Hyperglycemia disrupted the integrity of the blood-brain barrier following diffuse axonal injury through the sEH/NF-κB pathway.

OBJECTIVES: We aimed to investigate the role of soluble epoxide hydrolase for hyperglycemia induced-disruption of blood-brain barrier (BBB) integrity after diffuse axonal injury (DAI). METHODS: Rat DAI hyperglycemia model was established by a lateral head rotation device and intraperitoneal injection of 50% glucose. Glial fibrillary acidic protein, ionized calcium-binding adapter molecule-1, ß-amyloid precursor protein, neurofilament light chain, and neurofilament heavy chain was detected by immunohistochemistry. Cell apoptosis was examined by terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) assay. The permeability of blood-brain barrier (BBB) was assessed by expression of tight junction proteins, leakage of Evans blue and brain water content. The soluble epoxide hydrolase (sEH) pathway was inhibited by 1-trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl) urea (TPPU) and the nuclear transcription factor kappa B (NF-κB) pathway was inhibited by pyrrolidine dithiocarbamate and activated by phorbol-12-myristate-13-acetate in vivo and/or vitro, respectively. The inflammatory factors were detected by enzyme-linked immunosorbent assay. RESULTS: Hyperglycemia could exacerbate axonal injury, aggravate cell apoptosis and glial activation, worsen the loss of BBB integrity, increase the release of inflammatory factors, and upregulate the expression of sEH and NF-κB. Inhibition of sEH could reverse all these damages and protect BBB integrity by upregulating the expression of tight junction proteins and downregulating the levels of inflammatory factors in vivo and vitro, while the agonist of NF-κB pathway abrogated the protective effects of TPPU on BBB integrity in vitro. CONCLUSIONS: sEH was involved in mediating axonal injury induced by hyperglycemia after DAI by disrupting BBB integrity through inducing inflammation via the NF-κB pathway.

Development of pulsed magnetic field assisted supersonic plasma spraying.

This study designs a pulsed magnetic field assisted supersonic plasma spraying (PM-SPS) device. The instrument is divided into magnetic field generation and spraying modules, and they are connected by a dual control system and professional fixture. The PM-SPS system is simple to operate and has no contact with the spraying process. In addition, it can achieve high field intensity and stable pulse frequency in a short time. It has a strengthening effect on the whole coating forming process. The porosity, roughness, hardness, and tribological properties of the coatings prepared using the PM-SPS system were improved. The reported experiments and results can be generalized to other coating applications, which require high quality surfaces.

Bending Fatigue Behaviour and Fatigue Endurance Limit Prediction of 20Cr2Ni4A Gear Steel after the Ultrasonic Surface Rolling Process.

To study the effect of the surface properties on the bending fatigue performance of heavy-duty gear steel, the authors of this paper used the ultrasonic surface rolling process (USRP) to strengthen 20Cr2Ni4A carburized gear steel. USRP is a novel technique in which the ultrasonic technology is incorporated into the concept of conventional deep rolling. In this study, we illustrated how the surface properties and cross-section mechanical property influence the three-point bending fatigue life of the samples before and after USRP treatment. At the same time, the predicted failure probability-stress-number of cycles (P-S-N) curve was drawn, and the fatigue fracture was analysed. The results show that the fatigue limit increased from 651.36 MPa to 918.88 MPa after USRP treatment. The fatigue source is mainly from the sample interior or surface scratches, and the fatigue performance is positively correlated with the results of the material surface roughness, surface residual stress and surface hardness. At the same time, combined with the change in the phase structure, dislocation structure, residual stress and hardness of the cross section of the material, it is found that the USRP process turns the steel into a gradient material with five layers. Finally, the coupling mechanism between the ultrasonic surface strengthening deformation layer and the carburized layer of 20Cr2Ni4A carburized gear steel is presented, and the grain structure distribution diagram of the section of the 20Cr2Ni4A model after surface strengthening treatment was simulated. The mechanism that influenced the fatigue performance after USRP treatment is explained from the perspectives of the surface and cross section of the samples.

Recombinant osteopontin provides protection for cerebral infarction by inhibiting the NLRP3 inflammasome in microglia.

Neuroinflammation is one of the most important secondary pathological events after cerebral infarction. Activation of NLRP3 inflammasome is a pivotal form of neuroinflammation. Osteopontin (OPN) is expressed during the subacute phase after cerebral infarction and has an important chemotactic effect on microglia. The aim of this study was to reveal the effect of recombinant OPN on brain injury after cerebral infarction and the regulation of NLRP3 inflammasome. We used the middle cerebral artery occlusion (MCAO) method-established focal cerebral ischemia model and LPS-induced inflammation model on neonate rat primary microglia. The effects of OPN on cerebral ischemic injury, neural function, microglia inflammation and NLRP3 inflammasome function were studied by immunofluorescence, staining, enzyme-linked immunosorbent assay and Western blot assay. We established MCAO cerebral ischemia and reperfusion injury model, and found that recombinant OPN reduced the volume of cerebral infarction and alleviated the ischemic injury degree of cerebral tissues, neurons, and neurological function. We found that OPN was also involved in the negative regulation of inflammasome and microglia activity in cerebral ischemic injury, and that OPN inhibited the activation of NLRP3 inflammasome and the function of microglia in a LPS-induced inflammatory model. Our findings show that recombinant OPN can reduce the ischemic infarct size and alleviate the cerebral ischemic injury of rats, which may be related to its efficient involvement in the inhibitory regulation of inflammasome and microglia inflammatory activation.

Study of the Catalytic Strengthening of a Vacuum Carburized Layer on Alloy Steel by Rare Earth Pre-Implantation.

Conventional carburizing has disadvantages, such as high energy consumption, large deformation of parts, and an imperfect structure of the carburizing layer. Hence, a rare earth ion pre-implantation method was used to catalyze and strengthen the carburized layer of 20Cr2Ni4A alloy steel. In this study, X-ray diffraction (XRD), X-ray photoelectron spectroscopy (XPS), optical microscopy (OM), scanning electron microscopy (SEM), energy dispersive microanalysis (EDS), transmission electron microscopy (TEM), and Rockwell/Vickers hardness testing were used to analyze the microstructure, phase composition, retained austenite content, hardness, carburized layer thickness, and carbon diffusion. The results showed that lanthanum and yttrium ions implanted into the 20Cr2Ni4A steel formed solid solutions of rare earth ions and a large number of dislocations, which improved the diffusion coefficient of carbon elements on the carburized surface and the uniformity of the carbon distribution. Simultaneously, rare earth ion implantation improved the structure and hardness of the vacuum carburized layer. Compared to the lanthanum ion implantation, yttrium ion implantation caused the structure of the carburized layer to be finer, and the carbon diffusion coefficient increased by 1.17 times; in addition, the surface hardness of the carburized layer was 61.8 HRC.

Bending Fatigue Behaviors Analysis and Fatigue Life Prediction of 20Cr2Ni4 Gear Steel with Different Stress Concentrations near Non-metallic Inclusions.

To investigate the relationship between inclusions and bending fatigue behaviors in 20Cr2Ni4 steel under different stress concentrations. This paper designs a new experimental method to prefabricate different size stress concentrations near the inclusions, and then conducts a new type of bending fatigue test to study the inclusions and their surrounding stress distributions in 20Cr2Ni4 steel. A microhardness tester was combined with laser etching equipment to realize the prefabrication of different stress concentrations at arbitrary positions around any inclusion on the gear steel surface. This method provides an experimental basis for the quantitative analysis of the relationship between stress distribution and fatigue life around the inclusions of heavy-duty gear steels. We also predict the bending fatigue lives of heavy-duty gear steels with different types of inclusions, stress states, and spatial distributions. Then, based on the prefabricated notch parameters and the state of inclusions in the steel, a mathematical model of quantitative analysis is proposed, which can accurately predict the fatigue limit of heavy-duty gear steel. The research results can be applied to the actual use of heavy-duty gears and to the accurate life estimation based on the state of gear stress, thereby providing a quantitative reference model for subsequent gear steel production and gear part processing.

LncRNA SNHG6 functions as a ceRNA to regulate neuronal cell apoptosis by modulating miR-181c-5p/BIM signalling in ischaemic stroke.

Long non-coding RNAs (lncRNAs) play important roles in the pathogenesis of brain and neurodegenerative disorders. As far as we know, the functions and potential mechanisms of small nucleolar RNA host gene 6 (SNHG6) in ischaemic stroke have not been explored. This study aimed to examine the functional role of SNHG6 in the ischaemic stroke. Middle cerebral artery occlusion (MCAO) in mice and the oxygen glucose deprivation (OGD)-induced injury in neuronal cells were applied to mimic ischaemic stroke. TTC staining, quantitative real-time PCR, cell apoptosis assay, caspase-3 activity assay, Western blot, RNA immunoprecipitation and luciferase reporter assay were performed to evaluate the function and possible mechanisms of SNHG6 in the pathogenesis of ischaemic stroke. The results show that SNHG6 expression was significantly increased both OGD-induced neuronal cells and MCAO model mice. In vitro results showed that inhibition of SNHG6 increased cell viability, inhibited cell apoptosis and caspase-3 activity in OGD-induced neuronal cells. Consistently, knockdown of SNHG6 reduced brain infarct size and improved neurological scores in the MCAO mice. Mechanistic study further revealed that SNHG6 functioned as a competing endogenous RNA (ceRNA) for miR-181c-5p, which in turn repressed its downstream target of Bcl-2 interacting mediator of cell death (BIM) and inhibiting cell apoptosis. This study revealed a novel function of SNHG6 in the modulating neuronal apoptosis in the ischaemic stroke model, and the role of SNHG6 in the regulating of neuronal apoptosis was at least partly via targeting miR-181c-5p/BIM signalling pathway.

Hydrogen Peroxide-Induced Secreted Frizzled-Related Protein 1 Gene Demethylation Contributes to Hydrogen Peroxide-Induced Apoptosis in Human U251 Glioma Cells.

Glioblastoma multiforme is a type of central nervous system tumor with extremely poor prognosis. Previously, hydrogen peroxide (H2O2), which promotes the oxidative stress response, has been reported to induce the apoptosis of glioma cells. Recently, secreted frizzled-related protein 1 (SFRP1) has been shown to be associated with various types of malignant tumors and with H2O2-induced oxidative stress in cardiomyocytes by negatively regulating the Wnt signaling pathway. This study aimed to explore SFRP1 expression and its roles in H2O2-induced apoptosis in human glioma cells. We found that the SFRP1 level was decreased in several human glioma cell lines, including U87, U251, and SW1783 cells. In U251 cells, SFRP1 could function as a cancer suppressor gene, and the growth of U251 cells could be inhibited not only by H2O2 but also by the overexpression of SFRP1. Furthermore, we demonstrated that H2O2-induced SFRP1 gene demethylation partially contributed to H2O2-induced U251 cell apoptosis, which was verified by studies using an SFRP inhibitor (WAY-316606). Our research identified that H2O2-induced SFRP1 gene demethylation contributes to H2O2-induced apoptosis in human U251 glioma cells.

Comparative study among three different methods of bone marrow mesenchymal stem cell transplantation following cerebral infarction in rats.

The objective of this study was to investigate the effects of transplanted bone marrow mesenchymal stem cells (BMSCs) administered via internal jugular vein injection, carotid artery injection, or intraventricular transplantation for the treatment of cerebral infarction, which was modeled in rats. The neurological scores of the treated rats and the distribution of the transplanted cells (GFP-labeled) in the infarction area were evaluated. The cerebral infarction model was produced by inserting a modified Zea-longa suture, which generated middle cerebral artery occlusion (MCAO). The GFP-labeled BMSCs were transplanted through the jugular vein or the carotid artery or by stereotactic intraventricular delivery to the infarction models 1 week after the cerebral infarction was established. The 'Nerve Function Score' of the model rats was recorded before and after BMSC transplantation. Brain tissue sections were examined under a fluorescence microscope. We determined that the transplanted BMSCs rescued brain function, which was indicated by a decrease in the neurological scores (P<0·05) following BMSC transplantation. The effect of BMSC transplantation was reflected in decreases in the neurological score in the intraventricular transplantation group, the carotid artery transplantation group, and the jugular vein graft group*. The transplanted BMSCs were able to migrate to the brain injury area and the cortex and survived the infarction; thus, BMSCs may promote the recovery of nerve function.