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This paper proposes a novel spatial-temporal fusion deep neural network for soft sensing of industrial processes. Different from previous deep learning based methods, the proposed model considers a new structure by combining the gated recurrent unit(GRU) and deep convolutional neural network(DCNN). The temporal correlation is captured by the GRU framework and the spatial correlation/input-output relationship is revealed using the DCNN structure. The resultant features are then fused and fed into a dense layer to produce the final estimations. A backpropagating algorithm is used to optimize the parameters of the model. The developed soft sensor considers both the spatial and temporal information and hence are more accurate in soft sensing of important quality variables that are difficult to measure in industrial processes. The effectiveness and feasibility of the soft sensor is verified by an application to the sulfur recovery unit(SRU).

A previous study has revealed that oxidized low‑density lipoprotein (oxLDL)/β2‑glycoprotein I (β2GPI)/anti‑β2‑glycoprotein I (anti‑β2GPI), an immune complex, is able to activate the Toll‑like receptor 4 (TLR4)/nuclear factor κβ (NF‑κβ) inflammatory signaling pathway in macrophages, and consequently enhance foam cell formation and the secretion of prothrombin activators. However, the effects of the oxLDL/β2GPI/anti‑β2GPI complex on vascular smooth muscle cells have yet to be investigated. The present study investigated whether the oxLDL/β2GPI/anti‑β2GPI complex was able to reinforce the pro‑atherogenic activities of a rat thoracic aorta smooth muscle cell line (A7r5) and examined the underlying molecular mechanisms. The results revealed that the oxLDL/β2GPI/anti‑β2GPI complex treatment significantly (P

Objective To explore the effect of the oxidized low-density lipoprotein/β2 -glycoprotein I/β2 glycoprotein I antibody (oxLDL/β2GPI/β2GPI-Ab) complex on the migration, chemotaxis and lipid accumulation of rat thoracic aortic smooth muscle A7r5 cell line, and unveil the role of Toll-like receptor 4 (TLR4) pathway during the process. Methods A7r5 cells were cultured in vitro with or without the pretreatment of TAK-242, a TLR4 inhibitor. Then the cells were stimulated by oxLDL, oxLDL/β2GPI complex, β2GPI, β2GPI-Ab, β2GPI/β2GPI-Ab complex or oxLDL/β2GPI/β2GPI-Ab complex. Total RNA was extracted from the cells and the mRNA levels of monocyte chemoattractant protein-1 (MCP-1), matrix metalloproteinase-9 (MMP-9) and acetyl-CoA acetyltransferase 1 (ACAT1) were evaluated by real-time quantitative PCR. The cell supernatants were collected, and the protein levels of MCP-1 and MMP-9 were determined by ELISA. The migration of A7r5 was observed through wound-healing test. A7r5 cells pretreated with or without TAK-242 were stimulated by oxLDL or oxLDL/β2GPI/β2GPI-Ab complex, and the content of total cholesterol (TC) and free cholesterol (FC) in them were measured by corresponding test kits. Then the level of intracellular cholesterol ester (CE) was calculated. Results The oxLDL/β2GPI/β2GPI-Ab complex promoted the migration and cholesterol accumulation, and up-regulated the expressions of MCP-1, MMP-9 and ACAT1 in A7r5 cells. In addition, the application of TLR4 inhibitor, TAK-242, suppressed these effects. Conclusion oxLDL/β2GPI/β2GPI-Ab complex contributes to the process of atherosclerosis through promoting the migration, chemotaxis and lipid accumulation of a7r5 in a TLR4-dependent manner.

Objective To investigate the effect of oxidative low-density lipoprotein/β2 glycoprotein I/anti-β2 glycoprotein I antibody (oxLDL/β2GPI/anti-β2GPI-Ab) complex on the expressions of adhesion molecules in human umbilical vein endothelial cells (HUVECs), and the role of Toll-like receptor 4 (TLR4) signaling pathway during this process. Methods HUVECs were stimulated with simple medium, oxLDL, oxLDL/β2GPI complex, oxLDL/anti-β2GPI-Ab complex, oxLDL/β2GPI/anti-β2GPI-Ab complex and LPS separately, and then the total mRNA and protein were collected. The mRNA and protein expressions of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1) and von Willebrand factor (vWF) were detected by real-time quantitative PCR and Western blotting, respectively. Pre-treatment method was applied to explore the influence of TLR4 antagonist TAK-242 (5 μmol/L) and p38MAPK antagonist SB203580 (10 μmol/L) on the expressions of adhesion molecules in HUVECs. THP-1 cell adhesion test was employed to evaluate the effect of oxLDL/β2GPI/anti-β2GPI-Ab complex on the ability of attracting monocytes of HUVECs. Results Compared with simple medium, oxLDL/β2GPI/anti-β2GPI-Ab complex obviously upregulated the expressions of ICAM-1, VCAM-1 and vWF in HUVECs and promoted the adhesion of THP-1 cells to HUVECs. In addition, these effects were inhibited by the pre-treatment of TAK-242 or SB203580. Conclusion OxLDL/β2GPI/anti-β2GPI-Ab complex could up-regulate the expressions of adhesion molecules in HUVECs and promote the adhesion of THP-1 cells to HUVECs, in which TLR4 and p38 MAPK were closely involved.

Objective To study the effects of the complex of oxidized low density lipoprotein/β2-glycoprotein I/β2-glycoprotein I antibodies (oxLDL/β2GPI/β2GPI-Ab) on the migration of human umbilical vein endothelial cells (HUVECs) and the expression of inflammatory cytokines, and their underlying Toll-like receptor (TLR4) pathway. Methods HUVECs were treated with oxLDL, oxLDL/β2GPI complex, oxLDL/β2GPI-Ab complex, oxLDL/β2GPI/β2GPI-Ab complex, or lipopolysaccharide (LPS) for a period of time in their corresponding groups. The migration of HUVECs was observed by the wound-healing assay. The mRNA and protein levels of TLR4 in HUVECs were detected by real-time quantitative PCR (qRT-PCR) and Western blotting, respectively. The cells were pretreated with or without TAK-242 (the inhibitor of TLR4) 2 hours before stimulated by corresponding stimulus as described above. Then, the contents of monocyte chemotactic protein-1 (MCP-1), interleukin 1β (IL-1β) and IL-6 in cell culture supernatant were determined by ELISA, and their mRNAs were detected by qRT-PCR. Results The oxLDL/β2GPI/β2GPI-Ab complex promoted the migration of HUVECs effectively, and increased the expression of TLR4. The oxLDL/β2GPI/β2GPI-Ab complex increased the expressions of MCP-1, IL-1β, and IL-6. TAK-242 could reduce the effects of oxLDL/β2GPI/β2GPI-Ab complex. Conclusion The oxLDL/β2GPI/anti-β2GPI-Ab complex can promote the migration of HUVECs and the expression of related inflammatory cytokines, and TLR4 may be involved in this process.

Objective To investigate the roles of anti-beta 2 glycoprotein I antibodies (anti-β2GPI Ab) in the expressions of atherosclerosis(AS)-related inflammatory factors and pro-thrombosis molecules in apolipoprotein E-deficient (ApoE

In some industrial productions and precision instruments, it requires high-precision temperature control temperature, measurements is the basis of temperature control. This paper has made some theoretical error analysis and developed a high-precision temperature measurement circuit, based on the error analysis, the type and precision of the critical power supply chip power and precision resistance has been determined, ultimately through the simulation, the precision devices has been determined, and under the selected devices, a temperature test has done, after all, the temperature measurement circuit precision can reach 0.02 °C, it meets the needs of industrial production and a number of precision instruments.