Long non-coding RNA OIP5-AS1 suppresses multiple myeloma progression by sponging miR-27a-3p to activate TSC1 expression.

BACKGROUND: Multiple myeloma (MM) is a prevalent hematological malignancy. Long noncoding RNAs are correlated with the development of MM. In this project, the function of lncRNA opa interacting protein 5-antisense 1 (OIP5-AS1) in MM and the potential mechanistic pathway were explored. METHODS: The expression of OIP5-AS1, microRNA (miR)-27a-3p and tuberous sclerosis 1 (TSC1) was analyzed by quantitative real-time polymerase chain reaction (qRT-PCR) assay. Cell proliferation was assessed by Cell Counting Kit-8 (CCK-8) assay, colony formation assay and Bromodeoxyuridine (BrdU) staining. And cell apoptosis was evaluated by flow cytometry assay. Cell metastasis was assessed utilizing transwell assay. Western blot analysis was employed to detect protein level. The target relation between miR-27a-3p and OIP5-AS1 or TSC1 was confirmed via dual-luciferase reporter assay and RNA immunoprecipitation assay. Tumor xenograft assay was conducted to measure the function of OIP5-AS1 in vivo. RESULTS: The expression levels of OIP5-AS1 and TSC1 were decreased in MM, whereas miR-27a-3p was upregulated. High level of OIP5-AS1 could predict favourable prognosis of MM patients. Overexpression of OIP5-AS1 inhibited cell viability, colony formation ability, migration and invasion, induced cell cycle arrest in G1 phase and apoptosis of MM cells in vitro as well as repressed tumorigenesis in vivo. MiR-27a-3p was a target of OIP5-AS1, and reversed the impact of OIP5-AS1 on MM cells. MiR-27a-3p directly targeted TSC1. Silencing of miR-27a-3p repressed MM progression by elevating TSC1 expression. OIP5-AS1 upregulated TSC1 by sponging miR-27a-3p. CONCLUSION: OIP5-AS1 repressed multiple myeloma progression by regulating miR-27a-3p/TSC1 axis.

Triptolide improves spinal cord injury by promoting autophagy and inhibiting apoptosis.

We investigated the effect of triptolide (TP) on spinal cord injury (SCI), and its underlying mechanism. Following the establishment of the SCI model using YFP H-line transgenic mice, TP was intraperitoneally injected at a dose of 0.2 mg/kg once daily for 7 days. Behavioral tests, Nissl staining, and hematoxylin-eosin staining were employed to assess motor function recovery and neuronal cell death. Western blot and immunofluorescence staining were used to assess autophagy-associated proteins (LC3B, p62, Beclin-1) and the apoptosis-associated proteins (Bcl-2, caspase-3, Bax). The TP-treated group showed improved motor functions, and reduced neuronal cell death. Also, significant upregulation of Bcl-2 and LC3B expressions, with the downregulation of p62, Bax and caspase-3 expressions were found in the TP-treated group. Additionally, phosphorylation of extracellular signal-regulated protein kinases 1 and 2 (ERK1 and ERK2) was decreased in the TP-treated group. TP mediates its protective effect in SCI by promoting the autophagic pathway while inhibiting the MAPK/ERK1/2 signaling pathway. These results demonstrate the therapeutic potential of TP in SCI.

microRNA-29a inhibition induces Gab1 upregulation to protect OB-6 human osteoblasts from hydrogen peroxide.

The present study determines the role of the Gab1 in hydrogen peroxide (H2O2)-induced death of human osteoblasts. We show that Gab1 is required for H2O2-induced Akt activation to promote osteoblast survival. In OB-6 human osteoblasts, Gab1 silencing (by targeted-shRNA) or complete knockout (by CRISPR-Cas9 KO plasmid) largely attenuated Akt activation by H2O2. Gab1-depleted OB-6 cells were more vulnerable to H2O2. Conversely, forced over-expression of Gab1 by an adenovirus vector increased Akt activation to protect OB-6 cells from H2O2. Significantly, the anti-sense of microRNA-29a ("antagomiR-29a") induced Gab1 expression to facilitate H2O2-induced Akt activation, which protected OB-6 cells from apoptosis. AntagomiR-29a was however ineffective in Gab1-deficient and Akt-inhibited OB-6 cells. Forced over-expression of miR-29a induced Gab1 downregulation to inhibit H2O2-induced Akt activation, causing enhanced OB-6 cell death. miR-29a-induced actions were abolished by an adenovirus constitutively-active Akt1 (Ad-caAkt1) in OB-6 cells. Together, microRNA-29a inhibition induces Gab1 upregulation and Akt activation to protect OB-6 osteoblasts from H2O2.

Long noncoding RNA SNHG6 promotes osteosarcoma cell proliferation through regulating p21 and KLF2.

The effects of long non-coding RNAs (lncRNAs) on cellular biological processes and even the tumorigenesis have been widely reported. Small nucleolar RNA host gene 6 (SNHG6) has been reported to participate in regulating biological behaviors of multiple types of cancers. Nevertheless, the functions of SNHG6 in osteosarcoma still remain to be uncovered. This study intended to determine the clinical significance and biological functions of SNHG6 in osteosarcoma. It was confirmed by qRT-PCR that SNHG6 was highly expressed in osteosarcoma tissues and cell lines. Highly expressed SNHG6 predicted poor survival rate and advanced clinical stage for osteosarcoma patients, according to Kaplan-Meier method and Cox regression analysis. Loss-of-function assays were performed to examine the effects of silenced SNHG6 on the progression of osteosarcoma, indicating that silenced SNHG6 suppressed cell proliferation through inducing cell cycle arrest in G0/G1 phase and causing cell apoptosis. In vitro assays exposed the potential oncogenic role of SNHG6 in osteosarcoma, further affirmed by in vivo nude mice assays. Mechanistic assays demonstrated that SNHG6 was negatively correlated with p21 and KLF2 in osteosarcoma. And biological functions of SNHG6 in osteosarcoma were realized through regulating p21 and KLF2. Collectively, SNHG6 was a new type of molecule involving in the progression of osteosarcoma.

[Biomechanical and biocompatible enhancement of reinforced calcium phosphate cement via RGD peptide grafted chitosan nanofibers].

Objective: To analysis the biomechanical and biocompatible properties of calcium phosphate cement (CPC) enhanced by chitosan short nanofibers(CSNF) and Arg-Gly-Asp (RGD). Methods: Chitosan nanofibers were prepared by electrospinning, and cut into short fibers by high speed dispersion. CPC with calcium phosphorus ratio of 1.5:1 was prepared by Biocement D method. The composition and structure of CPC, CSNF, RGD modified CSNF (CSNF-RGD), CSNF enhanced CPC (CPC-CSNF), RGD modified CPC-CSNF (CPC-CSNF-RGD) were observed by infrared spectrum, X-ray diffraction (XRD) and scan electron microscopy (SEM). The mechanical properties were measured by universal mechanical testing instrument. The adhesion and proliferation of MC3T3 cells were assessed using immunofluorescence staining and MTT method. Results: The distribution of CSNF in the scaffold was homogeneous, and the porous structure between the nanofibers was observed by SEM. The infrared spectrum showed the characteristic peaks at 1633 nm and 1585 nm, indicating that RGD was successfully grafted on chitosan nanofibers. The XRD pattern showed that the bone cement had a certain curability. The stain-stress test showed that break strengths were (17.74±0.54) MPa for CPC-CSNF and (16.67±0.56) MPa for CPCP-CSNF-RGD, both were higher than that of CPC(all P<0.05). The immunofluorescence staining and MTT results indicated that MC3T3 cells grew better on CPC-CSNF-RGD after 240 min of culture(all P<0.05). Conclusion: CSNF-RGD can improve the biomechanical property and biocompatibility of CPC, indicating its potential application in bone tissue repair.

SC79 rescues osteoblasts from dexamethasone though activating Akt-Nrf2 signaling.

Dexamethasone (Dex) causes osteoblast cell injuries. In the present research, we tested the potential effect of SC79, a novel and specific Akt activator, against Dex in osteoblasts. In primary murine osteoblasts and osteoblastic MC3T3-E1 cells, pretreatment with SC79 significantly attenuated Dex-induced cell death. Further, Dex-induced mitochondrial permeability transition pore (mPTP) opening, cytochrome C release and apoptosis activation were dramatically alleviated with SC79 pretreatment in above cells. At the molecular level, SC79 activated Akt, which was indispensable for subsequent osteoblast protection against Dex. Akt inhibitors (LY294002, perifosine and MK-2206) blocked SC79-induced Akt activation and abolished its anti-Dex actions in osteoblasts. Further, SC79 activated Akt downstream Nrf2 (NF-E2-related factor 2) signaling and attenuated Dex-induced oxidative stress in osteoblasts. Nrf2 shRNA knockdown or S40T mutation almost reversed SC79-mediated anti-oxidant and cytoprotective activities in osteoblasts. Together, these results suggest that SC79 activates Akt-Nrf2 signaling to protect osteoblasts from Dex.

Krüppel-Like Factor 4 Is a Regulator of Proinflammatory Signaling in Fibroblast-Like Synoviocytes through Increased IL-6 Expression.

Human fibroblast-like synoviocytes play a vital role in joint synovial inflammation in rheumatoid arthritis (RA). Proinflammatory cytokines induce fibroblast-like synoviocyte activation and dysfunction. The inflammatory mediator Krüppel-like factor 4 is upregulated during inflammation and plays an important role in endothelial and macrophage activation during inflammation. However, the role of Krüppel-like factor 4 in fibroblast-like synoviocyte activation and RA inflammation remains to be defined. In this study, we identify the notion that Krüppel-like factor 4 is higher expressed in synovial tissues and fibroblast-like synoviocytes from RA patients than those from osteoarthritis patients. In vitro, the expression of Krüppel-like factor 4 in RA fibroblast-like synoviocytes is induced by proinflammatory cytokine tumor necrosis factor-α. Overexpression of Krüppel-like factor 4 in RA fibroblast-like synoviocytes robustly induced interleukin-6 production in the presence or absence of tumor necrosis factor-α. Conversely, knockdown of Krüppel-like factor 4 markedly attenuated interleukin-6 production in the presence or absence of tumor necrosis factor-α. Krüppel-like factor 4 not only can bind to and activate the interleukin-6 promoter, but also may interact directly with nuclear factor-kappa B. These results suggest that Krüppel-like factor 4 may act as a transcription factor mediating the activation of fibroblast-like synoviocytes in RA by inducing interleukin-6 expression in response to tumor necrosis factor-α.

Effect of B vitamin (folate, B6, and B12) supplementation on osteoporotic fracture and bone turnover markers: a meta-analysis.

BACKGROUND: B vitamins (including folate, B6, and B12) supplementation can effectively and easily modify high plasma homocysteine (Hcy). However, the role of Hcy in the pathogenesis of osteoporotic fracture and bone turnover is still controversial. This meta-analysis aimed to assess the impact of B vitamin supplementation on occurrence of any osteoporotic fracture and bone turnover by pooling the results of previous studies. MATERIAL AND METHODS: Relevant randomized controlled trials (RCTs) were searched in databases. Data integration and analysis were done by using Review Manager 5.3 (the Cochrane Collaboration). The risk ratio (RR) and corresponding 95% confidence intervals (CI) of fracture (intervention vs. control) were estimated. Changes in bone turnover indicators (continuous data), weighted mean difference (WMD), and corresponding 95% (CI) were pooled for estimation. RESULTS: Based on the results of 4 RCTs, this meta-analysis failed to identify a risk-reducing effect of daily supplementation of B vitamins on osteoporotic fracture in patients with vascular disease and with relatively normal plasma Hcy. In addition, we also did not find any positive effects of B vitamin supplementation on bone turnover. CONCLUSIONS: B vitamin supplementation might not be effective in preventing fracture and improving bone turnover. However, the possible benefits in selective populations, such as populations with very high plasma Hcy and from regions without B vitamin fortification should be explored in the future.

lncRNA myocardial infarction-associated transcript (MIAT) knockdown alleviates LPS-induced chondrocytes inflammatory injury via regulating miR-488-3p/sex determining region Y-related HMG-box 11 (SOX11) axis.

Long noncoding RNA (lncRNA) has been shown to be involved in the development of osteoarthritis (OA), an age-related bone and joint disease. However, the function and possible molecular mechanism of lncRNA myocardial infarction-associated transcript (MIAT) in lipopolysaccharide (LPS)-induced chondrocytes injury model remain unexplored. Cell viability and apoptosis were detected by methyl thiazolyl tetrazolium (MTT) and flow cytometry, respectively. Western blot was used to detect protein expression. The concentrations of inflammatory factors were estimated by enzyme-linked immunosorbent assay (ELISA). Abundances of MIAT, microRNA-488-3p (miR-488-3p), and sex determining region Y-related HMG-box 11 (SOX11) were examined by quantitative reverse transcriptase polymerase chain reaction (qRT-PCR). Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were performed to analyze the interaction between miR-488-3p and MIAT or SOX11. LPS caused chondrocytes injury by reducing cell activity and increasing apoptosis rate and inflammatory factor secretions. Higher levels of MIAT and SOX11 and lower miR-488-3p were observed in LPS-treated C28/I2 cells. Importantly, knockdown of MIAT attenuated the LPS-induced cell injury by targeting miR-488-3p, and miR-488-3p overexpression weakened the LPS-induced cell injury by targeting SOX11. Additionally, repression of MIAT inactivated the LPS-induced NF-κB signaling pathway by decreasing SOX11 and increasing miR-488-3p. Knockdown of MIAT alleviated the LPS-induced chondrocytes injury by inhibiting the NF-κB signaling pathway mediated by the miR-488-3p/SOX11 axis.

Prognostic factors for postoperative survival in melanoma patients with bone metastasis.

ABSTRACT: Melanoma can spread to the bone by metastasis and is relevant to a poor outcome. However, because of the rarity of melanoma patients with bone metastasis, the prognostic postoperative survival factors of them have not been elucidated. The aim of this special population-based cohort was to elucidate the prognostic factors associated with postoperative survival. The Surveillance, Epidemiology, and End Results database was used to extract postoperative survival data relating to patients with melanoma and bone metastasis at diagnosis between 2010 and 2016, along with data on a range of potential postoperative prognostic factors. We then investigated the potential postoperative prognostic roles of these factors using a Cox regression model and the Kaplan-Meier analysis. In all, the Surveillance, Epidemiology, and End Results database included 186 cases. Regarding overall survival, the 1-, 3-, and 5-year overall survival rates for the entire cohort were 36.2%, 15.4%, and 9.5%, respectively. Regarding cancer-specific survival, the 1-, 3-, and 5-year cancer-specific survival rates were 42.0%, 23.2%, and 16.6%, respectively. Within a cohort of melanoma patients with bone metastasis after surgery, our analysis showed that a smaller tumor size and the lack of metastases at other sites were predictors of survival.

Mechanism and regulation of pyroptosis-mediated in cancer cell death.

Pyroptosis, a form of programmed cell death, has garnered increasing attention as it relates to innate immunity and diseases. The discovery of caspase-1/3/4/5/8/11 function in sensing various challenges expands the spectrum of pyroptosis mediators and also reveals that pyroptosis is not cell type specific. Recent studies have identified that pyroptosis has become a new topic in cancer research because it may affect all stages of carcinogenesis. In this mini-review, we provided a primer on pyroptosis, discussed the induction of pyroptosis in cancer and its implications in cancer management. Moreover, its two important executioners, the gasdermin D (GSDMD) and gasdermin E (GSDME), the functions and mechanisms of them involved in the regulation of cancer therapy were focused on. Small molecules-mediated pyroptosis were found to effectively inhibit various tumor cells. In brief, the findings of pyroptosis-dependent cancer progression, new drugs and therapeutic targets may lead to a promising, novel therapeutic approach for cancer patients.

PI3K-Akt-mTOR inhibition by GNE-477 inhibits renal cell carcinoma cell growth in vitro and in vivo.

Sustained activation of PI3K-Akt-mTOR cascade is important for renal cell carcinoma (RCC) cell progression. GNE-477 is a novel and efficacious PI3K-mTOR dual inhibitor. The current study tested its anti-RCC cell activity. In the primary cultured human RCC cells, GNE-477 potently inhibited cell growth, viability and proliferation, as well as cell cycle progression, migration and invasion. Furthermore, it induced robust apoptosis activation in primary RCC cells, but being non-cytotoxic to HK-2 epithelial cells and primary human renal epithelial cells. In the primary RCC cells GNE-477 inactivated PI3K-Akt-mTOR cascade by blocking phosphorylation of p85, Akt1, p70S6K1 and S6. Restoring Akt-mTOR activation by a constitutively-active Akt1 reversed GNE-477-induced anti-RCC cell activity. In nude mice intraperitoneal injection of GNE-477 potently suppressed RCC xenograft tumor growth. Collectively, targeting PI3K-Akt-mTOR cascade by GNE-477 inhibits RCC cell growth in vitro and in vivo.

[Effect of changes of inflammatory factors on prognosis of tibia plateau Schatzker â ¢ fractures treated under arthroscopic or open reduction and internal fixation].

OBJECTIVE: To explore changes of inflammatory factors on prognosis of tibia plateau Schatzker Ⅲ fractures treated under arthroscopic or open reduction and internal fixation. METHODS: From November 2013 to November 2016, clinical data of 30 patients with tibia plateau Schatzker Ⅲ fractures were retrospectively analyzed, and divided into minimally invasive group and control group according to different surgical methods 15 patients in each group. Minimally invasive group were treated by arthroscopic internal fixation, including 8 males and 7 females, aged from 20 to 50 years old with an average of (35.0± 14.6) years old, the time from injury to operation ranged from 7 to 15 days with an average of (11.0±4.1) days. Control group were treated by open reduction and internal fixation, including 7 males and 8 females, aged from 18 to 48 years old with an average of (33.0±13.6) years old, the time from injury to operation ranged from 6 to 14 days with an average of (10.0±3.4) days.Operation time, length of incision, blood loss, postoperative loading time and fracture healing time, complications were compared between two groups. Level of IL-1ß, IL-6, TNF-α were detected at 3 days, 6 months and 12 months after operation, Lysholm knee function score at 6 and 12 months were compared between two groups. RESULTS: Allpatients were followed up, but there was no significant difference in following up between two groups. Operation time, length of incision, blood loss, postoperative loading time, fracture healing time and cases of complications in minimally invasive group were (80.3±9.7) min ,(4.2± 1.0) cm ,(102.2±26.4) ml ,(30.0±10.0) d ,(70.0±5.0) d and 0 case respectively; while in control group were (90.3±9.1) min, (10.5±1.1) cm ,(221.1±46.8) ml ,(50.0±15.0) d ,(90.0±6.0) d and 2 cases respectively; there were significant difference between two groups. Lysholm score in minimally invasive group 89.2±5.1 was higher than that of control group 80.1±3.1; and score of swelling, squat and pain in minimally invasive group was higher than that of control group at 6 months after opertaion. While there were no significant difference in each items and total score of Lysholm score between two groups at 12 months after operation. Level of IL-1ß, IL-6, and TNF-α in minimally invasive group at 3 days and 6 months were [(52.1±20.1) pg/L, (0.9±0.1) pg/L ],[(56.1±20.1) pg/L ,(1.1±1.3) pg/L ] and [(28.3±2.5) pg/L ,(8.4±1.5) pg/L ] respectively; while in control group were [(64.8±9.1) pg/L ,(8.1±2.1) pg/L ],[(65.8±12.3) pg/L ,(9.1±5.3) pg/L ] and [(38.5±2.3) pg/L ,(26.5± 1.4) pg/L ] respectively; there were statistically difference in level IL-1ß, IL-6 and TNF-α between two groups at 3 days and 6 months after operation; while there was no difference at 12 months after operation (P>0.05) . Inflammatory cytokines level at 3 days after operation IL-1ß [OR=1.279, 95%CI (1.047, 1.512), P<0.05 ], IL-6 [OR=1.687, 95%CI (1.478, 1.888), P<0.05 ], TFN-α [ OR=2.096, 95%CI (1.863, 2.316), P<0.05 ] was an independent risk factor for Lysholm knee function score at 6 months after operation. CONCLUSION: Arthroscopic surgery and open surgery also could obtain good clinical effects in treating tibia plateau Schatzker Ⅲ fractures. Arthroscopic internal fixation could shorten operation time, lessen the mount of blooding with minimally invasive, lower occurrence of postoperative complications, faster recovery of knee function.

The therapeutic value of the SphK1-targeting microRNA-3677 in human osteosarcoma cells.

Sphingosine kinase 1 (SphK1) is a potential therapeutic target for human osteosarcoma (OS). SphK1-targeting microRNAs (miRNAs) could have important therapeutic value for OS. We discovered that micorRNA-3677 (miR-3677) is a SphK1-targeting miRNA, inhibiting OS cell progression. The results of RNA-Pull down assay confirmed direct binding between biotinylated-miR-3677 and SphK1 mRNA in primary human OS cells. In established and primary human OS cells forced overexpression of miR-3677, by a lentiviral construct, decreased SphK1 3'-UTR (untranslated region) activity and downregulated SphK1 expression. Both were however enhanced with miR-3677 inhibition in OS cells. Function studies demonstrated that OS cell growth, proliferation and migration were inhibited with miR-3677 overexpression, but augmented with miR-3677 inhibition. MiR-3677 overexpression-induced anti-OS cell activity was reversed with re-expression of the 3'-UTR-depleted SphK1. Additionally, in SphK1 knockout OS cells (by CRISPR/Cas9 strategy), altering miR-3677 expression failed to further alter cell functions. Finally, we show that miR-3677 expression was significantly downregulated in primary human OS tissues, correlating with SphK1 mRNA upregulation. We conclude that targeting SphK1 by miR-3677 inhibits human OS cell progression.

Chemokines in bone-metastatic breast cancer: Therapeutic opportunities.

Due to non-response to chemotherapy, incomplete surgical resection, and resistance to checkpoint inhibitors, breast cancer with bone metastasis is notoriously difficult to cure. Therefore, the development of novel, efficient strategies to tackle bone metastasis of breast cancer is urgently needed. Chemokines, which induce directed migration of immune cells and act as guide molecules between diverse cells and tissues, are small proteins indispensable in immunity. These complex chemokine networks play pro-tumor roles or anti-tumor roles when produced by breast cancer cells in the tumor microenvironment. Additionally, chemokines have diverse roles when secreted by various immune cells in the tumor microenvironment of breast cancer, which can be roughly divided into immunosuppressive effects and immunostimulatory effects. Recently, targeting chemokine networks has been shown to have potential for use in treatment of metastatic malignancies, including bone-metastatic breast cancer. In this review, we focus on the role of chemokines networks in the biology of breast cancer and metastasis to the bone. We also discuss the therapeutic opportunities and future prospects of targeting chemokine networks, in combination with other current standard therapies, for the treatment of bone-metastatic breast cancer.

Sarsasapogenin Suppresses RANKL-Induced Osteoclastogenesis in vitro and Prevents Lipopolysaccharide-Induced Bone Loss in vivo.

INTRODUCTION: Osteoclasts are giant polynuclear cells; their main function is bone resorption. An increased number of osteoclasts and enhanced bone resorption exert significant effects on osteoclast-related bone-lytic diseases, including osteoporosis. Given the limitations of current therapies for osteolytic diseases, it is urgently required to develop safer and more effective alternatives. Sarsasapogenin, a major sapogenin from Anemarrhena asphodeloides Bunge, possesses potent antitumor effects and inhibits NF-κB and MAPK signaling. However, the manner in which it affects osteoclasts is unclear. METHODS: We investigated the effects of anti-osteoclastogenic and anti-resorptive of sarsasapogenin on bone marrow-derived osteoclasts. RESULTS: Sarsasapogenin inhibited multiple RANKL-induced signaling cascades, thereby inhibiting the induction of key osteoclast transcription factor NFATc1. The in vivo and in vitro results were consistent: sarsasapogenin treatment protected against bone loss in a mouse osteolysis model induced by lipopolysaccharide. CONCLUSION: Our research confirms that sarsasapogenin can be used as a new treatment for osteoclast-related osteolytic diseases.

Asymmetrical bilateral sternoclavicular joint dislocation combined with bilateral clavicular fracture: A case report.

RATIONALE: Asymmetrical bilateral sternoclavicular joint (SCJ) dislocation consists of posterior SCJ dislocation on one side and anterior SCJ dislocation on the other side. This is an extremely rare injury and only a few cases have been reported in the literature. If not been diagnosed timely and accurately, asymmetrical bilateral SCJ dislocation can be life-threatening. PATIENTS CONCERNS: We experienced a patient who has a life-threatening posterior dislocation of right SCJ and anterior dislocation on the left SCJ combined with bilateral clavicular fracture after a traffic accident. DIAGNOSES: A computed tomography (CT) scan with three-dimensional reconstructions of SCJ showed potentially life-threatening posterior dislocation of right SCJ and anterior dislocation on the left SCJ combined with bilateral clavicular fracture. INTERVENTIONS: Because of failed attempts at closed reduction, electively surgical intervention was made. We repaired the ruptured joint capsule and ligaments and fixed bilateral SCJ by Kirschner wire during the operation. OUTCOMES: Three-dimensional CT scans confirmed bilateral SCJ reduction and alignment after operation 1 week as well as at the 2-month follow-up. LESSONS: SCJ dislocation is an extremely rare and life-threatening injury. The aim of the operation is to repair the ruptured joint capsule and its ligaments and to fix the dislocated joints.

Simultaneous spontaneous bilateral quadriceps tendon rupture with secondary hyperparathyroidism in a patient receiving hemodialysis: A case report.

RATIONALE: Simultaneous spontaneous bilateral quadriceps tendon rupture is a rare orthopedic injury; its initial diagnosis is misdiagnosed in up to 50% of patients with secondary hyperparathyroidism. Early diagnosis and surgical repair are important to achieve an excellent functional outcome. PATIENT CONCERNS: We report a case of simultaneous spontaneous bilateral quadriceps tendon rupture associated with secondary hyperparathyroidism. DIAGNOSIS: Magnetic resonance imaging showed that the quadriceps tendon was completely ruptured at the osteotendinous junction. We then found bilateral quadriceps tendon rupture during the operation. INTERVENTIONS: The patient underwent successful tendon repair surgery. OUTCOMES: The 31-year-old female patient regained full active movement of both knee joints and was able to participate in her activities of daily living. LESSONS: Simultaneous spontaneous bilateral quadriceps tendon rupture in a patient with secondary hyperparathyroidism (undergoing hemodialysis) is a rare orthopedic injury that can be easily overlooked at the initial presentation. Early diagnosis and surgical repair is important to achieve an excellent functional outcome. For patients with secondary hyperparathyroidism receiving hemodialysis, strict systematic treatment of hyperparathyroidism is needed to prevent rupture or re-rupture of the quadriceps tendon.

Mobile thoracic schwannoma combined with intraosseous schwannomas: A case report.

RATIONALE: Mobile schwannomas have been rarely reported in the lumbar and thoracic spine. These entities are usually intradural extramedullary involving less than 3 vertebrae. Here, we present a rare case of thoracic schwannoma moving over 4 vertebral levels from the primary site combined with intraosseous schwannomas. PATIENT CONCERNS: A 64-year-old woman presented with back pain for several months. DIAGNOSES: Preoperative computed tomography (CT) and magnetic resonance imaging (MRI) showed 2 intraosseous tumors at the T7 and T8 levels and an intradural extramedullary tumor at the T5-6 levels. INTERVENTIONS: The patient underwent a surgical resection of the intraosseous tumors at the T7 and T8 levels, and the tumor at the T5-6 levels was not found. Postoperative MRI showed that the intradural extramedullary tumor had moved to the T3-4 levels. Subsequently, the patient developed gait disturbance and numbness on bilateral lower limbs. During the second operation, we found the tumor at the T1-2 levels. Eventually, the tumor was completely removed. OUTCOMES: Histopathological examination showed schwannomas. After a 3-month follow-up, the symptoms were significantly relieved, and there was no clinical or radiological recurrence. LESSONS: The clinicians should be aware of the coincidence of intraosseous schwannomas and mobile schwannoma. Careful preoperative MRIs are essential for early diagnosis of mobile tumors. Intraoperative localization of the mobile tumor is imperative to prevent unnecessary laminotomy.

Triptolide Suppressed the Microglia Activation to Improve Spinal Cord Injury Through miR-96/IKKß/NF-κB Pathway.

STUDY DESIGN: The effect of triptolide on spinal cord injury (SCI) and inflammatory response was observed by establishing SCI rat model. And in vitro experiments were conducted to determine the underlying mechanism of triptolide-mediated in murine microglial cell line BV2. OBJECTIVE: To determine the underlying mechanism of triptolide in suppressing the microglia activation to improve SCI. SUMMARY OF BACKGROUND DATA: Triptolide, as a major active ingredient of Chinese herb Tripterygium wilfordii, can promote spinal cord repair through inhibiting microglia activation, but the underlying mechanism is not clear. METHODS: Locomotion recovery was accessed by Basso, Beattie, and Bresnahan score, the number of footfalls, stride length, and angle of rotation analysis. Expressions of microRNA 96 (miR-96), microglia activation marker Iba-1, and IκB kinase (IKKß)/nuclear factor (NF)-κB-related proteins were detected by qRT-PCR or western blot. Inflammatory cytokines tumor necrosis factor-α and interleukin -1ß were measured by enzyme-linked immuno sorbent assay. The regulation of miR-96 on IKKß was confirmed by dual luciferase reporter assay. RESULTS: Triptolide promoted locomotion recovery of SCI rats, upregulated the expression of miR-96, decreased microglia activation marker Iba-1 and IKKß/NF-κB-related proteins, and inhibited inflammatory cytokines tumor necrosis factor-α and interleukin-1ß levels in spinal cord tissues and lipopolysaccharide -induced microglia. Triptolide suppressed the microglia activation and inflammatory cytokines secretion in BV2 cells through up-regulating miR-96. We confirmed the interaction between miR-96 and IKKß, and IKKß expression was negatively regulated by miR-96. Finally, we determined that triptolide suppressed the microglia activation and inflammatory cytokines secretion through miR-96/IKKß pathway. CONCLUSION: Triptolide suppressed microglia activation after SCI through miR-96/IKKß/NF-κB pathway. LEVEL OF EVIDENCE: N/A.