Comparison of Laminectomy with Fusion and Laminoplasty Treating Multilevel Cervical Spondylotic Myelopathy: A Single-Center Retrospective Study.

OBJECTIVE: Comparing laminectomy with fusion (LF) and laminoplasty (LP) for treating multilevel cervical spondylotic myelopathy (MCSM) and comparative analysis of neck pain and sagittal cervical parameters. METHODS: This single-center study retrospectively analyzed MCSM patients treated with LF or LP in our department between June 2018 and January 2023, with at least a 12-month follow-up. T-tests were used to identify operation time, hemoglobin, hospital stay, modified Japanese Orthopaedic Association (mJOA) score, C2-C7 Cobb angle, C2-C7 sagittal vertical axis, T1 slope, cervical range of motion (cROM), and C4/5 anterior and posterior spinal canal diameter (A-P diameter) and area. Nonparametric tests were used to identify visual analog scale (VAS) score (assessing neck pain). Pearson correlation analyses were used to identify the neck pain. RESULTS: Of all 67 patients (LF: 24, LP: 43), both groups' mJOA scores significantly improved (P < 0.001). The VAS scores had both significantly decreased, with the LF group exhibiting a more marked reduction (LF: P < 0.001, LP: P = 0.037). Both groups' C4/5 A-P diameters and areas increased significantly (P < 0.001). The cROM had both significantly decreased, with the LF group exhibiting a greater reduction. At the last follow-up, the LF group's T1 slope and C2-C7 Cobb angle considerably increased, and pain VAS scores substantially correlated with the C2-C7 Cobb angle (R = -0.451, P < 0.001). CONCLUSIONS: LF and LP were efficacious for MCSM. LF relieved neck pain better but caused greater reduction in cervical mobility. Cervical lordosis improvement was significantly correlated with neck pain alleviation.

Comparison of anterior cervical diskectomy with fusion (ACDF) and laminoplasty treating multilevel cervical spondylotic myelopathy with developmental canal stenosis: a retrospective study.

PURPOSE: To evaluate clinical effectiveness and radiologic results of anterior cervical diskectomy with fusion (ACDF) comparing with laminoplasty (LP) in treating multilevel cervical spondylotic myelopathy (MCSM) with developmental canal stenosis (DCS). METHODS: This was a retrospective analysis of 41 patients who had MCSM with DCS treated with ACDF or LP from December 2018 to April 2023. Patients were split into ACDF and LP groups for comparison, and patients were further separated into subgroups based on whether or not a reserving canal space was present. The operation time, hemoglobin, hospital stay, modified Japanese Orthopaedic Association (mJOA) score, and visual analog scale (VAS) score were used to assess clinical efficacy. The C2-C7 Cobb angle, C2-C7 sagittal vertical axis, T1 slope, and cervical range of motion were applied to evaluate imaging changes. RESULTS: Of the 41 patients, 19 received ACDF, and 22 received LP. At the final follow-up, both groups' mJOA scores significantly improved, and the intercomparison showed no differences; the VAS score was much lower in the ACDF group but remained unchanged in the LP group. At the final follow-up, the C2-C7 Cobb angle and T1 slope had significantly increased in the ACDF group, while the LP group showed no change; the cervical range of motion had significantly decreased in both groups, with the ACDF group exhibiting a more marked reduction. Within the ACDF subgroup, there was no postoperative symptom improvement for those with reserving space, whereas there was postoperative symptom resolution for those with non-reserving space; however, postoperative symptom in the LP subgroup was resolved. CONCLUSIONS: Both ACDF and LP were efficacious for MCSM patients with DCS. While ACDF could improve cervical lordosis and alleviate neck pain more effectively, it can also result in cervical sagittal imbalance and decreased mobility. Furthermore, the recovery from LP was superior to that from ACDF for patients with reserving space. In contrast, the recovery from both decompression techniques was comparable for individuals in non-reserving space.

Circular RNA HIPK2 Promotes A1 Astrocyte Activation after Spinal Cord Injury through Autophagy and Endoplasmic Reticulum Stress by Modulating miR-124-3p-Mediated Smad2 Repression.

Glial scarring formed by reactive astrocytes after spinal cord injury (SCI) is the primary obstacle to neuronal regeneration within the central nervous system, making them a promising target for SCI treatment. Our previous studies have demonstrated the positive impact of miR-124-3p on neuronal repair, but it remains unclear how miR-124-3p is involved in autophagy or ER stress in astrocyte activation. To answer this question, the expression of A1 astrocyte-related markers at the transcriptional and protein levels after SCI was checked in RNA-sequencing data and verified using quantitative polymerase chain reaction (qPCR) and Western blotting in vitro and in vivo. The potential interactions among circHIPK2, miR-124-3p, and Smad2 were analyzed and confirmed by bioinformatics analyses and a luciferase reporter assay. In the end, the role of miR-124-3p in autophagy, ER stress, and SCI was investigated by using Western blotting to measure key biomarkers (C3, LC3, and Chop) in the absence or presence of corresponding selective inhibitors (siRNA, 4-PBA, TG). As a result, SCI caused the increase of A1 astrocyte markers, in which the upregulated circHIPK2 directly targeted miR-124-3p, and the direct downregulating effect of Smad2 by miR-124-3p was abolished, while Agomir-124 treatment reversed this effect. Injury caused a significant change of markers for ER stress and autophagy through the circHIPK2/miR-124-3p/Smad2 pathway, which might activate the A1 phenotype, and ER stress might promote autophagy in astrocytes. In conclusion, circHIPK2 may play a functional role in sequestering miR-124-3p and facilitating the activation of A1 astrocytes through regulating Smad2-mediated downstream autophagy and ER stress pathways, providing a new perspective on potential targets for functional recovery after SCI.

Transcriptomics Provides Novel Insights into the Regulatory Mechanism of IncRNA HIF1 A-AS1 on Vascular Smooth Muscle Cells.

INTRODUCTION: Thoracic aortic aneurysm is a potentially fatal disease with a strong genetic contribution. The dysfunction of vascular smooth muscle cells (VSMCs) contributes to the formation of this aneurysm. Although previous studies suggested that long non-coding ribonucleic acid (RNA) hypoxia inducible factor 1 α-antisense RNA 1 (HIF1A-AS1) exerted a vital role in the progression and pathogenesis of thoracic aortic aneurysm, we managed to find a new regulatory mechanism of HIF1A-AS1 in VSMCs via transcriptomics. METHODS: Cell viability was detected by the cell counting kit-8 assay. Cell apoptosis was assessed by Annexin V-fluorescein isothiocyanate/propidium iodide double staining. Transwell migration assay and wound healing assay were performed to check the migration ability of HIF1A-AS1 on VSMCs. The NextSeq XTen system (Illumina) was used to collect RNA sequencing data. Lastly, reverse transcription-quantitative polymerase chain reaction confirmed the veracity and reliability of RNA-sequencing results. RESULTS: We observed that overexpressing HIF1A-AS1 successfully promoted apoptosis, significantly altered cell cycle distribution, and greatly attenuated migration in VSMCs, further highlighting the robust promoting effects of HIF1A-AS1 to thoracic aortic aneurysm. Moreover, transcriptomics was implemented to uncover its underlying mechanism. A total of 175 differently expressed genes were identified, with some of them enriched in apoptosis, migration, and cell cycle-related pathways. Intriguingly, some differently expressed genes were noted in vascular development or coagulation function pathways. CONCLUSION: We suggest that HIF1A-AS1 mediated the progression of thoracic aortic aneurysm by not only regulating the function of VSMCs, but also altering vascular development or coagulation function.

lncRNA XIST inhibition promotes M2 polarization of microglial and aggravates the spinal cord injury via regulating miR-124-3p / IRF1 axis.

Spinal cord injury (SCI) has a high disability rate and mortality rate. Recently, LncRNA XIST has been found to be involved in the regulation of inflammatory responses. Therefore, we aimed to investigate the role of XIST in the occurrence and development of SCI and the specific regulation mechanism. Methods: 100 ng/mL lipopolysaccharide (LPS) was used to treat mouse microglia BV2 cells. Hitting spinal cord was performed to C57BL/6 mice for establishing SCI model. Real-time reverse transcriptase-polymerase chain reaction (RT-qPCR), Western blot, Immunofluorescence (IF) and Enzyme linked immunosorbent assay (ELISA) experiments were used to explore the function of XIST, miR-124-3p and IRF1 in LPS-induced BV2 cells. RT-qPCR, Nissl staining, IF, Western blot and ELISA experiment were performed to study the function of XIST in SCI mice. Dual-luciferase reporter assay, RNA immunoprecipitation (RIP), RT-qPCR and Western blot assays were utilized to identify the interaction among XIST, miR-124-3p and IRF1. Results: XIST was upregulated in LPS-induced BV2 cells and spinal cord tissues of SCI mice. Overexpression of XIST promoted the M1 microphages polarization and cytokines concentration in LPS-stimulated BV2 cells, aggravated SCI of mice. Downregulated XIST promoted M1-to-M2 conversion of microglial and relieved the injury of SCI mice. Mechanism verification indicated that XIST acted as a molecular sponge of miR-124-3p and regulated IRF1 expression. Increased miR-124-3p or reduced IRF1 inhibited M1 polarization of microglial and decreased the production of inflammatory cytokines in LPS-induced BV2 cells. Increased XIST or decreased miR-124-3p had an opposite of on LPS-induced BV2 cells. Conclusion: Overexpression of XIST enhanced M1 polarization of microglia and promoted the level of inflammatory cytokines through sponging miR-124-3p and regulating IRF1 expression.

Transcriptomics Provides Novel Insights into the Regulatory Mechanism of IncRNA HIF1 A-AS1 on Vascular Smooth Muscle Cells

ABSTRACT Introduction: Thoracic aortic aneurysm is a potentially fatal disease with a strong genetic contribution. The dysfunction of vascular smooth muscle cells (VSMCs) contributes to the formation of this aneurysm. Although previous studies suggested that long non-coding ribonucleic acid (RNA) hypoxia inducible factor 1 α-antisense RNA 1 (HIF1A-AS1) exerted a vital role in the progression and pathogenesis of thoracic aortic aneurysm, we managed to find a new regulatory mechanism of HIF1A-AS1 in VSMCs via transcriptomics. Methods: Cell viability was detected by the cell counting kit-8 assay. Cell apoptosis was assessed by Annexin V-fluorescein isothiocyanate/propidium iodide double staining. Transwell migration assay and wound healing assay were performed to check the migration ability of HIF1A-AS1 on VSMCs. The NextSeq XTen system (Illumina) was used to collect RNA sequencing data. Lastly, reverse transcription-quantitative polymerase chain reaction confirmed the veracity and reliability of RNA-sequencing results. Results: We observed that overexpressing HIF1A-AS1 successfully promoted apoptosis, significantly altered cell cycle distribution, and greatly attenuated migration in VSMCs, further highlighting the robust promoting effects of HIF1A-AS1 to thoracic aortic aneurysm. Moreover, transcriptomics was implemented to uncover its underlying mechanism. A total of 175 differently expressed genes were identified, with some of them enriched in apoptosis, migration, and cell cycle-related pathways. Intriguingly, some differently expressed genes were noted in vascular development or coagulation function pathways. Conclusion: We suggest that HIF1A-AS1 mediated the progression of thoracic aortic aneurysm by not only regulating the function of VSMCs, but also altering vascular development or coagulation function.

ESG ratings, monetary policy uncertainty, and bond issuance premium.

Existing studies generally recognize the critical role played by macro monetary policy, of which the uncertainty will increase corporate bond issuance premiums at a micro level. However, relatively little is known about these relationships from the perspective of non-financial information in the corporation. So this study sets out to do further exploration. We use the database to obtain information, including the bond issuance of A-share listed corporations in China from 2015 to 2020. The findings suggest that high environmental, social, and governance (ESG) ratings from listed corporations significantly weaken the positive correlation between monetary policy uncertainty and bond issuance premiums. Specifically, it has a positive information pricing effect on China's primary debt issuance market, as well as a mitigating impact on macro-financial policy risk. We also find, through further mechanistic studies, that ESG ratings are more helpful in undermining the impact of monetary policy uncertainty on bond issuance premiums in the context of higher financial information quality. Our findings are conducive to enriching the research framework of the economic consequences of ESG ratings, meaningfully influencing the growing literature that exposed the mechanism of bond issuance premiums, and further, verifying the interaction of information at different levels (macro vs micro) in asset pricing.

Tranexamic acid dosage for spinal surgery: a meta-analysis.

PURPOSE: We conducted this meta-analysis of randomized controlled trials (RCTs) to compare the efficacy of different doses of intravenous tranexamic acid (TXA) in spinal surgery. METHODS: We searched relevant academic articles from PubMed, Embase, the Cochrane Library, and CNKI. Two reviewers independently selected studies, assessed quality, extracted data, and evaluated the risk of bias. RevMan 5.4 was used for data analysis. RESULTS: Ten randomized controlled trials (RCTs) met the inclusion criteria and were identified, including 740 patients. According to the different dose regimens of intravenous TXA, the included studies' patients were divided into the high dose of intravenous TXA group and the low dose of intravenous TXA group. Compared with the low-dose group, the high-dose group can reduce the intraoperative blood loss (MD = - 100.87, 95% CI: [- 147.81, - 53.92], P < 0.0001). For the postoperative Hb and HCT, the high-dose group can separately maintain 4.54 g/dL (MD = 4.54, 95% CI: [2.08, 6.99], P = 0.003) and 1.27% (MD = 1.27, 95% CI: [0.59, 1.94], P = 0.0002). There were no statistically significant differences in total blood loss, preoperative Hb and HCT, operative time, and blood transfusion rate between the high-dose group and the low-dose group. CONCLUSIONS: Based on the present meta-analysis, compared with the low-dose of intravenous TXA in spinal surgery, the high dose of intravenous TXA decreases the intraoperative blood loss and preserves higher postoperative Hb and HCT levels without increasing the operative time and blood transfusion rate.

LncRNA HIF1A-AS1 Regulates the Cellular Function of HUVECs by Globally Regulating mRNA and miRNA Expression.

BACKGROUND: Long non-coding RNA (lncRNA) hypoxia inducible factor 1α-antisense RNA 1 (HIF1A-AS1) serves critical roles in cardiovascular diseases (CVDs). Vascular endothelial cells (VECs) are vulnerable to stimuli. Our previous study revealed that knockdown of HIF1A-AS1 reduces palmitic acid-induced apoptosis and promotes the proliferation of human VECs (HUVECs); however, the underlying mechanism remains unclear. MATERIAL AND METHODS: Cell Counting Kit-8, flow cytometry, transwell invasion, and wound healing were applied to detect the function of HUVECs. Moreover, miRNA sequencing (miRNA-seq) and RNA sequencing (RNA-seq) were conducted to uncover its underlying mechanism. Quantitative Polymerase Chain Reaction (qPCR) was implemented to assess the accuracy of miRNA-seq. A co-expression network was generated to determine the relationship between differentially expressed miRNAs (DEmiRNAs) and differentially expressed genes (DEGs). RESULTS: Knockdown of HIF1A-AS1 promoted the proliferation, migration, and invasion but reduced the apoptosis of HUVECs, and the overexpression of this lncRNA had the opposite effect. Numerous DEmiRNAs and DEGs were identified, which might contribute to this phenomenon. Multiple target genes of DEmiRNAs were associated with cell proliferation and apoptosis, and overlapped with DEGs identified from RNA-seq. Finally, the network manifested that lncRNA HIF1A-AS1 moderated the function of HUVECs by not only regulating the expression of some genes directly but also by influencing a few miRNAs to indirectly mediate the expression of mRNAs. CONCLUSIONS: The results suggested that HIF1A-AS1 might regulate HUVEC function by not only regulating the expression of some genes directly but also by influencing some miRNAs to indirectly mediate the expression level of mRNA.

Statistical ankle-shape and pressure analysis for design of elastic tubular bandage.

Ankles can benefit from the elastic tube bandage (ETB) by providing the ankle joint with compression, but partial high- or low-pressure leads to body discomfort. The aim of this paper is to propose a method for analyzing the ankle shape with the fabric compression which is basis on the comfortable pressure on human body. First, a standard model of ankle is established from the scanned data of 306 samples, and the mapping of the fabric shape curves on ankle were constructed by the U-direction convex curves of the model. The positions or areas of maximum and minimum pressure are then marked by extracting the curvatures of the fabric shape curves. According to the Laplace's Law, the sizes of ETBs can be calculated given that the value of comfortable pressure on human body is the maximum one. The data of calculation is approximate to the relevant previous studies which has the same parameters of ETBs. Nine groups of the ankle shapes from the database are discussed, each group has a proportional coefficient to the standard model, and the result shows that six sizes of ETBs with comfort pressure match for the nine groups. These can be applied to the comfort design, and the method proposed can boost size customization of ETBs, as well as will inspire the research on other elastic compression garments.

[Effects of HOXA1 Gene Antisense Oligonucleotides on Growth of Esophageal Cancer Cells].

OBJECTIVE: To investigate the effect of antisense oligodeoxynucleotides (ASODN) of Homeobox A1 gene ( HOXA1) on proliferation, apoptosis, invasion and migration of esophageal carcinoma cells. METHODS: The expression of HOXA1 protein in normal esophageal epithelial cells Het-1A and esophageal cancer TE-1, EC9706 and Eca109 cells was detected by Western blot. Screening of highly expressed of HOXA1 protein esophageal squamous cell carcinoma cells for follow-up experiments. HOXA1 antisense oligonucleotide (ASODN) chains, sense oligodeoxynucleotides (SODN) chain, and nonsense oligodeoxy nucleotides (N-ODN) chain were designed. The screened esophageal squamous cell carcinoma cells with high expression were divided into HOXA1 ASODN group (5, 10, 15 µmol/L HOXA1 ASODN transfected Eca109 cells), control group (conventional culture medium, no cell transfection), SODN group (cells transfected with 15 µmol/L of SODN) and N-ODN group (cells transfected with 15 µmol/L N-ODN). Cell viability, apoptosis rate and invasion and migration ability were detected by methylthiazolyldiphenyl-tetrazolium bromide (MTT) method, flow cytometry, transwell chamber respectively; The expression of HOXA1, phosphorylation serine/threonine kinase (p-AKT), proliferating cell nuclear antigen (PCNA), matrix metalloproteinase 2 (MMP-2) and B-cell lymphoma2 (Bcl-2) associated X protein (Bax) protein was detected by Western blot. RESULTS: Compared with normal esophageal epithelial cells Het-1A, the expression of HOXA1 protein in human esophageal squamous cell carcinoma cells TE-1, EC9706 and Eca109 was significantly higher ( P<0.05). The expression of HOXA1 protein was the highest in Eca109 cells, therefore, Eca109 cells were selected for follow-up experiments. The expression of HOXA1 protein in Eca109 cells transfected with HOXA1 ASODN was significantly decreased ( P<0.05). After transfection of Eca109 cells with HOXA1 ASODN, the viability of Eca109 cells decreased with the increase of concentration and time, the difference was significant compared with the control, SODN and N-ODN groups ( P<0.05). 15 µmol/L HOXA1 ASODN significantly inhibited cell viability. After 15 µmol/L HOXA1 ASODN was transfected into Eca109 cells, the invasion and migration abilities of cells were significantly decreased, the apoptosis rate was increased, the expressions of p-AKT, PCNA and MMP-2 were significantly decreased, and the expression of Bax was significantly increased ( P<0.05). CONCLUSION: Antisense oligodeoxynucleotides of HOXA1 gene can inhibit the proliferation, invasion and migration of esophageal cancer cells, and induce apoptosis. The mechanism is related to the inhibition of PI3K/AKT signaling pathway.

MicroRNA485-3p negatively regulates the transcriptional co-repressor CtBP1 to control the oncogenic process in osteosarcoma cells.

Carboxyl-terminal binding protein 1 (CtBP1), a well-known transcriptional co-repressor, is highly expressed in a number of cancer types. However, it is still absent in osteosarcoma cells. Here, we found that CtBP1, but not CtBP2, is overexpressed in invasive osteosarcoma tissues and cells. The overexpressed CtBP1 in turn represses its downstream targets, such as the pro-apoptotic regulators Bax, Bim and p53 upregulated modulator of apoptosis (PUMA), cell adhesion molecule E-cadherin, and the cell cycle regulators p16, p21 and phosphatase and tensin homolog (PTEN). To explore the molecular mechanism of CtBP1 overexpression, we subjected three independent clinical samples to miRNA microarray analysis and found that miR-485-3p could specifically bind to the 3'-untranslated region (3'-UTR) of CtBP1, thereby negatively controlling CtBP1 expression. The overexpression of miR-485-3p in osteosarcoma cells significantly repressed CtBP1 levels and inhibited cell proliferation, colony formation, cell migration and sphere formation. Further analysis indicated that DNA hypermethylation in the promoter region of miR-485-3p caused the downregulation of miR-485-3p. Treatment with the DNA methylation inhibitor 5-aza-2'-deoxycytidine (AZA) resulted in the upregulation of miR-485-3p and the downregulation of CtBP1 as well as inhibited osteosarcoma cell growth. This study provides evidence that CtBP1 is also overexpressed in osteosarcoma cells and demonstrates the underlying mechanism regarding its overexpression. Thus, therapeutically targeting CtBP1 may represent an effective strategy for osteosarcoma therapy.

Effects of pre-incubation with C-type natriuretic peptide on nuclear maturation, mitochondrial behavior, and developmental competence of sheep oocytes.

In vitro produced mammalian embryos suffer from developmental failure, with a large proportion showing embryonic retardation, degradation, or apoptosis. This failure is due, in part, to incomplete oocyte cytoplasmic maturation. C-type natriuretic peptide (CNP) has been reported to act as a meiotic inhibitor. Here we explored the potential effects of CNP pre-treatment sheep oocytes on nuclear maturation, changes in mitochondrial behavior and developmental competence of in vitro fertilized embryos. Sheep cumulus-oocyte complexes (COCs) were aspirated from abattoir-derived ovaries. Nuclear progression was assessed using DAPI chromatin staining, the expression of natriuretic peptide receptor 2 (NPR2) was evaluated by RT-qPCR, active mitochondria localization was assessed with a confocal laser scanning microscopy using MitoTracker Red, and the developmental competence of sheep oocytes subjected to one-step IVM or two-step IVM with or without CNP pretreatment was also investigated. Our results showed that 200 nM CNP could effectively maintain meiotic arrest of sheep COCs in vitro within 4 h. Furthermore, NPR2 mRNA was mainly expressed in cumulus cells. COCs pre-treated with 200 nM CNP for 4 h followed by 24 h IVM showed significantly higher (P < 0.05) cleavage rate and blastocyst rate after in vitro fertilization (IVF), and significantly lower (P < 0.05) proportion of DNA-fragmented nuclei in blastocysts when compared to the conventional 24 h IVM (standard IVM). Non-matured oocytes mainly displayed brilliant circumferential and fine diffuse distribution of mitochondria throughout the cytoplasm. By comparison, 200 nM CNP pre-treated COCs for 4 h led to cytoplasmic mitochondrial granule localization to the peripheral and perinuclear regions. Moreover, oocytes pre-treated with 200 nM CNP for 4 h followed by 24 h IVM, showed mitochondrial organization were similar to those of conventional 24 h matured oocytes in which mitochondria were aggregated more toward the cortical regions of the oocytes, but with larger clumps of stained mitochondria. These results indicate that CNP pre-treatment improves the quality and developmental competence of sheep oocytes and has great potential for facilitating in vitro embryo production.

Iron deficiency accelerates intervertebral disc degeneration through affecting the stability of DNA polymerase epsilon complex.

Iron serves as an important cofactor of iron-containing proteins that play critical roles in the maintenance of DNA stability and cell cycle progression. The disturbed iron homeostasis results in the pathogenesis of many diseases such as cancer and anemia. In this study, we found a clear correlation between iron deficiency and intervertebral disc degeneration (IDD). Through microarray experiments, we found that a large number of genes were differentially expressed in tissues with different degrees of degeneration. Among them, an iron-containing gene, PolE, the catalytic subunit of DNA polymerase epsilon (Polε), and the other two Polε subunits, including PolE2 and PolE3, were markedly downregulated, while some proteins involved in apoptosis such as Caspase-3 and -8 were significantly upregulated. By supplementation with an iron chelator deferoxamine (DFO) or knocking down either iron divalentmetal transporter 1 (DMT1) or transferrin receptor 1 (TfR1) in the nucleus pulposus (NP) cells, we found that the protein levels of PolE complex members were dramatically reduced, whereas the intrinsic apoptotic pathway was activated. Interestingly, overexpression of PolE in NP cells knocked down with either DMT1 or TfR could not reverse the stability of PolE complex and apoptosis status. In summary, our study suggests that iron deficiency is an important factor in the aggravation of IDD. Proper iron supplementation may be an effective strategy to alleviate the symptoms of patients with IDD.

Transpedicular Excision of a Thoracic Intraspinal Osteochondroma in a Patient with Hereditary Multiple Exostoses and Brown-Séquard Syndrome.

BACKGROUND: Spinal osteochondroma is a rare but recognized cause of myelopathy. Brown-Séquard syndrome is a form of severe myelopathy characterized by a clinical picture of hemisection of the spinal cord. Brown-Séquard syndrome caused by osteochondroma is extremely rare, calling for individualized surgical procedures. CASE DESCRIPTION: We report a 16-year-old girl with hereditary multiple exostoses and a rare case of thoracic osteochondroma causing partial Brown-Séquard syndrome. Customized surgical procedures were designed to avoid iatrogenic spinal cord injury. The patient underwent neural decompression and tumor excision through a transpedicular approach. The surgical procedure consisted of 4 consecutive steps: 1) laminectomy, 2) costotransversectomy and pediculectomy, 3) extracavitary removal of the mass, and 4) pedicular fixation with fusion. Total resection of the tumor was achieved macroscopically without intraoperative spinal cord injury. The postoperative recovery was uneventful, and the patient returned to a normal life without evidence of recurrence at 24-month follow-up. CONCLUSIONS: For patients with hereditary multiple exostosis and new onset of neurologic symptoms, the possibility of a spinal osteochondroma should be considered. In the situation of an intraspinal exostosis protruding from the lateral side, customized surgical procedures with a transpedicular approach may be a valid way to minimize intraoperative neural injury and achieve a satisfactory outcome.

Effect of C-type natriuretic peptide pretreatment on in vitro bovine oocyte maturation.

C-type natriuretic peptide (CNP) has been considered as a physiological meiotic inhibitor that stimulates the cGMP production by cumulus cell natriuretic peptide receptor 2 (NPR2), which inhibits oocyte phosphodiesterase type 3 activity and increases cAMP. In this study, we explored the effect of CNP pretreatment on the in vitro maturation (IVM) of bovine oocytes by examining changes in cleavage rate, blastocyst formation, mitochondrial DNA (mtDNA) copy number, reactive oxygen species (ROS) level, glutathione (GSH) content, and redox state. Our results showed that 200 nM CNP could effectively maintain meiotic arrest of bovine oocytes in vitro within 6 h. The two-step IVM system in which oocytes were pretreated with 200 nM CNP for 6 h and then cultured IVM for 28 h yielded a significantly (P < 0.05) increased blastocyst rate and cell number after in vitro fertilization (IVF) while compared to the conventional one-step IVM method. In addition, in comparison with the conventional 24-h matured oocyte, oocytes pretreated with 200 nM CNP for 6 h followed by 28 h IVM resulted in significantly (P < 0.05) higher mtDNA copy number and ROS levels in oocytes, while GSH level significantly (P < 0.05) decreased. Remarkably, regardless of treatment, no changes were observed in FAD++, NAD(P)H autofluorescence intensity, and redox ratio (FAD++/NAD(P)H) within the oocytes, maintaining a healthy metabolic equilibrium of redox throughout the two-step IVM. In conclusion, these results indicate that CNP pretreatment could dramatically improve the quality of bovine oocytes during in vitro maturation.

miR-10b promotes invasion by targeting KLF4 in osteosarcoma cells.

OBJECTIVE: Osteosarcoma is a common malignancy with high rate of metastasis. miR-10b has been reported to be expressed in many types of tumors abnormally and be associated with cancer carcinogenesis and progression. But the function of miR-10b in osteosarcoma is still unknown. So this study was aimed to investigate the role of miR-10b in osteosarcoma development. METHODS: miR-10b expression in osteosarcoma tissues and osteosarcoma cells were detected using real time PCR. The effects of miR-10b on osteosarcoma cells proliferation, apoptosis, migration and invasion were detected using CCK-8 assay, flow cytometry, wound-healing assay and transwell assay, respectively. The relationship between miR-10b and KLF4 was evaluated using dual-luciferase assay, correlation analysis. RESULTS: miR-10b was highly expressed in osteosarcoma tissues and osteosarcoma cells. Furthermore, inhibition of miR-10b in osteosarcoma cells depressed the cells proliferation, migration and invasion but promoted cells apoptosis. In addition, KLF4 was down-regulated by miR-10b and miR-10b expression was negatively related to KLF4 expression in osteosarcoma tissue, miR-10b participated in the process of osteosarcoma cells invasion by regulating KLF4 expression. CONCLUSION: miR-10b is overexpressed in osteosarcoma and KLF4 is the direct target gene of miR-10b. Furthermore, miR-10b promotes osteosarcoma cells progression by downregulating KLF4 expression. These results suggest that miR-10b functions as an oncomiR and play an important role in osteosarcoma cellular processes at least partially through regulating KLF4; miR-10b may be a therapeutic target for osteosarcoma treatment.