Efficacy and safety of en-bloc resection versus debulking for spinal tumor: a systematic review and meta-analysis.

BACKGROUND: This systematic review and meta-analysis aimed to consolidate the existing evidence regarding the comparison between en-bloc resection surgery and debulking surgery for spinal tumors, including both primary and metastatic tumors. MATERIALS AND METHODS: The databases of PubMed, Embase, Cochrane database, Web of Science, Scopus, Chinese National Knowledge Infrastructure (CNKI), Chongqing VIP Database (VIP), and Wan Fang Database was carried out and included all studies that directly compared en-bloc resection surgery with debulking surgery for spinal tumors in patients through March 2024. The primary outcomes included recurrence rate, postoperative metastasis rate, mortality rate, overall survival (OS), recurrence-free survival (RFS), complication, and so on. The statistical analysis was conducted using Review Manager 5.3. RESULTS: We systematically reviewed 868 articles and included 27 studies involving 1135 patients who underwent either en-bloc resection surgery (37.89%) or debulking surgery (62.11%). Our meta-analysis demonstrated significant advantages of en-bloc resection over debulking surgery. Specifically, the en-bloc resection group had a lower recurrence rate (OR = 0.19, 95%CI: 0.13-0.28, P < 0.00001), lower postoperative metastasis rate (P = 0.002), and lower mortality rate (P < 0.00001). Additionally, en-bloc resection could improve OS and RFS (HR = 0.45, 95%CI: 0.32-0.62, P < 0.00001 and HR = 0.37, 95%CI: 0.17-0.80, P = 0.01, respectively). However, en-bloc resection required longer operative times and was associated with a higher overall complication rate compared to debulking surgery (P = 0.0005 and P < 0.00001, respectively). CONCLUSION: The current evidence indicates that en-bloc surgical resection can effectively control tumor recurrence and mortality, as well as improve RFS and OS for patients with spinal tumors. However, it is crucial not to overlook the potential risks of perioperative complications. Ultimately, these findings should undergo additional validation through multi-center, double-blind, and large-scale randomized controlled trials (RCTs).

Culture and identification of neonatal rat brain-derived neural stem cells.

BACKGROUND: Timing of passaging, passage number, passaging approaches and methods for cell identification are critical factors influencing the quality of neural stem cells (NSCs) culture. How to effectively culture and identify NSCs is a continuous interest in NSCs study while these factors are comprehensively considered. AIM: To establish a simplified and efficient method for culture and identification of neonatal rat brain-derived NSCs. METHODS: First, curved tip operating scissors were used to dissect brain tissues from new born rats (2 to 3 d) and the brain tissues were cut into approximately 1 mm3 sections. Filter the single cell suspension through a nylon mesh (200-mesh) and culture the sections in suspensions. Passaging was conducted with TrypLTM Express combined with mechanical tapping and pipetting techniques. Second, identify the 5th generation of passaged NSCs as well as the revived NSCs from cryopreservation. BrdU incorporation method was used to detect self-renew and proliferation capabilities of cells. Different NSCs specific antibodies (anti-nestin, NF200, NSE and GFAP antibodies) were used to identify NSCs specific surface markers and muti-differentiation capabilities by immunofluorescence staining. RESULTS: Brain derived cells from newborn rats (2 to 3 d) proliferate and aggregate into spherical-shaped clusters with sustained continuous and stable passaging. When BrdU was incorporated into the 5th generation of passaged cells, positive BrdU cells and nestin cells were observed by immunofluorescence staining. After induction of dissociation using 5% fetal bovine serum, positive NF200, NSE and GFAP cells were observed by immunofluorescence staining. CONCLUSION: This is a simplified and efficient method for neonatal rat brain-derived neural stem cell culture and identification.

Attapulgite-MXene Hybrids with Ti3C2Tx Lamellae Surface Modified by Attapulgite as a Mechanical Reinforcement for Epoxy Composites.

As a member of two-dimensional (2D) materials, MXene is an ideal reinforcement phase for modified polymers due to its large number of polar functional groups on the surface. However, it is still relatively difficult to modify any functional groups on the surface of MXene at present, which limits its application in enhancing some polymers. Herein, one-dimensional (1D) attapulgite (ATP) nanomaterials were introduced onto the surface of MXene to form ATP-MXene hybrids, which successfully improved the mechanical properties of the epoxy composites. ATP with appropriate content can increase the surface roughness of the MXene lamellae to obtain better interface interaction. Therefore, remarkable enhancement on the mechanical property was achieved by adding M02A025 (0.2 wt % MXene and 0.25 wt % ATP), which is the optimum composition in the hybrids for composite mechanical properties. Compared to neat epoxy, the tensile strength, flexural strength and critical stress intensity factor (KIC) of M02A025/epoxy are increased by 88%, 57%, and 195%, respectively, showing a high application prospect.

Extracellular vesicles derived from mesenchymal stem cells containing microRNA-381 protect against spinal cord injury in a rat model via the BRD4/WNT5A axis.

AIMS: Non-coding microRNA (miRNA) in extracellular vesicles (EVs) derived from mesenchymal stem cells (MSCs) may promote neuronal repair after spinal cord injury (SCI). In this paper we report on the effects of MSC-EV-microRNA-381 (miR-381) in a rodent model of SCI. METHODS: In the current study, the luciferase assay confirmed a binding site of bromodomain-containing protein 4 (BRD4) and Wnt family member 5A (WNT5A). Then we detected expression of miR-381, BRD4, and WNT5A in dorsal root ganglia (DRG) cells treated with MSC-isolated EVs and measured neuron apoptosis in culture by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining. A rat model of SCI was established to detect the in vivo effect of miR-381 and MSC-EVs on SCI. RESULTS: We confirmed an interaction between miR-381 and BRD4, and showed that miR-381 overexpression inhibited the expression of BRD4 in DRG cells as well as the apoptosis of DRG cells through WNT5A via activation of Ras homologous A (RhoA)/Rho-kinase activity. Moreover, treatment of MSC-EVs rescued neuron apoptosis and promoted the recovery of SCI through inhibition of the BRD4/WNT5A axis. CONCLUSION: Taken altogether, miR-381 derived from MSC-EVs can promote the recovery of SCI through BRD4/WNT5A axis, providing a new perspective on SCI treatment. Cite this article: Bone Joint Res 2021;10(5):328-339.

miR-27a promotion resulting from silencing of HDAC3 facilitates the recovery of spinal cord injury by inhibiting PAK6 expression in rats.

AIMS: Spinal cord injury (SCI) is one of the most devastating diseases that challenges neurology and medicine, leading to paraplegia or quadriplegia worldwide. Neuroprotection conferred by histone deacetylase (HDAC) inhibitors against various insults and deficits in the central nervous system has been reported previously. Herein, we set out to ascertain whether HDAC3 inhibition exerts neuroprotective effects against SCI. MAIN METHODS: A modified Allen's weight-drop method was performed to induce experimental SCI in rats. Basso-Beattie-Bresnahan (BBB) scores were used to assess locomotor function. Flow cytometric analysis of AnnexinV-FITC/PI double staining, TUNEL staining, and immunoblotting analysis of apoptosis-related proteins were performed to determine apoptosis in H2O2-induced cell injury of primary rat neurons. KEY FINDINGS: Upregulated HDAC3 and downregulated miR-27a were observed in spinal cord tissues of SCI rats and H2O2-injured neurons. HDAC3 knockdown by its specific shRNA restored the locomotor function of SCI rats and prevented rat neurons from H2O2-induced apoptosis through promotion of miR-27a. miR-27a targeted PAK6 (encoding P21-activated kinase 6) and inhibited its expression. The effects of HDAC3 knockdown on the locomotor function of SCI rats and H2O2-induced apoptosis of rat neurons were lost upon further PAK6 overexpression. SIGNIFICANCE: The present study uncovers that silencing HDAC3 inhibited PAK6 expression by upregulating miR-27a, eventually inhibiting neuron apoptosis and promoting the recovery of SCI, which might provide a novel therapeutic target for SCI.

[Effect of percutaneous kyphoplasty with different phases bone cement for treatment of osteoporotic vertebral compression fractures].

OBJECTIVE: To compare the effect of percutaneous kyphoplasty (PKP) with different phases bone cement for treatment of osteoporotic vertebral compression fracture (OVCF). METHODS: The clinical data of 219 OVCF patients who treated with PKP and met the selection criteria between June 2016 and May 2018 were retrospectively analyzed. According to the different time of intraoperative injection of bone cement, they were divided into observation group [116 cases, intraoperative injection of polymethyl methacrylate (PMMA) bone cement in low-viscosity wet-sand phase)] and control group (103 cases, intraoperative injection of PMMA bone cement in low-viscosity wire-drawing phase). There was no significance in general date of gender, age, disease duration, body mass index, bone mineral density T value, fracture vertebral body, preoperative fracture severity of the responsible vertebral body, anterior height ratio of the responsible vertebral body, preoperative pain visual analogue scale (VAS) score, and Oswestry disability index (ODI) between the two groups ( P>0.05). The VAS score and ODI score were used to evaluate the improvement of patients' symptoms at immediate, 2 days, 3 months after operation and at last follow-up. At 1 day, 3 months after operation, and at last follow-up, X-ray film and CT of spine were reexamined to observe the distribution of bone cement in the vertebral body, bone cement leakage, and other complications. During the follow-up, the refracture rate of the responsible vertebral body and the fracture rate of the adjacent vertebral body were recorded. RESULTS: The injection amount of bone cement in the observation group and control group were (4.53±0.45) mL and (4.49±0.57) mL, respectively, showing no significant difference between the two groups ( t=1.018, P=0.310). Patients in both groups were followed up 6-18 months (mean, 13.3 months). There were 95 cases (81.9%) and 72 cases (69.9%) of the bone cement distribution range more than 49% of the cross-sectional area of the vertebral body in the observation group and the control group, respectively, showing significant difference in the incidence between the two groups ( χ 2=4.334, P=0.037). The VAS score and ODI score of the postoperative time points were significantly improved compared with those before operation ( P<0.05), and there were significant differences among the postoperative time points ( P<0.05). The VAS score and ODI score of the observation group were significantly better than those of the control group ( P<0.05) at immediate, 2 days, and 3 months after operation, and there was no significant difference between the two groups at last follow-up ( P>0.05). At 1 day after operation, the cement leakage occurred in 18 cases of the observation group (8 cases of venous leakage, 6 cases of paravertebral leakage, 4 cases of intradiscal leakage) and in 22 cases of the control group (9 cases of venous leakage, 8 cases of paravertebral leakage, 5 cases of intradiscal leakage). There was no significant difference between the two groups ( P>0.05). During the follow-up, 5 cases (4.3%) in the observation group, 12 cases (11.7%) in the control group had responsible vertebral refracture, and 6 cases (5.2%) in the observation group and 14 cases (13.6%) in the control group had adjacent vertebral fracture, the differences were significant ( χ 2=4.105, P=0.043; χ 2=4.661, P=0.031). CONCLUSION: Bone cement injection with wet-sand phase in PKP is beneficial for the bone cement evenly distributed, strengthening the responsible vertebral, relieving the short-term pain after operation, decreasing the rate of responsible vertebral refracture and adjacent vertebral fracture without increasing the incidence of relevant complications and can enhance the effectiveness.

LncRNA FER1L4 induces apoptosis and suppresses EMT and the activation of PI3K/AKT pathway in osteosarcoma cells via inhibiting miR-18a-5p to promote SOCS5.

Previous studies have determined that long non-coding RNA (lncRNA) Fer-1-like protein 4 (FER1L4) is suppressed in osteosarcoma (OS) and inhibits the tumorigenesis in a variety of cancer. However, the precise biological of FER1L4 in OS has not been cleared. The aim of this study is to investigate the roles and potential mechanisms of FER1L4 in apoptosis and epithelial-mesenchymal transition (EMT) in OS. In the present study, the levels of FER1L4 were decreased significantly in OS tissues and cell lines compared with non-tumorous tissues or hFOB1.19. Knockdown of FER1L4 in OS cells decreased the apoptosis rate, but increased the OS cell proliferation, upregulated the expression levels of CD133 and Nanog, as well as promoted Twist1 expression, increased the N-cadherin and Vimentin expression. In turn, the opposite trends were observed upon overexpression of FER1L4. In addition, the expression of PI3K, p-AKT (Ser470) and p-AKT (Thr308) was upregulated by siFER1L4, while decreased upon overexpression of FER1L4. MicroRNA (miRNA) -18a-5p, an osteosarcoma-promoting miRNA which was suggested a target of FER1L4 in osteosarcoma, was identified to be a functional target of FER1L4 on the regulating of cell apoptosis and EMT, presently. The effects of FER1L4 overexpression on the markers of cell apoptosis, proliferation, EMT, and stemness and PI3K/AKT signaling were all reversed by miR-18a-5p upregulation. Furthermore, the suppressor of cytokine signaling 5 (SOCS5) was confirmed a target gene of miR-18a-5p by luciferase gene reporter assay and SOCS5 suppression by miR-18a-5p attenuated the effects of FER1L4 overexpression on the OS cells apoptosis and the expressed levels of PI3K, AKT, Twist1, N-cadherin and Vimentin. In conclusion, our data indicated thatthe overexpression of FER1L4 promoted apoptosis and inhibited the EMT markers expression and PI3K/AKT signaling pathway activation in OS cells via downregulating miR-18a-5p to promote SOCS5.

GSK-3 Inhibitor Promotes Neuronal Cell Regeneration and Functional Recovery in a Rat Model of Spinal Cord Injury.

The reparative process following spinal cord injury (SCI) is extremely complicated. Cells in the microenvironment express multiple inhibitory factors that affect axonal regeneration over a prolonged period of time. The axon growth inhibitory factor glycogen synthase kinase-3 (GSK-3) is an important factor during these processes. TDZD-8 (4-benzyl-2-methyl-1,2,4-thiadiazolidine-3,5-dione) is the most effective and specific non-ATP-competitive inhibitor of GSK-3. Here, we show that administering TDZD-8 after SCI was associated with significantly inhibited neuronal apoptosis, upregulated GAP-43 expression, increased density of cortical spinal tract fibers around areas of injury, and increased Basso, Beattie, and Bresnahan (BBB) scores in the lower limbs. These findings support the notion that GSK-3 inhibitors promote neuronal cell regeneration and lower limb functional recovery.

Spinal cord extracts from injured spinal cord impede differentiation of rat embryonic neural stem cells into neurons through regulating Notch signaling pathway.

SCI (spinal cord injury) is a complex and serious neurological disease with no efficient treatment. NSC (neural stem cells) have the potential for self-renewal, proliferation and differentiation into all types of nerve cells. The aim of our study is to evaluate the effect of SCE (spinal cord extracts) from injured spinal cord on the differentiation of rat embryonic NSC and to clarify its potential mechanism. Here, NSC were isolated and cultured with SCE. The experiments were divided into four groups, including NSC + sham, NSC + SCE, NSC + SCE + DMSO (dimethyl sulfoxide), NSC + SCE + DAPT (N-[N-(3,5-difluorophenacetyl)-1-alanyl]-S-Phenyl-glycinet-butylester). The Notch1 (notch receptor 1) and Hes1 (hes family bHLH transcription factor 1) mRNA expression was analyzed by qPCR (quantitative real-time PCR) analysis. The protein expression levels of GFAP (glial fibrillary acidic protein) and NSE (nestin) were evaluated by immunofluorescence staining. Cell differentiation of NSC was induced by using neurobasal medium. The results showed that the NSC were successfully identified, and could proliferate to form spherical aggregates and was passaged continuously and steadily in vitro. The NSC at fifth generation were positively stained with NSE, and was capable of differentiating into NSE-positive cells and GFAP-positive cells. SCE treatment could upregulate the mRNA expression levels of Notch1 and Hes1, but inhibited the differentiation of NSC into neurons. DAPT could down-regulate the mRNA expression of Notch1 and Hes1 in NSC. Mechanically, DAPT targeting Notch signal pathway could facilitate NSC differentiation into neurons. Together, our data highlighted that SCE suppresses the differentiation of rat embryonic NSC by regulating the Notch signaling pathway, and DAPT treatment can reverse the effect of SCE related differentiation.

Comparison of the Anteroposterior and Posterior Approaches for Percutaneous Catheter Drainage of Tuberculous Psoas Abscess.

BACKGROUND Tuberculous infection of the lumbar spine may be associated with psoas abscess. The aim of this clinical study was to compare the outcome of posterior lumbar debridement and spinal fusion, combined with either a one-stage anteroposterior (AP) or posterior (P) approach to percutaneous catheter drainage (PCD) for the treatment of lumbar tuberculosis with psoas abscess. MATERIAL AND METHODS From January 2008 to June 2012, 74 patients were diagnosed at our hospital with lumbar tuberculosis with unilateral or bilateral psoas abscess. Forty-three patients underwent P-PCD (group A), and 31 patients underwent AP-PCD (group B). Operative duration, blood loss, the length of hospital stay, spinal correction, clinical cure rate, and other clinical outcomes in the two groups were compared. RESULTS Comparison of the outcome for the P-PCD and AP-PCD patients showed that there was no significant difference in outcome for spinal bone fusion, correction of spinal deformity, or cure rate from tuberculosis infection (P>0.05). Blood loss, operative time, and the length of hospital stay for patients in group A, the P-PCD group, were significantly less than for group B, the AP-PCD group (P<0.05). Also, group B, the AP-PCD group, had an increased incidence of complications than group A, the P-PCD group, leading to increased hospital stay (OR 3.04, CI 0.52-17.75). CONCLUSIONS For the treatment of tuberculous psoas abscess using PCD, the posterior approach may achieve the same clinical efficacy as the anteroposterior approach, but is associated with reduced length of hospital stay, and lower risk of complications.

The protective effect of berberine hydrochloride on LPS­induced osteoclastogenesis through inhibiting TRAF6­Ca2+­calcineurin­NFATcl signaling pathway.

The present study investigated the protective effect of berberine hydrochloride on lipopolysaccharide (LPS) ­induced acute bone destruction through inhibition of the TNF receptor associated factor 6 (TRAF6)­Ca2+­calcineurin­nuclear factor of activated T­cell 1 (NFATc1) signaling pathway. An osteoclast culture system of RAW264.7 cells induced by LPS in vitro was established. A polymerase chain reaction (PCR) assay was applied to determine the effect of berberine hydrochloride on the mRNA expression levels of fos­related antigen 2 (Fra­2), tartrate­resistant acid phosphatase (TRAP), ß3­integrin, cathepsin K, dendritic cell­specific transmembrane protein (DC­STAMP), V­type proton ATPase subunit d 2 (Atp6v0d2) and NFATcl. An ELISA assay was performed to measure the release of tumor necrosis factor­α (TNF­α). Western blot analysis was used to measure the effect of berberine hydrochloride on the expression of calcineurin in the LPS­induced NFATc1 signaling pathway, as well as the expression levels of phosphoinositide phospholipase C­Î³l (PLC­Î³1), toll like receptor 4 (TLR4) and TRAF6. The effect of berberine hydrochloride on Ca2+ concentration was detected using a confocal technique with a Flou­3/acetoxymethyl ester Ca2+ probe. The PCR results demonstrated that berberine hydrochloride inhibited the mRNA expression levels of Fra­2, TRAP, ß3­integrin, cathepsin K, DC­STAMP, Atp6v0d2 and NFATc1. Furthermore, the ELISA results demonstrated that TNF­α expression was decreased. The western blot analysis revelead that berberine hydrochloride treatment results in decreased expression levels of PLC­Î³1, TLR4 and TRAF6, and inhibition of Ca2+ influx. In conclusion, the results of the present study suggest that berberine hydrochloride targets TRAF6 and NFATc1, thus inhibiting osteoclastogenesis and bone destruction via inhibition of the TRAF6­Ca2+­calcineurin­NFATcl signaling pathway.

IGF-1R promotes the expression of cyclin D1 protein and accelerates the G1/S transition by activating Ras/Raf/MEK/ERK signaling pathway.

OBJECTIVE: The objective of study was to detect the expression level of IGF-1R in breast cancer tissues and investigate the effect of IGF-1R expression on the proliferation and apoptosis of breast cancer cells. METHODS: The expression of IGF-1R protein in breast cancer tissues and the adjacent normal tissues was detected by immunohistochemistry. By IGF-1R inhibitor mediated repression of IGF-1R expression in MCF-7 cells, the cell proliferation rate, cell cycle and the expression of Ras/Raf/MEK/ERK signaling pathway proteins as well as cyclin D1 protein were examined in the IGF-1R-inhibited cells. RESULTS: The proportion of IGF-1R, cyclin D1, Ras and p-ERK1/2 positive cells in breast cancer tissues were (69.8±12.7)%, (38.0±6.2)%, (71.6±10.3)% and (3.1±5.7)%, respectively, which were all significantly higher than those in the adjacent normal tissues [(16.2±6.7)%, (0.5±0.7)%, (7.1±0.9)% and (12.2±5.4)%] (P<0.05). Compared to normal MCF-7 cells, the MCF-7 cells treated with IGF-1R inhibitor showed no expression of IGF-1R protein, increased apoptosis rate (370.3%), increased proportion of cells in G1 phase (81.1%), decreased proportion of cells in S phase (66.8%), decreased proportion of cells in G2/M phase (52.9%), decreased Ras protein expression (70.9%), decreased p-ERK1/2 protein expression (53.3%), decreased cyclin D1 protein expression (59.5%), and substantially unchanged expression of ERK1/2 protein (P<0.05). CONCLUSIONS: IGF-1R is overexpressed in breast cancer tissues. The overexpressed IGF-1R promotes the expression of cyclin D1 protein and accelerates the G1/S transition by activating Ras/Raf/MEK/ERK signaling pathway, thus further promoting cell proliferation and the carcinogenesis of breast cancer.

Combined application of Rho-ROCKII and GSK-3ß inhibitors exerts an improved protective effect on axonal regeneration in rats with spinal cord injury.

Previous studies have reported that the Rho-associated coiled-coil containing protein kinase 2 (ROCKII) and glycogen synthase kinase­3ß (GSK)­3ß signaling pathways are involved in axonal regeneration. The present study investigated the effects of the combined application of Y27632 (a ROCKII inhibitor) and 4-benzyl-2­methyl-1,2,4-thiadiazolidine-3,5-dione (TDZD-8; a GSK­3ß inhibitor) on neurite outgrowth and functional recovery in rats with spinal cord injury (SCI). A total of 90 female Sprague­Dawley rats were randomly allocated into six groups, and the SCI rats received daily administration of 1.6 mg/kg Y27632 for 2 weeks and/or 1 mg/kg TDZD­8 for 3 weeks via a catheter. Cellular apoptosis in the injured spinal cords was measured at each time point using a terminal deoxynucleotidyl transferase­mediated dUTP nick end labeling assay. The expression levels of growth­associated protein­43 (GAP­43) were determined by immunohistochemical staining. In addition, an anterograde tracer was used to analyze axonal regeneration, the Basso Beattie Bresnahan locomotor rating scale (BBB) was analyzed, and the somatosensory evoked potential (SEP) test was conducted. The results demonstrated that SCI upregulated the number of apoptotic cells, increased GAP­43 expression and enhanced the latent periods of SEP, as compared with in mice that underwent a sham operation. Furthermore, SCI decreased the BBB scores and the SEP amplitudes. These injuries in the spinal cord were reduced following treatment with Y27632, TDZD­8, or their combined application, as detected by decreased apoptosis, the induction of axonal regeneration, and the promotion of functional recovery of the lower limbs. Although the BBB scores, and SEP amplitudes and latent periods were not significantly different among the three drug treatment groups, the combined application of Y27632 and TDZD­8 resulted in stronger axonal regenerative potency and a greater protective effect on secondary SCI. These results indicated that the combined application of Y27632 and TDZD­8 may more effectively protect against secondary SCI by inhibiting cellular apoptosis, enhancing GAP-43 expression and promoting neurite outgrowth in SCI rats, compared with Y27632 or TDZD-8 alone.

[COMPARISON OF SHORT SEGMENTAL FIXATION WITH AND WITHOUT FUSION IN TREATMENT OF THORACOLUMBAR BURST FRACTURE BY POSTERIOR APPROACH].

OBJECTIVE: To compare the effectiveness of short segmental pedicle screw fixation with and without fusion in the treatment of thoracolumbar burst fracture. METHODS: A retrospective analysis was made on the clinical data of 57 patients with single segment thoracolumbar burst fractures, who accorded with the inclusion criteria between February 2012 and February 2014. The patients underwent posterior short segmental pedicle screw fixation with fusion in 27 cases (fusion group) and without fusion in 30 cases (non-fusion group). There was no significant difference in gender, age, cause of injury, time between injury and admission, fracture segment and classification, and neurologic function America Spinal Injury Association (ASIA) classification between 2 groups, which had the comparability (P>0.05). The operative time, blood loss, and hospitalization days were compared between 2 groups. The height of the injured vertebra, the kyphotic angle, and the range of motion (ROM) were measured on the X-ray film. The functional outcomes were evaluated by using the Greenough low-back outcome score and the visual analogue scale (VAS) for back pain. The neurologic functional recovery was assessed by ASIA grade. RESULTS: The operative time was significantly shortened and the blood loss was significantly reduced in the non-fusion group when compared with the fusion group (P<0.05), but no significant difference was found in hospitalization days between 2 groups (P>0.05). The patients were followed up for 2.0-3.5 years (mean, 3.17 years) in the fusion group and for 2-4 years (mean, 3.23 years) in the non-fusion group. X-ray films showed that 2 cases failed bone graft fusion, the fusion time was 12-17 weeks (mean, 15.6 weeks) in the other 25 cases. Complication occurred in 2 cases of the fusion group (1 case of incision deep infection and 1 case of hematoma at iliac bone donor site) and in 1 case of the non-fusion group (fat liquefaction); primary healing of incision was obtained in the others. The Cobb angle, the height of injured vertebrae showed no significant difference between 2 groups at pre-operation, immediate after operation, and last follow-up (P>0.05). The ROM of injured vertebrae showed no significant difference between 2 groups at 1 year after operation (before implants were removed) (P>0.05). The implants were removed at 1 year after operation in all cases of the non-fusion group, and in 11 cases of the fusion group. At last follow-up, the ROM of injured vertebrae in the non-fusion group was significantly higher than that in the fusion group (P<0.05), but no significant difference was found in Greenough low-back outcome score, VAS score, and ASIA grade between 2 groups (P>0.05). CONCLUSIONS: Fusion is not necessary when thoracolumbar burst fracture is treated by posterior short segmental pedicle screw fixation, which can preserve regional segmental motion, shorten the operative time, decrease blood loss, and eliminate bone graft donor site complications.

Effect of spinal cord extracts after spinal cord injury on proliferation of rat embryonic neural stem cells and Notch signal pathway in vitro.

OBJECTIVE: To investigate the effect of the spinal cord extracts (SCE) after spinal cord injuries (SCIs) on the proliferation of rat embryonic neural stem cells (NSCs) and the expressions of mRNA of Notch1 as well as of Hes1 in this process in vitro. METHODS: The experiment was conducted in 4 different mediums: NSCs+PBS (Group A-blank control group), NSCs+SCE with healthy SD rats (Group B-normal control group), NSCs+SCE with SD rats receiving sham-operation treatment (Group C-sham-operation group) and NSCs+ SCE with SCIs rats (Group D-paraplegic group). Proliferative abilities of 4 different groups were analyzed by MTT chromatometry after co-culture for 1, 2, 3, 4 and 5 d, respectively. The expressions of Notch1 and Hes1 mRNA were also detected with RT-PCR after co-culture for 24 and 48 h, respectively. RESULTS: After co-culture for 1, 2, 3, 4 and 5 d respectively, the MTT values of group D were significantly higher than those of group A, group B and group C (P<0.05). However, there were no significantly differences regarding MTT values between group A, group B and group C after co-culture for 1, 2, 3, 4 and 5 d, respectively (P>0.05). Both the expressions of Notch1 and Hes1 mRNA of group D were significantly higher than those of other 3 groups after co-culture for 24 h and 48 h as well (P<0.05). But there was no difference oin expressions of Notch1 and Hes1 mRNA among group A, group B and group C after co-culture for 24 h and 48 h (P>0.05). There was no difference in expressions of Notch1 and Hes1 mRNA between 24 h and 48 h treatment in group D. CONCLUSIONS: SCE could promote the proliferation of NSCs. It is demonstrated that the microenvironment of SCI may promote the proliferation of NSCs. Besides, SCE could increase the expression of Notch1 and Hes1 mRNA of NSC. It can be concluded that the Notch signaling pathway activation is one of the mechanisms that locally injured microenvironment contributes to the proliferation of ENSC after SCIs. This process may be performed by up-regulating the expressions of Notch1 and Hes1 gene.

Up-regulation of Smurf1 after spinal cord injury in adult rats.

Smad ubiquitination regulatory factor 1 (Smurf1) is one of members of the Hect family of proteins, which also includes the ubiquitin E3-type ligases Nedd3 and E6-AP. As an E3 ligase, Smurf1 selectively interacts with receptor-regulated Smads to trigger their ubiquitination and degradation. Recently, a report indicates that Smurf1 can inhibit apoptosis by regulating p53 negatively, which depends on the effect of Smurf1 stabilizing the MDM2-MDMX complex. However, the roles of Smurf1 in central nervous system injury remain to be unknown. In our study, we finished acute spinal cord injury (SCI) in adult rats to research the protein expression and cellular localization of Smurf1 in spinal cord. Western blot analysis showed that Smurf1 was low expressed in normal spinal cord. It was increased at 6 h after SCI, peaked at 1 day, remained for 3 days, and then declined gradually during the following days. Immunohistochemistry further confirmed that Smurf1 immunoactivity was expressed at low levels in the gray matter and white matter in normal condition and increased after SCI. Double immunofluorescence staining showed that Smurf1 was co-expressed NeuN (neuronal marker), CNPase (oligodendroglial marker), and active caspase-3 at 1 day post-injury. Additionally, p53 and MDM2 levels were up-regulated after SCI consistently. All these findings suggest that Smurf1 might be involved in the pathophysiology of spinal cord after SCI.

Regulating function of coenzymization and decoenzymization of the lactate dehydrogenase isozymes in the mouse tissues during hypoxia / 中国医学科学杂志(英文版)

<p><b>OBJECTIVE</b>To study the characteristics of changes of LDH enzyme patterns of mice under slight hypoxia.</p><p><b>METHODS</b>Mice treated with artificial hypoxia, various tissues were made for the test of LDH enzymatic activity by the specific staining technique. LDH (1-5) relative percentage enzymatic activity (RPEA) were measured with CS-910 dual-wavelength thin layer chromatography scanner.</p><p><b>RESULTS</b>The RPEA of LDH isozymes of various tissues after slight hypoxia shifted to the isozymes LDH1 and LDH2, whose principal subunits are H subunits, and the RPEA of LDH1 (H4), LDH2 (H3M) increased, while RPEA of LDH5 (M4) in various tissues decreased prominently except the cardiac muscle, and that of LDH4 (HM3) decreased as well. After polyacrylamide gel electrophoresis (PAGE) of the hypoxia treated cardiac muscle specimen was made, activity subbands originated regularly in the isoyme patterns of LDH, with the regularity of LDH1 (0 subband), LDH2 (0-1 subbands), LDH3 (0-2 subbands), LDH4 (1-3 subbands), LDH5 (2-4 subbands). After adding appropriate amount of NAD+ to the hypoxia treated cardiac muscle specimen, PAGE showed the subbands of four isoymes (LDH2-LDH5) reduced or even totally disappeared in the isozyme patterns.</p><p><b>CONCLUSIONS</b>The negative feedback regulation of coenzymization and decoenzymization of LDH isozymes is one of the mouse stress responses to slight hypoxia.</p>