The Acceleration/Deceleration Control Algorithm Based on Trapezoid-Curve Jerk in CNC Machining

Abstract: In this study, we put forward an Acc/Dec control algorithm based on trapezoid-curve jerk in order to avoid step change in jerk curve. Moreover, the motion profile smooth control approach based on continuous jerk is developed in details to decrease machine tools impact according to various kinematics constraint conditions, such as the maximum acceleration, the maximum jerk, the machining program segment displacement, the instruction feed rate and so on; Finally, the developed Acc/Dec approach and the traditional linear Acc/Dec approach are compared in the CNC experimental table. The results reveal that the developed approach can achieve more smooth and flexible motion profile, which is helpful to minish machine tools impact and enhance parts machining surface quality

Automatic Microassembly of Tissue Engineering Scaffold

Ph.DDOCTOR OF PHILOSOPH

The role of mitochondria-associated membranes mediated ROS on NLRP3 inflammasome in cardiovascular diseases

Reactive oxygen species (ROS) metabolism is essential for the homeostasis of cells. Appropriate production of ROS is an important signaling molecule, but excessive ROS production can damage cells. ROS and ROS-associated proteins can act as damage associated molecular pattern molecules (DAMPs) to activate the NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome in cardiovascular diseases. Previous studies have shown that there are connected sites, termed mitochondria-associated membranes (MAMs), between mitochondria and the endoplasmic reticulum. In cardiovascular disease progression, MAMs play multiple roles, the most important of which is the ability to mediate ROS generation, which further activates the NLPR3 inflammasome, exacerbating the progression of disease. In this review, the following topics will be covered: 1. Molecular structures on MAMs that can mediate ROS generation; 2. Specific mechanisms of molecule-mediated ROS generation and the molecules' roles in cardiovascular disease, 3. The effects of MAMs-mediated ROS on the NLRP3 inflammasome in cardiovascular disease. The purpose of this review is to provide a basis for subsequent clinical treatment development

Survival of esophageal cancer in China: A pooled analysis on hospital-based studies from 2000 to 2018

Background: Esophageal cancer (EC) causes more than 400 thousand deaths per year, and half of them occur in China. There are discrepancies regarding the survival of EC patients between population-based surveillance studies and hospital-based studies. Objectives: We aimed to synthesize the survival data from hospital-based EC studies in the Chinese population from 2000 to 2018 and to compare the survival rates between EC patients with different clinical classifications. Methods: The protocol of this systematic review was registered in PROSPERO (CRD-42019121559). We searched Embase, PubMed, CNKI, and Wanfang databases for studies published between January 1, 2000 and December 31, 2018. We calculated the pooled survival rates and 95% confidence intervals (CIs) by Stata software (V14.0). Results: Our literature search identified 933 studies, of which 331 studies with 79,777 EC patients met the inclusion criteria and were included in meta-analyses. The pooled survival rates were 74.1% (95% CI: 72.6–75.7%) for 1-year survival, 49.0% (95% CI: 44.2–53.8%) for 2-years survival, 46.0% (95% CI: 42.6–49.5%) for 3-years survival, and 40.1% (95% CI: 33.7–46.4%) for 5-years survival. An increased tendency toward EC survival was verified from 2000 to 2018. In addition, discrepancies were observed between EC patients with different clinical classifications (e.g., stages, histologic types, and cancer sites). Conclusions: Our findings showed a higher survival rate in hospital-based studies than population-based surveillance studies. Although this hospital-based study is subject to potential representability and publication bias, it offers insight into the prognosis of patients with EC in China

Down-regulation of microRNA-23b aggravates LPS-induced inflammatory injury in chondrogenic ATDC5 cells by targeting PDCD4

Objective(s): Osteoarthritis (OA), characterized by degradation of articular cartilage, is a leading cause of disability. As the only cell type present in cartilage, chondrocytes play curial roles in the progression of OA. In our study, we aimed to explore the roles of miR-23b in the lipopolysaccharide (LPS)-induced inflammatory injury. Materials and Methods: LPS-induced cell injury of ATDC5 cells was evaluated by the loss of cell viability, enhancement of cell apoptosis, alteration of apoptosis-associated proteins, and release of inflammatory cytokines. Then, miR-23b level after LPS treatment was assessed by qRT-PCR. Next, the effects of aberrantly expressed miR-23b on the LPS-induced inflammatory injury were explored. The possible target genes of miR-23b were virtually screened by informatics and verified by luciferase assay. Subsequently, whether miR-23b functioned through regulating the target gene was validated. The involved signaling pathways were investigated finally.Results: Cell viability was decreased but cell apoptosis, as well as release of inflammatory cytokines, was enhanced by LPS treatment. MiR-23b was down-regulated by LPS and its overexpression alleviated LPS-induced inflammatory injury. PDCD4, negatively regulated by miR-23b expression, was verified as a target gene of miR-23b. Following experiments showed miR-23b alleviated LPS-induced cell injury through down-regulating PDCD4 expression. Phosphorylated levels of key kinases in the NF-κB pathway, as well as expressions of key kinases in the Notch pathways, were increased by PDCD4 overexpression.Conclusion: MiR-23b was down-regulated after LPS treatment, and its overexpression ameliorated LPS-induced inflammatory injury in ATDC5 cells by targeting PDCD4, which could activate the NF-κB/Notch pathways

Cloning and Comparative Studies of Seaweed Trehalose-6-Phosphate Synthase Genes

The full-length cDNA sequence (3219 base pairs) of the trehalose-6-phosphate synthase gene of Porphyra yezoensis (PyTPS) was isolated by RACE-PCR and deposited in GenBank (NCBI) with the accession number AY729671. PyTPS encodes a protein of 908 amino acids before a stop codon, and has a calculated molecular mass of 101,591 Daltons. The PyTPS protein consists of a TPS domain in the N-terminus and a putative TPP domain at the C-terminus. Homology alignment for PyTPS and the TPS proteins from bacteria, yeast and higher plants indicated that the most closely related sequences to PyTPS were those from higher plants (OsTPS and AtTPS5), whereas the most distant sequence to PyTPS was from bacteria (EcOtsAB). Based on the identified sequence of the PyTPS gene, PCR primers were designed and used to amplify the TPS genes from nine other seaweed species. Sequences of the nine obtained TPS genes were deposited in GenBank (NCBI). All 10 TPS genes encoded peptides of 908 amino acids and the sequences were highly conserved both in nucleotide composition (>94%) and in amino acid composition (>96%). Unlike the TPS genes from some other plants, there was no intron in any of the 10 isolated seaweed TPS genes