Evaluation of Factors Underlying Sex-Based Disparities in Cardiovascular Care in Adults With Self-reported Premature Atherosclerotic Cardiovascular Disease.

Importance: There are limited data regarding sex-based differences in physical and mental health domains and health care access in adults with premature atherosclerotic cardiovascular disease (ASCVD).

Objective: To study the association of sex with physical and mental health domains as well as health care access-related factors among adults with self-reported premature ASCVD.

Design, Setting, And Participants: Retrospective cohort analysis of 748 090 adults aged 18 to 55 years in the Behavioral Risk Factor Surveillance System 2016 to 2019 in the US.

FAT10 protects against ischemia-induced ventricular arrhythmia by decreasing Nedd4-2/Nav1.5 complex formation.

The human leukocyte antigen F-associated transcript 10 (FAT10) is a member of the small ubiquitin-like protein family that binds to its target proteins and subjects them to degradation by the ubiquitin-proteasome system (UPS). In the heart, FAT10 plays a cardioprotective role and affects predisposition to cardiac arrhythmias after myocardial ischemia (MI). However, whether and how FAT10 influences cardiac arrhythmias is unknown.

Clinical and economic outcomes of ProGlide compared with surgical repair of large bore arterial access.

This study compared real-world complication rates, hospitalization duration and costs, among patients undergoing arterial repair using the Perclose ProGlide (ProGlide) versus surgical cutdown (Cutdown). Retrospective study of matched patients who underwent transcatheter aortic valve replacement/repair, endovascular abdominal aortic aneurysm repair, thoracic endovascular aortic repair or balloon aortic valvuloplasty with arterial repair by either ProGlide or Cutdown between 1 January 2013 and 24 April 2017. Infections and blood transfusions were lower in the ProGlide cohort.

Cardiac repair and the putative role of stem cells.

Stem cell biology has informed and energized cardiac regenerative medicine. The field is linked to a construct that challenges long-standing concepts and advances the basic tenets that: 1) the mammalian heart has the capacity for significant regeneration of cardiomyocytes (CMC) by reentry of CMC into the cell cycle and by activation of endogenous cardiac stem cells and 2) the administration of exogenous stem cell preparations can result in significant myocardial repair and regeneration in cardiac diseases. Based on the latter, major resources have been invested in clinical trials of stem cell therapy.

Diagnostic and Prognostic Relevance of Red Blood Cell Distribution Width for Vascular Aging and Cardiovascular Diseases.

Evidence suggests association of red blood cell distribution width (RDW) with cardiovascular diseases (CVDs). On the contrary, we underline that the sole RDW values cannot represent a valid CVD biomarker. High RDW values are expression of biological effects of a lot of both endogenous and exogenous factors (.

Dissertation of ST elevation causation.

ECG Quiz: Diffuse ST elevations with broad differential in 57 year old man.

Genome-wide analysis yields new loci associating with aortic valve stenosis.

Aortic valve stenosis (AS) is the most common valvular heart disease, and valve replacement is the only definitive treatment. Here we report a large genome-wide association (GWA) study of 2,457 Icelandic AS cases and 349,342 controls with a follow-up in up to 4,850 cases and 451,731 controls of European ancestry. We identify two new AS loci, on chromosome 1p21 near PALMD (rs7543130; odds ratio (OR) = 1.

Correction to: Disruption of endothelial adherens junctions by high glucose is mediated by protein kinase C-β-dependent vascular endothelial cadherin tyrosine phosphorylation.

This article was unintentionally published twice in this journal, by the same authors. The following should be considered the version of record and used for citation purposes: "Mehran Haidari, Wei Zhang, James T Willerson and Richard AF Dixon, Disruption of endothelial adherens junctions by high glucose is mediated by protein kinase C-β-dependent vascular endothelial cadherin tyrosine phosphorylation, Cardiovascular Diabetology, Volume 13, Issue 1, doi: 10.1186/1475-2840-13-112 ".

Quantification of Embryonic Myofiber Development by Immunofluorescence.

Mammalian myogenesis occurs in two distinct phases, primary and secondary, which are temporally separated. The primary wave occurs shortly after somitogenesis producing embryonic myofibers. The secondary wave occurs after somitogenesis producing fetal myofibers that form adjacent to the embryonic myofibers.

Toll-like receptor-4 signaling pathway in aorta aging and diseases: "its double nature".

Recent advances in the field of innate immunity have revealed a complex role of innate immune signaling pathways in both tissue homeostasis and disease. Among them, the Toll-like receptor 4 (TLR-4) pathways has been linked to various pathophysiological conditions, such as cardiovascular diseases (CVDs). This has been interrogated by developing multiple laboratory tools that have shown in animal models and clinical conditions, the involvement of the TLR-4 signaling pathway in the pathophysiology of different CVDs, such as atherosclerosis, ischemic heart disease, heart failure, ischemia-reperfusion injury and aorta aneurysm.

HIRA deficiency in muscle fibers causes hypertrophy and susceptibility to oxidative stress.

Nucleosome assembly proceeds through DNA replication-coupled or replication-independent mechanisms. For skeletal myocytes, whose nuclei have permanently exited the cell cycle, replication-independent assembly is the only mode available for chromatin remodeling. For this reason, any nucleosome composition alterations accompanying transcriptional responses to physiological signals must occur through a DNA replication-independent pathway.

Novel SUMO-Protease SENP7S Regulates β-catenin Signaling and Mammary Epithelial Cell Transformation.

SUMO post-translational modification of proteins or SUMOylation ensures normal cell function. Disruption of SUMO dynamics prompts various pathophysiological conditions, including cancer. The burden of deSUMOylating the large SUMO-proteome rests on 6 full-length mammalian SUMO-proteases or SENP.

Development of diagnostic SCAR markers for genomic DNA amplifications in breast carcinoma by DNA cloning of high-GC RAMP-PCR fragments.

Cancer is genetically heterogeneous regarding to molecular genetic characteristics and pathogenic pathways. A wide spectrum of biomarkers, including DNA markers, is used in determining genomic instability, molecular subtype determination and disease prognosis, and estimating sensitivity to different drugs in clinical practice. In a previous study, we developed highly effective DNA markers using improved random amplified polymorphic DNA (RAPD) with high-GC primers, which is a valuable approach for the genetic authentication of medicinal plants.

Genetic Variants in LRP1 and ULK4 Are Associated with Acute Aortic Dissections.

Acute aortic dissections are a preventable cause of sudden death if individuals at risk are identified and surgically repaired in a non-emergency setting. Although mutations in single genes can be used to identify at-risk individuals, the majority of dissection case subjects do not have evidence of a single gene disorder, but rather have the other major risk factor for dissections, hypertension. Initial genome-wide association studies (GWASs) identified SNPs at the FBN1 locus associated with both thoracic aortic aneurysms and dissections.

Mesp1 Marked Cardiac Progenitor Cells Repair Infarcted Mouse Hearts.

Mesp1 directs multipotential cardiovascular cell fates, even though it's transiently induced prior to the appearance of the cardiac progenitor program. Tracing Mesp1-expressing cells and their progeny allows isolation and characterization of the earliest cardiovascular progenitor cells. Studying the biology of Mesp1-CPCs in cell culture and ischemic disease models is an important initial step toward using them for heart disease treatment.

miR-322/-503 cluster is expressed in the earliest cardiac progenitor cells and drives cardiomyocyte specification.

Understanding the mechanisms of early cardiac fate determination may lead to better approaches in promoting heart regeneration. We used a mesoderm posterior 1 (Mesp1)-Cre/Rosa26-EYFP reporter system to identify microRNAs (miRNAs) enriched in early cardiac progenitor cells. Most of these miRNA genes bear MESP1-binding sites and active histone signatures.

Fast-track endovascular aortic repair: Interim report from the prospective LIFE registry.

Objective: To assess the feasibility, safety, and clinical utility of a fast-track endovascular aneurysm repair (EVAR) protocol.

Background: Despite recent advances in EVAR technology and techniques, considerable opportunity exists to further improve EVAR efficiency and outcomes.

Methods: Eligible patients underwent elective EVAR with the Ovation Prime stent graft.

Patients Awaiting Heart Transplantation on HVAD Support for Greater Than 2 Years.

Advanced heart failure patients who are classified as bridge to transplant (BTT) often remain on mechanical circulatory support (MCS) for long durations because of the limited supply of donor organs. Here, we present the outcomes of patients who have been supported by the HeartWare ventricular assist device system for more than 2 years. In the HeartWare BTT and continued access protocol trial, 74 of the 382 total patients (19.

4D Contrast-enhanced MR Angiography with the Keyhole Technique in Children: Technique and Clinical Applications.

Unlike in adults, contrast agent-enhanced magnetic resonance (MR) angiography in the pediatric population raises unique challenges such as faster heart rates, more rapid arteriovenous transit, smaller structures, smaller volumes of contrast agent used, and more complex disease processes. A need exists for a rapid contrast-enhanced MR angiographic technique that can separate the arterial and venous phases of contrast enhancement in sedated pediatric patients breathing freely during the course of an examination. In time-resolved contrast-enhanced MR angiography with the keyhole method (four-dimensional [4D] contrast-enhanced MR angiography), various spatial and temporal frequency undersampling schemes are used to substantially reduce the time of acquisition without markedly compromising spatial resolution.

Mouse myofibers lacking the SMYD1 methyltransferase are susceptible to atrophy, internalization of nuclei and myofibrillar disarray.

The Smyd1 gene encodes a lysine methyltransferase specifically expressed in striated muscle. Because Smyd1-null mouse embryos die from heart malformation prior to formation of skeletal muscle, we developed a Smyd1 conditional-knockout allele to determine the consequence of SMYD1 loss in mammalian skeletal muscle. Ablation of SMYD1 specifically in skeletal myocytes after myofiber differentiation using Myf6(cre) produced a non-degenerative myopathy.

Cardiomyocyte-specific conditional knockout of the histone chaperone HIRA in mice results in hypertrophy, sarcolemmal damage and focal replacement fibrosis.

HIRA is the histone chaperone responsible for replication-independent incorporation of histone variant H3.3 within gene bodies and regulatory regions of actively transcribed genes, and within the bivalent promoter regions of developmentally regulated genes. The HIRA gene lies within the 22q11.

Defective myogenesis in the absence of the muscle-specific lysine methyltransferase SMYD1.

The SMYD (SET and MYND domain) family of lysine methyltransferases harbor a unique structure in which the methyltransferase (SET) domain is intervened by a zinc finger protein-protein interaction MYND domain. SMYD proteins methylate both histone and non-histone substrates and participate in diverse biological processes including transcriptional regulation, DNA repair, proliferation and apoptosis. Smyd1 is unique among the five family members in that it is specifically expressed in striated muscles.