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phosphatidic acid/infart

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1. We have re-examined the lipids from myocardial infarcts of cat, dog, rabbit and man, mainly through TLC methods, and confirm the identity of cat and dog "infarct plasmalogen" as an N-acyl phosphatidyl ethanolamine (NAPE). This substance was not detected in infarcts of rabbit and man. 2. We have
BACKGROUND Low plasma levels of high-density lipoprotein-cholesterol (HDL-C) are typical of acute myocardial infarction (MI) and predict risk of recurrent cardiovascular events. The potential relationships between modifications in the molecular composition and the functionality of HDL subpopulations

Depressed phosphatidic acid-induced contractile activity of failing cardiomyocytes.

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The effects of phosphatidic acid (PA), a known inotropic agent, on Ca(2+) transients and contractile activity of cardiomyocytes in congestive heart failure (CHF) due to myocardial infarction were examined. In control cells, PA induced a significant increase (25%) in active cell shortening and Ca(2+)

Depressed responsiveness of phospholipase C isoenzymes to phosphatidic acid in congestive heart failure.

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The cardiac sarcolemmal membrane cis -unsaturated fatty acid-sensitive phospholipase D hydrolyzes phosphatidylcholine to form phosphatidic acid. The functional significance of phosphatidic acid is indicated by its ability to increase [Ca(2+)](i)and augment cardiac contractile performance via the

Expression of phospholipase D isozymes in scar and viable tissue in congestive heart failure due to myocardial infarction.

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The phospholipase D (PLD) associated with the cardiac sarcolemmal (SL) membrane hydrolyses phosphatidylcholine to produce phosphatidic acid, an important phospholipid signaling molecule known to influence cardiac function. The present study was undertaken to examine PLD isozyme mRNA expression,
Lethal ventricular tachyarrhythmia (LVTA) is the most prevalent electrophysiological underpinning of sudden cardiac death (SCD), a condition that occurs in response to multiple pathophysiological abnormalities. The aim of this study was to identify common lipid features of LVTA that were induced by

Hepatokine α1-Microglobulin Signaling Exacerbates Inflammation and Disturbs Fibrotic Repair in Mouse Myocardial Infarction.

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Acute cardiac rupture and adverse left ventricular (LV) remodeling causing heart failure are serious complications of acute myocardial infarction (MI). While cardio-hepatic interactions have been recognized, their role in MI remains unknown. We treated cultured cardiomyocytes with conditioned media

Common disbalance in the brain parenchyma of dementias: Phospholipid profile analysis between CADASIL and sporadic Alzheimer's disease.

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Sporadic Alzheimer's disease (SAD) is the most common form of dementia, and cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is the most frequent hereditary ischemic small vessel disease of the brain. Relevant biomarkers or specific metabolic
A 51 year old man with Waldenström's macroglobulinaemia presented with a malabsorptive syndrome related to extensive small bowel lymphangiectasia caused by immunoglobulin accumulation. The patient's plasma had strong lupus anticoagulant activity and the IgM lambda paraprotein displayed specificity

Antibody to phosphatidylethanolamine in a patient with lupus anticoagulant and thrombosis.

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Most patients with lupus anticoagulant (LA) activity have coincident antibodies to a group of negatively charged phospholipids, and its is suggested that LA and anticardiolipin tests detect antibodies with overlapping specificities. Some discordance between the two assays has been described,
OBJECTIVE To detect antiphosphatidylethanolamine antibodies (aPE) as the only antiphospholipid antibodies (aPL) in 122 patients we investigated for aPL and to correlate the presence of aPL with clinical manifestations. METHODS Patients with autoimmune diseases (n = 41), thromboembolic episodes (TEE)

Redistribution and abnormal activity of phospholipase A(2) isoenzymes in postinfarct congestive heart failure.

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Cardiac sarcolemmal (SL) cis-unsaturated fatty acid sensitive phospholipase D (cis-UFA PLD) is modulated by SL Ca(2+)-independent phospholipase A(2) (iPLA(2)) activity via intramembrane release of cis-UFA. As PLD-derived phosphatidic acid influences intracellular Ca(2+) concentration and contractile

Alterations of sarcolemmal phospholipase D and phosphatidate phosphohydrolase in congestive heart failure.

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Phospholipase D 2 (PLD2) is the major PLD isozyme associated with the cardiac sarcolemmal (SL) membrane. Hydrolysis of SL phosphatidylcholine (PC) by PLD2 produces phosphatidic acid (PA), which is then converted to 1,2 diacylglycerol (DAG) by the action of phosphatidate phosphohydrolase type 2

Role of diacylglycerol kinase in cellular regulatory processes: a new regulator for cardiomyocyte hypertrophy.

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Diacylglycerol (DAG) kinase (DGK) phosphorylates and converts DAG to phosphatidic acid. DGK regulates cellular DAG levels and attenuates DAG signaling. The 10 mammalian DGK isoforms have been identified to date. In cardiac myocytes, DGKalpha, epsilon, and zeta are expressed, and DGKzeta is the
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