Adipose triglyceride lipase promotes prostaglandin-dependent actin remodeling by regulating substrate release from lipid droplets.

Lipid droplets (LDs), crucial regulators of lipid metabolism, accumulate during oocyte development. However, their roles in fertility remain largely unknown. During Drosophila oogenesis, LD accumulation coincides with the actin remodeling necessary for follicle development.

Absence of significant myocardial injury following elective direct current cardioversion for atrial fibrillation.

Background: Direct current (DC) cardioversion is used to terminate cardiac arrhythmias. Current guidelines list cardioversion as a cause of myocardial injury.

Objective: This study determined whether external DC cardioversion results in myocardial injury measured by serial changes in high-sensitivity cardiac troponin T (hs-cTnT) and high-sensitivity cardiac troponin I (hs-cTnI).

Visualizing Lipid Droplets in Drosophila Oogenesis.

Lipid droplets (LDs) are fat storage organelles highly abundant in oocytes and eggs of many vertebrates and invertebrates. They have roles both during oogenesis and in provisioning the developing embryo. In Drosophila, large numbers of LDs are generated in nurse cells during mid-oogenesis and then transferred to oocytes.

From Dynamics to Novelty: An Agent-Based Model of the Economic System.

The modern economy is both a complex self-organizing system and an innovative, evolving one. Contemporary theory, however, treats it essentially as a static equilibrium system. Here we propose a formal framework to capture its complex, evolving nature.

Characterization of sp. nov., and its taxonomic relatedness to other polyhydroxybutyrate-degrading streptomycetes.

A polyhydroxybutyrate (PHB)-degrading actinomycete, strain SFB5A, was identified as a species of based on its membrane fatty acid profile and the presence of ll-diaminopimelic acid in the cell wall. It formed sporulating mycelia on most agar media, but flat or wrinkled, moist colonies on trypticase soy agar. Spores were smooth, cylindrical, and borne on long, straight to flexuous chains.

Peptides as Therapeutic Agents for Atherosclerosis.

More than three decades ago, as a test for the amphipathic helix theory, an 18 amino acid residue peptide and its analogs were designed with no sequence homology to any of the exchangeable apolipoproteins. Based on the apolipoprotein A-I (the major protein component of high density lipoproteins, HDL) mimicking properties, they were termed as ApoA-I mimicking peptides. Several laboratories around the world started studying such de novo-designed peptides for their antiatherogenic properties.

Sequestration to lipid droplets promotes histone availability by preventing turnover of excess histones.

Because both dearth and overabundance of histones result in cellular defects, histone synthesis and demand are typically tightly coupled. In Drosophila embryos, histones H2B, H2A and H2Av accumulate on lipid droplets (LDs), which are cytoplasmic fat storage organelles. Without LD binding, maternally provided H2B, H2A and H2Av are absent; however, how LDs ensure histone storage is unclear.

Apolipoprotein Mimetic Peptides: An Emerging Therapy against Diabetic Inflammation and Dyslipidemia.

Obesity has achieved epidemic status in the United States, resulting in an increase in type 2 diabetes mellitus, dyslipidemia, and cardiovascular disease. Numerous studies have shown that inflammation plays a key role in the development of insulin resistance and diabetic complications. HDL cholesterol levels are inversely associated with coronary heart disease in humans.

Bovine HDL and Dual Domain HDL-Mimetic Peptides Inhibit Tumor Development in Mice.

A growing body of literature supports the role of apolipoproteins present in HDL in the treatment of pro-inflammatory diseases including cancer. We examined whether bovine HDL (bHDL) and three dual-domain peptides, namely AEM-28 and its analog AEM-28-2, and HM-10/10, affect tumor growth and development in mouse models of ovarian and colon cancer. We demonstrate that bHDL inhibits mouse colorectal cancer cell line CT26-mediated lung tumor development, and mouse ovarian cancer cell line ID8-mediated tumor burden.

The Apolipoprotein A-I Mimetic L-4F Attenuates Monocyte Activation and Adverse Cardiac Remodeling after Myocardial Infarction.

Excessive inflammation after myocardial infarction (MI) can promote infarct expansion and adverse left ventricular (LV) remodeling. L-4F, a mimetic peptide of apolipoprotein A-I (apoA-I), exhibits anti-inflammatory and anti-atherogenic properties; however, whether L-4F imparts beneficial effects after myocardial infarction (MI) is unknown. Here we demonstrate that L-4F suppresses the expansion of blood, splenic, and myocardial pro-inflammatory monocytes and macrophages in a mouse model of reperfused MI.

Epidemiology of in-hospital cardiac arrest complicating non-ST-segment elevation myocardial infarction receiving early coronary angiography.

In the period between 2000 and 2014, 584,704 admissions with non-ST-segment elevation myocardial infarction that received early coronary angiography (day zero) were identified from the National Inpatient Sample. In-hospital cardiac arrest was noted in 4349 (0.8%), of which ~47% were from ventricular arrhythmias and ~90% of occurred within ≤4 days.

Early vs. delayed in-hospital cardiac arrest complicating ST-elevation myocardial infarction receiving primary percutaneous coronary intervention.

Background: There are limited data on the timing and outcomes of in-hospital cardiac arrest (IHCA) in patients with ST-elevation myocardial infarction (STEMI) receiving primary percutaneous coronary intervention (pPCI). This study sought to examine the in-hospital mortality, temporal trends and resource utilization in early vs. delayed IHCA in STEMI.

Reduced Size Profile of Amniotic Membrane Particles Decreases Osteoarthritis Therapeutic Efficacy.

Osteoarthritis (OA) is a widespread disease that continues to lack approved and efficacious treatments that modify disease progression. Micronized dehydrated human amnion/chorion membrane (μ-dHACM) has been shown to be effective in reducing OA progression, but many of the engineering design parameters have not been explored. The objectives of this study were to characterize the particle size distributions of two μ-dHACM formulations and to investigate the influence of these distributions on the therapeutic efficacy of μ-dHACM.

Direct Current Cardioversion of Atrial Arrhythmias in Adults With Cardiac Amyloidosis.

Background: Arrhythmias, conduction abnormalities, and intracardiac thrombus are common in patients with cardiac amyloidosis (CA). Outcomes of direct-current cardioversion (DCCV) for atrial arrhythmias in patients with CA are unknown.

Objectives: This study sought to examine DCCV procedural outcomes in patients with CA.

The apoA-I mimetic peptide 4F protects apolipoprotein A-I from oxidative damage.

High density lipoprotein (HDL) is prone to modification by the oxidizing and chlorinating agent hypochlorite anion (OCl). Oxidation of apolipoprotein (apo) A-I, the major protein in HDL, reduces ABCA-1 mediated cholesterol efflux and other protective responses to HDL. The apoA-I mimetic peptide 4F has been shown to undergo oxidation; however, the ability of the peptide to mediate cholesterol efflux remains intact.

Novel fatty acyl apoE mimetic peptides have increased potency to reduce plasma cholesterol in mice and macaques.

Ac-hE18A-NH is a dual-domain apoE mimetic peptide that possesses the putative receptor binding domain from apoE (LRKLRKRLLR, denoted hE; residues 141-150) covalently attached to lipid-associating peptide 18A. Like apoE, Ac-hE18A-NH reduces plasma cholesterol in animal models and exhibits anti-inflammatory properties independent of its cholesterol-reducing effect. Ac-hE18A-NH has already undergone phase I clinical trials as a lipid-lowering agent.

The Apolipoprotein E Mimetic Peptide AEM-2 Attenuates Mitochondrial Injury And Apoptosis In Human THP-1 Macrophages.

Cardiovascular disease, specifically atherosclerosis, is exacerbated by hypercholesterolemia. Current therapies that target lipid lowering, however, are not effective in all patients. Apolipoprotein E (apoE) plays an important role in mediating the clearance of plasma cholesterol and also exerts numerous cytoprotective responses.

Echocardiographic left ventricular diastolic dysfunction predicts hospital mortality after out-of-hospital cardiac arrest.

Purpose: To determine whether systolic or diastolic dysfunction on transthoracic echocardiogram (TTE) predicts mortality after out-of-hospital cardiac arrest (OHCA).

Methods: Retrospective cohort study of 173 OHCA subjects undergoing targeted temperature management who underwent TTE during hospitalization. Univariate analysis and multivariate logistic regression were used to determine associations between TTE measurements of systolic and diastolic function and systemic hemodynamics with all-cause mortality.

Changes in left ventricular systolic and diastolic function on serial echocardiography after out-of-hospital cardiac arrest.

Aim: Reversible myocardial dysfunction is common after out-of-hospital cardiac arrest (OHCA). The aim of this study was to determine if changes on serial transthoracic echocardiography (TTE) can predict long-term mortality in OHCA subjects.

Methods: This is a single-center historical cohort study of OHCA subjects undergoing targeted temperature management who received >1 TTE during hospitalization.

Improving trend in ventricular fibrillation/pulseless ventricular tachycardia out-of-hospital cardiac arrest in Rochester, Minnesota: A 26-year observational study from 1991 to 2016.

Background: Mortality from out-of-hospital cardiac arrest (OHCA) is characterized by substantial regional variation. The Institute of Medicine (IOM) recently recommended enhancing the capabilities of EMS systems to improve outcome. In this study, we analyzed the trend in outcome from ventricular fibrillation/pulseless ventricular tachycardia (VF/pVT) OHCA in Rochester, MN.

Cholesterol reduction and macrophage function: role of paraoxonases.

Purpose Of Review: Unregulated uptake of oxidized LDL by macrophages to form foam cells is the hallmark for atherosclerosis. The paraoxonase (PON) family of enzymes plays a critical role in attenuating atherosclerotic lesion formation by hydrolyzing lipid peroxides (LOOHs) and preventing the oxidation of LDL particles and by enhancing HDL-mediated cholesterol efflux. Findings in recent years suggest novel mechanisms by which PON isoforms interact with macrophages to regulate cholesterol metabolism and cellular function.

High-Density Lipoprotein Regulation of Mitochondrial Function.

Lipoproteins play a key role in regulating plasma and tissue levels of cholesterol. Apolipoprotein B (apoB)-containing lipoproteins, including chylomicrons, very-low density lipoprotein (VLDL) and low-density lipoprotein (LDL), serve as carriers of triglycerides and cholesterol and deliver these metabolites to peripheral tissues. In contrast, high-density lipoprotein (HDL) mediates Reverse Cholesterol Transport (RCT), a process by which excess cholesterol is removed from the periphery and taken up by hepatocytes where it is metabolized and excreted.

Electroencephalography Predicts Poor and Good Outcomes After Cardiac Arrest: A Two-Center Study.

Objective: The prognostic role of electroencephalography during and after targeted temperature management in postcardiac arrest patients, relatively to other predictors, is incompletely known. We assessed performances of electroencephalography during and after targeted temperature management toward good and poor outcomes, along with other recognized predictors.

Design: Cohort study (April 2009 to March 2016).