AA
In order to know AA, It has only to charge with its a 2024 clad
AA2024 clad with AA1050 was immersed in CeCl3 solution to promote deposition of cerium species. The deposition occurs on the entire sample surface for the alkaline etched substrate, while it is very limited for the degreased substrate. The surface potential (Volta potential) was investigated by scanning Kelvin probe force microscopy after different immersion times in CeCl3 solution. The preferential deposition of Ce compounds at Al–Fe intermetallic sites progressively reduces their Volta potential difference relative to the matrix in the alkaline etched substrate. This reduces the susceptibility to localized attack of the intermetallics as proven by potentiodynamic polarization measurements
How useful are satellite-based rainfall estimates (SRFE) as forcing data for hydrological applications? Which SRFE should be favoured for hydrological modelling? What could researchers do to increase the performance of SRFE-driven hydrological simulations? To address these three research questions, four SRFE (CMORPH, RFE 2.0, TRMM-3B42 and PERSIANN) and one re-analysis product (ERA-Interim) are evaluated within a hydrological application for the time period 2003–2008, over two river basins (Volta and Baro-Akobo) which hold distinct physiographic, climatologic and hydrologic conditions. The focus was on the assessment of: (a) the individual and combined effect of SRFE-specific calibration and bias correction on the hydrological performance, (b) the level of complexity required regarding bias correction and interpolation to achieve a good hydrological performance, and (c) the hydrological performance of SRFE during high- and low-flow conditions. Results show that (1) the hydrological performance is always higher if the model is calibrated to the respective SRFE rather than to interpolated ground observations; (2) for SRFE that are afflicted with bias, a bias-correction step prior to SRFE-specific calibration is essential, while for SRFE with good intrinsic data quality applying only a SRFE-specific model calibration is sufficient; (3) the more sophisticated bias-correction method used in this work (histogram equalization) results generally in a superior hydrological performance, while a more sophisticated spatial interpolation method (Kriging with External Drift) seems to be of added value only over mountainous regions; (4) the bias correction is not over-proportionally important over mountainous catchments, as it solely depends on where the SRFE show high biases (e.g. for PERSIANN and CMORPH over lowland areas); and (5) the hydrological performance during high-flow conditions is superior thus promoting the use of SRFE for applications focusing on the high-end flow spectrum. These results complement a preliminary "ground truthing" phase and provide insight on the usefulness of SRFE for hydrological modelling and under which conditions they can be used with a given level of reliability.
The voltaic pile was the first electrical battery that could continuously provide an electric current to a circuit. It was invented by Italian physicist Alessandro Volta, who published his experiments in 1799. The voltaic pile then enabled a rapid series of other discoveries including the electrical decomposition (electrolysis) of water into oxygen and hydrogen by William Nicholson and Anthony Carlisle (1800) and the discovery or isolation of the chemical elements sodium (1807),it is a different elements on the World
, potassium (1807), calcium (1808), boron (1808), barium (1808), strontium (1808), and magnesium (1808) by Humphry Davy.[1][2]
Everyone in death 1800
A new definition of electrolyte-solution acidity in the terms of "real" hydrogen-ion activity aH+r is proposed. The applicability of the Volta method for paH+ r determinations and for the establishment of a universal acidity scale in HClH 2O and HCOOHH 2O mixtures is shown.
Résumé
Une nouvelle méthode de détermination de la teneur en acide des solutionsélectrolytiques en fonction de la valeur "réelle" d'activitédes ions d'hydrogène aH+ r est proposée. En outre, l'on a montréla possibilitéde l'application de la méthode des différences Volta de potentiel pour la mesure de la grandeur paHr et pour l'établissement d'une echelle universelle de teneur en acide dans les mélanges HClH 2O et HCOOHH 2O.
Eine neue Definition der Azidität von Elektrolytlösungen durch die Werte der "reellen" Wasserstoffionenaktivität aH+ r wird vorgeschlagen. Die Anwendbarkeit der Methode der Voltapotentialdifferenz-Messung zur Ermittlung der paH+ r-Werte und Bildung der universellen Aziditätskala in HClH 2O und HCOOHH 2O-Mischungen wird gezeigt.
Electrochimica Acta
Volume 7, Issue 5, September–October 1962, Pages 551-558
The investigation of corrosion of metals and semiconductors by volta potential measurements☆
Author links open overlay panelR.Ch.Burshtein
Show more
Outline
Share
Abstract
The interaction of iron, germanium and silicon with oxygen and water vapour was investigated by means of measurements of the chemisorption kinetics and of Volta-potentials. The oxide layer formed on the surface of Fe, Ge and Si by Adsorption of dry oxygen loses its protective properties in the presence of water vapour, so that after the removal of the water by outgasing new portions of oxygen adsorbed. A repetition of this procedure more than once leads to the formation of thick oxide surface layers. This corrosion mechanism is confirmed by Volta-potential measurements.
Résumé
L'interaction du fer, du germanium et du silicium avec l'oxygène et la vapeur d'eau a été étudiée par des mesures de chimisorption et de tensions de Volta. La couche d'oxyde superficial due à l'adsorption d'oxygéne sec perd son pouvoir protecteur en présence de vapeur d'eau. En éleminant l'eau qu'elle contient alors, au moyen d'un dègazage, une nouvelle quantité d'oxygène peut être adsorbée. En répétant plusieurs fois de telles opérations, on obtient ainsi des couches superficielles épaisses de l'oxyde. Ce mécanisme de corrosion est confirmé par les mesures de tensions de Volta.
Zusammenfassung
Die Einwirkung von Sauerstoff und Wasserdampf auf Eisen, Germanium und Silicium wurde durch Messung der Kinetik der Chemisorption und der Voltaspannung untersucht. Die Oxydschicht, die auf der Oberfläche von Fe, Ge und Si durch Adsorption von trockenem Sauerstoff gebildet wird, verliert in Anwesenheit von Wasserdampf ihre Schutzwirkung, sodass nach Entfernung des Wassers durch Entgasung Sauerstoff von neuem asdorbiert wird. Die Wiederholung dieses Prozesses mehr als einmal führt zur Bildung dicker oberflächlicher Oxydschichten. Messungen der Voltaspannung bestätigen diesen Korrosionsmechanismus.
This paper deals with the fractional-order Volta's system. It is based on the concept of chaotic system, where the mathematical model of system contains fractional order derivatives. This system has simple structure and can display a double-scroll attractor. The behavior and stability analysis of the integer-order and the fractional commensurate and non-commensurate order Volta's system with total order less than 3 which exhibits chaos are presented as well.
Skip to Main content
Arachidonic Acid
Related terms:
Fatty Acids
Eicosanoid Receptor
Enzymes
Cyclooxygenase
Platelet
Lipid
Protein
Docosahexaenoic Acid
Phospholipase A2
Cyclooxygenase 2
View all Topics
Arachidonic Acid
Stefano Fiore, in Encyclopedia of Gastroenterology, 2004
Introduction
Various pathways using arachidonic acid (AA) as the initial substrate are composed of dioxygenases that carry out a complex reaction involving abstraction of selected hydrogens and insertion of molecular oxygen. Two major classes of enzymes, cyclooxygenases (COX) and lipoxygenases (LOX), are recognized for their prominent role in generating a number of important biological mediators. Among these, prostaglandins (PGs) and leukotrienes (LTs) are widely studied given their recognized role in human disease conditions as well as physiological and/or pathophysiological activities. Of these biological actions, one of the most significant is the major role played by eicosanoids in inflammation, where they contribute to all of the clinical symptoms associated with the inflammatory condition, namely, pain, redness, and swelling. The ever-growing number of molecules derived from AA includes other families such as lipoxins (LXs), hepoxilins, hepoxides, monohydroxyeicosatretraenoic acids (HETEs), dihydroxyeicosatretraenoic acids, and their hydroperoxy precursors. Whereas synthesis of most of these mediators involves the non-heme iron catalytic center typical of cyclo- and lipoxygenases, hepoxilins and hepoxides originate via heme proteins such as hematin and cytochrome P450.
View chapterPurchase book
Thermal Sensors
Jialie Luo, Hongzhen Hu, in Current Topics in Membranes, 2014
4.3 Arachidonic acid
AA, a polyunsaturated fatty acid present in the phospholipids of cell membrane, is an important inflammatory mediator involved in many molecular and cellular functions under physiological and pathological conditions (Meves, 2008). Although AA signaling regulates activities of many TRP channels including TRPV1 and TRPV4 (Nilius, Vriens, Prenen, Droogmans, & Voets, 2004), different AA metabolic pathways are involved. For instance, activation of bradykinin B2 receptors produces 12-lipoxygenase metabolites such as 12-HPETE to activate TRPV1 and increase the excitability of sensory nerve endings (Hwang et al., 2000; Shin et al., 2002). On the other hand, the endocannabinoid anandamide and AA use the cytochrome P450 epoxygenase-dependent formation of epoxyeicosatrienoic acids such as 5′, 6′-epoxyeicosatrienoic acid (EET) and 11′, 12′-EET to activate TRPV4 (Sonkusare et al., 2012; Watanabe, et al., 2003). Interestingly, previous studies have suggested that TRPV3 may contribute to AA-mediated inflammatory responses since AA dramatically increased membrane current and intracellular Ca2+ response mediated by heterologously or endogenously expressed TRPV3, but not TRPV1 and TRPV2 (Hu et al., 2006). In addition to AA, many other unsaturated fatty acids exhibited similar potentiating effects on TRPV3 channel activity. AA was shown to increase the affinity of TRPV3 to 2-APB as evidenced by a leftward shift of the concentration–response curve of 2-APB in the presence of AA. The potentiating effect of TRPV3 by AA was mediated by an increase of the single-channel open probability but not the channel conductance. Neither AA metabolic blockers nor protein kinase inhibitors against protein kinase C (PKC) or calmodulin-dependent protein kinase II affected the potentiating effect of AA, suggesting that AA directly acts on TRPV3 channels.
View chapterPurchase book
Eicosanoids in Cerebrovascular Diseases
K. van Leyen, in Primer on Cerebrovascular Diseases (Second Edition), 2017
Production of Eicosanoids
AA is not produced in the human body, and thus must be taken up exogenously from various food sources. Once processed, most AA is not present as the free acid, but incorporated into phospholipids, typically in the sn-2 position. These AA-containing phospholipids are especially abundant in the brain, where they make up around 30% of all phospholipids. Under conditions of ischemia, phospholipases A2 (PLA2s) are activated, which liberate AA from the membrane phospholipids. Chief among these is the cytosolic calcium-dependent PLA2, but others may contribute.
With its four double bonds, free AA is highly reactive and prone to oxidation. This is especially relevant in stroke, because oxidative stress is known to be a major injury mechanism.
View chapterPurchase book
Molecular Mechanisms of Drug Actions
Catherine Litalien, Pierre Beaulieu, in Pediatric Critical Care (Fourth Edition), 2011
Arachidonic Acid and Its Metabolites
Arachidonic acid and its metabolites (prostaglandins and leukotrienes) are now considered intracellular messengers.31 Arachidonic acid is a component of membrane phospholipids released either in a one-step process, after phospholipase A2 (PLA2) action, or a two-step process, after phospholipase C and DAG lipase actions. Arachidonic acid is then metabolized by cyclooxygenase (COX) and 5-lipoxygenase, resulting in the synthesis of prostaglandins and leukotrienes, respectively. These intracellular messengers play an important role in the regulation of signal transduction implicated in pain and inflammatory responses. Corticosteroids inhibit PLA2 activity, whereas nonsteroidal antiinflammatory drugs inhibit COX activity.
View chapterPurchase book
Chagas Disease, Part B
Fabiana S. Machado, ... Anthony W. Ashton, in Advances in Parasitology, 2011
1.2.1 AA metabolism
AA is a 20-carbon polyunsaturated fatty acid derived from linoleic acid. Once synthesized, AA is stored as a part of glycerophospholipids that compose the lipid bilayer of the plasma membrane and can be released via the action of phospholipases A2, C and D (PLA2, PLC and PLD, respectively; Fig. 1.1). AA can be reincorporated into cellular lipids via reacylation and recombination with lysophospholipid. AA is metabolized predominantly by the following three independent metabolic pathways:

Sign in to download full-size image
Figure 1.1. Production and use of free arachidonic acid from various intracellular sources.
1.
The cyclooxygenase (COX) pathway: producing prostaglandins (PGs) and thromboxane A2 (TXA2).
2.
The lipoxygenase (LO) pathway: producing leukotrienes (LTs), lipoxins (LXs), hydroxyeicosatetraenoic acids (HETE) and hydroperoxyeicosatetraenoic acids (HPETE).
3.
Cytochrome P-450 monooxygenase pathway: producing epoxides and hydroxyeicosatetraenoic acids.
In addition to its role in eicosanoid synthesis, AA itself is capable of regulating cellular responses. AA controls the activity of PLA2 and PLC via a negative feedback mechanism (Sumida et al., 1993), triggers mobilization of intracellular calcium stores in a manner similar to that of inositol 1,4,5-phosphate (Chow and Jondal, 1990) and activates the classical isoforms of protein kinase C (PKC) (Naor, 1991). Activation of PKC by fatty acids may form a positive feedback loop to enhance fatty acid liberation through amplification of PLA2 activity (Sumida et al., 1993). AA also suppresses tumour necrosis factor (TNF)-α, interleukin (IL)-1α and lipopolysaccharide (LPS)-induced activation of endothelial cells (Stuhlmeier et al., 1996), indicating that AA may negatively regulate endothelial cell activation.
View chapterPurchase book
Mood Stabilizers
H.K. Manji, ... J. Du, in Encyclopedia of Neuroscience, 2009
AA Metabolism
AA functions as an important mediator of second-messenger pathways within the brain. It is released from membrane phospholipids via receptor/G-protein-initiated activation of phospholipase A2. This action results in release of AA from the cellular membrane and cyclooxygenase-mediated production of eicosanoid metabolites such as prostaglandins and thromboxanes. These metabolites mediate numerous subsequent intracellular responses and transynaptic responses.
Chronic lithium and valproate treatment of rats results in selective reductions in the turnover rate in the brain phospholipids of AA. In addition, lithium downregulates the gene expression and protein levels of an AA-specific phospholipase A2 (cPLA2) and the protein levels of cycloxygenase-2 (COX-2). Valproate decreases turnover of AA and protein levels of COX-1 and COX-2. These findings suggest that effects of mood stabilizers on cell membranes, and specifically AA turnover, might be relevant to the pharmacological action of lithium and valproate. Further general support for the involvement of the AA signaling pathway in bipolar disorder comes from other preclinical and clinical studies. Administration of nonselective cycloxygenase inhibitors indomethacin and piroxicam in rats prevented amphetamine-stimulated locomotor activity and blocked cocaine sensitization (both are rodent models of mania). Furthermore, inhibition of COX-2 with NS-398 attenuates restraint stress (a model of depression)-induced oxidative changes. In humans cyclooxygenase-2 inhibitor celecoxib was recently found to have antidepressant effects in a double-blind, placebo-controlled trial.
View chapterPurchase book
Chemoprevention of Barrett's Esophagus and Adenocarcinoma
Ebubekir Şenateş, in Barrett's Esophagus, 2016
14.2.1.2 Arachidonic Acid Pathway
Arachidonic acid pathway is a central regulator of inflammatory response. Gastric acid and duodenal bile acids may contribute to carcinogenesis in BE through activation of this pathway. Low pH and bile acids induce cyclooxygenase-2 (COX-2), which is a central enzyme of the arachidonic acid pathway both in the human BE ex vivo culture model and the EAC cell lines [32,33]. Expression of COX-2 increases concomitantly with neoplastic progression in BE and this increase supports an association between the arachidonic acid pathway and the development of EAC [32–35]. The COX-2 enzyme catalyzes conversion of arachidonic acid to different prostaglandins such as prostaglandin E2 (PGE2). PGE2 induces proliferation of Barret's epithelial cells and its inhibition may slow their growth [36]. PGE2-induced cell proliferation leads to accumulation of replicative errors in premalignant Barrett's cells. Furthermore, it inhibits tumor surveillance through natural killer cell activity of PGE2. Chronic induction of PGE2 might facilitate accumulation of abnormal cells that have genomic instability and thus inhibition of components of arachidonic acid pathway probably will inhibit carcinogenesis [37].
View chapterPurchase book
Omega-3 polyunsaturated fatty acids: Nutrigenetic and Nutrigenomic Aspects in the Determination of Dietary Requirements, Development, and Chronic Diseases
A.P. Simopoulos, in Encyclopedia of Human Nutrition (Third Edition), 2013
Genetic Variants of the FADS1 and FADS2 Gene Cluster Influence Omega-6 and Omega-3 Fatty Acids Composition in Both Plasma and Red Cell Membrane Phospholipids During Pregnancy and Lactation
AA, EPA, and DHA play central roles in infant growth, neural development, and immune function. The maternal status of AA, EPA, and DHA during gestation influences maternal to infant transfer via the placenta and breast milk provides fatty acids to infants after birth. FADS1 and FADS2 single nucleotide polymorphisms influence plasma phospholipid and erythrocyte ethanolamine phosphoglyceride (EPG) omega-6 and omega-3 fatty acids during pregnancy and their breast milk during lactation. Minor allele homozygotes of rs 174553 (GG), rs 99780 (TT), and rs 174583 (TT) had lower AA but higher LA in plasma phospholipids and erythrocyte EPG and decreased omega-6 and omega-3 fatty acids product to precursor ratio at 16 and 36 weeks gestation P<0.001. Breast milk fatty acids were influenced by genotype, with significantly lower 14.0, AA and EPA, but higher 20:2ω-6 in the minor allele homozygotes of rs 174553 (GG), rs 99780 (TT), and rs 174583 (TT) and lower AA, EPA, DPA 22:5ω-3, and DHA in the minor allele homozygotes GG of rs 174575. The results indicate a robust association between minor alleles of the 4 SNPs and lower AA and other omega-6 fatty acids relative to precursor LA. Similar results were found for the omega-3 series. Genetic variation in the FADS1 and FADS2 gene cluster is important for the composition of fatty acids provided to breastfed infants in mother's milk.
View chapterPurchase book
Synthesis, Metabolism, and Actions of Bioregulators
David O. Norris Ph.D., James A. Carr Ph.D., in Vertebrate Endocrinology (Fifth Edition), 2013
B Biosynthesis and Actions of Eicosanoids
Arachidonic acid is synthesized from α-linolenic acid derived from linoleic acid, an essential fatty acid, by the enzyme Δ6-desaturase. Once formed, arachidonic acid can be converted to any of the eicosanoids (Figure 3-36). Cyclooxygenase is an enzyme that transforms arachidonic acid into endoperoxides which are used to synthesize prostaglandins, prostacyclin, or thromboxanes. Drugs such as aspirin and indomethacin inhibit cyclooxygenase and block the synthesis of prostaglandins and thromboxanes. Certain flavenoids obtained from plants also block cyclooxygenase. A separate enzyme, 5-lipoxygenase, forms the leucotrienes from arachidonic acid. This enzyme is not inhibited by aspirin or indomethacin but can be inhibited by specific lipoxygenase inhibitors as well as by plant flavenoids.
Eicosanoids produce their effects by binding to the peroxisome proliferator-activated (PPAR) receptor. PPARs are also members of the same superfamily of nuclear receptors that includes steroids and TRs and are in the same subgrouping as the TRs. Occupied PPARs, like occupied TRs, form heterodimers with RXRs prior to binding to gene response elements.
View chapterPurchase book
Dietary Interventions in Infancy
M.M. Vonk, ... J. Garssen, in Allergy, Immunity and Tolerance in Early Childhood, 2016
Abbreviations
AA
Arachidonic acid
AD
Atopic dermatitis
ALA
α-Linolenic acid
APC
Antigen-presenting cells
BLG
β-Lactoglobulin
CMA
Cow's milk allergy
DHA
Docosahexaenoic acid
EPA
Eicosapentaenoic acid
FOS
Fructo-oligosaccharides
GALT
Gut-associated lymphoid tissue
GI
Gastrointestinal tract
GOS
Galacto-oligosaccharides
GPR120
G-protein coupled receptor 120
HMOS
Human milk oligosaccharides
IEC
Intestinal epithelial cells
LA
Linoleic acid
LCPUFA
Long-chain polyunsaturated fatty acids
MLN
mesenteric lymph nodes
OVA
Ovalbumin
Peripheral blood mononuclear cells
PGE2
Prostaglandin E2
PUFA
Polyunsaturated fatty acids
SCFA
Short-chain fatty acids
Skip to Main content

AA Amyloidosis
AA amyloidosis develops in association with an enhanced and prolonged inflammation that leads to a sustained upregulated production of its precursor and, subsequently, to its incomplete degradation, misfolding, and deposition in the tissues.
From: Pathobiology of Human Disease, 2014
Related terms:
Prion
Amyloid
Transthyretin
Prions
Serum Amyloid A
AL Amyloidosis
Nested Gene
Amyloidosis
Mutation
View all Topics
Renal Amyloidosis and Glomerular Diseases with Monoclonal Immunoglobulin Deposition
Pierre M. Ronco, ... Bruno Moulin, in Comprehensive Clinical Nephrology (Fourth Edition), 2010
Epidemiology
AA amyloidosis develops in 5% of patients with sustained elevation of serum amyloid A protein (SAA). Patients at risk are those with a long duration of chronic inflammatory disease (median, 17 years),29 high magnitude of acute-phase SAA response, homozygosity for SAA1 isotype, familial Mediterranean fever (FMF) trait (heterozygosity for variant pyrin), and family history of AA amyloidosis.
An important epidemiologic aspect of AA amyloidosis is the changing spectrum of underlying diseases. Pyogenic and granulomatous infections, especially tuberculosis, account for far fewer cases today (15%) than previously.29 Thus, antibiotic treatment efficiently prevents AA amyloidosis by suppressing its cause. In contrast, the prevalence of chronic inflammatory arthritis has increased dramatically (60%).29 AA amyloidosis in patients with Hodgkin's disease has virtually disappeared with more efficient treatment of the hematologic disease. Hereditary AA amyloidoses associated with familial recurrent fever syndromes account for an increasing proportion of cases, about 10% in recent series.
View chapterPurchase book
Amyloidosis
Ralph C. Budd, David C. Seldin, in Kelley and Firestein's Textbook of Rheumatology (Tenth Edition), 2017
AA Amyloidosis
AA amyloidosis can occur at any age. The primary clinical manifestation is proteinuria, renal insufficiency, or both.5 A study from Finland found AA amyloidosis to be the most common cause of nephrotic syndrome in patients with rheumatoid arthritis.64 Hepatomegaly, splenomegaly, and autonomic neuropathy frequently occur as the disease progresses; cardiomyopathy occurs rarely. With chronic inflammatory diseases, amyloid progression is slow, and survival is often longer than 10 years, particularly with treatment for end-stage renal disease. In contrast, untreated infections, such as osteomyelitis, tuberculosis, or leprosy, can produce a more rapidly progressive amyloid syndrome, which remits with effective medical or surgical treatment of the infection.
The major therapy in AA amyloidosis is treatment of the underlying inflammatory or infectious disease. Treatment that suppresses or eliminates the inflammation or infection also decreases the SAA protein. For familial Mediterranean fever, colchicine, 1.2 to 1.8 mg/day, is the appropriate treatment. Colchicine has not been helpful for AA amyloidosis of other causes or for other amyloidoses. A multicenter randomized trial using a new antiamyloid drug, eprodisate, has been completed; the drug was found to significantly delay worsening of renal function in patients with AA amyloidosis.65 A second multicenter trial requested by the Food and Drug Administration is now under way. Eprodisate interferes with the interaction of AA amyloid protein and glycosaminoglycans in tissues and prevents fibril formation and deposition.
View chapterPurchase book
Nonsuppurative Manifestations of Infections
Carlos Franco-Paredes MD, MPH, in Core Concepts in Clinical Infectious Diseases (CCCID), 2016
Amyloidosis
Amyloidosis (AA type) may complicate chronic infections processes or chronic inflammatory diseases such as rheumatoid arthritis. Chronic infectious diseases classically associated with AA amyloidosis include tuberculosis, leprosy, and brucellosis given the long-term inflammation associated with M. tuberculosis and M. leprae, respectively. Chronic parasitic infections can also lead to renal amyloidosis such as Schistosoma mansoni or Schistosoma haematobium.5 It usually manifests as an organ-specific amyloidosis, such as nephritic or nephrotic syndrome, cardiac amyloidosis, hepatic amyloidosis, or nerve infiltration. Chronic osteomyelitis and bronchiectasis can also be associated with renal amyloidosis. HIV infection has also been associated with amyloidosis cardiac amyloidosis.6,7
View chapterPurchase book
Amyloidosis
Philip N. Hawkins, in Rheumatology (Sixth Edition), 2015
Disease associations
AA amyloidosis occurs in association with chronic inflammatory disorders, chronic local or systemic microbial infections, and occasionally neoplasms, all of remarkable variety. In Western Europe and the United States the most frequent predisposing conditions are idiopathic rheumatic diseases. The lifetime incidence of AA amyloidosis in patients with rheumatoid arthritis and juvenile idiopathic arthritis in Europe is between 1% and 5%, is rather lower in the United States for reasons that are not clear, and is probably decreasing, generally due to improved treatments. Tuberculosis and leprosy are important causes of AA amyloidosis in some areas. Chronic osteomyelitis, bronchiectasis, chronically infected burns and decubitus ulcers, and the chronic pyelonephritis of paraplegia are other well-recognized associations. Hodgkin disease and renal carcinoma, which often cause a major acute-phase response, are the malignancies most commonly associated with systemic AA amyloid. Perhaps surprisingly, up to 10% of patients with AA amyloidosis do not have a clinically obvious chronic inflammatory disease, and these patients are often erroneously assumed to have AL amyloidosis. Although it may remain impossible to identify the of the precipitating acute-phase response in many such patients, the most common identifiable pathologic conditions in such cases in series at the author's own institution have been hitherto undiagnosed inherited periodic fever syndromes9 and cytokine-secreting Castleman disease tumors of the solitary plasma cell type, located in either the mediastinum or gut mesentery.10
View chapterPurchase book
A worldwide yearly survey of new data in adverse drug reactions
Ashakumary Lakshmikuttyamma, Abigail Kay, in Side Effects of Drugs Annual, 2015
Urinary Tract
AA amyloidosis, or secondary amyloidosis, is characterized by abnormal protein deposits, which can result in damage to an organ, as well as its ability to function normally. Cooper et al. [68C] present a patient who was determined to have developed AA renal amyloidosis due to subcutaneous injection (i.e. "skin popping") of heroin. The patient was a 37-year-old woman with a medical history significant for heroin use, cocaine use, HCV, DVT, and a recent admission 2 weeks earlier for a left axilla abscess of her breast. She represented with continued pain from her abscess and a bilateral lower extremity edema since her last admission. She had dysuria, fever, flank pain, shortness of breath, and urinary frequency. On physical exam she had evidence of multiple lesions due to her injection drug use, bilateral edema, which extended to knee level, but no evidence of lymphadenopathy. Her lab results demonstrated multiple abnormalities including a hemoglobin of 8.5 g/dL, a hematocrit of 26.7%, a blood urea nitrogen of 33 mg/dL, a C reactive protein of 5.47 mg/L, an erythrocyte sedimentation rate of 137 mm/h, and greater than 300 mg/dL of protein in her urinalysis. Her abscess was cultured and determined to be methicillin-resistant Staphylococcus aureus and her blood cultures were negative. She was started on anti-microbial therapy and a renal biopsy was done, whose pathology was consistent with secondary amyloidosis. The authors conclude that AA amyloidosis should be considered in the differential diagnosis of any patient with heroin use disorder with proteinuria and renal impairment.
View chapterPurchase book
Bone Marrow, Blood Cells, and the Lymphoid/Lymphatic System1
Katie M. Boes, Amy C. Durham, in Pathologic Basis of Veterinary Disease (Sixth Edition), 2017
E-Glossary 13-1 Glossary of Abbreviations and Terms
AA amyloidosis—Serum amyloid A amyloidosis
ACT—Activated clotting time
ADP—Adenosine diphosphate
AL amyloidosis—Amyloid–light chain amyloidosis
ALL—Acute lymphoblastic leukemia
AML—Acute myeloid leukemia
AP3—Adaptor protein complex
ATALT—Auditory tube–associated lymphoid tissue
ATP—Adenosine triphosphate
BALT—Bronchus-associated lymphoid tissue
BCR-ABL—Breakpoint cluster region-Abelson
BLAD—Bovine leukocyte adhesion deficiency
BLL—Burkitt-like lymphoma
BLP—B lymphocyte progenitor
BLV—Bovine leukemia virus
BNP—Bovine neonatal pancytopenia
BVD—Bovine viral diarrhea
BVDV—Bovine viral diarrhea virus
CalDAG-GEFI—Calcium diacylglycerol guanine nucleotide exchange factor I
CALT—Conjunctiva-associated lymphoid tissue
CBC—Complete blood count
C-bilirubin—Conjugated bilirubin
CD—Cluster of differentiation
CH—Cutaneous histiocytosis
CHS—Chédiak-Higashi syndrome
CLAD—Canine leukocyte adhesion deficiency
CLL—Chronic lymphocytic leukemia
CLP—Common lymphoid progenitor
CML—Chronic myeloid leukemia
CMP—Common myeloid progenitor
CPV-2—Canine parvovirus type 2
CTCL—Cutaneous T lymphocyte lymphoma
DC—Dendritic cell
DIC—Disseminated intravascular coagulation
DLBCL—Diffuse large B cell lymphoma
DNA—Deoxyribonucleic acid
DNA-PKcs—DNA-dependent protein kinase catalytic subunit
2,3-DPG—2,3-diphosphoglycerate
EATCL—Enteropathy-associated T cell lymphoma
EBL—Enzootic bovine leukosis
EBV—Epstein-Barr virus
EHV-1—Equine herpes virus 1
EHV-5—Equine herpes virus 5
EIAV—Equine infectious anemia virus
EMH—Extramedullary hematopoiesis
EMP—Extramedullary plasmacytoma
EP—Erythroid progenitor
Epo—Erythropoietin
FAD—Flavin adenine dinucleotide
FAE—Follicle-associated epithelium
FcaGHV1—Felis catus gammaherpesvirus 1
Fe3+—Ferric iron
FeLV—Feline leukemia virus
FIV—Feline immunodeficiency virus
FL—Follicular lymphoma
FPV—Feline parvovirus
GALT—Gut-associated lymphoid tissue
GMP—Granulocyte-macrophage progenitor
GP—Glycoprotein
GP—Granulocyte progenitor
G6PD—Glucose-6-phosphate dehydrogenase
Gr.—Greek
GSH—Reduced glutathione
GT—Glanzmann thrombasthenia
H&E—Hematoxylin and eosin
HEV—High endothelial venule
Hgb—Hemoglobin
Hpt—Haptoglobin
Hpx—Hemopexin
HS—Histiocytic sarcoma
HSC—Hematopoietic stem cell
IBD—Inflammatory bowel disease
iDC—Interstitial dendritic cell
Ig—Immunoglobulin
IgA—Immunoglobulin A
IgG—Immunoglobulin G
IgM—Immunoglobulin M
IL—Interleukin
IMHA—Immune-mediated hemolytic anemia
IMTP—Immune-mediated thrombocytopenia
INF—Interferon
IRF4—Interferon regulatory factor 4
LAD—Leukocyte adhesion deficiency
LALT—Larynx-associated lymphoid tissue
LBL—Lymphoblastic lymphoma
LC—Langerhans cell
LGL—Large granular lymphocyte
LYST—Lysosomal trafficking regulator
MAC—Membrane attack complex
MALT—Mucosa-associated lymphoid tissue
MAP—Mycobacterium avium ssp. paratuberculosis
M cell—Microfold cell
MCF—Malignant catarrhal fever
MCH—Mean cell hemoglobin
MCHC—Mean cell hemoglobin concentration
MCL—Mantle cell lymphoma
MCP—Mast cell progenitor
MCT—Mast cell tumor
MCV—Mean cell volume
MDS—Myelodysplastic syndrome
MEP—Megakaryocyte-erythroid progenitor
MetHgb—Methemoglobin
MHC—Major histocompatibility complex
miRNA—MicroRNA
MKP—Megakaryocyte progenitor
MM—Multiple myeloma
MP—Macrophage progenitor
MPV—Mean platelet volume
MUM1—Melanoma-associated antigen (mutated) 1
MZL—Marginal zone lymphoma
NADH—Reduced nicotinamide adenine dinucleotide
NADPH—Reduced nicotinamide adenine dinucleotide phosphate
NALT—Nasal-associated lymphoid tissue
NCI—National Cancer Institute
NI—Neonatal isoerythrolysis
NK cell—Natural killer cell
NKP—Natural killer cell progenitor
nRBC—Nucleated red blood cell
PALS—Periarteriolar lymphoid sheath
PAMS—Periarteriolar macrophage sheath
PARR—Polymerase chain reaction for antigen receptor rearrangement
PCR—Polymerase chain reaction
PCV2—Porcine circovirus type 2
PCVAD—Porcine circovirus–associated disease
PFK—Phosphofructokinase
PHA—Pelger-Huët anomaly
PK—Pyruvate kinase
PL—Persistent lymphocytosis
PMWS—Postweaning multisystemic wasting syndrome
PPP—Pentose phosphate pathway
PRCA—Pure red cell aplasia
PRDC—Porcine respiratory disease complex
PrPSc—Scrapie prion protein
PRRS—Porcine reproductive and respiratory syndrome
PT—Prothrombin time
PTCL—Peripheral T cell lymphoma
PTT—Partial thromboplastin time
RBC—Red blood cell
REAL—Revised European-American Classification of Lymphoid Neoplasms
rhEpo—Recombinant human erythropoietin
SCID—Severe combined immunodeficiency disease
SFHN—Splenic fibrohistiocytic nodule
SH—Systemic histiocytosis
SPF—Specific pathogen–free
TCRLBCL—T cell–rich large B cell lymphoma
TGF-β—Transforming growth factor-β
TLP—T lymphocyte progenitor
TNF—Tumor necrosis factor
TNKP—T lymphocyte–natural killer cell progenitor
Tpo—Thrombopoietin
TZL—T zone lymphoma
U-bilirubin—Unconjugated bilirubin
vWD—von Willebrand disease
vWF—von Willebrand factor
WHO—World Health Organization
View chapterPurchase book
Amyloid Cardiomyopathy
T. Sher, M.A. Gertz, in Encyclopedia of Cardiovascular Research and Medicine, 2018
Secondary Systemic Amyloid (AA) Cardiomyopathy
Secondary systemic (AA) amyloidosis results from excessive production and misfolding of the acute-phase reactant serum amyloid A protein. AA is common in developing countries and in the Mediterranean basin due to a high prevalence of chronic infections and auto-inflammatory disorders, such as familial periodic fever syndromes (van der Hilst et al., 2005). In the United States and Western Europe, it is rare and usually results from unrecognized or treatment refractory chronic autoimmune disorders such as rheumatoid arthritis and inflammatory bowel disease (Hazenberg and van Rijswijk, 2000). Nephrotic syndrome is the most common presentation, but involvement of gastrointestinal and hepatobiliary systems leading to malabsorption syndrome and/or hepatosplenomegaly can be seen. Involvement of endocrine organs, such as thyroid and adrenal gland, can be seen and may result in adrenal insufficiency (Hazenberg and van Rijswijk, 2000). Cardiac involvement in AA is rare and even if severe by echocardiogram, seldom results in clinically significant cardiomyopathy.
View chapterPurchase book
Systemic autoinflammatory syndromes
Jeroen C.H. van der Hilst, ... Anna Simon, in Clinical Immunology (Fourth Edition), 2013
Amyloidosis
Reactive or type AA amyloidosis is a serious complication of all autoinflammatory syndromes.35 It is caused by the deposition of insoluble fibrils in the extracellular matrix of organs and tissues, most notably the kidneys, spleen, and liver. The fibrils are composed of a degradation product of SAA. Since SAA is an acute-phase reactant there is a close relationship between the continuous elevation of SAA and the development of amyloidosis. Before the recognition of colchicine as an effective treatment for FMF, amyloidosis occurred in up to 75% of patients. Even before the advent of effective treatment, not all FMF patients developed amyloidosis, suggesting that other factors contribute to the risk of developing amyloidosis.
In FMF there is a strong correlation between ethnicity and risk of amyloidosis, with the highest risk for Sephardic Jews. Another identified risk factor for developing amyloidosis is single nucleotide polymorphisms (SNPs) in the SAA gene. Two SNPs define three different SAA proteins: SAA 1.1, 1.3, and 1.5. Patients with the SAA 1.1/1.1genotype have a three- to sevenfold increased risk of developing amyloidosis.
Up to a quarter of TRAPS patients develop amyloidosis, if the disease is left untreated. There seems to be a strong family predilection. In some families almost all adults are affected whereas in other families no cases of amyloidosis are found. In CAPS, an estimated one-third of patients develop amyloidosis if the disease is left untreated, although exact numbers are missing.
Patients with HIDS have a relatively small risk of developing amyloidosis: only 4–5 cases of HIDS patients with amyloidosis are known world-wide. This is a remarkably lower incidence of amyloidosis in HIDS compared to the other periodic fever syndromes, despite a similar acute-phase response.36
A diagnosis of amyloidosis is confirmed by Congo red staining of affected tissues, showing a typical apple-green birefringence under polarized light microscopy (Fig. 59.5). Biopsy of subcutaneous fat or rectal tissue can be used to detect amyloid fibrils. If these are negative and there is a high index of suspicion, a direct biopsy from an affected organ can be considered.
The natural history of amyloidosis is progression to renal failure. If inflammation cannot be controlled, amyloid deposits in a variety of organs (liver, spleen, gastrointestinal tract, heart) occur. As a consequence malabsorption with severe diarrhea may ensue. Cardiac failure and rhythm disturbances are typical manifestations of cardiac involvement. The prognosis of patients with established amyloidosis is grave, with a median survival of 24–53 months. However, the progression of amyloidosis is strongly dependent on the ability to control the underlying inflammatory process.
If the SAA concentration can be kept under 10 mg/L, progression of amyloidosis can be halted in many cases, and in some the amyloid mass even slowly regresses.36 The recent advances in therapy will likely improve the survival in patients with autoinflammatory syndromes complicated by amyloidosis.
View chapterPurchase book
The Pharmacology and Therapeutic Aspects of Colchicine
Claire Le Hello, in The Alkaloids: Chemistry and Biology, 1999
2 Secondary A A Amyloidosis Outside the Context of Familial Mediterranean Fever
The principal treatment of AA amyloidosis is that of its cause. However, based on its beneficial effect on familial Mediterranean fever and several cases of AL amyloidosis, colchicine could be added to this etiological therapy. Several isolated successes have been reported. An amyloid nephrotic syndrome secondary to granulomatous colitis regressed in 7 months under 1 mg of colchicine daily and remained stable over 61 months of follow-up (103). Two nephrotic syndromes caused by amyloidosis secondary to ulcerative colitis disappeared after 108 and 8 months of treatment with colchicine (1.2 mg/day), intermittently combined with corticosteroids, independently of the evolution of the causal disease (142). Another patient's nephrotic syndrome regressed after intestinal resection for Crohn's disease and 5 years of colchicine (1.5 mg/day) (143). After 2 years of colchicine (1 mg/day) and sulfasalazine, a nephrotic syndrome secondary to ankylosing spondylarthritis disappeared (144). A nephrotic syndrome that persisted after excision of a tumoral mass of Castleman's disease was attenuated after 9 months of treatment with colchicine (1.5 mg/day) and was immediately followed by a pregnancy with a favorable evolution (145).
The outcomes of two patients with cystic fibrosis complicated by AA amyloid nephropathy were less evident and should be seen in light of the fact that, at this stage, the prognosis for this pathology is dismal with a mean survival of < 1 year. Colchicine was able to stabilize the nephrotic syndrome for one patient and delay the appearance of renal insufficiency for the other, but the latter patient died, nonetheless, shortly thereafter (146).
Several failures of colchicine have been published, but their real frequency is probably underestimated. The drug was unable to attenuate the amyloid nephropathy of Muckle-Wells syndrome (147), a genetic disorder characterized by recurrent urticarial rashes, arthralgias, and progressive sensorineural deafness, and complicated by amyloidosis. Likewise, colchicine does not seem to prevent the development of the b2-microglobulin amyloidosis in hemodialysis patients (148),and did not modify the serum b2-microglobulin concentrations in a group of 15 hemodialyzed patients (149).
These observations should be interpreted with caution because of the short duration of treatment and the small number of patients studied. Nevertheless, generally speaking, adding colchicine to any therapeutic regimen for secondary amyloidosis should be considered.
Skip to main contentSkip to article

Access through your institution
Get Access
Journal of Substance Abuse
Volume 7, Issue 3, 1995, Pages 281-292
AA and other helpseeking for alcohol problems: Former drinkers in the U.S. general population
Author links open overlay panelDeborah S.HasinBridget F.Grant
Show more
Outline
Share
Cite
https://doi.org/10.1016/0899-3289(95)90022-5Get rights and content
Abstract
Former drinkers comprise 18.5% of the adult U.S. population. However, no epidemiologic data has been published on the histories of seeking help for alcohol problems from Alcoholics Anonymous (AA) or professional or informal sources of help. Using a sample of 8,057 former drinkers surveyed in the 1988 National Health Interview Survey, prevalence and characteristics associated with histories of such helpseeking were investigated. About 7% of the former drinkers had gone to AA or sought other types of help. Characteristics associated with such helpseeking were a diagnosis of DSM-IV alcohol dependence or abuse, a sense of compulsion to drink, social pressure to cut down, and highest ever alcohol consumption. The effects of alcohol consumption were stronger among younger respondents than older ones for professional or informal helpseeking