We present an alternative technique for the repair of a high partially anomalous pulmonary venous connection to the superior vena cava.
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cSTAR analysis identifies endothelial cell cycle as a key regulator of flow-dependent artery remodeling.
Sci Adv
January 2025
Yale Cardiovascular Research Center, Yale School of Medicine, New Haven, CT 06511, USA.
Fluid shear stress (FSS) from blood flow sensed by vascular endothelial cells (ECs) determines vessel behavior, but regulatory mechanisms are only partially understood. We used cell state transition assessment and regulation (cSTAR), a powerful computational method, to elucidate EC transcriptomic states under low shear stress (LSS), physiological shear stress (PSS), high shear stress (HSS), and oscillatory shear stress (OSS) that induce vessel inward remodeling, stabilization, outward remodeling, or disease susceptibility, respectively. Combined with a publicly available database on EC transcriptomic responses to drug treatments, this approach inferred a regulatory network controlling EC states and made several notable predictions.
View Article and Find Full Text PDFTherapeutic effect of fully human anti-Nrp-1 antibody on non-small cell lung cancer in vivo and in vitro.
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January 2025
Public Center of Experimental Technology, The School of Basic Medical Sciences, Southwest Medical University, Luzhou, 646000, Sichuan Province, China.
Although immune checkpoint inhibitors have changed the treatment paradigm for non-small cell lung cancer (NSCLC), not all patients benefit from them. Therefore, there is an urgent need to explore novel immune checkpoint inhibitors. Neuropilin-1 (Nrp-1) is a unique immune checkpoint capable of exerting antitumor effects through CD8 T cells.
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December 2024
Barcelonaβeta Brain Research Center (BBRC), Pasqual Maragall Foundation, Barcelona, Spain.
Background: Current evidence suggests that hippocampal subfields have partially different genetic architecture and may improve the sensitivity of the detection of Alzheimer's disease (AD). In this study, we investigated whether genetic predisposition to AD contributes to the accelerated rate of hippocampal volume atrophy across sex and AD stages and how this contribution is specifically driven by functional variants located in the APOE gene.
Methods: The study comprised 1,051 participants from ADNI cohort (75.
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Columbia University, New York, NY, USA.
Background: Alzheimer's disease (AD) missing heritability remains extensive despite numerous genetic risk loci identified by genome-wide association or sequencing studies. This has been attributed, at least partially, to mechanisms not currently investigated by traditional single-marker/gene approaches. Polygenic Risk Scores (PRS) aggregate sparse genetic information across the genome to identify individual genetic risk profiles for disease prediction and patient risk stratification.
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Cleveland Institute for Computational Biology, Department of Population and Quantitative Health Sciences, Case Western Reserve University, Cleveland, OH, USA.
Background: While there are numerous genome-wide association studies (GWAS) assessing the genetic basis of Alzheimer's disease (AD), there are far fewer studies examining genetic factors for cognitive and global resilience to AD neuropathology. By focusing on a gene-level rather than a single-variant basis, transcriptome-wide association studies (TWAS) have increased statistical power relative to GWAS and can assess the role of genetically regulated gene expression in AD resilience. We leveraged the largest available cis-eQTL meta-analysis summary statistics from brain tissue (MetaBrain Brain-Cortex; N = 2,547) and whole blood (eQTLGen; N = 31,684) and applied them to the largest cognitive and global resilience to AD neuropathology summary statistics from Dumitrescu et al.
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