progression and development of EWS, while the putative role of miR-638 in EWS remains uncertain. Accordingly, we detected the expression of miR-638 and explored its putative biological effects on the malignant phenotype of EWS cells. As expected, miR-638 was significantly down-regulated in EWS cells. Moreover, overexpression of miR-638 suppressed cell growth, induced cell apoptosis, and inhibited tubule formation of EWS cells in vitro Among the putative target genes of miR-638 predicted by the miRNA target prediction tools, vascular endothelial cell growth factor A (VEGFA) attracted out attention most. The luciferase reporter assays reaffirmed that VEGFA was a targeted gene of miR-638 in EWS cells. Furthermore, miR-638 suppressed the mRNA and protein level of VEGFA, and restored the expression of VEGFA reversed the suppressed effects of miR-638 in EWS cells. Taken together, the results suggested that miR-638 might perform tumor suppressive effects in EWS, which might be mediated, at least partially, through suppressing the activity of VEGFA.

MiR-107 suppresses cell proliferation and tube formation of Ewing sarcoma cells partly by targeting HIF-1ß.

MicroRNAs serve a crucial role in the regulation of malignant biological behavior of Ewing's sarcoma (ES). Abnormal expression of miR-107 has been reported in a cohort of cancers, while its exact function in ES remains unclear. Hence, we explored the expression of miR-107 in ES cells and detected its effects on the malignant phenotype of ES cells. Firstly, we perceived the under-expression of miR-107 in human ES cells contrast with the human mesenchymal stem cells. Over-expression of miR-107 restrained cell proliferation and tube formation, arrested cell cycle progression, and facilitated cell apoptosis in SK-ES-1 and RD-ES cell lines. Furthermore, hypoxia inducible factor-1ß (HIF-1ß) was assumed as a target gene of miR-107. We confirmed the target role of HIF-1ß in ES cells. Finally, restoring the expression of HIF-1ß could partly abolish miR-107-mediated tumor suppression in ES cells. In conclusion, our results advised that miR-107 suppressed the malignant biological ability of ES cells through targeting HIF-1ß.

miR-124 represses the mesenchymal features and suppresses metastasis in Ewing sarcoma.

Metastasis is the most powerful predictor of poor outcome of Ewing sarcoma (ES). Thus, identification of new molecules involved in tumor metastasis is of crucial importance to reduce morbidity and mortality of this devastating disease. In this study, we found that miR-124, a highly conserved miRNA, was suppressed in ES tissues and might be associated with tumor metastasis through suppressing its mesenchymal features. Overexpression of miR-124 suppressed the invasion of ES cells in vitro and tumor metastasis in vivo, which might be achieved through suppressing its mesenchymal features, as overexpression of miR-124 could repress the mesenchymal genes expression, and inhibit cell differentiation to mesenchymal lineages in ES cells. However, when SLUG was experimentally restored in these cells, mesenchymal features including suppressed expression of mesenchymal genes and decreased invasive ability were observed. We also found that cyclin D2 (CCND2) was a novel target gene of miR-124, and was directly involved in miR-124-mediated suppressive effects on cell growth. Lastly, we found that treatment with 5-Aza-CdR restored the expression of miR-124, accompanied with suppressed cell proliferation, invasion and mesenchymal features of ES cells, which demonstrated that hypermethylation might be involved in the regulation of miR-124 expression. Collectively, our data suggest that hypermethylation-mediated suppression of miR-124 might be involved in the tumor initiation and metastasis through suppressing the mesenchymal features of ES cells.

Comparing Single Versus Double Screw-Rod Anterior Instrumentation for Treating Thoracolumbar Burst Fractures with Incomplete Neurological Deficit: A Prospective, Randomized Controlled Trial.

BACKGROUND Following a thoracolumbar burst fracture (TCBF), anterior screw-rods apply pressure upon the graft site. However, there is limited evidence comparing single screw-rod anterior instrumentation (SSRAI) to double screw-rod anterior instrumentation (DSRAI) for TCBFs. Our objective was to compare SSRAI versus DSRAI for TCBFs with incomplete neurological deficit. MATERIAL AND METHODS A total of 51 participants with T11-L2 TCBFs (AO classification: A3) were randomly assigned to receive SSRAI or DSRAI. Key preoperative, perioperative, and postoperative data were collected. Statistical analysis was conducted to determine the independent factors associated with inferior clinical outcomes, as well as the comparative efficacy of SSRAI and DSRAI. RESULTS There were no significant differences in the key demographic and clinical characteristics between the two groups (all p>0.05). Smoking status was significantly associated with inferior three-month and six-month Denis pain scores (Wald statistic=4.246, p=0.039). Both SSRAI and DSRAI were significantly effective in improving three-month and six-month postoperative degree of kyphosis, three-month and six-month postoperative ASIA impairment scale scores, three-month and six-month postoperative Denis pain score, and three-month and six-month postoperative Denis work score (all p<0.001). Although there were no significant differences between DSRAI and SSRAI with respect to all outcomes (all p>0.05), DSRAI displayed significantly longer operating times, as well as significantly larger operative blood losses (both p<0.001). CONCLUSIONS SSRAI may be preferable over DSRAI for TCBFs with incomplete neurological deficit due to its lower operating time and amount of operative blood loss.

Vitamin D and Sunlight Exposure in Newly-Diagnosed Parkinson's Disease.

Circulating vitamin D has previously been found to be lower in patients with Parkinson's disease (PD), while the effects of sunlight exposure have not yet been fully investigated. Therefore, we evaluated the associations between serum vitamin D, vitamin D intake, sunlight exposure, and newly-diagnosed PD patients in a Chinese population. This case-control study measured serum 25-hydroxyvitamin D (25(OH)D) levels and sunlight exposure in 201 patients with newly-diagnosed PD and 199 controls without neurodegenerative diseases. Data on vitamin D intake and sunlight exposure were obtained using a self-report questionnaire. Multivariable logistic regressions were employed to evaluate the associations between serum 25(OH)D levels, sunlight exposure, and PD. Adjustments were made for sex, age, smoking, alcohol use, education, BMI, and vitamin D intake. There were significantly lower levels of serum 25(OH)D (20.6 ± 6.5 ng/mL), daily vitamin D intake (8.3 ± 3.7 g/day), and sunlight exposure (9.7 ± 4.1 h/week) in patients with PD compared to healthy controls (p < 0.05). Crude odds ratios (ORs) for PD in the quartiles of serum 25(OH)D were 1 (reference), 0.710 (0.401, 1.257), 0.631 (0.348, 1.209), and 0.483 (0.267, 0.874), respectively. Crude ORs for PD in quartiles of sunlight exposure were 1 (reference), 0.809 (0.454, 1.443), 0.623 (0.345, 1.124) and 0.533 (0.294, 0.966), respectively. A significant positive correlation between serum 25(OH)D and sunlight exposure was found, but serum 25(OH)D was not correlated with daily vitamin D intake. This study indicates that lower levels of serum 25(OH)D and sunlight exposure are significantly associated with an increased risk for PD.

[Influence of isobar ttl dynamic internal fixation system on adjacent segment degeneration by mri measurement of lumbar nucleus pulposus volume].

OBJECTIVE: ?To investigate the influence of ISOBAR TTL dynamic internal fixation system on degeneration of adjacent intervertebral disc by MRI measurement of lumbar nucleus pulposus volume in treating lumbar degenerative disease after operation. METHODS: ?Between March 2010 and October 2011, 34 patients with lumbar intervertebral disc herniation (23 cases of paracentral type and 11 cases of lateral type) underwent operation with ISOBAR TTL dynamic internal fixation system for fixation of single segment, and the clinical data were analyzed retrospectively. There were 20 males and 14 females, aged 39-62 years (mean, 47.5 years). The disease duration was 6-18 months (mean, 14 months). Involved segments included L4, 5 in 21 cases and L5, S1 in 13 cases. The X-ray films and MRI images were taken at 6, 12, 18, 24, 36, and 48 months after surgery. Based on X-ray films, the height of intervertebral space was measured using angle bisectrix method. The nucleus pulposus volume was measured based on the MRI scan. The postoperative change of nucleus pulposus volume and intervertebral disc height were used to evaluate the influence of ISOBAR TTL system on degeneration of adjacent intervertebral disc nucleus pulposus. RESULTS: ?Thirty patients were followed up 48 months. The height of intervertebral space showed no significant difference between at pre-and post-operation (P>0.05). The nucleus pulposus volume increased after operation, showing no significant difference at 6, 12, and 18 months when compared with preoperative value (P>0.05), but significant difference was found at 24, 36, and 48 months when compared with preoperative value (P<0.05). The height of nucleus pulposus increased after operation but the width was decreased; the values showed no significant difference at 6, 12, and 18 months when compared with preoperative ones, but showed significant difference at 24, 36, and 48 months when compared with preoperative ones (P<0.05). The diameter of nucleus pulposus at 18, 24, 36, and 48 months after operation was significantly langer than that at preoperation (P<0.05). CONCLUSIONS: ?ISOBAR TTL dynamic internal fixation system can prevent or delay the degeneration of intervertebral discs.

Risk factors contributing to postoperative delirium in geriatric patients postorthopedic surgery.

INTRODUCTION: Postoperative delirium is a common clinical manifestation in geriatric patients, resulting in prolonged hospitalization and increased economic burden, in addition to higher morbidity and mortality rates. Therefore, identifying non-obvious risk factors that contribute to the development of postoperative delirium in geriatric patients is crucial. METHODS: From January 2011 to June 2013, 200 geriatric patients of over 65 years of age scheduled for orthopedic surgery were randomly selected and statistically analyzed with respect to the effects of the following 12 factors on postoperative delirium: sex, age, anesthesia type, surgical type (i.e. spine, hip replacement, and pelvic or femoral fracture repair), operative duration, intraoperative hypoxia, intraoperative hypercapnia, intraoperative hypotension, intraoperative blood loss, preoperative affective state, postoperative sleep disorders, and underlying disease (i.e. hypertension, coronary heart disease, diabetes, hyperlipidemia, and chronic bronchitis). RESULTS: Seven factors--age, anesthesia type, duration of operation, intraoperative hypercapnia, intraoperative hypotension, preoperative affective state, and postoperative sleep disorders--were found to be significantly differentiated, suggesting that these factors have an impact on the development of postoperative delirium. Sex, surgical type, intraoperative hypoxia, intraoperative blood loss (with 300 ml as a cutoff value), and underlying disease were not directly related to the development of postoperative delirium. DISCUSSION: Advanced age (>70 years), the use of general anesthesia, longer surgical duration (>3 hours), the presence of intraoperative hypercapnia and hypotension, the presence of preoperative affective dysfunction, and the presence of postoperative sleep disorders appear to be associated with the development of postoperative delirium in geriatric patients after orthopedic surgery.

[Failure cause of posterior approach orthopaedic operation of thoracolumbar hemivertebra and strategies of revision].

OBJECTIVE: To explore the failure cause of posterior approach orthopaedic operation of thoracolumbar hemivertebra, and to summary strategies of revision. METHODS: The clinical data from 9 cases undergoing posterior approach orthopaedic operation failure of thoracolumbar hemivertebra between June 2003 and June 2008, were retrospectively analyzed. There were 5 males and 4 females with a median age of 12 years (range, 1 year and 10 months to 24 years). All malformations were identified as fully segmented hemivertebra from the original medical records and X-ray films, including 2 cases in thoracic vertebra, 5 cases in thoracolumbar vertebra, and 2 cases in lumbar vertebra. The preoperative scoliotic Cobb angle was (45.4 +/- 17.4) degrees, and kyphotic Cobb angle was (29.8 +/- 22.0) degrees. The reason of primary surgical failure were analyzed and spinal deformity was corrected again with posterior revision. RESULTS: All surgeries were finished successfully. The operation time was 3.0-6.5 hours (mean, 4.5 hours), and the perioperative bleeding was 400-2 500 mL (mean, 950 mL). All incisions healed by first intention; no infection or deep venous thrombosis occurred. Numbness occurred in unilateral lower extremity of 1 case postoperatively, and the symptom was relieved completely after treatment of detumescence and neural nutrition. All cases were followed up 12-30 months (mean, 18 months). No pseudoarthrosis and implant failure occurred. The X-ray films showed that the bone grafts completely fused within 8-14 months (mean, 11 months) after operation. The Cobb angles of scoliosis and kyphosis at 1 week after operation and the last follow-up were obviously improved when compared with preoperative ones, showing significant differences (P < 0.05). No obvious correction loss was observed either in coronal or sagittal plane. CONCLUSION: The failure causes of posterior approach orthopaedic operation are hemivertebra processing, selection of fixation and fusion range, and selection of internal fixation. If the strategies of revision are made after the above-mentioned failure causes are considered, the clinical results will be satisfactory.

[Confidence high viscosity bone cement system and postural reduction in treating acute severe osteoporotic vertebral compression fractures].

OBJECTIVE: To evaluate the effectiveness of Confidence high viscosity bone cement system and postural reduction in treating acute severe osteoporotic vertebral compression fracture (OVCF). METHODS: Between June 2004 and June 2009, 34 patients with acute severe OVCF were treated with Confidence high viscosity bone cement system and postural reduction. There were 14 males and 20 females with an average age of 72.6 years (range, 62-88 years). All patients had single thoracolumbar fracture, including 4 cases of T11, 10 of T12, 15 of L1, 4 of L2, and 1 of L3. The bone density measurement showed that T value was less than -2.5. The time from injury to admission was 2-72 hours. All cases were treated with postural reduction preoperatively. The time of reduction in over-extending position was 7-14 days. All patients were injected unilaterally. The injected volume of high viscosity bone cement was 2-6 mL (mean, 3.2 mL). RESULTS: Cement leakage was found in 3 cases (8.8%) during operation, including leakage into intervertebral space in 2 cases and into adjacent paravertebral soft tissue in 1 case. No clinical symptom was observed and no treatment was performed. No pulmonary embolism, infection, nerve injury, or other complications occurred in all patients. All patients were followed up 12-38 months (mean, 18.5 months). Postoperatively, complete pain relief was achieved in 31 cases and partial pain relief in 3 cases; no re-fracture or loosening at the interface occurred. At 3 days after operation and last follow-up, the anterior and middle vertebral column height, Cobb angle, and visual analogue scale (VAS) score were improved significantly when compared with those before operation (P < 0.05); and there was no significant difference between 3 days and last follow-up (P > 0.05). CONCLUSION: Confidence high viscosity bone cement system and postural reduction can be employed safely in treating acute severe OVCF, which has many merits of high viscosity, long time for injection, and easy-to-control directionally.

[Preliminary report for treatment of discogenic low back pain with combined percutaneous laser and O2-O3 mixture].

OBJECTIVE: To evaluate the efficacy of percutaneous laser and O2-O3 mixture in treating chronic discogenic low back pain. METHODS: There were 48 patients included 32 male and 16 female with the mean age of 43.5 years (range, from 21 to 66 years). The duration of symptoms was more than 6 months, all patients were treated with percutaneous laser and O2-O3 mixture under TV monitoring. RESULTS: Forty-eight patients followed-up showed no severe complications. At 1 week follow up, 8 cases were evaluated as excellent, 28 as good, 8 as fair and 4 as poor by Macnab standard. The excellent and good rate reached 75%. At 3 months follow up, 17 cases were evaluated as excellent, 23 as good, 6 as fair and 2 as poor with the excellent and good rate of 83.3%. At 6 months follow up, 20 cases were evaluated as excellent, 22 as good, 4 as fair and 2 as poor with a total effective rate of 87.5%. At 12 months follow up, 21 cases were evaluated as excellent, 22 as good, 4 as fair and 1 as poor with a total effective rate of 89.6%. CONCLUSION: Combined percutaneous laser and O3-O3 mixture is an effective and safe method in treating discogenic low back pain.