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This article discusses a study on the estimation of regurgitation in patients with percutaneous left ventricular assist devices (PLVAD) during full support. The study proposes an estimation system based on a regurgitation model and uses an unscented Kalman filter (UKF) as an estimation approach. The research findings demonstrate that the proposed system can accurately estimate regurgitation during PLVAD full support, providing valuable information for clinical practitioners. The text also discusses the use of the UKF algorithm to estimate regurgitation caused by positional abnormalities after the implantation of a partial left ventricular assist device (PLVAD). The study analyzes experimental data for different degrees of positional offset and finds that the estimation error is minor for moderate and severe offsets, but slightly larger for mild offset. The UKF algorithm is shown to accurately estimate regurgitation in cases of cardiogenic shock. However, further research is needed to improve the accuracy of estimation and validate the results in larger animal models and clinical patient populations. The text also discusses the use of the UKF algorithm to estimate regurgitation status in patients with cardiogenic shock. The algorithm shows relatively accurate estimation, but further consideration is needed to improve accuracy by accounting for the impact of myocardial contractility on pump performance. Real-time observation of flow waveforms can assist in detecting regurgitation events and improving patient safety. The study is limited to a computational approach and a mock circuit, but future developments should incorporate animal and human data for [Extracted from the article]

To detect the expression of inflammatory factors such as interleukin-1β (IL-1β), interleukin-6 (IL-6), transforming growth factor (TGF-β), and tumor necrosis factor (TNF-α) in the tumor tissue of ventricular septal defect (VSD) in congenital heart disease and to explore the role of inflammatory response in the formation of aneurysmal perimembranous VSD(APVSD). Children with APVSD of congenital heart disease treated by surgery were selected and divided into true aneurysmal perimembranous group (TAP group) and pseudoaneurysmal perimembranous group (PAP group) according to echocardiography and surgical findings. There were 15 children in the TAP group and 31 in the PAP group. The aneurysmal perimembranous tissue of the two groups of children was collected during the operation. IL-1β, IL-6, TGF-β, and TNF-α were positively expressed in the aneurysmal perimembranous tissue of the two groups, and the expression levels of all inflammatory factors in the PAP group were higher than those in the TAP group, and the difference was statistically significant (P < 0.05). The expression levels of IL-1β, IL-6, TGF-β, and TNF-α in the aneurysmal perimembranous tissue of the two groups were negatively correlated with the width of the APVSD breach. IL-1β, IL-6, TGF-β, and TNF-α may be involved in the occurrence and development of APVSD through inflammatory mechanism. [ABSTRACT FROM AUTHOR]

As a non-invasive assisted circulation therapy, enhanced external counterpulsation (EECP) has demonstrated potential in treatment of lower-extremity arterial disease (LEAD). However, the underlying hemodynamic mechanism remains unclear. This study aimed to conduct the first prospective investigation of the EECP-induced responses of blood flow behavior and wall shear stress (WSS) metrics in the femoral artery. Twelve healthy male volunteers were enrolled. A Doppler ultrasound-based approach was introduced for the in vivo determination of blood flow in the common femoral artery (CFA) and superficial femoral artery (SFA) during EECP intervention, with incremental treatment pressures ranging from 10 to 40 kPa. Three-dimensional subject-specific numerical models were developed in 6 subjects to quantitatively assess variations in WSS-derived hemodynamic metrics in the femoral bifurcation. A mesh-independence analysis was performed. Our results indicated that, compared to the pre-EECP condition, both the antegrade and retrograde blood flow volumes in the CFA and SFA were significantly augmented during EECP intervention, while the heart rate remained constant. The time average shear stress (TAWSS) over the entire femoral bifurcation increased by 32.41%, 121.30%, 178.24%, and 214.81% during EECP with treatment pressures of 10 kPa, 20 kPa, 30 kPa, and 40 kPa, respectively. The mean relative resident time (RRT) decreased by 24.53%, 61.01%, 69.81%, and 77.99%, respectively. The percentage of area with low TAWSS in the femoral artery dropped to nearly zero during EECP with a treatment pressure greater than or equal to 30 kPa. We suggest that EECP is an effective and non-invasive approach for regulating blood flow and WSS in lower extremity arteries. [ABSTRACT FROM AUTHOR]

Sepsis-associated encephalopathy (SAE) is a common complication of sepsis that may seriously affect the prognosis and quality of life of patients with sepsis. Microglial activation is vital to the neuroinflammation and the pathology of SAE. In the present study, in vitro cultured BV-2 microglial cells stimulated with lipopolysaccharide (LPS) were employed as a model of microglia activation. The altered profiles of long noncoding (lnc)RNAs, circular (circ)RNAs and mRNAs in BV-2 cells after 4 h of LPS exposure were arrayed by using the Agilent competing endogenous (ce)RNA Microarray Chip. Using fold change >2 and P<0.05 as the cutoff criteria, 1,135 mRNAs and 2,488 lncRNAs were determined to be upregulated and 630 mRNAs and 744 lncRNAs to be downregulated. The number of differentially expressed circRNAs was lower, with 140 upregulated and 123 downregulated. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis of DE mRNAs suggested that inflammatory responses, as well as lipid metabolism, were involved in microglial activation. Furthermore, analyses of ceRNA networks of the lncRNA-miRNA-mRNA or circRNA-miRNA-mRNA interrelations were performed. The present study revealed a multitude of novel candidate mRNAs, lncRNAs and circRNAs involved in microglial activation, which may improve the current knowledge on neuroinflammation and provide potential therapeutic targets for SAE. [ABSTRACT FROM AUTHOR]