Search

Early-life psychological stress (ELPS) can cause anxiety, pessimism, and a decrease of cognitive ability in adult individuals. In this study, a psychological stress model (a terrified sound stress) was applied to new-born Sprague-Dawley rats for 21 days. And then, we separately evaluated the impact of ELPS on their spatial learning and memory abilities and hippocampal proteome from early-stage to the adult-stage. The Morris Water Maze (MWM) test was employed to evaluate their spatial learning and memory abilities after ELPS till to the adult-stage. Two-dimensional gel electrophoresis (2DE) as well as matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF-MS) were used to uncover the protein expression profile of the hippocampus from both ELPS-young and ELPS-adult as well as their control groups. We found that the rats had a dysfunction of spatial learning and memory after the ELPS till to the adult-stage. The proteomic analysis revealed that 51 proteins were significant differentially expression, and 25 of them were down-regulated, while the other 26 proteins were up-regulated in the hippocampus of the ELPS-young rats compared with the controls. In the ELPS-adult rats, there were 56 significant differentially expression proteins, and 42 of them were down-regulated, the other 14 proteins were up-regulated in the hippocampus compared with their controls. Thirteen of the most significant differentially expressed proteins in ELPS-adult hippocampus were identified as SPTAN1, MYH4, HSPA8, HS90A, DYN1, DLDH, ARP3, GLNA, SAHH, HBB1, ACLY, TBB2A and GBB1, that demonstrated the greatest stress-induced changes. Furthermore, western blotting analyses consistently showed that the reduced expression of SPTAN1 and MYH4 whereas the expression of HSPA8 was up-regulated in the hippocampus after ELPS till to the adult-stage. The current study showed the impaired spatial learning and memory and changed hippocampal gene expressions induced by ELPS from early-stage to adult-stage in rats. This study shows that ELPS plays an important role in behavioral cognition and hippocampal protein expression in adult rats.

The surface shape and accuracy of the metal lapping pad are important factors that affect the performance of the lapping process for flat optical components. A real-time control system for metal-lapping-pad surface shape (RCLPS) based on the bimetal thermal-deformation effect is proposed. Unlike traditional dressing methods (e.g., turning dressing with a diamond tool), real-time dressing based on the RCLPS system is a material-loss-free and in-process dressing method. A full-aperture lapping turntable based on the RCLPS system was designed, and the working heat was analyzed. A thermal-deformation model was established through regression analysis. Finally, experiments were conducted to verify the functionality of the RCLPS system. During turning dressing (turntable rotational speed nm = 100 rpm), the thermal-deformation error caused by the working heat of the turntable-shaft system was compensated by the RCLPS system. During the lapping process for optical elements (nm ≤ 20 rpm), the real-time dressing of the lapping-pad surface shape was controlled by the coolant temperature of the RCLPS system, permitting optimization and adjustment of the process performance of the plane optical component. The effectiveness and practicality of the RCLPS system were demonstrated experimentally.

BackgroundAutism spectrum disorder (ASD) is a prevalent developmental disorder that appears in early childhood and manifests repetitive behavioral and social deficits. Reported biomarkers for ASD cannot directly and specifically reflect the abnormality of brain neurons which are preferentially affected and correlated with clinical severity of the disease. Neuron-derived exosomes (NDEs), which carry proteins, lipids and nucleic acids can reflect a variety of brain diseases. However, little research has been reported about NDEs in children with ASD. MethodsSerum samples were collected from 100 ASD children and 60 age-matched typically developed (TD) children, and were pooled into 5 ASD groups and 3 TD groups (n=20). NDEs from the pooled sera in each group were isolated using L1CAM antibody mediated immunosorbent assay and characterized by nanoparticle tracking analysis, transmission electron microscopy and western blot. Whole-transcriptome of NDEs was detected by lncRNA microarray and RNA-Sequencing. RNAs expressed differently in NDEs from ASD sera as versus those from TD sera were screened, analyzed, and validated. ResultsSerum NDEs were isolated successfully. A total of 1418 mRNAs, 1745 lncRNAs and 11 miRNAs were identified to be differentially expressed, and most of them were down-regulated in ASD. The differentially expressed RNAs were prone to be distributed on chromosome 17. Target gene prediction and bioinformatic analysis revealed that a large portion of RNAs were involved in neuron- and glycan-related networks implicated in ASD. qRT-PCR identified that the levels of EDNRA, SLC17A6, HTR3A, OSTC, TMEM165, PC-5p-139289_26, and hsa-miR-193a-5p changed significantly in ASD, indicating them as potential biomarkers for the disease. LimitationsThe correlation between the expression of candidate biomarkers and disease severity were not examined. Some of our participants were not medication-free. Samples were mainly from a single hospital. ConclusionsWhole-transcriptome analysis of serum NDEs reveals specific signature for ASD in Chinese children, which may help detect predictive biomarkers and molecular mechanisms of ASD, and provide reference for diagnoses and therapeutic management of the disease.

In this work, a theoretical analysis of surface generation numerical model is presented to predict the surface roughness achieved by side milling operations with cylindrical tools. This work is focused on the trajectory of tools with two teeth by influencing of tool errors such as radial runouts, as well as straightness with dynamic effects. A computational system was developed to simulate roughness topography in contour milling with cylindrical tool. Finally, the PSO (particle swarm optimization) algorithm is employed to find the optimal machining position for the best surface roughness. Experimental data is satisfied with the the novel pretiction model for the tooth’s trajectory, and the the final prediction accuracy is high enough, i.e. that the prediction surface roughness. Low prediction surface roughness error (1.37 ~ 15.04%) and position error (0.95 ~ 1.25 mm) indicate effectiveness of the model built in this work. The novel model may be used to determine the variation in surface roughness.

Background: Methyl-CpG-binding protein 2 (MECP2), an epigenetic regulatory factor, promotes the carcinogenesis and progression of a number of cancers. However, its role in the migration and invasion of gastric cancer (GC) as well as the underlying molecular mechanisms remain unclear.Methods: Immunohistochemistry (IHC), Western blot, and quantitative real-time PCR (qRT-PCR) were performed to measure the expressions of MECP2, FBXW7, c-Myc, mTOR and Notch1 in GC tissues and cell lines, respectively. The effects of MECP2 silencing and overexpression on GC cell migration and invasion were detected by wound healing assay and transwell assay. The mechanisms of MECP2-mediated migration and invasion were further investigated using chromatin immunoprecipitation sequencing (ChIP-Seq) and luciferase reporter gene assay.Results: In this study, we found that MECP2 facilitated the migration and invasion of GC cells. Investigation of the molecular mechanism revealed that MECP2 restrained FBXW7 transcription in GC by binding to the methylated CpG sites of FBXW7’s promoter region. MECP2 expression was remarkably negatively correlated with the FBXW7 level in GC tissues. FBXW7 expression was significantly downregulated in GC tissues and cell lines, and low FBXW7 expression was correlated with the clinicopathologic features. FBXW7 repressed cell migration and invasion by regulating the Notch1/c-Myc/mTOR signaling pathways, and knockdown of FBXW7 reversed the effects of silencing MECP2. Moreover, MECP2 upregulated the Notch1/c-Myc/mTOR signaling pathways by inhibiting FBXW7 expression at the transcription level.Conclusion: This study demonstrates that MECP2 promotes migration and invasion of GC cells via modulating the Notch1/c-Myc/mTOR signaling pathways by suppressing FBXW7 transcription. The findings suggest that MECP2 may be a novel effective therapeutic target for GC patients.