Roy L. Silverstein
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FVIII-associated LDL circulates longer and participates in blood clot formation Open
Background and rationale. Hemophilia A is a bleeding disorder caused by deficient or absent in coagulation factor VIII (FVIII). Several clinical studies reported overall lower prevalence of atherosclerotic cardiovascular diseases in hemoph…
Macrophage PIM1 Drives Atherosclerosis by Enhancing Foam Cell Formation Via CD36 Open
Background Atherosclerosis is characterized by the buildup of fatty plaques that thicken and stiffen arterial walls. Macrophages (Mφs) significantly contribute to this process through their scavenger receptor CD36. PIM1 is a serine/threoni…
View article: Na/K-ATPase Signaling in Adipocytes Promotes Atherosclerosis
Na/K-ATPase Signaling in Adipocytes Promotes Atherosclerosis Open
BACKGROUND Adipocyte dysfunction is closely associated with oxidative stress and chronic inflammation, which contribute to systemic metabolic disturbances and atherosclerosis. We previously identified Na/K-ATPase (NKA) α1 as a signal trans…
Chronic diseases alter the platelet rheostat to promote hyperreactivity and thrombosis Open
Platelet hyperreactivity, defined as enhanced sensitivity to activation in response to classical agonists, contributes to the increased risk of arterial thrombosis associated with chronic inflammatory diseases. In this issue of the JCI, Ko…
View article: CD36 restricts lipid-associated macrophages accumulation in white adipose tissues during atherogenesis
CD36 restricts lipid-associated macrophages accumulation in white adipose tissues during atherogenesis Open
Visceral white adipose tissues (WAT) regulate systemic lipid metabolism and inflammation. Dysfunctional WAT drive chronic inflammation and facilitate atherosclerosis. Adipose tissue-associated macrophages (ATM) are the predominant immune c…
View article: Distinguishing ASH clinical practice guidelines from other forms of ASH clinical advice
Distinguishing ASH clinical practice guidelines from other forms of ASH clinical advice Open
The American Society of Hematology (ASH) develops a variety of resources that provide guidance to clinicians on the diagnosis and management of blood diseases. These resources include clinical practice guidelines (CPGs) and other forms of …
Targeting Cysteine Oxidation in Thrombotic Disorders Open
Oxidative stress increases the risk for clinically significant thrombotic events, yet the mechanisms by which oxidants become prothrombotic are unclear. In this review, we provide an overview of cysteine reactivity and oxidation. We then h…
Intracellular tPA–PAI-1 interaction determines VLDL assembly in hepatocytes Open
Apolipoprotein B (apoB)–lipoproteins initiate and promote atherosclerotic cardiovascular disease. Plasma tissue plasminogen activator (tPA) activity is negatively associated with atherogenic apoB-lipoprotein cholesterol levels in humans, b…
View article: Contribution of adipocyte Na/K-ATPase α1/CD36 signaling induced exosome secretion in response to oxidized LDL
Contribution of adipocyte Na/K-ATPase α1/CD36 signaling induced exosome secretion in response to oxidized LDL Open
Introduction Adipose tissue constantly secretes adipokines and extracellular vesicles including exosomes to crosstalk with distinct tissues and organs for whole-body homeostasis. However, dysfunctional adipose tissue under chronic inflamma…
View article: Supplemental Figures 1-8 from Targeting PIM1-Mediated Metabolism in Myeloid Suppressor Cells to Treat Cancer
Supplemental Figures 1-8 from Targeting PIM1-Mediated Metabolism in Myeloid Suppressor Cells to Treat Cancer Open
Supplemental Figures 1-8 plus Legends
View article: Data from Targeting PIM1-Mediated Metabolism in Myeloid Suppressor Cells to Treat Cancer
Data from Targeting PIM1-Mediated Metabolism in Myeloid Suppressor Cells to Treat Cancer Open
There is a strong correlation between myeloid-derived suppressor cells (MDSC) and resistance to immune checkpoint blockade (ICB), but the detailed mechanisms underlying this correlation are largely unknown. Using single-cell RNA sequencing…
View article: Data from Targeting PIM1-Mediated Metabolism in Myeloid Suppressor Cells to Treat Cancer
Data from Targeting PIM1-Mediated Metabolism in Myeloid Suppressor Cells to Treat Cancer Open
There is a strong correlation between myeloid-derived suppressor cells (MDSC) and resistance to immune checkpoint blockade (ICB), but the detailed mechanisms underlying this correlation are largely unknown. Using single-cell RNA sequencing…
View article: Supplementary Table 1 from Targeting PIM1-Mediated Metabolism in Myeloid Suppressor Cells to Treat Cancer
Supplementary Table 1 from Targeting PIM1-Mediated Metabolism in Myeloid Suppressor Cells to Treat Cancer Open
Supplementary Table 1
View article: Supplementary Table 1 from Targeting PIM1-Mediated Metabolism in Myeloid Suppressor Cells to Treat Cancer
Supplementary Table 1 from Targeting PIM1-Mediated Metabolism in Myeloid Suppressor Cells to Treat Cancer Open
Supplementary Table 1
View article: Supplemental Figures 1-8 from Targeting PIM1-Mediated Metabolism in Myeloid Suppressor Cells to Treat Cancer
Supplemental Figures 1-8 from Targeting PIM1-Mediated Metabolism in Myeloid Suppressor Cells to Treat Cancer Open
Supplemental Figures 1-8 plus Legends
Supplementary Note from Vasculostatin Inhibits Intracranial Glioma Growth and Negatively Regulates <i>In vivo</i> Angiogenesis through a CD36-Dependent Mechanism Open
Supplementary Note from Vasculostatin Inhibits Intracranial Glioma Growth and Negatively Regulates In vivo Angiogenesis through a CD36-Dependent Mechanism
Supplementary Figure 1 from Vasculostatin Inhibits Intracranial Glioma Growth and Negatively Regulates <i>In vivo</i> Angiogenesis through a CD36-Dependent Mechanism Open
Supplementary Figure 1 from Vasculostatin Inhibits Intracranial Glioma Growth and Negatively Regulates In vivo Angiogenesis through a CD36-Dependent Mechanism
Data from Vasculostatin Inhibits Intracranial Glioma Growth and Negatively Regulates <i>In vivo</i> Angiogenesis through a CD36-Dependent Mechanism Open
Angiogenesis is a critical physiologic process that is appropriated during tumorigenesis. Little is known about how this process is specifically regulated in the brain. Brain angiogenesis inhibitor-1 (BAI1) is a brain-predominant seven-tra…
Supplementary Figure Legends 1-2 from Vasculostatin Inhibits Intracranial Glioma Growth and Negatively Regulates <i>In vivo</i> Angiogenesis through a CD36-Dependent Mechanism Open
Supplementary Figure Legends 1-2 from Vasculostatin Inhibits Intracranial Glioma Growth and Negatively Regulates In vivo Angiogenesis through a CD36-Dependent Mechanism
Supplementary Note from Vasculostatin Inhibits Intracranial Glioma Growth and Negatively Regulates <i>In vivo</i> Angiogenesis through a CD36-Dependent Mechanism Open
Supplementary Note from Vasculostatin Inhibits Intracranial Glioma Growth and Negatively Regulates In vivo Angiogenesis through a CD36-Dependent Mechanism
Supplementary Figure Legends 1-2 from Vasculostatin Inhibits Intracranial Glioma Growth and Negatively Regulates <i>In vivo</i> Angiogenesis through a CD36-Dependent Mechanism Open
Supplementary Figure Legends 1-2 from Vasculostatin Inhibits Intracranial Glioma Growth and Negatively Regulates In vivo Angiogenesis through a CD36-Dependent Mechanism
Data from Vasculostatin Inhibits Intracranial Glioma Growth and Negatively Regulates <i>In vivo</i> Angiogenesis through a CD36-Dependent Mechanism Open
Angiogenesis is a critical physiologic process that is appropriated during tumorigenesis. Little is known about how this process is specifically regulated in the brain. Brain angiogenesis inhibitor-1 (BAI1) is a brain-predominant seven-tra…
Supplementary Figure 2 from Vasculostatin Inhibits Intracranial Glioma Growth and Negatively Regulates <i>In vivo</i> Angiogenesis through a CD36-Dependent Mechanism Open
Supplementary Figure 2 from Vasculostatin Inhibits Intracranial Glioma Growth and Negatively Regulates In vivo Angiogenesis through a CD36-Dependent Mechanism
Supplementary Figure 1 from Vasculostatin Inhibits Intracranial Glioma Growth and Negatively Regulates <i>In vivo</i> Angiogenesis through a CD36-Dependent Mechanism Open
Supplementary Figure 1 from Vasculostatin Inhibits Intracranial Glioma Growth and Negatively Regulates In vivo Angiogenesis through a CD36-Dependent Mechanism
Supplementary Figure 2 from Vasculostatin Inhibits Intracranial Glioma Growth and Negatively Regulates <i>In vivo</i> Angiogenesis through a CD36-Dependent Mechanism Open
Supplementary Figure 2 from Vasculostatin Inhibits Intracranial Glioma Growth and Negatively Regulates In vivo Angiogenesis through a CD36-Dependent Mechanism