Pretrained subtraction and segmentation model for coronary angiograms.

This study introduces a novel self-supervised learning method for single-frame subtraction and vessel segmentation in coronary angiography, addressing the scarcity of annotated medical samples in AI applications. We pretrain a U-Net model on a large dataset of unannotated coronary angiograms using an image-to-image translation framework, then fine-tune it on a limited set of manually annotated samples. The pretrained model excels at comprehensive single-frame subtraction, outperforming existing DSA methods.

Exploration and validation of signature genes and immune associations in septic cardiomyopathy.

An early and accurate diagnosis of septic cardiomyopathy is vital for improving the overall prognosis of sepsis. In our research, we aimed to identify signature genes and their immune connections in septic cardiomyopathy. By analyzing the mouse myocardial transcriptome from sepsis induced by cecum ligation and puncture (CLP), we identified four distinct k-means clusters.

Preparation and Properties of Medium-Density Fiberboards Bonded with Vanillin Crosslinked Chitosan.

An eco-friendly medium-density fiberboard (MDF) was prepared using vanillin (V) crosslinked chitosan (CS) adhesive through a hot-pressing process. The cross-linking mechanism and the effect of different proportions of added chitosan/vanillin on the mechanical properties and dimensional stability of MDF were investigated. The results showed that vanillin and chitosan are crosslinked to form a three-dimensional network structure due to the Schiff base reaction between the aldehyde group of vanillin and the amino group of chitosan.

Triphenyl phosphate induced apoptosis of mice testicular Leydig cells and TM3 cells through ROS-mediated mitochondrial fusion inhibition.

Triphenyl phosphate (TPHP) is a widely used organophosphate flame retardant and has biological toxicity. Previous studies showed TPHP can restrain testosterone biosynthesis in Leydig cells, while the underlying mechanisms remain unclear. In this study, C57BL/6J male mice were exposed to 0, 5, 50, and 200 mg/kg B.

Retracted: Wnt-C59 Attenuates Pressure Overload-Induced Cardiac Hypertrophy via Interruption of Wnt Pathway.

This publication has been retracted by the Editor due to the identification of non-original figure images and manuscript content that raise concerns regarding the credibility and originality of the study and the manuscript. Reference: Zhengbo Zhao, Han Liu, Yu Li, Jingxiu Tian, Songbai Deng. Wnt-C59 Attenuates Pressure Overload-Induced Cardiac Hypertrophy via Interruption of Wnt Pathway.

Using the VQ-VAE to improve the recognition of abnormalities in short-duration 12-lead electrocardiogram records.

Background And Objective: Morphological diagnosis is a basic clinical task of the short-duration 12-lead electrocardiogram (ECG). Due to the scarcity of positive samples and other factors, there is currently no algorithm that is comparable to human experts in ECG morphological recognition. Our objective is to develop an ECG specialist-level deep learning method that can accurately identify ten ECG morphological abnormalities in real scene data.

Wnt-C59 Attenuates Pressure Overload-Induced Cardiac Hypertrophy via Interruption of Wnt Pathway.

BACKGROUND Cardiac hypertrophy usually results in heart failure and is an important cause of mortality worldwide. Wnt/ß-catenin signaling pathway hyper-activation is involved in the pathogenesis and progression of cardiac hypertrophy. Wnt-C59 is a small molecular compound, which strongly and specifically targets at Porcupine to pharmacologically inhibit Wnt palmitoylation, secretion, and other biological activities.

Aliskiren attenuates cardiac dysfunction by modulation of the mTOR and apoptosis pathways.

Aliskiren (ALS) is well known for its antihypertensive properties. However, the potential underlying the molecular mechanism and the anti-hypertrophic effect of ALS have not yet been fully elucidated. The aim of the present study was to investigate the role of ALS in mammalian target of rapamycin (mTOR) and apoptosis signaling using in vivo and in vitro models of cardiac hypertrophy.