RESUMO
Intracardiac wireless communication is crucial for the development of multi-chamber leadless cardiac pacemakers (LCP). However, the time-varying characteristics of intracardiac channel pose major challenges. As such, mastering the dynamic conduction properties of the intracardiac channel and modeling the equivalent time-varying channel are imperative for realizing LCP multi-chamber pacing. In this article, we present a limiting volume variational approach based on the electrical properties of cardiac tissues and trends in chamber volume variation. This approach was used to establish a quasi-static and a continuous time-varying equivalent circuit model of an intracardiac channel. An equivalence analysis was conducted on the model, and a discrete time-varying equivalent circuit phantom grounded on the cardiac cycle was subsequently established. Moreover, an ex vivo cardiac experimental platform was developed for verification. Results indicate that in the frequency domain, the congruence between phantom and ex vivo experimental outcomes is as high as 94.3%, affirming the reliability of the equivalent circuit model. In the time domain, the correlation is up to 75.3%, corroborating its effectiveness. The proposed time-varying equivalent circuit model exhibits stable and standardized dynamic attributes, serving as a powerful tool for addressing time-varying challenges and simplifying in vivo or ex vivo experiments.
Assuntos
Modelos Cardiovasculares , Marca-Passo Artificial , Animais , Desenho de Equipamento , HumanosRESUMO
The mining and smelting site soils in South China present excessive Cd pollution. However, the transport behavior of Cd in the highly weathered acidic soil layer at the lead-zinc smelting site remains unclear. Here, under different conditions of simulated infiltration, the migration behavior of Cd2+ in acid smelting site soils at different depths was examined. The remodeling effect of Cd2+ migration behavior on microbial community structure and the dominant microorganisms in lead-zinc sites soils was analyzed using high-throughput sequencing of 16S rRNA gene amplicons. The results revealed a specific flow rate in the range of 0.3-0.5 mL/min that the convection and dispersion have no obvious effect on Cd2+ migration. The variation of packing porosity could only influence the migration behavior by changing the average pore velocity, but cannot change the adsorption efficiency of soil particles. The Cd has stronger migration capacity under the reactivation of acidic seepage fluid. However, in the alkaline solution, the physical properties of soil, especially pores, intercept the Cd compounds, further affecting their migration capacity. The acid-site soil with high content of SOM, amorphous Fe oxides, crystalline Fe/Mn/Al oxides, goethite, and hematite has stronger ability to adsorb and retain Cd2+. However, higher content of kaolinite in acidic soil will increase the potential migration of Cd2+. Besides, the migration behavior of Cd2+ results in simplified soil microbial communities. Under Cd stress, Cd-tolerant genera (Bacteroides, Sphingomonas, Bradyrhizobium, and Corynebacterium) and bacteria with both acid-Cd tolerance (WCHB 1-84) were distinguished. The Ralstonia showed a high enrichment degree in alkaline Cd2+ infiltration solution (pH 10.0). Compared to the influence of Cd2+ stress, soil pH had a stronger ability to shape the microbial community in the soil during the process of Cd2+ migration.
Assuntos
Microbiota , Poluentes do Solo , Solo/química , Cádmio/toxicidade , RNA Ribossômico 16S , Poluentes do Solo/toxicidade , Poluentes do Solo/análise , Zinco/análise , ÓxidosRESUMO
This study aimed to investigate effects of pulmonary fractalkine (FKN/CX3CL1) on angiogenesis and tube formation. Tube forming capability of pulmonary vascular endothelial cells (PVECs) was evaluated. CCK-8 assay was used to evaluate proliferation of PVECs. RT-PCR assay was used to determine angiogenesis specific biomarkers. Western blot was applied to identify CX3CR1, Akt, phosphorylated Akt (p-Akt), Erk1/2, phosphorylated Erk1/2 (p-Erk1/2), vascular endothelial growth factor A (VEGFA), and inducible nitric oxide synthase (iNOS) expression. VEGF-A and platelet-derived growth factor (PDGF) levels were examined using ELISA. FKN was safe and triggered tube formation in PVECs. FKN significantly enhanced VEGF-A, PDGF, and iNOS gene transcription compared to the Control group (p < 0.05). CX3CR1 interfering (LV5-CX3CR1 shRNA) remarkably reduced CX3CR1 expression compared to those in LV5 blank group (p < 0.05). Ratios of p-Akt/Akt and p-Erk/Erk were significantly decreased in CX3CR1 shRNA-treated PVECs administered Akt inhibitor (or Erk inhibitor) and 10 ng/mL FKN compared to CX3CR1 shRNA-treated PVECs administered 10 ng/mL FKN (p < 0.05). FKN increased VEGF-A and iNOS expression through activating Akt/Erk pathway. FKN promoted VEGF-A/iNOS expression and triggered p-Akt/Akt and p-Erk/Erk pathway through modulating CX3CR1. FKN-treated macrophages enhanced activation of Akt/Erk pathway. FKN-treated macrophages enhanced PDGF and VEGF-1 expression in PVECs. FKN modulated pulmonary angiogenesis and tube formation through modulating CX3CR1 and growth factors and activating p-Akt/Akt and p-Erk/Erk signaling pathway.