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The Role of Tumor Necrosis Associated Factor (TRAF)-1 in Cardio-metabolic Disease
Abstract: Cardiovascular disease (CVD), such as atherosclerosis, myocardial infarction (MI) and stroke, represents the most common cause of death globally and is driven by a cluster of risk factors - obesity, hypertension, hyperlipidemia, and insulin resistance - that is referred to as the Metabolic Syndrome (MS). Chronic, low-grade inflammation fuels not only atherosclerosis, but also critically contributes to adipose tissue dysfunction in MS. Inflammatory pathways also determine acute complications of atherosclerosis, such as arterial thrombosis causing MI and stroke. Despite their potent role in mediating CVD, common underlying pathways that simultaneously drive the development of risk fa...
A Ligand-specific Blockade of the Integrin Mac-1 Selectively Targets Pathologic Inflammation While Maintaining Protective Host-defense
Abstract: Integrin-based therapeutics have garnered considerable interest in the medical treatment of inflammation. Integrins mediate the fast recruitment of monocytes and neutrophils to the site of inflammation, but are also required for host defense, limiting their therapeutic use. Here, we report a novel monoclonal antibody, anti-M7, that specifically blocks the interaction of the integrin Mac-1 with its pro-inflammatory ligand CD40L, while not interfering with alternative ligands. Anti-M7 selectively reduces leukocyte recruitment in vitro and in vivo. In contrast, conventional anti-Mac-1 therapy is not specific and blocks a broad repertoire of integrin functionality, inhibits phagocytosis, promotes apoptosis, and fuels a cytokine storm in vivo. Whereas conventional anti-integrin therapy potentiates bacterial sepsis, bacteremia, and mortality, a ligand-specific intervention with anti-M7 is protective. These findings deepen our understanding of ligand-specific integrin functions and open a path for a new field of ligand-targeted anti-integrin therapy to prevent inflammatory conditions
Atheroprotection Through SYK Inhibition Fails in Established Disease when Local Macrophage Proliferation Dominates Lesion Progression
Abstract: Macrophages in the arterial intima sustain chronic inflammation during atherogenesis. Under hypercholesterolemic conditions murine Ly6Chigh monocytes surge in the blood and spleen, infiltrate nascent atherosclerotic plaques, and differentiate into macrophages that proliferate locally as disease progresses. Spleen tyrosine kinase (SYK) may participate in downstream signaling of various receptors that mediate these processes. We tested the effect of the SYK inhibitor fostamatinib on hypercholesterolemia-associated myelopoiesis and plaque formation in Apoe−/− mice during early and established atherosclerosis. Mice consuming a high cholesterol diet supplemented with fostamatinib fo...
AHA Scientific Sessions 2016: Program Information
The American Heart Association’s Scientific Sessions 2016 is bringing big science, big technology, and big networking opportunities to New Orleans, Louisiana this November. This event features five days of the best in science and cardiovascular clinical practice covering all aspects of basic, clinical, population and translational content.
Glucose Lowering by SGLT2-inhibitor Empagliflozin Accelerates Atherosclerosis Regression in Hyperglycemic STZ-diabetic Mice
Abstract: Diabetes worsens atherosclerosis progression and leads to a defect in repair of arteries after cholesterol reduction, a process termed regression. Empagliflozin reduces blood glucose levels via inhibition of the sodium glucose cotransporter 2 (SGLT-2) in the kidney and has been shown to lead to a marked reduction in cardiovascular events in humans. To determine whether glucose lowering by empagliflozin accelerates atherosclerosis regression in a mouse model, male C57BL/6J mice were treated intraperitoneally with LDLR- and SRB1- antisense oligonucleotides and fed a high cholesterol diet for 16 weeks to induce severe hypercholesterolemia and atherosclerosis progression. At week 14 al...
ATP and the Heart
ATP plays a central role in the two leading causes of cardiac morbidity and mortality in the western world: ischemia and heart failure. We are in our infancy applying what is known about biology and chemistry of ATP toward developing effective therapies for these diseases. In this volume, the current understanding of the chemistry and biology of ATP specifically in the cardiomyocyte is presented. New insights into ATP have been gleaned using biophysical techniques allowing dynamic measurement of chemical events in the intact beating heart and using new animal models in which cardiac proteins are either over expressed, deleted or harbor specific mutations. This book provides a summary of the basic understanding and includes illustrations of why ATP and the Heart is important to both the clinician and scientist.
