High Impact Resistance of 2D MXene with Multiple Fracture Modes.

Two-dimensional (2D) transition metal carbides/nitrides (MXenes) are promising nanomaterials due to their remarkable mechanical and electrical properties. However, the out-of-plane mechanical properties of MXene under impact loading remain unclear. Here, particular impact-resistant fracture behaviors and energy dissipation mechanisms of MXene were systemically investigated via molecular dynamics (MD) simulation. Specifically, it was found that the specific penetration energy of MXene exceeds most conventional impact-resistant materials, such as aluminum and polycarbonate. Two kinds of novel energy dissipation mechanisms, including radial fracture and crushed fracture under different impact velocities, are revealed. In addition, the sandwiched atomic-layer structure of MXene can deflect cracks and restrain their propagation to some extent, enabling the cracked MXene to retain remarkable resistance. This work provides in-depth insights into the impact-resistance of MXene, laying a foundation for its future applications.

Silence of URI in gastric cancer cells promotes cisplatin-induced DNA damage and apoptosis.

URI, a prefoldin family member, has been implicated roles in cancer development. We have previously shown that URI can attenuate DNA damage in gastric cancer cells treated with potassium dichromate. The aim of this study was to investigate how URI involves cisplatin-induced DNA damage response (DDR) in gastric cancer cells and its possible mechanism relating to the ATM/CHK2 pathway. Here, MGC-803 and SGC-7901 gastric cancer cells were treated with different concentrations of cisplatin. Comet assay was used to detect DNA damage and the results confirmed the dose-effect of cisplatin-induced DNA damage in gastric cancer cells. URI knockdown cell lines were established with siRNA transfection. Cell viability and proliferation were detected by counting kit 8 (CCK-8) and 5-ethynyl-2'-deoxyuridine (EdU) assays respectively. Apoptosis and cell cycle were analyzed by flow cytometry. The results indicated that URI knockdown increased the sensitivity of cells to cisplatin by inhibiting proliferation and promoting apoptosis. The levels of P-ATM, P-CHK2 and γH2AX were detected by Western blot. Increased levels of P-ATM, P-CHK2, and γH2AX were observed in cisplatin treated cells, indicating that cisplatin induced a DNA damage response (DDR). URI knockdown in cisplatin-treated cells significantly decreased the levels of P-ATM and P-CHK2 at 12 hours, but not at 0 and 6 hours after drug withdrawal, while significantly increased γH2AX levels were detected at 6 hours, but not at 0 and 12 hours after drug withdrawal compared with the control cells. However, the levels of γH2AX were significantly increased in URI knockdown cells after cisplatin treatment for 12 hours. The cell cycle analysis showed that the number of cells entering S phase was significantly reduced and the cells were arrested in the G1 phase in URI-silenced cisplatin-exposed cells, indicating that cell cycle progression was inhibited. In conclusion, our results suggest that URI is involved in the cisplatin-induced DNA damage response via the ATM/CHK2 pathway, and silencing URI can increase cisplatin-induced DNA damage and enhance drug sensitivity in gastric cancer cells.

Thermal Transport Properties of Sulfur-Loaded Carbon-Based Nanotubes and Composite Sulfur Cathodes in Lithium-Sulfur Batteries.

The thermal management of lithium-sulfur batteries with high specific energy has become one of the critical issues for their applications. Carbon-based nanotubes are widely used to construct composite sulfur cathodes. This paper focuses on the thermal transport properties of sulfur-coated and sulfur-embedded boron carbide nanotubes (BCNTs) and carbon nanotubes (CNTs) and their composites using molecular dynamics. It is found that phonon softening and localization play a role in making BCNT exhibit a lower thermal conductivity (TC) than CNT. Furthermore, it is discovered that the sulfur embedded inside the carbon-based nanotube has a greater negative impact on carbon-based nanotube phonon transport. Moreover, the effective medium theory model is not suitable for predicting the effective thermal conductivity of coated sulfur composites, in contrast to its good applicability to embedded sulfur composites. These findings provide an in-depth understanding of the thermal transport properties of composite sulfur cathodes in lithium-sulfur batteries.

Modulation of the thermal conductivity, interlayer thermal resistance, and interfacial thermal conductance of C2N.

C2N, a novel 2D semiconductor with orderly distributed holes and nitrogen atoms, has attracted significant attention due to its possible practical applications. This paper investigates the in-plane thermal conductivity and interlayer thermal resistance of C2N and the interfacial thermal conductance of in-plane heterostructures assembled by C2N and carbonized C2N(C-C2N) using molecular dynamics simulations. The in-plane thermal conductivities of C2N monolayers along zigzag and armchair directions are 73.2 and 77.3 W m-1 K-1, respectively, and can be effectively manipulated by point defects, chemical doping, and strain engineering. Remarkably, nitrogen vacancies have a more substantial impact on reducing the thermal conductivity than carbon vacancies because of the more pronounced suppression of the high-frequency peaks. The difference in doping sites leads to a change in phonon mode localization. When the C2N size is small, as the tensile strain increases, ki is affected by dimensional lengthening due to stretching in addition to tensile strain. The interlayer thermal resistance decreases with increasing layer number and interlayer coupling strength. The AA stacking gives rise to a lower thermal resistance than the AB stacking when the heat flow passes through the multilayer due to the weaker in-plane bonding strength. Moreover, various possible atomic structures of C2N/C-C2N in-plane heterojunctions and the effect of carbon and nitrogen vacancies on interfacial thermal conductance are explored. The results provide valuable insights into the thermal transport properties in the application of C2N-based electronic devices.

Flame-retardant MXene/polyimide film with outstanding thermal and mechanical properties based on the secondary orientation strategy.

With the development of multifunction and miniaturization in modern electronics, polymeric films with strong mechanical performance and high thermal conductivity are urgently needed. Two-dimensional transition metal carbides and nitrides (MXenes) have attracted extensive attention due to their tunable surface chemistry, layered structure and charming properties. However, there are few studies on using MXenes as fillers to enhance polymer properties. In this paper, we fabricate a three-dimensional foam by the freeze-drying method to enhance the interfacial interaction between adjacent MXene sheets and polyimide (PI) macromolecules, and then a composite film with a dense and well-ordered layer-by-layer structure is produced by the hot-pressing process. Based on the secondary orientation strategy, the resultant MXene/PI film exhibits an enhanced thermal conductivity of 5.12 ± 0.37 W m-1 K-1 and tensile strength of 102 ± 3 MPa. Moreover, the composite film has good flexibility and flame retardancy owing to the synergistic effect of MXene sheets and PI chains. Hence, the MXene/PI composite film with the properties of flexibility, flame-retardancy, high mechanical strength and efficient heat transmission is expected to be used as the next thermal management material in a variety of applications.

Downregulation of circular RNA HECTD1 induces neuroprotection against ischemic stroke through the microRNA-133b/TRAF3 pathway.

AIMS: Circular RNAs (circRNAs) have been shown to play crucial roles in various biological processes and human diseases. However, their exact functions in ischemic stroke remain largely unknown. In this study, we explored the functional role of circRNA HECTD1 (circ-HECTD1) and its underlying mechanism in cerebral ischemia/reperfusion injury. METHODS: Mouse middle cerebral artery occlusion (MCAO) model and oxygen-glucose deprivation (OGD) model in HT22 cells were used to mimic the cerebral ischemia/reperfusion injury. Brain infarct volume, flow cytometry, caspase 3 activity, NF-κB activity, and TUNEL staining were performed to evaluate the function of circ-HECTD1. Luciferase report assay was used to explore the regulatory mechanism. FINDINGS: The results showed that the expression of circ-HECTD1 and tumor necrosis factor receptor-associated factor 3 (TRAF3) was remarkably up-regulated, while miR-133b was down-regulated in oxygen-glucose deprivation (OGD)-induced HT22 cells and mouse middle cerebral artery occlusion (MCAO) model. circ-HECTD1 knockdown relieved OGD-caused neuronal cell death in vitro. Simultaneously, circ-HECTD1 knockdown improved cerebral infarction volume and neuronal apoptosis in MCAO mice. circ-HECTD1 was able to negatively regulate the expression of miR-133b, and TRAF3 is one of the targets of miR-133b. Upregulation of miR-133b inhibited the expression of TRAF3 in OGD-stimulated cells, whereas circ-HECTD1 upregulation reversed this effect. Furthermore, upregulation of miR-133 was able to inhibit OGD-caused cell apoptosis and NF-κB activation, whereas upregulation of circ-HECTD1 attenuated these effects of miR-133b mimics. SIGNIFICANCE: Taken together, circ-HECTD1 knockdown inhibited the expression of TRAF3 by targeting miR-133b, thereby attenuating neuronal injury caused by cerebral ischemia.

Thermal transport properties of graphite carbon nitride.

Graphite carbon nitride (GCN), which can be regarded as a nitrogen heteroatom-substituted graphite framework, has attracted great attention as a new 2D layered structure material with semiconductor electronic characteristics. Using molecular dynamics simulations, the in-plane thermal conductivity and cross-plane thermal resistance of two GCN structures (i.e., triazine-based and heptazine-based) are investigated. Our results show that the in-plane thermal conductivities of the triazine-based and heptazine-based GCN monolayers along the armchair direction are 55.39 and 17.81 W m-1 K-1, respectively. The cross-plane thermal resistance decreases with increasing layer number and reaches asymptotic values of 3.6 × 10-10 and 9.3 × 10-10 m2 K W-1 at 40 layers for triazine-based and heptazine-based GCN, respectively. The in-plane thermal conductivity can be effectively manipulated by changing the temperature and applying strain, while it is insensitive to the number of layers, which is in sharp contrast to that of graphene. Moreover, the cross-plane thermal resistance decreases monotonically with temperature and coupling strength, and can be modulated by external strain. Surprisingly, the cross-plane tensile strain can reduce the thermal resistance of the heptazine-based GCN. Our study serves as a guide to groups interested in the physical properties of GCN.

Effect of strain and defects on the thermal conductance of the graphene/hexagonal boron nitride interface.

In-plane heterojunctions, obtained by seamlessly joining two or more nanoribbon edges of isolated two-dimensional atomic crystals such as graphene and hexagonal boron nitride, are emerging as nanomaterials for the development of future multifunctional devices. The thermal transport behavior at the interface of these heterojunctions plays a pivotal role in determining their functional performance. Using molecular dynamics simulations, the interfacial thermal conductance of graphene/hexagonal boron nitride (GE/BN) in-plane heterojunctions was investigated. The GE/BN heterostructure has a remarkably high interfacial thermal conductance, and thermal rectification occurs at the interface. The results also show that the interfacial thermal conductance is effectively modulated by strain and defect engineering. The atomic defect location can affect the phonon transmission at the interface. Interestingly, compared with the nitrogen doping effect, the boron doping defect can more effectively facilitate vibrational coupling at the interface in the graphene sheet. Stress distribution and vibrational spectral analyses are performed to elucidate the thermal transport mechanism. The results of this study may provide a foundation for future research attempting to manipulate the interfacial thermal conductance in other two-dimensional heterostructures.

Leiomyosarcoma with osteoclast-like (LMS-OGC) giant cells the breast: A report of a rare case.

Leiomyosarcoma with osteoclast-like giant cells (LMS-OGC) has seldom been reported clinically. LMS-OGC of the breast is extremely rare according to the literature. Here, we report a case of LMS-OGC leiomyosarcoma with osteoclast-like giant cells of the breast. A 51-year-old female patient presented with a breast mass which was treated surgically and the pathological examination of the tumor indicated LMS-OGC. Microscopically, the tumor was composed of spindle cells arranged in bundles or spokes with giant tumor cells and mitosis. Eosinophilic cytoplasm and morphologically benign osteoclast-like cells were mixed together. Immunohistochemistry examination revealed SMA and desmin were positive with a Ki-67 proliferation index of 40%. However, CK (AE1/AE3), E-cadherin, ER, PR, CD34, S-100 and CD10 were negatively expressed in the tumor tissue. LMS-OGC is a soft tissue malignant tumor which develops extremely rarely in the breast. It should be differentiated and diagnosed according to the history, histological characteristics and immunohistochemical staining.

Thermal conductivity of two-dimensional BC3: a comparative study with two-dimensional C3N.

The thermal conductivities of single-layer BC3 (SLBC) sheets and their responses to environmental temperature, vacancy defects and external strain have been studied and compared with those of single-layer C3N (SLCN) sheets by molecular dynamics (MD) simulations. We found that SLBC and SLCN are isotropic in the basal plane and that their predicted thermal conductivities for infinite length sheets are 488.54 W m-1 K-1 and 799.87 W m-1 K-1, respectively. Despite many similar features in the structures of these materials, SLBC exhibits a lower thermal conductivity than SLCN due to stronger flexural acoustic phonon-defect scattering rates and weaker interatomic bonding stiffnesses. The vibrational density of states (VDOS) are calculated in both structures to elucidate their thermal conductivity differences. SLBC exhibits a more substantial redshift phenomenon in the high- and low-frequency domains than SLCN. In addition, the thermal conductivities of these materials exhibit decreasing trends in response to increases in temperature and defect ratio, and the temperature effect in SLBC is more substantial than that in SLCN, while the defect effect in SLBC is less substantial than that in SLCN. The influences of uniaxial compressive and tensile strains on the thermal conductivities of these materials are analysed separately. These two deformation modes cause different effects on the thermal transport behaviours of SLBC and SLCN: the effect of uniaxial compressive strain is slightly negative, while the effect of uniaxial tensile strain is initially positive and then negative. Moreover, the biaxial strains result in a more severe reduction in thermal conductivity than the uniaxial strains. Remarkably, the impact of uniaxial and biaxial tensile strains on thermal transport was stronger in SLBC than in SLCN. We propose that SLBC nanomembranes are promising candidates for various thermal applications.

URI knockdown induces autophagic flux in gastric cancer cells.

URI, a member of the prefoldin family of molecular chaperones, functions in the regulation of nutrient-sensitive, mTOR-dependent transcription signaling pathways. Previous studies of several tumor types demonstrated that URI exhibits characteristics similar to those of an oncoprotein. URI has been shown as a mitochondrial substrate of S6 kinase 1 (S6K1), which acts to integrate nutrient and growth factor signals to promote cell growth and survival. Notably, the Akt/mTOR/p70S6K signaling pathway constitutes major negative regulatory mechanism of autophagy. However, the role of URI in autophagy has not been explored. Here, we investigated the involvement of URI in autophagy by manipulating its expression in MGC-803 and HGC-27 cells using siRNA and transfection approaches. GFP-LC3 punctum aggregation was assessed by confocal microscopy, whereas formation of autophagic vesicles was assessed using transmission electron microscopy. NH4Cl was used to inhibit autophagosome-lysosome fusion and to monitor autophagic flux. Expression of LC3-I, LC3-II, beclin1, total and phosphorylated mTOR, and p70S6k was assessed by Western blotting. The results showed that knockdown of URI induced significant autophagic flux in gastric cancer cells. URI regulates the expression of beclin1, which is essential for initiation of conventional autophagy. Levels of p-mTOR (Ser2448) and p-p70S6K (Thr389) increased in URI-overexpressing cells treated with the mTOR inhibitor rapamycin but decreased in URI-silenced cells. The inhibitory effect of URI silencing on mTOR and p70S6K phosphorylation was antagonized by the autophagy inhibitor 3-methyladenine. These results suggest that URI knockdown-induced autophagy is associated with the mTOR/p70S6K signaling pathway, indicating the potential existence of a novel autophagy regulatory mechanism mediated by URI.

Study on Damage Evaluation and Machinability of UD-CFRP for the Orthogonal Cutting Operation Using Scanning Acoustic Microscopy and the Finite Element Method.

Owing to high specific strength and designability, unidirectional carbon fiber reinforced polymer (UD-CFRP) has been utilized in numerous fields to replace conventional metal materials. Post machining processes are always required for UD-CFRP to achieve dimensional tolerance and assembly specifications. Due to inhomogeneity and anisotropy, UD-CFRP differs greatly from metal materials in machining and failure mechanism. To improve the efficiency and avoid machining-induced damage, this paper undertook to study the correlations between cutting parameters, fiber orientation angle, cutting forces, and cutting-induced damage for UD-CFRP laminate. Scanning acoustic microscopy (SAM) was employed and one-/two-dimensional damage factors were then created to quantitatively characterize the damage of the laminate workpieces. According to the 3D Hashin's criteria a numerical model was further proposed in terms of the finite element method (FEM). A good agreement between simulation and experimental results was validated for the prediction and structural optimization of the UD-CFRP.

URI promotes the migration and invasion of human cervical cancer cells potentially via upregulation of vimentin expression.

URI is known to act as an oncoprotein in several tumors. Our previous studies have shown that URI is associated with the migration process in cervical and gastric cancer cells, but the mechanisms remain to be determined. Given the fact that URI positively regulates vimentin expression, we therefore investigated how URI regulated vimentin expression affects the migration and invasion of cells from two human cervical cancer cell lines HeLa and C33A, which differentially express URI. We have shown that knock-down of URI in HeLa cells using URI siRNA caused decreased vimentin mRNA and protein levels along with attenuated cell motility. Meanwhile, overexpression of URI by transfection of PCMV6-URI in C33A cells resulted in increased vimentin expression and enhanced cell migration and invasion. We have also used TGF-ß to induce vimentin expression, which enhanced the cell migration and invasion abilities affected by URI, while inhibition of vimentin by siRNA attenuated URI's effect on cell migration and invasion. In addition, we have performed luciferase reporter and ChIP assays, and the results support that URI indirectly enhances the activity of vimentin promoter. Taken together, our results suggest that URI plays essential roles in the migration and invasion of human cervical cancer cells, possibly via targeting vimentin expression.

URI promotes gastric cancer cell motility, survival, and resistance to adriamycin in vitro.

Unconventional prefoldin RPB5 interactor (URI), a RNA polymerase II Subunit 5-Interacting protein, is known to participate in the regulation of nutrient-sensitive mTOR-dependent transcription programs. Multiple studies have recently demonstrated that URI functions as an oncoprotein, possibly through the mTOR pathway, and regulates tumor cell motility, invasion, and metastasis. However, whether and how URI plays a role in gastric oncogenesis has not been elucidated. Due to drug resistance, recurrence and metastasis, the prognosis of gastric cancer remains poor. This study aims to explore the effects of URI on gastric cancer cells by focusing on their migratory ability and resistance to adriamycin. URI was over-expressed or knocked-down in MGC-803 and HGC-27 gastric cancer cells using URI plasmid or siRNA transfection approach. The cell viability, apoptosis, and migration ability were then examined by the CCK-8 assay, flow cytometer Annexin V/PI staining, and the Transwell cell migration assay respectively. The protein levels of apoptosis and EMT related genes were detected by western blot. The results showed that overexpression of URI promoted while knock-down of URI inhibited gastric cancer cell proliferation. URI overexpression resulted in increased Bcl-2 expression but decreased levels of Bax, cleaved PARP-1 and cleaved caspase-3. Conversely, cells treated with URI siRNA showed increased adriamycin induced apoptosis, along with reduced Bcl-2, but increased Bax, cleaved PARP-1 and cleaved caspase-3 expression. We have also shown that overexpression of URI enhanced cancer cell proliferation and migration with higher levels of Snail and Vimentin, whereas knockdown of URI in MGC-803 and HGC-27 cells inhibited proliferation and migration with decreased Snail and Vimentin expression. Together, our results support that URI promotes cell survival and mobility and acts as a chemotherapeutics resistant protein in MGC-803 and HGC-27 cells. URI might be a potential biomarker for gastric cancer diagnostics and prognostics.

URI prevents potassium dichromate-induced oxidative stress and cell death in gastric cancer cells.

Chromium VI can provoke oxidative stress, DNA damage, cytotoxicity, mutagenesis and carcinogenesis. Aberrantly high level of reactive oxygen species (ROS) has been associated with oxidative stress and subsequent DNA damage. Notably, multiple previous studies have shown the increased level of ROS in chromium (VI) induced oxidative stress, but its effect on cell death and the underlying mechanism remain to be determined. In this study, we aimed to investigate the role of URI, an unconventional prefoldin RBP5 interactor, in potassium dichromate induced oxidative stress and cell death through in vitro loss-of-function studies. We have shown that knockdown of URI in human gastric cancer SGC-7901 cells by URI siRNA enhanced potassium dichromate-induced production of ROS. The level of rH2AX, a marker of DNA damage, was significantly increased, along with a reduced cell viability in URI siRNA treated cells that were also exposed to potassium dichromate. Comet assay showed that URI knockdown increased the tail moment in potassium dichromate-treated SGC-7901 cells. Accordingly, the cell rates of apoptosis and necrosis were also increased in URI knockdown cells treated with potassium dichromate at different concentrations. Together, these results suggest that URI is preventive for the oxidative stress and cell death induced by potassium dichromate, which potentially leads to cancer cell survival and therapeutic resistance.

Zbed3 contributes to malignant phenotype of lung cancer via regulating ß-catenin and P120-catenin 1.

Our previous studies indicate that abnormal expression of several Wnt signaling molecules including Axin, Dvl and ß-catenin are involved in proliferation, invasion and metastasis of lung cancer. Zbed3 was found to inhibit function of Axin-GSK3ß complex and thus lead to accumulation of ß-catenin in NIH3T3 and HEK293T cells. However its function in malignant tumors is largely unknown. Here we investigate the clinico-pathological significance of Zbed3 expression and its function in non-small cell lung cancer. We use immunohistochemistry and Western blotting to examine Zbed3 expression in non-small cell lung cancer and lung tissues. Transfection of siRNA and plasmid was used to study the function of Zbed3 in lung cancer cells in vitro. We found Zbed3 expression was elevated in cancer tissues compared to normal lung tissues. Increased Zbed3 expression is significantly associated with lymph node metastasis, advanced TNM stages, higher Ki67 status and patients' poor clinical outcome. Higher Zbed3 expression was also found in lung cancer cell lines compared to bronchial epithelial cell line HBE. Downregulation of Zbed3 by siRNA significantly inhibits cancer cell proliferation and invasion in vitro. Downregulation of Zbed3 also significantly inhibits expression of ß-catenin, downstream molecules of Wnt signaling and P120ctn-1 in lung cancer cells. These results suggest that Zbed3 may contribute to lung cancer cell invasion through regulating ß-catenin and p120ctn-1 and may be a promissing cancer marker in non-small cell lung cancer.

Btbd7 contributes to reduced E-cadherin expression and predicts poor prognosis in non-small cell lung cancer.

BACKGROUND: Disorders of cell adhesion are critical steps in cancer progression in which varieties of markers including cadherins are involved in.Btbd7 was found to inhibit E-cadherin expression in MDCK cells and play important roles during branching morphogenesis of embryonic salivary glands and lungs. However its function in malignant tumors is largely unknown. The aim of this study is to investigate the clinicopathological significance and possible function of Btbd7 in non-small cell lung cancer. METHODS: Immunohistochemistry and Western blotting were used to investigate Btbd7 expression in non-small cell lung cancer and lung tissues. The clinicopathological association and the overall survival was analyzed. In vitro experiments were performed using siRNA to investigate the function of Btbd7 in lung cancer cells. RESULTS: Btbd7 expression was elevated in non-small cell lung cancer tissues compared to normal lung tissues. Increased Btbd7 expression was significantly associated with lymph node metastasis, reduced E-cadherin expression and patients' poor clinical outcome. Downregulation of Btbd7 expression in lung cancer cells by siRNA significantly inhibits cancer cell invasion and effectively restores E-cadherin expression in cancer cell membrane. CONCLUSIONS: Btbd7 contributes to reduced expression of E-cadherin and may be a promising cancer marker in non-small cell lung cancer.

Diversin increases the proliferation and invasion ability of non-small-cell lung cancer cells via JNK pathway.

The expression and significance of Diversin in human tumors remains unclear. We found that Diversin was overexpressed in NSCLC, and exhibited direct correlation to poor differentiation, advanced TNM stage, lymph node metastasis and survival time. Overexpression of Diversin lead to a significant increase in proliferation and invasion of NSCLC cells, possibly through activation of JNK, cyclin B and MMP9, and the effects were blocked by JNK inhibitor. These results suggest Diversin is overexpressed in NSCLC and predict poor prognosis. Diversin may promote cell proliferation and invasion through JNK pathway.

DIXDC1 increases the invasion and migration ability of non-small-cell lung cancer cells via the PI3K-AKT/AP-1 pathway.

DIX domain containing 1 (DIXDC1), is a human homolog of Ccd1, a recently identified DIX domain containing protein in zebrafish. DIXDC1 protein was detected in human colorectal adenocarcinoma tissues and was found to be correlated with a high cell proliferation index. We demonstrated DIXDC1 overexpression in 55% (92/167) of non-small cell lung cancer (NSCLC) cases, compared to adjacent noncancerous lung tissues (P < 0.01). Overexpression of DIXDC1 was associated with lymph node metastasis and more advanced TNM stage (P < 0.001 and P = 0.001, respectively). Kaplan-Meier survival curves and log-rank testing indicated that overexpression of DIXDC1 correlated with worse overall survival in NSCLC (P = 0.031). DIXDC1 was more abundant in seven NSCLC lines than the bronchial cell line HBE, and modulation of its expression regulated AP-1 activity; MMP2, MMP7, and MMP9 protein and mRNA; and invasion ability. Metalloproteinase induction was reversed by PI3K/AKT and AP-1 inhibition. These results suggest DIXDC1 is associated with stage and prognosis in NSCLC, and may promote invasion and migration through PI3K-AKT/AP-1-dependent activation of metalloproteinases.

[Surgical treatment of ossification of ligamentum flavum in thoracic spine and its therapeutic effect analysis].

OBJECTIVE: To explore the correlation between CT classification and operative method and to discuss its therapeutic effect. METHODS: From January of 2001 to June of 2010, 30 patients with thoracic ossification of ligamentum flavum were reviewed retrospectively, including 22 males and 8 females with an average age of 52.8 years old (ranged from 37 to 68 years old). The course of duration ranged from 2 months to 6 years. Single segment lesion was in 11 cases and multiple segments were in 19 cases. Two patients were accompanied by cervical ossification of ligamentum flavum and 1 was accompanied by ossification of posterior longitudinal ligament. The ossified lesions were located at T1,2 to T4,5 in 5 cases,T5,6 to T8,9 in 7 cases, T9,10 to T11,12 in 12 cases, at the upper and middle thoracic levels in 2 cases, at the middle and lower thoracic levels in 4 cases. They were divided into 2 types according to the morphologic features of the CT scan:simple type, 18 segments with lateral, slice or unfused type; complex type, 42 segments with thickened, fused or nodular type. The clinical manifestation was paralysis of upper motor neuron in 21 cases, and of upper and lower motor neuron in other 9 cases. Sphincter dysfunction was found in 26 cases. Preoperative JOA sphincter function score was 1.97 +/- 0.56. Preoperative modified JOA motor function score of lower limb was 1.20 +/- 0.76. Different surgical procedure was applied to one of the 2 types. For the simple type, an en bloc laminectomy was performed. However,for the complex type, a laminar shelling decompression was done. Laminectomy combined with internal fixation and lateral fusion was performed in patients whose decompressive areas were wider. RESULTS: The mean decompression length was 3.1 lamina (2 to 6 lamina). Cerebrospinal fluid leakage was found in 3 cases and hematoma in incision was found in 1 case. The mean follow-up duration was 26 months (12 to 96 months). Twenty-two patients with the feel of constriction of trunk or lower limbs were completely recovered; 18 cases with sensation disturbance, numbness and pain of the lower limb were totally recovered, and relived in 10 cases. Postoperative JOA sphincter function score was 2.73 +/- 0.45, comparing with the preoperative score, and the difference was significant (P < 0.01). Postoperative JOA motor function score was 3.57 +/- 0.77, comparing with the preoperative score, and the difference was significant (P < 0.01 ). The lower limb function relief rate was 86.1%, 24 patients got an excellent results, 3 good, 2 poor and 1 bad. CONCLUSION: Different surgical procedures will be safely and effectively applied to treat thoracic ossification of ligamentum flavum according to CT classification.