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Got glycogen? An energy resource in HIF-mediated prevention of ischemic kidney injury.
Haase VH
(2020) Kidney Int 97: 645-647
MeSH Terms: Glycogen, Kidney, Procollagen-Proline Dioxygenase, Prolyl Hydroxylases, Up-Regulation
Show Abstract · Added March 24, 2020
Hypoxia-inducible factor activation reprograms glucose metabolism and leads to glycogen accumulation in multiple cell types. In this issue of Kidney International, Ito and colleagues demonstrate that pharmacologic inhibition of hypoxia-inducible factor-prolyl hydroxylase domain oxygen sensors in renal epithelial cells enhances glycogen synthesis and protects from subsequent hypoxia and glucose deprivation. In vivo studies advance the concept that renal glycogen metabolism contributes to cytoprotection afforded by pre-ischemic hypoxia-inducible factor-prolyl hydroxylase domain inhibition.
Copyright © 2020 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.
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5 MeSH Terms
Recognition and Initial Management of Fulminant Myocarditis: A Scientific Statement From the American Heart Association.
Kociol RD, Cooper LT, Fang JC, Moslehi JJ, Pang PS, Sabe MA, Shah RV, Sims DB, Thiene G, Vardeny O, American Heart Association Heart Failure and Transplantation Committee of the Council on Clinical Cardiology
(2020) Circulation 141: e69-e92
MeSH Terms: American Heart Association, Arrhythmias, Cardiac, Extracorporeal Membrane Oxygenation, Female, Heart Transplantation, Humans, Multiple Organ Failure, Myocarditis, Practice Guidelines as Topic, Shock, Cardiogenic, United States
Show Abstract · Added January 15, 2020
Fulminant myocarditis (FM) is an uncommon syndrome characterized by sudden and severe diffuse cardiac inflammation often leading to death resulting from cardiogenic shock, ventricular arrhythmias, or multiorgan system failure. Historically, FM was almost exclusively diagnosed at autopsy. By definition, all patients with FM will need some form of inotropic or mechanical circulatory support to maintain end-organ perfusion until transplantation or recovery. Specific subtypes of FM may respond to immunomodulatory therapy in addition to guideline-directed medical care. Despite the increasing availability of circulatory support, orthotopic heart transplantation, and disease-specific treatments, patients with FM experience significant morbidity and mortality as a result of a delay in diagnosis and initiation of circulatory support and lack of appropriately trained specialists to manage the condition. This scientific statement outlines the resources necessary to manage the spectrum of FM, including extracorporeal life support, percutaneous and durable ventricular assist devices, transplantation capabilities, and specialists in advanced heart failure, cardiothoracic surgery, cardiac pathology, immunology, and infectious disease. Education of frontline providers who are most likely to encounter FM first is essential to increase timely access to appropriately resourced facilities, to prevent multiorgan system failure, and to tailor disease-specific therapy as early as possible in the disease process.
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11 MeSH Terms
Pharmacological closure of the patent ductus arteriosus: when treatment still makes sense.
Gillam-Krakauer M, Hagadorn JI, Reese J
(2019) J Perinatol 39: 1439-1441
MeSH Terms: Acetaminophen, Cyclooxygenase Inhibitors, Decision Making, Ductus Arteriosus, Patent, Humans, Indomethacin, Infant, Infant, Low Birth Weight, Infant, Newborn, Infant, Premature
Added July 28, 2020
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MeSH Terms
Increased Epithelial Oxygenation Links Colitis to an Expansion of Tumorigenic Bacteria.
Cevallos SA, Lee JY, Tiffany CR, Byndloss AJ, Johnston L, Byndloss MX, Bäumler AJ
(2019) mBio 10:
MeSH Terms: Aerobiosis, Animals, Carcinogenesis, Colitis, Colorectal Neoplasms, Dextran Sulfate, Escherichia coli, Escherichia coli Infections, Female, Gastrointestinal Microbiome, Mice, Mice, Inbred C57BL, Oxygen, Peptides, Polyketides
Show Abstract · Added March 30, 2020
Intestinal inflammation is a risk factor for colorectal cancer formation, but the underlying mechanisms remain unknown. Here, we investigated whether colitis alters the colonic microbiota to enhance its cancer-inducing activity. Colitis increased epithelial oxygenation in the colon of mice and drove an expansion of within the gut-associated microbial community through aerobic respiration. An aerobic expansion of colibactin-producing was required for the cancer-inducing activity of this pathobiont in a mouse model of colitis-associated colorectal cancer formation. We conclude that increased epithelial oxygenation in the colon is associated with an expansion of a prooncogenic driver species, thereby increasing the cancer-inducing activity of the microbiota. One of the environmental factors important for colorectal cancer formation is the gut microbiota, but the habitat filters that control its cancer-inducing activity remain unknown. Here, we show that chemically induced colitis elevates epithelial oxygenation in the colon, thereby driving an expansion of colibactin-producing , a prooncogenic driver species. These data suggest that elevated epithelial oxygenation is a potential risk factor for colorectal cancer formation because the consequent changes in the gut habitat escalate the cancer-inducing activity of the microbiota.
Copyright © 2019 Cevallos et al.
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15 MeSH Terms
Arachidonic Acid Kills Staphylococcus aureus through a Lipid Peroxidation Mechanism.
Beavers WN, Monteith AJ, Amarnath V, Mernaugh RL, Roberts LJ, Chazin WJ, Davies SS, Skaar EP
(2019) mBio 10:
MeSH Terms: Animals, Anti-Bacterial Agents, Arachidonic Acid, Brain, Dose-Response Relationship, Drug, Drug Resistance, Bacterial, Female, Kidney, Lipid Peroxidation, Lipids, Mice, Mice, Inbred BALB C, Microbial Sensitivity Tests, Mutation, Neutrophils, Oxidative Stress, Reactive Oxygen Species, Spleen, Staphylococcal Infections, Staphylococcus aureus, Teichoic Acids
Show Abstract · Added March 11, 2020
infects every niche of the human host. In response to microbial infection, vertebrates have an arsenal of antimicrobial compounds that inhibit bacterial growth or kill bacterial cells. One class of antimicrobial compounds consists of polyunsaturated fatty acids, which are highly abundant in eukaryotes and encountered by at the host-pathogen interface. Arachidonic acid (AA) is one of the most abundant polyunsaturated fatty acids in vertebrates and is released in large amounts during the oxidative burst. Most of the released AA is converted to bioactive signaling molecules, but, independently of its role in inflammatory signaling, AA is toxic to Here, we report that AA kills through a lipid peroxidation mechanism whereby AA is oxidized to reactive electrophiles that modify macromolecules, eliciting toxicity. This process is rescued by cotreatment with antioxidants as well as in a strain genetically inactivated for (USA300 mutant) that produces lower levels of reactive oxygen species. However, resistance to AA stress in the USA300 mutant comes at a cost, making the mutant more susceptible to β-lactam antibiotics and attenuated for pathogenesis in a murine infection model compared to the parental methicillin-resistant (MRSA) strain, indicating that resistance to AA toxicity increases susceptibility to other stressors encountered during infection. This report defines the mechanism by which AA is toxic to and identifies lipid peroxidation as a pathway that can be modulated for the development of future therapeutics to treat infections. Despite the ability of the human immune system to generate a plethora of molecules to control infections, is among the pathogens with the greatest impact on human health. One class of host molecules toxic to consists of polyunsaturated fatty acids. Here, we investigated the antibacterial properties of arachidonic acid, one of the most abundant polyunsaturated fatty acids in humans, and discovered that the mechanism of toxicity against proceeds through lipid peroxidation. A better understanding of the molecular mechanisms by which the immune system kills , and by which avoids host killing, will enable the optimal design of therapeutics that complement the ability of the vertebrate immune response to eliminate infections.
Copyright © 2019 Beavers et al.
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21 MeSH Terms
Aspects of Prostaglandin Glycerol Ester Biology.
Kingsley PJ, Rouzer CA, Morgan AJ, Patel S, Marnett LJ
(2019) Adv Exp Med Biol 1161: 77-88
MeSH Terms: Animals, Arachidonic Acids, Cyclooxygenase 2, Endocannabinoids, Glycerides, Glyceryl Ethers, Prostaglandins
Show Abstract · Added March 12, 2020
The Cyclooxygenase enzymes (COX-1 and COX-2) incorporate 2 molecules of O into arachidonic acid (AA), resulting in an array of bioactive prostaglandins. However, much work has been done showing that COX-2 will perform this reaction on several different AA-containing molecules, most importantly, the endocannabinoid 2-arachidonoylglycerol (2-AG). The products of 2-AG oxygenation, prostaglandin glycerol esters (PG-Gs), are analogous to canonical prostaglandins. This chapter reviews the literature detailing the production, metabolism, and bioactivity of these compounds, as well as their detection in intact animals.
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is associated with indomethacin treatment failure for patent ductus arteriosus.
Rooney SR, Shelton EL, Aka I, Shaffer CM, Clyman RI, Dagle JM, Ryckman K, Lewis TR, Reese J, Van Driest SL, Kannankeril PJ
(2019) Pharmacogenomics 20: 939-946
MeSH Terms: Cohort Studies, Cyclooxygenase Inhibitors, Cytochrome P-450 CYP2C9, Ductus Arteriosus, Patent, Female, Gestational Age, Humans, Indomethacin, Infant, Infant, Newborn, Infant, Premature, Male, Treatment Failure, Treatment Outcome
Show Abstract · Added July 28, 2020
To identify clinical andgenetic factors associated with indomethacin treatment failure in preterm neonates with patent ductus arteriosus (PDA). This is a multicenter cohort study of 144 preterm infants (22-32 weeks gestational age) at three centers who received at least one treatment course of indomethacin for PDA. Indomethacin failure was defined as requiring subsequent surgical intervention. In multivariate analysis, gestational age (AOR 0.76, 95% CI 0.60-0.96), surfactant use (AOR 9.77, 95% CI 1.15-83.26), and (AOR 3.74; 95% CI 1.34-10.44) were each associated with indomethacin failure. Age, surfactant use, and influence indomethacin treatment outcome in preterm infants with PDA. This combination of clinical and genetic factors may facilitate targeted indomethacin use for PDA.
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IRE1α-XBP1 signaling in leukocytes controls prostaglandin biosynthesis and pain.
Chopra S, Giovanelli P, Alvarado-Vazquez PA, Alonso S, Song M, Sandoval TA, Chae CS, Tan C, Fonseca MM, Gutierrez S, Jimenez L, Subbaramaiah K, Iwawaki T, Kingsley PJ, Marnett LJ, Kossenkov AV, Crespo MS, Dannenberg AJ, Glimcher LH, Romero-Sandoval EA, Cubillos-Ruiz JR
(2019) Science 365:
MeSH Terms: Animals, Cells, Cultured, Cyclooxygenase 2, Dinoprostone, Endoribonucleases, Humans, Leukocytes, Mice, Mice, Inbred C57BL, Myeloid Cells, Pain, Postoperative, Promoter Regions, Genetic, Prostaglandin-E Synthases, Protein-Serine-Threonine Kinases, Signal Transduction, Unfolded Protein Response, Visceral Pain, X-Box Binding Protein 1
Show Abstract · Added March 12, 2020
Inositol-requiring enzyme 1[α] (IRE1[α])-X-box binding protein spliced (XBP1) signaling maintains endoplasmic reticulum (ER) homeostasis while controlling immunometabolic processes. Yet, the physiological consequences of IRE1α-XBP1 activation in leukocytes remain unexplored. We found that induction of prostaglandin-endoperoxide synthase 2 (/Cox-2) and prostaglandin E synthase (/mPGES-1) was compromised in IRE1α-deficient myeloid cells undergoing ER stress or stimulated through pattern recognition receptors. Inducible biosynthesis of prostaglandins, including the pro-algesic mediator prostaglandin E2 (PGE), was decreased in myeloid cells that lack IRE1α or XBP1 but not other ER stress sensors. Functional XBP1 transactivated the human and genes to enable optimal PGE production. Mice that lack IRE1α-XBP1 in leukocytes, or that were treated with IRE1α inhibitors, demonstrated reduced pain behaviors in PGE-dependent models of pain. Thus, IRE1α-XBP1 is a mediator of prostaglandin biosynthesis and a potential target to control pain.
Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.
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18 MeSH Terms
Characterization of the hemodynamic response function in white matter tracts for event-related fMRI.
Li M, Newton AT, Anderson AW, Ding Z, Gore JC
(2019) Nat Commun 10: 1140
MeSH Terms: Adult, Cerebral Cortex, Cerebrovascular Circulation, Female, Gray Matter, Healthy Volunteers, Hemodynamics, Hemoglobins, Humans, Magnetic Resonance Imaging, Male, Nerve Net, Oxygen, Pattern Recognition, Visual, Stroop Test, White Matter
Show Abstract · Added March 26, 2019
Accurate estimates of the BOLD hemodynamic response function (HRF) are crucial for the interpretation and analysis of event-related functional MRI data. To date, however, there have been no comprehensive measurements of the HRF in white matter (WM) despite increasing evidence that BOLD signals in WM change after a stimulus. We performed an event-related cognitive task (Stroop color-word interference) to measure the HRF in selected human WM pathways. The task was chosen in order to produce robust, distributed centers of activity throughout the cortex. To measure the HRF in WM, fiber tracts were reconstructed between each pair of activated cortical areas. We observed clear task-specific HRFs with reduced magnitudes, delayed onsets and prolonged initial dips in WM tracts compared with activated grey matter, thus calling for significant changes to current standard models for accurately characterizing the HRFs in WM and for modifications of standard methods of analysis of functional imaging data.
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16 MeSH Terms
Regulation of leukocyte function by citric acid cycle intermediates.
Patil NK, Bohannon JK, Hernandez A, Patil TK, Sherwood ER
(2019) J Leukoc Biol 106: 105-117
MeSH Terms: Animals, Citric Acid, Citric Acid Cycle, Fumarates, Humans, Leukocytes, Reactive Oxygen Species, Succinates, Succinic Acid
Show Abstract · Added March 18, 2020
Cellular metabolism is a means of generating ATP to provide energy for key cellular functions. However, recent research shows that citric acid cycle intermediates target vital cellular functions of the innate immune system. Succinate, itaconate, citrate, and fumarate have been shown to mediate or regulate important myeloid cell functions during infection and inflammation. This review covers the regulatory functions of citric acid cycle intermediates in myeloid cells and discusses potential translational applications, key mechanistic questions, and future research directions.
©2019 Society for Leukocyte Biology.
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9 MeSH Terms