A lipoprotein-associated PHOSPHOLIPASE A2 which modulates the action of PLATELET ACTIVATING FACTOR by hydrolyzing the SN-2 ester bond to yield the biologically inactive lyso-platelet-activating factor. It has specificity for phospholipid substrates with short-chain residues at the SN-2 position, but inactive against long-chain phospholipids. Deficiency in this enzyme is associated with many diseases including ASTHMA, and HYPERCHOLESTEROLEMIA.
Enzymes which catalyze the hydrolysis of carboxylic acid esters with the formation of an alcohol and a carboxylic acid anion.
Hydrolytic enzyme activity used as a histocytochemical test for the presence of esterases in tissue. Substrate used is 3-hydroxy-4'-nitro-2-naphthanilide chloroacetate (naphthol AS-D).
An enzyme that catalyzes the hydrolysis of CHOLESTEROL ESTERS and some other sterol esters, to liberate cholesterol plus a fatty acid anion.
An enzyme that catalyzes the conversion of acetate esters and water to alcohols and acetate. EC 3.1.1.6.
Carboxylesterase is a serine-dependent esterase with wide substrate specificity. The enzyme is involved in the detoxification of XENOBIOTICS and the activation of ester and of amide PRODRUGS.
A di-isopropyl-fluorophosphate which is an irreversible cholinesterase inhibitor used to investigate the NERVOUS SYSTEM.
The covalent bonding of an alkyl group to an organic compound. It can occur by a simple addition reaction or by substitution of another functional group.
Collections of illustrative plates, charts, etc., usually with explanatory captions.
The systematic study of the complete complement of proteins (PROTEOME) of organisms.
A "smooth brain" malformation of the CEREBRAL CORTEX resulting from abnormal location of developing neurons during corticogenesis. It is characterized by an absence of normal convoluted indentations on the surface of the brain (agyria), or fewer and shallower indentations (pachygryia). There is a reduced number of cortical layers, typically 4 instead of 6, resulting in a thickened cortex, and reduced cerebral white matter that is a reversal of the normal ratio of cerebral white matter to cortex.
The first cervical vertebra.
A multi-functional catenin that participates in CELL ADHESION and nuclear signaling. Beta catenin binds CADHERINS and helps link their cytoplasmic tails to the ACTIN in the CYTOSKELETON via ALPHA CATENIN. It also serves as a transcriptional co-activator and downstream component of WNT PROTEIN-mediated SIGNAL TRANSDUCTION PATHWAYS.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
The use of statistical methods in the analysis of a body of literature to reveal the historical development of subject fields and patterns of authorship, publication, and use. Formerly called statistical bibliography. (from The ALA Glossary of Library and Information Science, 1983)
Copies of a work or document distributed to the public by sale, rental, lease, or lending. (From ALA Glossary of Library and Information Science, 1983, p181)
"The business or profession of the commercial production and issuance of literature" (Webster's 3d). It includes the publisher, publication processes, editing and editors. Production may be by conventional printing methods or by electronic publishing.
Critical and exhaustive investigation or experimentation, having for its aim the discovery of new facts and their correct interpretation, the revision of accepted conclusions, theories, or laws in the light of newly discovered facts, or the practical application of such new or revised conclusions, theories, or laws. (Webster, 3d ed)
A subspecialty of internal medicine concerned with the study of the physiology and diseases of the digestive system and related structures (esophagus, liver, gallbladder, and pancreas).
Research that involves the application of the natural sciences, especially biology and physiology, to medicine.
A bibliographic database that includes MEDLINE as its primary subset. It is produced by the National Center for Biotechnology Information (NCBI), part of the NATIONAL LIBRARY OF MEDICINE. PubMed, which is searchable through NLM's Web site, also includes access to additional citations to selected life sciences journals not in MEDLINE, and links to other resources such as the full-text of articles at participating publishers' Web sites, NCBI's molecular biology databases, and PubMed Central.
Organizations representing specialized fields which are accepted as authoritative; may be non-governmental, university or an independent research organization, e.g., National Academy of Sciences, Brookings Institution, etc.
An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.
Phospholipases that hydrolyze the acyl group attached to the 2-position of PHOSPHOGLYCERIDES.
NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).
Studies in which individuals or populations are followed to assess the outcome of exposures, procedures, or effects of a characteristic, e.g., occurrence of disease.
Observation of a population for a sufficient number of persons over a sufficient number of years to generate incidence or mortality rates subsequent to the selection of the study group.

Lipoprotein-associated phospholipase A2, platelet-activating factor acetylhydrolase, generates two bioactive products during the oxidation of low-density lipoprotein: use of a novel inhibitor. (1/562)

A novel and potent azetidinone inhibitor of the lipoprotein-associated phospholipase A2 (Lp-PLA2), i.e. platelet-activating factor acetylhydrolase, is described for the first time. This inhibitor, SB-222657 (Ki=40+/-3 nM, kobs/[I]=6. 6x10(5) M-1.s-1), is inactive against paraoxonase, is a poor inhibitor of lecithin:cholesterol acyltransferase and has been used to investigate the role of Lp-PLA2 in the oxidative modification of lipoproteins. Although pretreatment with SB-222657 did not affect the kinetics of low-density lipoprotein (LDL) oxidation by Cu2+ or an azo free-radical generator as determined by assay of lipid hydroperoxides (LOOHs), conjugated dienes and thiobarbituric acid-reacting substances, in both cases it inhibited the elevation in lysophosphatidylcholine content. Moreover, the significantly increased monocyte chemoattractant activity found in a non-esterified fatty acid fraction from LDL oxidized by Cu2+ was also prevented by pretreatment with SB-222657, with an IC50 value of 5.0+/-0.4 nM. The less potent diastereoisomer of SB-222657, SB-223777 (Ki=6.3+/-0.5 microM, kobs/[I]=1.6x10(4) M-1.s-1), was found to be significantly less active in both assays. Thus, in addition to generating lysophosphatidylcholine, a known biologically active lipid, these results demonstrate that Lp-PLA2 is capable of generating oxidized non-esterified fatty acid moieties that are also bioactive. These findings are consistent with our proposal that Lp-PLA2 has a predominantly pro-inflammatory role in atherogenesis. Finally, similar studies have demonstrated that a different situation exists during the oxidation of high-density lipoprotein, with enzyme(s) other than Lp-PLA2 apparently being responsible for generating lysophosphatidylcholine.  (+info)

Association of the inflammatory state in active juvenile rheumatoid arthritis with hypo-high-density lipoproteinemia and reduced lipoprotein-associated platelet-activating factor acetylhydrolase activity. (2/562)

OBJECTIVE: To investigate the relationship between the quantitative and qualitative abnormalities of apolipoprotein B (Apo B)- and Apo A-I-containing lipoproteins and between lipoprotein-associated platelet-activating factor acetylhydrolase (PAF-AH) activity in patients with juvenile rheumatoid arthritis (JRA) as a function of the inflammatory state. METHODS: Twenty-six JRA patients and 22 age- and sex-matched control subjects with normal lipid levels participated in the study. Fourteen patients had active disease, and 12 had inactive disease. Plasma lipoproteins were fractionated by gradient ultracentrifugation into 9 subfractions, and their chemical composition and mass were determined. The PAF-AH activity associated with lipoprotein subfractions and the activity in plasma were also measured. RESULTS: Patients with active JRA had significantly lower plasma total cholesterol and high-density lipoprotein (HDL) cholesterol levels as compared with controls, due to the decrease in the mass of both the HDL2 and HDL3 subfractions. Patients with active JRA also had higher plasma triglyceride levels, mainly due to the higher triglyceride content of the very low-density lipoprotein plus the intermediate-density lipoprotein subfraction. The plasma PAF-AH activity in patients with active JRA was lower than that in controls, mainly due to the decrease in PAF-AH activity associated with the intermediate and dense low-density lipoprotein subclasses. The lipid abnormalities and the reduction in plasma PAF-AH activity were significantly correlated with plasma C-reactive protein levels and were not observed in patients with inactive JRA. CONCLUSION: This is the first study to show that patients with active JRA exhibit low levels of HDL2 and HDL3 and are deficient in plasma PAF-AH activity. These alterations suggest that active JRA is associated with partial loss of the antiinflammatory activity of plasma Apo B- and Apo A-I-containing lipoproteins.  (+info)

Glutamate receptor signaling interplay modulates stress-sensitive mitogen-activated protein kinases and neuronal cell death. (3/562)

Glutamate receptors modulate multiple signaling pathways, several of which involve mitogen-activated protein (MAP) kinases, with subsequent physiological or pathological consequences. Here we report that stimulation of the N-methyl-D-aspartate (NMDA) receptor, using platelet-activating factor (PAF) as a messenger, activates MAP kinases, including c-Jun NH2-terminal kinase, p38, and extracellular signal-regulated kinase, in primary cultures of hippocampal neurons. Activation of the metabotropic glutamate receptor (mGluR) blocks this NMDA-signaling through PAF and MAP kinases, and the resultant cell death. Recombinant PAF-acetylhydrolase degrades PAF generated by NMDA-receptor activation; the hetrazepine BN50730 (an intracellular PAF receptor antagonist) also inhibits both NMDA-stimulated MAP kinases and neuronal cell death. The finding that the NMDA receptor-PAF-MAP kinase signaling pathway is attenuated by mGluR activation highlights the exquisite interplay between glutamate receptors in the decision making process between neuronal survival and death.  (+info)

Molecular basis of the interaction between plasma platelet-activating factor acetylhydrolase and low density lipoprotein. (4/562)

The platelet-activating factor acetylhydrolases are enzymes that were initially characterized by their ability to hydrolyze platelet-activating factor (PAF). In human plasma, PAF acetylhydrolase (EC 3.1.1.47) circulates in a complex with low density lipoproteins (LDL) and high density lipoproteins (HDL). This association defines the physical state of PAF acetylhydrolase, confers a long half-life, and is a major determinant of its catalytic efficiency in vivo. The lipoprotein-associated enzyme accounts for all of the PAF hydrolysis in plasma but only two-thirds of the protein mass. To characterize the enzyme-lipoprotein interaction, we employed site-directed mutagenesis techniques. Two domains within the primary sequence of human PAF acetylhydrolase, tyrosine 205 and residues 115 and 116, were important for its binding to LDL. Mutation or deletion of those sequences prevented the association of the enzyme with lipoproteins. When residues 115 and 116 from human PAF acetylhydrolase were introduced into mouse PAF acetylhydrolase (which normally does not associate with LDL), the mutant mouse PAF acetylhydrolase associated with lipoproteins. To analyze the role of apolipoprotein (apo) B100 in the formation of the PAF acetylhydrolase-LDL complex, we tested the ability of PAF acetylhydrolase to bind to lipoproteins containing truncated forms of apoB. These studies indicated that the carboxyl terminus of apoB plays a key role in the association of PAF acetylhydrolase with LDL. These data on the molecular basis of the PAF acetylhydrolase-LDL association provide a new level of understanding regarding the pathway for the catabolism of PAF in human blood.  (+info)

Deficiency of platelet-activating factor acetylhydrolase is a severity factor for asthma. (5/562)

Asthma, a family of airway disorders characterized by airway inflammation, has an increasing incidence worldwide. Platelet-activating factor (PAF) may play a role in the pathophysiology of asthma. Its proinflammatory actions are antagonized by PAF acetylhydrolase. A missense mutation (V279F) in the PAF acetylhydrolase gene results in the complete loss of activity, which occurs in 4% of the Japanese population. We asked if PAF acetylhydrolase deficiency correlates with the incidence and severity of asthma in Japan. We found that the prevalence of PAF acetylhydrolase deficiency is higher in Japanese asthmatics than healthy subjects and that the severity of this syndrome is highest in homozygous-deficient subjects. We conclude that the PAF acetylhydrolase gene is a modulating locus for the severity of asthma.  (+info)

Platelet-activating factor may act as an endogenous pulse generator for sheep of luteolytic PGF2alpha release. (6/562)

Pulsatile release of uterine prostaglandin F2alpha (PGF2alpha) induces luteolysis in ruminants. However, the mechanism(s) that initiates and maintains luteolysis has not been defined. The present study tested the hypothesis that the endogenous PGF2alpha pulse generator is uterine-derived platelet-activating factor (PAF). Ovariectomized ewes were given exogenous progesterone (P), estradiol (E), or both (P+E, mimicking the normal luteal phase). Only ewes treated with steroids released PAF into the uterine lumen and had increased PAF:acetylhydrolase activity in the uterine lumen. Steroid treatment also influenced the capacity of the uterus to release PGF2alpha in response to exogenous PAF. PAF infusion did not affect plasma PGF2alpha metabolite (PGFM) levels in control (no steroid treatment) ewes but increased plasma PGFM levels in P+E ewes (P < 0.001) and ewes treated with P or E alone (P < 0.05). Infusion of PAF followed by or coincident with oxytocin (OT) acted in a synergistic manner to increase plasma PGFM levels. Repeated infusion of PAF into the uterus at 1-h intervals induced tachyphylaxis of the PGFM response to PAF; however, sensitivity of the uterus to PAF returned spontaneously by the 6th h. Interferon-tau (IFN-tau) inhibits pulsatile release of PGF2alpha during pregnancy to prevent luteolysis. Exogenous recombinant ovine IFN-tau (50 microgram) inhibited the uterine response to PAF alone or the combined effects of PAF and OT. These results indicate that uterine PAF fulfills many of the criteria for an endogenous PGF2alpha pulse-generator: steroid induction of PAF production and uterine responsiveness to PAF-induced release of PGF; synergistic stimulation of PAF-induced PGF release by OT; inhibition of PAF effects by IFN-tau; and PAF's ability to induce pulses of PGF with a periodicity during a period of chronic exposure of the uterus to PAF.  (+info)

Molecular analysis of an unstable genomic region at chromosome band 11q23 reveals a disruption of the gene encoding the alpha2 subunit of platelet-activating factor acetylhydrolase (Pafah1a2) in human lymphoma. (7/562)

A region of 150 kb has been analysed around a previously isolated, lymphoma associated, translocation breakpoint located at chromosome band 11q23. This balanced and reciprocal translocation, t(11;14)(q32;q23), has been shown to result in the fusion between chromosome 11 specific sequence and the switch gamma4 region of the IGH locus. The LPC gene, encoding a novel proprotein convertase belonging to the furin family, has been identified in this region. In order to characterize further the region surrounding the translocation, we have determined the detailed structure of LPC. Here we show that LPC consists of at least 16 exons covering 25 kb, and that there is a partial duplication, involving mobile genetic elements and containing LPC exons 13-17 in a tail-tail configuration at 65 kb downstream. Since the chromosomal breakpoint lay between these two structures, the intervening region was further analysed and shown to contain at least two unrelated genes. The previously known SM22 gene was localized close to the 3' tail of LPC. Furthermore, we identified the gene encoding the alpha2 subunit of platelet-activating factor acetylhydrolase (Pafah1a2) at the chromosomal breakpoint. The position of another previously identified breakpoint was also located to within the first intron of this gene. Altogether, our results give evidence of a genomic instability of this area of 11q23 and show that Pafah1a2 and not LPC is the gene disrupted by the translocation, suggesting that deregulated Pafah1a2 may have a role in lymphomagenesis.  (+info)

All ApoB-containing lipoproteins induce monocyte chemotaxis and adhesion when minimally modified. Modulation of lipoprotein bioactivity by platelet-activating factor acetylhydrolase. (8/562)

Mildly oxidized LDL has many proinflammatory properties, including the stimulation of monocyte chemotaxis and adhesion, that are important in the development of atherosclerosis. Although ApoB-containing lipoproteins other than LDL may enter the artery wall and undergo oxidation, very little is known regarding their proinflammatory potential. LDL, IDL, VLDL, postprandial remnant particles, and chylomicrons were mildly oxidized by fibroblasts overexpressing 15-lipoxygenase (15-LO) and tested for their ability to stimulate monocyte chemotaxis and adhesion to endothelial cells. When conditioned on 15-LO cells, LDL, IDL, but not VLDL increased monocyte chemotaxis and adhesion approximately 4-fold. Chylomicrons and postprandial remnant particles were also bioactive. Although chylomicrons had a high 18:1/18:2 ratio, similar to that of VLDL, and should presumably be less susceptible to oxidation, they contained (in contrast to VLDL) essentially no platelet-activating factor acetylhydrolase (PAF-AH) activity. Because PAF-AH activity of lipoproteins may be reduced in vivo by oxidation or glycation, LDL, IDL, and VLDL were treated in vitro to reduce PAF-AH activity and then conditioned on 15-lipoxygenase cells. All 3 PAF-AH-depleted lipoproteins, including VLDL, exhibited increased stimulation of monocyte chemotaxis and adhesion. In a similar manner, lipoproteins from Japanese subjects with a deficiency of plasma PAF-AH activity were also markedly more bioactive, and stimulated monocyte adhesion nearly 2-fold compared with lipoproteins from Japanese control subjects with normal plasma PAF-AH. For each lipoprotein, bioactivity resided in the lipid fraction and monocyte adhesion could be blocked by PAF-receptor antagonists. These data suggest that the susceptibility of plasma lipoproteins to develop proinflammatory activity is in part related to their 18:1/18:2 ratio and PAF-AH activity, and that bioactive phospholipids similar to PAF are generated during oxidation of each lipoprotein. Moreover, LDL, IDL, postprandial remnant particles, and chylomicrons and PAF-AH-depleted VLDL all give rise to proinflammatory lipids when mildly oxidized.  (+info)

In this study, we demonstrate the presence of a transacetylase activity in human plasma low-density lipoprotein (LDL) that transfers short-chain fatty acids from platelet-activating factor (PAF) and its close ether- and ester-linked analogues to ether/ester-linked lysophospholipids (lyso-PL). We show evidence that both PAF acetylhydrolase (PAF-AH) and transacetylase activities are inhibited to the same extent by serine esterase inhibitors, are resistant to heat treatment, and exhibit identical distributions in lipoprotein classes and in LDL subfractions. Additionally, the competitive inhibition of PAF-AH by lyso-PL, and the evidence that the recombinant PAF-AH also showed a similar transacetylase activity, suggest that PAF-AH is responsible for both activities. Using PAF as a donor molecule and lyso-PAF (1-O-alkyl-sn-glycero-3-phosphocholine) as an acceptor, the transacetylase activity showed typical allosteric kinetics, due to the positive co-operativity of the substrates, with apparent Vmax = ...
Lipoprotein-associated phospholipase A2 (Lp-PLA2) also known as platelet-activating factor acetylhydrolase (PAF-AH) is a phospholipase A2 enzyme that in humans is encoded by the PLA2G7 gene. Lp-PLA2 is a 45-kDa protein of 441 amino acids. It is one of several PAF acetylhydrolases. In the blood it travels mainly with low-density lipoprotein (LDL). Less than 20% is associated with high-density lipoprotein HDL. It is an enzyme produced by inflammatory cells and hydrolyzes oxidized phospholipids in LDL. Lp-PLA2 is platelet-activating factor (PAF) acetylhydrolase (EC 3.1.1.47), a secreted enzyme that catalyzes the degradation of PAF to inactive products by hydrolysis of the acetyl group at the sn-2 position, producing the biologically inactive products LYSO-PAF and acetate. Lp-PLA2 is involved in the development of atherosclerosis, an observation that has prompted interest as a possible therapeutic target (see, e.g. the investigational drug Darapladib). In human atherosclerotic lesions, 2 main ...
Title: The Role of Lipoprotein-Associated Phospholipase A2 (Lp-PLA2) in Cardiovascular Disease. VOLUME: 6 ISSUE: 2. Author(s):Ignatios Ikonomidis, Christos A. Michalakeas, John Lekakis, John Parissis and Maria Anastasiou-Nana. Affiliation:2nd Cardiology Department, University of Athens, Attikon Hospital, Perikleous 19, N. Chalkidona, Athens 14343, Greece.. Keywords:Lp-PLA2, PAF-AH, inflammatory biomarkers, cardiovascular disease. Abstract: Lipoprotein-associated Phospholipase A2 (Lp-PLA2) is an enzyme that belongs to the A2 Phospholipase superfamily and is produced by inflammatory cells that are involved in the process of atherogenesis. Even though there is controversy in current bibliography whether Lp-PLA2 exerts proatherogenic or anti-atherogenic properties, the weight of evidence suggests a pro-atherogenic role for this protein. Lp-PLA2 is detected in human atherosclerotic lesions and elevated Lp-PLA2 levels are associated with an increased risk of cardiovascular events and adverse events in ...
Platelet-activating factor acetylhydrolase 2, cytoplasmic is an enzyme that in humans is encoded by the PAFAH2 gene. It is one of several PAF acetylhydrolases. This gene encodes platelet-activating factor acetylhydrolase isoform 2, a single-subunit intracellular enzyme that catalyzes the removal of the acetyl group at the SN-2 position of platelet-activating factor (identified as 1-O-alkyl-2-acetyl-sn-glyceryl-3-phosphorylcholine). However, this lipase exhibits a broader substrate specificity than simply platelet activating factor. Two other isoforms of intracellular platelet-activating factor acetylhydrolase exist, and both are multi-subunit enzymes. Additionally, there is a single-subunit serum isoform of this enzyme. GRCh38: Ensembl release 89: ENSG00000158006 - Ensembl, May 2017 GRCm38: Ensembl release 89: ENSMUSG00000037366 - Ensembl, May 2017 Human PubMed Reference:. Mouse PubMed Reference:. Hattori K, Adachi H, Matsuzawa A, Yamamoto K, Tsujimoto M, Aoki J, Hattori M, Arai H, Inoue K ...
Πανεπιστήμιο Ιωαννίνων. Ιδρυματικό Αποθετήριο Ολυμπιάς.1999 . Creators: Milionis, H. J.. Contributors: Πανεπιστήμιο Ιωαννίνων. Σχολή Θετικών Επιστημών. Τμήμα Χημείας, Milionis, H. J..Background. Platelet-activating factor (PAF) is a potent inflammatory mediator associated with several physiopathological conditions, including renal diseases. PAF is degraded to the inactive metabolite lyso-PAF by PAF-acetylhydrolase (PAF-AH), which is considered as a potent anti-inflammatory and anti-atherogenic enzyme associated with lipoproteins. In this study, we evaluated the plasma- and lipoprotein(a) [Lp(a)]associated PAF-AH activity in relationship to plasma lipid parameters and Lp(a) isoform size in patients with mild/moderate chronic renal failure (CRF), as well as in hemodialysis (HD) and chronic ambulatory peritoneal dialysis (CAPD) patients. Methods. We studied 74 patients undergoing maintenance HD, 44
1ES9: The functional implications of the dimerization of the catalytic subunits of the mammalian brain platelet-activating factor acetylhydrolase (Ib).
Background and Objectives Darapladib is a lipoprotein-associated phospholipase A2 (Lp-PLA2) inhibitor. This study evaluated the pharmacokinetics, pharmacodynamics and safety of darapladib in healthy Chinese subjects. Methods Twenty-four subjects received darapladib 160 mg orally, approximately 1 hour after a standard breakfast, as a single dose and once daily for 28 days. Non-compartmental methods were used to determine the single and multiple dose pharmacokinetics of darapladib and its metabolite SB-553253. Repeat dose Lp-PLA2 activity and safety were evaluated. Results Systemic exposure (AUC(0-T), Cmax geometric mean (CVb%)) of darapladib was higher after multiple-dosing (519 ng.h/mL (33.3%), 34.4 ng/mL (49.9%)) compared to single-dose administration (153 ng.h/mL (69.0%), 17.9 ng/mL (55.2%). The steady-state accumulation ratio was less than unity (Rs = 0.80), indicating time-dependent pharmacokinetics of darapladib. Darapladib steady-state was reached by Day 14 of once daily dosing. Systemic
1] Sudhir K: Clinical review: Lipoprotein-associated phospholipase A2, a novel inflammatory biomarker and independent risk predictor for cardiovascular disease. J Clin Endocrinol Metab 2005; 90(5):3100-3105. [2] Koenig W, Khuseyinova N, Lowel H, et al: Lipoprotein-associated phospholipase A2 adds to risk prediction of incident coronary events by C-reactive protein in apparently healthy middle-aged men from the general population: results from the 14-year follow-up of a large cohort from southern Germany. Circulation 2004; 110(14):1903-1908. [3] Ballantyne CM, Hoogeveen RC, Bang H, et al: Lipoprotein-associated phospholipase A2, high-sensitivity C-reactive protein, and risk for incident coronary heart disease in middle-aged men and women in the Atherosclerosis Risk in Communities (ARIC) study. Circulation 2004; 109(7):837-842. [4] Brilakis ES, McConnell JP, Lennon RJ, et al: Association of lipoprotein-associated phospholipase A2 levels with coronary artery disease risk factors, angiographic ...
Background This study sought to determine the relation between and discriminative capability of lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) and coronary heart disease (CHD) in a large population of disease-free women.Methods Among participants of the Nurses Health Study who provided a blood sample, there were 421 cases of incident myocardial infarction during 14 years of follow-up. Controls were matched to cases 2:1 using risk set sampling based on age, smoking, and blood draw date.Results After conditioning on the matching factors, Lp-PLA(2) activity was significantly associated with myocardial infarction (relative risk [RR] 2.86 for extreme quartiles, 95% CI 1.98-4.12). Upon additional adjustment for lipid, inflammatory, and clinical risk factors, the RR remained statistically significant (RR 1.75, 95% CI 1.09-2.84). The discriminative capability of Lp-PLA(2) was assessed by comparing the area below the receiver operating characteristic curves for models with and without Lp-PLA(2) ...
AIMS: Lipoprotein-associated phospholipase A2 (Lp-PLA2) generates proinflammatory and proatherogenic compounds in the arterial vascular wall and is a potential therapeutic target in coronary heart disease (CHD). We searched for genetic loci related to Lp-PLA2 mass or activity by a genome-wide association study as part of the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Consortium. METHODS AND RESULTS: In meta-analyses of findings from five population-based studies, comprising 13 664 subjects, variants at two loci (PLA2G7, CETP) were associated with Lp-PLA2 mass. The strongest signal was at rs1805017 in PLA2G7 [P = 2.4 × 10(-23), log Lp-PLA2 difference per allele (beta): 0.043]. Variants at six loci were associated with Lp-PLA2 activity (PLA2G7, APOC1, CELSR2, LDL, ZNF259, SCARB1), among which the strongest signals were at rs4420638, near the APOE-APOC1-APOC4-APOC2 cluster [P = 4.9 × 10(-30); log Lp-PLA2 difference per allele (beta): -0.054]. There were no significant gene
To the Editor:. Previous reports have demonstrated that lipoprotein-associated phospholipase A2 (Lp-PLA2), an enzymatic inflammatory biomarker, is associated with increased risk of cardiovascular events (1). Lp-PLA2 mediates formation of bioactive mediators (lysophosphatidyl choline and oxidized nonesterified fatty acids) known to elicit several deleterious inflammatory responses involved in the pathobiology of atherosclerosis. Lysophosphatidyl choline serves as a potent chemoattractant for monocytes, resulting in foam cell accumulation within the arterial wall. Additionally, Lp-PLA2 has been detected in rupture-prone and ruptured atherosclerotic plaques. Taken together, the data suggests that inhibition of Lp-PLA2 may attenuate intimal macrophage accumulation and consequently stabilize atherosclerotic plaque.. Positron emission tomography (PET) imaging with 18F-fluorodeoxyglucose (FDG) is a validated imaging technique widely used to quantify vascular inflammation within atheroma. In vivo ...
Objective. Lipoprotein-associated phospholipase A2 (Lp-PLA2), a marker of vascular inflammation, is associated with cardiovascular disease. This prospective study of an inception cohort aimed to investigate whether the level of Lp-PLA2 is associated with subclinical atherosclerosis in patients with rheumatoid arthritis (RA). Methods. Patients from northern Sweden diagnosed with early RA were consecutively recruited into an ongoing prospective study. From these, all patients ,= 60 years (n = 71) were included for measurements of subclinical atherosclerosis at inclusion (T0) and five years later (T5). Forty age-and sex-matched controls were included. The patients were clinically assessed, SCORE, Reynolds Risk Score, and Larsen score were calculated, and blood samples were drawn from all individuals at T0 and T5. Results. There was no significant difference in the level of Lp-PLA2 between patients with RA and controls (p , 0.05). In simple linear regression models among patients with RA, Lp-PLA2 at ...
AIMS: To identify factors that influence plasma levels and assess the prognostic value of lipoprotein-associated phospholipase A2 (Lp-PLA2) activity in a prospective, population-based survey of the epidemiology and pathogenesis of atherosclerosis.. METHODS AND RESULTS: The Bruneck study is a prospective, population-based survey initiated in 1990. Lp-PLA2 activity and baseline variables for the current analysis were measured in 765 subjects aged 45-84 years in 1995. Incident cardiovascular disease (CVD) (cardiovascular death, myocardial infarction, stroke, and transient ischaemic attack) and rates of non-CVD mortality were assessed between 1995 and 2005. Subjects with incident CVD had higher levels of Lp-PLA2 activity (884 +/- 196 vs. 771 +/- 192 micromol/min/L, P , 0.001). Increased Lp-PLA2 activity was significantly related to incident CVD [age- and sex-adjusted hazard ratio (95%CI) 2.9 (1.6-5.5); third vs. first tertile group; P , 0.001] and with vascular mortality but not with non-CVD ...
Purpose: : Lipoprotein-associated phospholipase A2 (Lp-PLA2) plays a major role in macrophage infiltration, pro-inflammatory cytokine expression and adhesion molecule upregulation in macrovascular disease. Since diabetic macular edema (DME) is recognised to have an inflammation-linked aetiology it was hypothesized that inhibition of this enzyme could be protective against blood retinal barrier (BRB) breakdown. Methods: : Localization of Lp-PLA2 in human retina was analyzed by immunohistology. In parallel, brown Norwegian (BN) rats had diabetes induced using streptozotocin (65mg/Kg). After 4 weeks hyperglycemia, animals were treated for 4 weeks with either vehicle or SB435495 (a specific inhibitor of Lp-PLA2)(10mg/Kg/day) by intra-peritoneal injection. An additional group of hyperglycemic animals were maintained treatment free for 4 weeks prior to initiating the 4 wk treatment regimen. An age and sex-matched group of non-diabetic NDb) BN rats were used as controls. Following drug treatment, BRB ...
A Lipoprotein-associated phospholipase A2 test is used to assess risk for heart disease. Request A Tests convenient, affordable lab testing makes it easy to take charge of your own health.
|i|Background:|/i| Whether lipoprotein-associated phospholipase A2 (Lp-PLA2) levels are associated with kidney function decline has not been well studied. |i|Me
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1FXW: Preparation and crystal structure of the recombinant alpha(1)/alpha(2) catalytic heterodimer of bovine brain platelet-activating factor acetylhydrolase Ib.
The present study compares for the first time the effect of 3 hypolipidemic drugs (ezetimibe, rosuvastatin, fenofibrate), which exert their action through different mechanisms, on plasma Lp-PLA2 activity and mass. All drugs reduce Lp-PLA2 activity and mass associated with the atherogenic apoB-containing lipoproteins. Furthermore, fenofibrate increases the specific activity of the enzyme associated with these lipoproteins and specifically that of the most atherogenic dense LDL-5 subfraction.. Fenofibrate reduces Lp-PLA2 activity and mass associated with apoB-containing lipoproteins, an effect that could be mainly attributed to the preferential reduction of the enzyme associated with LDL-5 particles,24 ie, those particles carrying the majority of LDL-associated enzyme.2,6 In accordance with our previously published results,24 the present study shows that the above reduction is attributed to the fenofibrate action to decrease sdLDL and to increase large buoyant LDL particles, which have a higher ...
Lipoprotein-associated phospholipase A2 (Lp-PLA2), specifically Group VIIA PLA2, is an associate from the phospholipase A2 superfamily and is available mainly connected with LDL and HDL in individual plasma. apoproteins Xarelto in HDL, and also, residues 360C368 are just suffering from HDL.The full total results claim that apoA-I and phospholipid membranes play crucial roles in Lp-PLA2 localization to HDL. 14: 2032C2039. [PubMed] 20. Okamura K., Miura S., Zhang B., Uehara Y., Matsuo K., Kumagai K., Saku K.2007. Proportion of LDL- to HDL-associated platelet-activating aspect acetylhydrolase could be a marker of irritation in sufferers with paroxysmal atrial fibrillation. Circ. J.71: 214C219. [PubMed] 21. Tsimihodimos V., Karabina S. A., Tambaki A. P., Bairaktari E., Miltiadous G., Goudevenos J. A., Cariolou M. A., Chapman M. J., Tselepis A. D., Elisaf M. 2002. Changed distribution of platelet-activating aspect- acetylhydrolase activity between LDL and HDL being a function of the severe nature of ...
Objective: The current assumption is that the majority of the pro-oxidant enzyme Lipoprotein-Associated Phospholipase A2 (LpPLA2) resides on LDL-C, however the actual distribution of LpPLA2 on lipoproteins is unknown. We sought to determine the distribution of LpPLA2 mass and activity on different lipoproteins and the association with progression of coronary artery calcification (CAC).. Methods: From the Coronary Artery Calcification in Type 1 Diabetics (CACTI) study, we chose men with type 1 diabetes (not on statins, HDL-C in the 95th percentile by diabetes status) with and without CAC progression and matched controls (n=45). Lipoproteins were separated by Fast Protein Liquid Chromatography (FPLC). Individual samples of total plasma and pooled subfractions of LDL and HDL underwent LpPLA2 mass (PLAC) assays to measure accessible LpPLA2 mass on the surface of lipoprotein particles and activity (CAM) assays to measure total LpPLA2 activity dissociating from lipoprotein particles under denaturing ...
BACKGROUND: Both increased lipoprotein-associated phospholipase A2 (Lp-PLA2) concentrations and atherogenic lipoprotein subfractions have been shown to reflect unfavourable cardiovascular risk. However, the correlation between Lp-PLA2 and lipoprotein subfractions in patients with coronary artery disease (CAD) has not been assessed yet.. METHODS: A total of 324 consecutive subjects who were not treated with lipid-lowering drugs were enrolled (angiographically proven CAD: n = 253; non-CAD: n = 71). Plasma Lp-PLA2 concentrations were measured using ELISA. The low-density lipoprotein (LDL) and high-density lipoprotein (HDL) subfractions were determined by Lipoprint System.. RESULTS: Plasma Lp-PLA2 concentrations were higher in patients with CAD compared with those without CAD (153.61 ± 78.73 vs. 131.41 ± 65.49 ng/ml, p = 0.028). The univariable correlation analysis revealed that Lp-PLA2 concentrations were positively correlated with the cholesterol concentrations of each LDL subfractions and the ...
PAFAH1B2 - PAFAH1B2 (GFP-tagged) - Human platelet-activating factor acetylhydrolase 1b, catalytic subunit 2 (30kDa) (PAFAH1B2), transcript variant 1 available for purchase from OriGene - Your Gene Company.
Pafah1b2 - Pafah1b2 (untagged) - Mouse platelet-activating factor acetylhydrolase, isoform 1b, subunit 2 (Pafah1b2), (10ug) available for purchase from OriGene - Your Gene Company.
The main goal of AIM III is to assess and quantify the effect of long-term administration of darapladib 160 mg once a day, a selective, reversible, orally active inhibitor of plasma and vascular Lp-PLA2, on coronary endothelial function, progression of coronary atherosclerosis as determined by intravascular ultrasound (IVUS), and atherosclerosis in patients with early atherosclerosis. Patients with evidence of coronary endothelial dysfunction, as determined by intracoronary administration of acetylcholine during angiography and IVUS, will be followed for 6 months during once daily dosing of darapladib. Coronary endothelial function is determined by the changes in coronary artery diameter and coronary blood flow response to the intracoronary administration of acetylcholine and adenosine. The patients will be followed in clinic 6 months. They will have follow-up angiography, assessment of endothelial function, and IVUS during the six month visit ...
Inflammation is increasingly recognized to play an important role in atherosclerosis and stroke.1,15 Macrophages, cytokines, and leukocyte adhesion molecules contribute to vascular injury, endothelial dysfunction, plaque formation, plaque rupture, and coagulopathy.16 Because of this, serum levels of inflammatory biomarkers such as hsCRP, an acute phase protein, have been used as nonspecific measures of vascular inflammation. Lp-PLA2 is an enzyme derived from leukocytes, particularly macrophages, that is involved in metabolism of LDL to the proinflammatory mediators lysophosphatidylcholine and oxidized fatty acids.3,11 Lysophosphatidylcholine increases expression of vascular adhesion molecules, upregulates cytokines and CD40 ligand, and stimulates macrophage proliferation.. Our findings provide evidence that hsCRP and LpPLA2 activity levels are stable when repeated annually. Our findings are similar to findings of stability for hsCRP from other populations.17,18 In one study among patients with ...
In the present study of older community-dwelling individuals, Lp-PLA2 levels were significantly higher in those who developed CHD compared with those who did not. Associations between Lp-PLA2 and LDL, HDL, total cholesterol, and triglycerides were especially strong, and the magnitude of the correlations was in good agreement with previous studies (7,19). Despite these associations, Lp-PLA2 remained a strong and independent predictor of fatal and nonfatal CHD events, over and above these and other traditional risk factors. Thus, Lp-PLA2 added information to lipid and lipoprotein prediction of future CHD and may identify subpopulations at risk for CHD who would not be identified otherwise.. A similar independent association of Lp-PLA2 with CHD risk was reported in the younger participants from the WOSCOPS (5) and ARIC (7,19) studies and in a nested case-control study from the Rotterdam study (9). We now confirm these results for the first time in a cohort of apparently healthy older men and women ...
sPLA2 [odds ratio 1.23 for 1 standard deviation (SD) increase, p = 0.007], but not Lp-PLA2 (p = 0.26), activity was related to carotid atherosclerosis and to the amount of stenosis by WBMRA (p = 0.006) following adjustment for multiple risk factors. sPLA2 [hazard ratio (HR) 1.45 for 1 SD increase, p = 0.001], but not Lp-PLA2 (HR, 0.95; p = 0.55), activity was a significant risk factor for all-cause mortality during 7.0 years follow-up after adjustment for other risk factors. In a sample of 1,029 post-MI patients, sPLA2 (adjusted HR 1.32 for 1 unit increase, p = 0.036), but not Lp-PLA2 (HR, 1.03; p = 0.90), activity predicted death or recurrent MI during 1-year follow-up.. ...
This test looks for a specific lipoprotein, Lp-PLA2, in your blood. The test is used to help predict your risk for cardiovascular disease and stroke.
This test looks for a specific lipoprotein, Lp-PLA2, in your blood. The test is used to help predict your risk for cardiovascular disease and stroke.
This test looks for a specific lipoprotein, Lp-PLA2, in your blood. The test is used to help predict your risk for cardiovascular disease and stroke.
This test looks for a specific lipoprotein, Lp-PLA2, in your blood. The test is used to help predict your risk for cardiovascular disease and stroke.
This test looks for a specific lipoprotein, Lp-PLA2, in your blood. The test is used to help predict your risk for cardiovascular disease and stroke.
This test looks for a specific lipoprotein, Lp-PLA2, in your blood. The test is used to help predict your risk for cardiovascular disease and stroke.
This test looks for a specific lipoprotein, Lp-PLA2, in your blood. The test is used to help predict your risk for cardiovascular disease and stroke.
This test looks for a specific lipoprotein, Lp-PLA2, in your blood. The test is used to help predict your risk for cardiovascular disease and stroke.
This test looks for a specific lipoprotein, Lp-PLA2, in your blood. The test is used to help predict your risk for cardiovascular disease and stroke.
This test looks for a specific lipoprotein, Lp-PLA2, in your blood. The test is used to help predict your risk for cardiovascular disease and stroke.
Journal of Diabetes Research is a peer-reviewed, Open Access journal that publishes research articles, review articles, and clinical studies related to type 1 and type 2 diabetes. The journal welcomes submissions focusing on the epidemiology, etiology, pathogenesis, management, and prevention of diabetes, as well as associated complications, such as diabetic retinopathy, neuropathy and nephropathy.
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Each laboratory should check if the reference ranges are transferable to its own patient population and determine own reference ranges if necessary. For diagnostic purposes, the results should always be assessed with the patients medical history, clinical examinations and other findings ...
Create a standard curve by reducing the data using computer software capable of generating a four parameter logistic (4-PL) curve-fit. As an alternative, construct a standard curve by plotting the mean absorbance for each standard on the x-axis against the concentration on the y-axis and draw a best fit curve through the points on the graph. The data may be linearized by plotting the log of the PLA2G7 concentrations versus the log of the O.D. and the best fit line can be determined by regression analysis. This procedure will produce an adequate but less precise fit of the data ...
Alyssa Frank is a Marketing Associate at Mayo Medical Laboratories. She supports marketing strategies for product management and specialty testing. Alyssa has worked at Mayo Clinic since 2015 ...
Definition : Immunoassay reagents intended to perform quantitative analyses of body fluids (typically plasma or serum) to determine the level of the lipoprotein-associated enzyme phospholipase A2 (Lp-PLA2). These tests are usually based on turbidimetric or ELISA tests that use specific antibodies to identify the level of (Lp-PLA2). They may be used as an aid to assess vascular inflammation and the risk for coronary heart disease and ischemic stroke associated with atherosclerosis.. Entry Terms : Lipoprotein-Associated Phospholipase A2 Determination Reagents , Lp-PLA2 Determination Reagents , PLAC Test ELISA Kits , PLAC Test Reagent Kits. UMDC code : 32900 ...
Summary There is increasing evidence that lipoprotein-associated phospholipase A2 (LpPLA2) is associated with cardiovascular disease. However, it is still unclear whether LpPLA2 is simply a marker or has a causal role as either a pro- or anti-atherogenic factor. We analyzed the association of five...
Academic Journals Database is a universal index of periodical literature covering basic research from all fields of knowledge, and is particularly strong in medical research, humanities and social sciences. Full-text from most of the articles is available. Academic Journals Database contains complete bibliographic citations, precise indexing, and informative abstracts for papers from a wide range of periodicals.
In patients who experienced an acute coronary syndrome event -- such as heart attack or unstable angina -- use of the drug darapladib to inhibit the enzyme lipoprotein-associated phospholipase A2 -- believed to play a role in the development of atherosclerosis -- did not reduce the risk of recurrent major coronary events, according to a study published by JAMA. The study is being released early online to coincide with its presentation at the European Society of Cardiology Congress.
Пппп Page 20 пппп12 Ch. Efectos proscar alopecia Targeted disruption of intracellular type I platelet activating factor-acetylhydrolase catalytic subunits causes severe impairment in sperm- atogenesis. Efec tos Ideally, all children with CNS tumours undergoing aloecia.
In this study, 421 individuals who were blood related to and/or living with a person recently hospitalized due to cardiovascular disease were screened for traditional cardiovascular risk factors (such as elevated blood pressure and abnormal cholesterol levels), inflammatory markers associated with disease risk (high-sensitivity c-reactive protein (hsCRP) and lipoprotein-associated phospholipase A2 (Lp-PLA2)). They were also asked standardized questions about their oral health status, including whether they had ever been diagnosed with periodontal (gum) disease, whether they had ever been treated for periodontal disease, whether they used partial or complete removable dentures, and the date of their last teeth cleaning. The oral health history was then correlated with standard markers of inflammation ...
TY - JOUR. T1 - Corrigendum to Lipoprotein-associated phospholipase A2 is related to risk of subclinical atherosclerosis but is not supported by Mendelian randomization analysis in a general Japanese population. [Atherosclerosis 246 (March 2016) 141-147](S0021915015302562)(10.1016/j.atherosclerosis.2015.12.027). AU - the ACCESS and SESSA Research Groups. AU - Ueshima, Hirotsugu. AU - Kadowaki, Takashi. AU - Hisamatsu, Takashi. AU - Fujiyoshi, Akira. AU - Miura, Katsuyuki. AU - Ohkubo, Takayoshi. AU - Sekikawa, Akira. AU - Kadota, Aya. AU - Kadowaki, Sayaka. AU - Nakamura, Yasuyuki. AU - Miyagawa, Naoko. AU - Okamura, Tomonori. AU - Kita, Yoshikuni. AU - Takashima, Naoyuki. AU - Kashiwagi, Atsunori. AU - Maegawa, Hiroshi. AU - Horie, Minoru. AU - Yamamoto, Takashi. AU - Kimura, Takeshi. AU - Kita, Toru. N1 - Publisher Copyright: © 2015 Elsevier B.V.. PY - 2018/11. Y1 - 2018/11. N2 - The authors of the above paper have realized that an error has occurred in the number of eligible individuals ...
Methods: Forty chronic periodontitis (CP) subjects with hyperlipidaemia (CP/HPL group), 40 systemically healthy CP subjects (CP group) and 20 systemically and periodontally healthy subjects (control group) were enrolled. The clinical periodontal parameters, the serum concentrations of Lp-PLA2, lipid profiles including total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-c), low-density lipoprotein cholesterol (LDL-c) and white blood cell (WBC) counts were determined and compared between different groups. Linear regression analysis was performed to identify the contributing factors of Lp-PLA2 ...
This test looks for a specific lipoprotein, Lp-PLA2, in your blood. The test is used to help predict your risk for cardiovascular disease and stroke.
Platelet-activating factor is a potent mediator of inflammation, which has untoward effects on cerebrovascular and neural elements. While several investigators have reported attenuation of ischemic damage after treatment with antagonists of platelet-activating factor, no study has proved endogenous production of platelet-activating factor in ischemia of the central nervous system. We hypothesized that endogenous production of platelet-activating factor participates in the early pathologic manifestations of deteriorating stroke. In 12 rabbits, we found tissue levels of platelet-activating factor measured by the release of serotonin from washed platelets to be elevated by approximately 20-fold in spinal cord injured by 25 minutes of ischemia and 2 hours of reperfusion (2.80 +/- 0.98 ng/g) compared with that in normal spinal cord (0.15 +/- 0.06 ng/g, p less than 0.01). Given during ischemia to seven rabbits, 10 mg/kg i.p. of a highly selective and potent antagonist of platelet-activating factor (BN ...
The majority of the acute coronary events are caused by coronary artery segments with minimal luminal disease, but with potentially significant vascular wall inflammation and oxidative stress leading to plaque vulnerability. It has become apparent that an initial injury at the endothelial surface, is the primary site of the mechanisms involved and a role for vascular inflammation and the interaction with oxidative stress continues to emerge. Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a novel biomarker for vascular wall inflammation that circulates in the blood bound to both low density (LDL) and high density (HDL) lipoprotein and promotes vascular inflammation. Circulating levels of Lp-PLA2 mass and activity are an independent risk factor for cardiovascular events. Recent studies, demonstrating that Lp-PLA2 is also associated with coronary endothelial dysfunction. However, the relationship between Lp-PLA2 and early atherosclerotic changes in the coronary arteries, and the contribution ...
The omega-3 fatty acid eicosapentaenoic acid (EPA) has multiple actions potentially conferring cardiovascular benefit, including lowering serum triglyceride (TG) and non-high-density lipoprotein cholesterol (non-HDL-C) levels and potentially reducing key steps in atherogenesis. Dietary supplements are a common source of omega-3 fatty acids in the US, but virtually all contain docosahexaenoic acid (DHA) in addition to EPA, and lipid effects differ between DHA and EPA. Contrary to popular belief, no over-the-counter omega-3 products are available in the US, only prescription products and dietary supplements. Among the US prescription omega-3 products, only one contains EPA exclusively (Vascepa); another closely related prescription omega-3 product also contains highly purified EPA, but is approved only in Japan and is provided in different capsule sizes. These high-purity EPA products do not raise low-density lipoprotein cholesterol (LDL-C) levels, even in patients with TG levels |500 mg/dL, in contrast
Recent studies showed that the phospholipase subunits of Platelet Activating Factor Acetylhydrolase (PAFAH) Ib, α1 and α2 partially localize to the Golgi complex and regulate its structure and function. Using siRNA knockdown of individual subunits, we find that α1 and α2 perform overlapping and unique roles in regulating Golgi morphology, assembly, and secretory cargo trafficking. Knockdown of either α1 or α2 reduced secretion of soluble proteins, but neither single knockdown reduced secretion to the same degree as knockdown of both. Knockdown of α1 or α2 inhibited reassembly of an intact Golgi complex to the same extent as knockdown of both. Transport of VSV-G was slowed but at different steps in the secretory pathway: reduction of α1 slowed trans Golgi network to plasma membrane transport, whereas α2 loss reduced endoplasmic reticulum to Golgi trafficking. Similarly, knockdown of either subunit alone disrupted the Golgi complex but with markedly different morphologies. Finally, ...
What is the definition of platelet-activating factor? What is the meaning of platelet-activating factor? How do you use platelet-activating factor in a sentence? What are synonyms for platelet-activating factor?
Proper development of the mammalian cerebral cortex relies on the integrated control of neurogenesis and neuronal migration. Proliferation of neuronal progenitor cells during early stages of brain development is critical to expand the progenitor pool at the ventricular surface and later mitotic divisions result in the generation of postmitotic neural precursors, which then migrate to the cortical plate (Gupta et al., 2002; Götz and Huttner, 2005). Defective neurogenesis or neuronal migration leads to brain malformations, and are often associated with different forms of mental retardation or cognitive disabilities and severe epilepsy Guerrini et al., 2008). For example, classical lissencephaly (or smooth brain) is due to a reduced number or absence of gyri and sulci of the cortical surface, resulting in severe mental retardation, seizures and early death (Kato and Dobyns, 2003). Mutations in two genes, LIS1 (Reiner et al., 1993; Lo Nigro et al., 1997) and DCX (Gleeson et al., 1998; des Portes ...
An increased level of low-density lipoprotein (LDL) is a very well established risk factor of coronary artery disease (CAD). Unoxidized LDL is an inert transport vehicle of cholesterol and other lipids in the body and is thought to be atherogenic. Recently it has been appreciated that oxidized...
In 1963, Miller reported two siblings with a specific pattern of malformations in which lissencephaly was a key feature. Later in 1969, Dieker et al. described a similar condition. Jones et al. in ...
Expression of PAFAH1B1 (LIS1, MDCR, MDS, NudF, PAFAH) in lung tissue. Antibody staining with HPA020036 and CAB004489 in immunohistochemistry.
Human PAFAH1B1 full-length ORF ( AAH64638.1, 1 a.a. - 410 a.a.) recombinant protein with GST-tag at N-terminal. (H00005048-P01) - Products - Abnova
Summary of PAFAH1B3 () expression in human tissue. Cytoplasmic and membranous expression in several tissues, including a subsets of immune cells.
Ischaemiás-reperfusiós károsodások funkcionális és strukturális változásainak kivédése különböző (máj, vékonybél, szabad lebeny, amputatum) experimentalis sebészi modelleken
Jelenleg sem egy rtelm , hogy mi tekinthet a n triumbevitel optim lis szintj nek. A k zlem nyben azt vizsg lt k, vajon a bal kamra longitudin lis deform l d sa (longitudinal strain - LS), circumferenci lis deform l d sa s az e′ sebess g alapj n van-e a becs lt n triumbevitelnek (e...
A Willis-körök morfológiai analízisét végeztük nem stroke-os betegpopulációban. A száztíz eltávolított Willis-körből huszonöt esetben (22,7%) találtunk inkomplett kört, vagyis olyan rendszert, mikor egy vagy több ér hiánya, vagy eltérő lefutása miatt az ív nem zárult be. A teljesnek Willis-köröknek leírtuk az anatómiai variációit, ahol valamelyik ér rendellenes helyen szájazott vagy duplikációk voltak fellelhetőek. Ezek a variációk nyilvánvalóan nem befolyásolták a kollaterális kapacitást, minthogy mindegyik esetben teljes körről volt szó. Megállapítottuk az egyes érszegmentumok átlagos átmérőit, hosszát valamint összehasonlítottuk a páros erek esetén a két oldal átmérőit is. Matematikai keringés-élettani modellt alkalmaztunk a Willis-köri kollaterálisok funkcionális képességének vizsgálatára. A prémortem készült színkódolt transcranialis Doppler vizsgálatok eredményei alapján osztályoztuk a Willis-köri ...
Lis information about active ingredients, pharmaceutical forms and doses by Lisapharma, Lis indications, usages and related health products lists
QUICK FIX BLISTER Univerzális pillanatragasztó - cianoakrilát 3 g, .cs95E872D0{text-align:left;text-indent:0pt;margin:0pt 0pt 0pt 0pt} .cs1B16EEB5{color:#
A gasztrointsztinális, más néven gyomorbél-traktust a szájüreg, a garat, a nyelőcső, a gyomor, valamint a vékony- és vastagbél alkotja. A gyomorbél-tr...
Tämä sivusto käyttää evästeitä analytiikkaan sekä mukautetun sisällön ja mainosten näyttämiseen. Jatkamalla sivuston käyttöä hyväksyt tällaisen käytön. Lisätietoja ...
... naphthol as d esterase MeSH D08.811.277.352.100.680 - phospholipases MeSH D08.811.277.352.100.680.510 - lysophospholipase MeSH ... cholesterol esterase MeSH D08.811.277.352.100.170 - cholinesterases MeSH D08.811.277.352.100.170.176 - acetylcholinesterase ... endo-1,4-beta xylanases MeSH D08.811.277.450.950.500 - xylan endo-1,3-beta-xylosidase MeSH D08.811.277.656.149 - atp-dependent ... glucan 1,4-beta-glucosidase MeSH D08.811.277.450.420.200.600 - glucan endo-1,3-beta-d-glucosidase MeSH D08.811.277.450.420.375 ...
256 (1): 175-8. PMID 7451433. PAF+acetylhydrolase at the US National Library of Medicine Medical Subject Headings (MeSH) EC 3.1 ... In enzymology, a 1-alkyl-2-acetylglycerophosphocholine esterase (EC 3.1.1.47) is an enzyme that catalyzes the chemical reaction ... The systematic name of this enzyme class is 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine acetohydrolase. Other names in common ... Blank ML, Lee T, Fitzgerald V, Snyder F (1981). "A specific acetylhydrolase for 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine (a ...
... acetylxylan esterase EC 3.1.1.73: feruloyl esterase EC 3.1.1.74: cutinase EC 3.1.1.75: poly(3-hydroxybutyrate) depolymerase EC ... polyneuridine-aldehyde esterase EC 3.1.1.79: hormone-sensitive lipase EC 3.1.1.80: acetylajmaline esterase EC 3.1.1.81: quorum- ... methyl ester esterase EC 3.1.1.86: rhamnogalacturonan acetylesterase EC 3.1.1.87: fumonisin B1 esterase EC 3.1.1.88: pyrethroid ... alpha-amino-acid esterase EC 3.1.1.44: 4-methyloxaloacetate esterase EC 3.1.1.45: carboxymethylenebutenolidase EC 3.1.1.46: ...
256 (1): 175-8. PMID 7451433. PAF+acetylhydrolase at the US National Library of Medicine Medical Subject Headings (MeSH) EC 3.1 ... In enzymology, a 1-alkyl-2-acetylglycerophosphocholine esterase (EC 3.1.1.47) is an enzyme that catalyzes the chemical reaction ... The systematic name of this enzyme class is 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine acetohydrolase. Other names in common ... Blank ML, Lee T, Fitzgerald V, Snyder F (1981). "A specific acetylhydrolase for 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine (a ...
Yashashwi Pokharel 1 , Wensheng Sun 2 , Linda M Polfus 3 , Aaron R Folsom 4 , Gerardo Heiss 5 , A Richey Sharrett 6 , Eric ... 2015 Aug;241(2):641-8. doi: 10.1016/j.atherosclerosis.2015.06.033. Epub 2015 Jun 18. ... 1 Section of Cardiovascular Research, Department of Medicine, Baylor College of Medicine, Houston, TX, USA; Center for ... 2 Section of Cardiovascular Research, Department of Medicine, Baylor College of Medicine, Houston, TX, USA. Electronic address ...
M Niethammer 1 , D S Smith, R Ayala, J Peng, J Ko, M S Lee, M Morabito, L H Tsai ... DOI: 10.1016/s0896-6273(00)00147-1 Abstract Disruption of one allele of the LIS1 gene causes a severe developmental brain ... 1 Department of Pathology, Harvard Medical School, 200 Longwood Avenue, Boston, Massachussetts 02115, USA. ...
Has a marked selectivity for phospholipids with short acyl chains at the sn-2 position. May share a common physiologic function ... Belongs to the serine esterase family.Curated. Phylogenomic databases. evolutionary genealogy of genes: Non-supervised ... O-alkyl-2-acetyl-sn-glycero-3-phosphocholine*Search proteins in UniProtKB for this molecule. ... O-alkyl-2-acetyl-sn-glycero-3-phosphocholine*Search proteins in UniProtKB for this molecule. ...
NTERA-2. PC-3. REH. RH-30. RPMI-8226. RPTEC TERT1. RT4. SCLC-21H. SH-SY5Y. SiHa. SK-BR-3. SK-MEL-30. T-47d. THP-1. TIME. U-138 ... NTERA-2. PC-3. REH. RH-30. RPMI-8226. RPTEC TERT1. RT4. SCLC-21H. SH-SY5Y. SiHa. SK-BR-3. SK-MEL-30. T-47d. THP-1. TIME. U-138 ... CACO-2. CAPAN-2. Daudi. EFO-21. FHDF/TERT166. HaCaT. HAP1. HBEC3-KT. HBF TERT88. HDLM-2. HEK 293. HEL. HeLa. Hep G2. HHSteC. HL ... CACO-2. CAPAN-2. Daudi. EFO-21. FHDF/TERT166. HaCaT. HAP1. HBEC3-KT. HBF TERT88. HDLM-2. HEK 293. HEL. HeLa. Hep G2. HHSteC. HL ...
2004 Apr 1;428(6982):529-35. [PubMed:15057824 ] *Adachi H, Tsujimoto M, Hattori M, Arai H, Inoue K: cDNA cloning of human ... 2-Acetyl-1-alkyl-sn-glycero-3-phosphocholine + Water → 1-Organyl-2-lyso-sn-glycero-3-phosphocholine + Acetic acid. details ... 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine + Water → 1-alkyl-sn-glycero-3-phosphocholine + Acetic acid. details ... Inactivates paf by removing the acetyl group at the sn-2 position. This is a catalytic subunit. Plays an important role during ...
SSF53774, SSF53774, 1 hit. PROSITEi. View protein in PROSITE. PS00917, ASN_GLN_ASE_2, 1 hit. PS51732, ASN_GLN_ASE_3, 1 ... 3.40.50.1170, 1 hit. InterProi. View protein in InterPro. IPR036152, Asp/glu_Ase-like_sf. IPR006034, Asparaginase/ ... H0YHG5-1 [UniParc]FASTAAdd to basketAdded to basket. « Hide. 10 20 30 40 50. XPASRNQRIL YTVLECQPLF DSSDMTIAEW VCLAQTIKRH ... Annotation score:1 out of 5. ,p>The annotation score provides a heuristic measure of the annotation content of a UniProtKB ...
Exhibits also esterase activity toward p-nitrophenyl. May act on the brush border membrane to facilitate the absorption of ... InChI=1S/C18H38NO7P/c1-5-6-7-8-9-10-11-12-18(21)24-15-17(20)16-26-27(22,23)25-14-13-19(2,3)4/h17,20H,5-16H2,1-4H3/p+1/t17-/m1/ ... 1. Cytosolic phospholipase A2. General function:. Involved in metabolic process. Specific function:. Selectively hydrolyzes ... 2. Eosinophil lysophospholipase. General function:. Involved in sugar binding. Specific function:. May have both ...
2. FANTOM5 Ensembl ENCODE CraniofacialAtlas 10.6. +288.6. 288617. 4.3. SP1 PRDM10 ZNF629 RFX1 ZNF692 POLR2A BACH1 ETV6 LARP7 ... ABHD4 ENSG00000275552 lnc-ABHD4-1 NGDN PRMT5 ACIN1 LOC102724814 SLC7A8 C14orf93 MMP14 ... DAD1 lnc-OR6J1-2 ACIN1 RBM23 LOC102724814 MMP14 NGDN ABHD4 C14orf93 PABPN1 ... 1-(1-Enyl-stearoyl)-2-arachidonoyl-sn-glycero-3-phosphoethanolamine. *1-(1Z-Octadecenyl)-2-(5Z,8Z,11Z,14Z-eicosatetraenoyl)-sn- ...
EC 3.1.1.43: a-amino-acid esterase * EC 3.1.1.44: 4-methyloxaloacetate esterase ... EC 3.3.2.8: limonene-1,2-epoxide hydrolase EC 3.4: act on peptide bonds - Peptidase. 3.4.1. * EC 3.4.1.1: leucine ... 2 EC 3.2: Glycosylases *2.1 EC 3.2.1: Glycosidases, i.e. enzymes hydrolysing O- and S-glycosyl compounds ... EC 3.2.1: Glycosidases, i.e. enzymes hydrolysing O- and S-glycosyl compounds. * EC 3.2.1.1: α-amylase ...
Kim, J., Choi, J., Kwon, S. Y., McEvoy, J. W., Blaha, M., Blumenthal, R. S., Guallar, E., Zhao, D. & Michos, E. D., Jul 1 2018 ... Zhao, D., Guallar, E. & Michos, E. D., Oct 16 2018, In : Journal of the American College of Cardiology. 72, 16, 1 p.. Research ... Zhao, D., Guallar, E., Bowie, J., Swenor, B., Gajwani, P., Kanwar, N. & Friedman, D. S., Apr 1 2018, In : American Journal of ... Awotoye, J., Fashanu, O. E., Lutsey, P. L., Zhao, D., ONeal, W. T. & Michos, E. D., Feb 20 2020, In : Open Heart. 7, 1, ...
Hu, E. A., Steffen, L. M., Grams, M., Crews, D., Coresh, J., Appel, L. & Rebholz, C., Sep 1 2019, In : The American journal of ... Hu, E. A., Steffen, L. M., Coresh, J., Appel, L. J. & Rebholz, C. M., Feb 1 2020, In : The Journal of nutrition. 150, 2, p. 312 ... Wong, E., Ballew, S., Daya, N., Ishigami, J., Rebholz, C., Matsushita, K., Grams, M. & Coresh, J., Jan 1 2019, In : American ... Hu, E. A., Lazo-Elizondo, M., Rosenberg, S. D., Grams, M., Steffen, L. M., Coresh, J. & Rebholz, C., Jan 1 2019, In : Journal ...
Keywords: 1-Alkyl-2-acetylglycerophosphocholine Esterase, Alleles, Blood Pressure, Cholesterol, Cooperative Behavior, Coronary ... Darapladib is a potent and reversible oral inhibitor of Lp-PLA2.6 Darapladib has been shown to reduce levels of Lp-PLA2 in ... Figure 1: Kaplan-Meier curves for the primary end point of death from cardiovascular causes, myocardial infarction, or stroke ( ... Figure 2: Cumulative Kaplan-Meier estimates of the secondary end point of major coronary events (a composite of death from ...
... naphthol as d esterase MeSH D08.811.277.352.100.680 - phospholipases MeSH D08.811.277.352.100.680.510 - lysophospholipase MeSH ... cholesterol esterase MeSH D08.811.277.352.100.170 - cholinesterases MeSH D08.811.277.352.100.170.176 - acetylcholinesterase ... endo-1,4-beta xylanases MeSH D08.811.277.450.950.500 - xylan endo-1,3-beta-xylosidase MeSH D08.811.277.656.149 - atp-dependent ... glucan 1,4-beta-glucosidase MeSH D08.811.277.450.420.200.600 - glucan endo-1,3-beta-d-glucosidase MeSH D08.811.277.450.420.375 ...
2-acetyl-1-alkylglycerophosphocholine esterase, EC 3.1.1, EC 3.1.1.47,1-alkyl-2-acetylglycerophosphocholine esterase, Group- ... Produced in rabbits immunized with purified, recombinant PLA2G7/PAF-AH/Lp-PLA2 (Q13093-1; Met1-Asn441).. ... PAFAHPAF 2-acylhydrolase, phospholipase A2, group VII (platelet-activating factor acetylhydrolase, plasma), platelet-activating ... VIIA phospholipase A2, gVIIA-PLA2, LDL-associated phospholipase A2, LDL-PLA(2), LDL-PLA2, lipoprotein-associated phospholipase ...
LIS-1 is homologous to the fungal genes NudF and PAC1, which are involved in cytoplasmic dynein mediated nuclear transport, but ... Overexpression of LIS-1 interferes with cell division, with noteworthy effects on chromosome attachment to the mitotic spindle ... Together, these results suggest a role for LIS-1 in cytoplasmic dynein functions involving microtubule plus-ends. Furthermore, ... Recent evidence has implicated the human LIS-1 gene in Miller-Dieker lissencephaly and isolated lissencephaly sequence. ...
TY - JOUR. T1 - Assessment of clinical performance without adequate analytical validation. T2 - A prescription for confusion. AU - Oliver, Lawrence K.. AU - Voskoboev, Nikolay. AU - Heser, Don. AU - McConnell, Joseph P.. AU - Hodel-Hanson, Shannon. AU - Callanan, Heidi. AU - Jaffe, Allan S. PY - 2011/10. Y1 - 2011/10. N2 - Objectives: Lp-PLA2 is a biomarker with promise for predicting cardiac risk. The lack of reproducible results has limited its use. In evaluating a new reagent kit, we investigated conditions for optimal reproducibility. Methods: The Auto-PLAC reagents were evaluated on the Cobas instrument. Performance characteristics, stability, and population ranges were determined. Results: Analytical performance characteristics replicated manufacturers claims. The stability profile of the analyte was unusual, with increasing results observed with storage at 4 °C or - 20 °C. Only storage at -70 °C gave acceptable stability. Population median values with properly preserved samples were ...
In a sample of 1,029 post-MI patients, sPLA2 (adjusted HR 1.32 for 1 unit increase, p = 0.036), but not Lp-PLA2 (HR, 1.03; p = ... sPLA2 [hazard ratio (HR) 1.45 for 1 SD increase, p = 0.001], but not Lp-PLA2 (HR, 0.95; p = 0.55), activity was a significant ... sPLA2 [odds ratio 1.23 for 1 standard deviation (SD) increase, p = 0.007], but not Lp-PLA2 (p = 0.26), activity was related to ... 0.90), activity predicted death or recurrent MI during 1-year follow-up. ...
2 years. 3 years. 5 years. 10 years. Or published in the following date range: From (yyyy/mm/dd - month and day are optional) ... A1.1.3.1.1. Vertebrate. A1.1.3.1.1.1. Amphibian. A1.1.3.1.1.2. Bird. A1.1.3.1.1.3. Fish. A1.1.3.1.1.4. Mammal. A1.1.3.1.1.4.1. ... 2. Sandberg-Wollheim M, Ciusani E, Salmaggi A, Pociot F: An evaluation of tumor necrosis factor microsatellite alleles in ... 1 multiple sclerosis 383908 results Searchbox Export PDF RSS Email Delete Email this search result to the following email ...
Store at 4°C if entire vial will be used within 2-4 weeks. Store, frozen at -20°C for longer periods of time. Please avoid ... PLA2G7 alters the action of PAF (platelet-activating factor) by hydrolyzing the sn-2 ester bond to yield the biologically ... PLA2G7 has specificity for substrates with a short residue at the sn-2 position. PLA2G7 is inactive against long-chain ... Platelet-activating factor acetylhydrolase, PAF acetylhydrolase, PAF 2-acylhydrolase, LDL-associated phospholipase A2, LDL-PLA( ...
TY - JOUR. T1 - Relation of markers of inflammation (C-reactive protein, white blood cell count, and lipoprotein-associated phospholipase A2) to the ankle - Brachial index. AU - Santos, Simone. AU - Rooke, Thom W. AU - Bailey, Kent R. AU - McConnell, Joseph P.. AU - Kullo, Iftikhar Jan. PY - 2004. Y1 - 2004. N2 - Markers of inflammation are predictive of cardiovascular events but their association with atherosclerotic burden remains poorly defined. We hypothesized that markers of inflammation, including C-reactive protein (CRP), white blood cell (WBC) count, and lipoprotein-associated phospholipase A2 (Lp-PLA2), would be associated with the ankle-brachial index (ABI), a marker of atherosclerotic burden. Subjects were 247 patients referred for lower extremity arterial evaluation to the non-invasive vascular laboratory excluding those with active infection or lower extremity revascularization within the previous year. ABI was measured at two sites in both legs and the lowest of four measurements ...
Katzenellenbogen, J., Sanfilippo, F., Hobbs, M., Briffa, T., Knuiman, M., Dimer, L., Thompson, P. & Thompson, S., 1 Dec 2012, ... Chapman, C. M. L., Mcquillan, B., Beilby, J. P., Thompson, P. & Hung, J., 2006, In : Atherosclerosis. 189, 2, p. 414 - 419. ... Thompson, P. L. & Nidorf, S. M., 1 Dec 2018, In : Current Opinion in Lipidology. 29, 6, p. 467-473 7 p.. Research output: ... Bradshaw, P., Wilkes, E. T. & Thompson, P., 2007, In : Atherosclerosis. 192, 1, p. 218-223. Research output: Contribution to ...
1-Alkyl-2-acetylglycerophosphocholine Esterase. Wassertheil-Smoller S, Kooperberg C, McGinn AP, Kaplan RC, Hsia J, Hendrix SL, ...
1-Alkyl-2-acetylglycerophosphocholine esterase Current Synonym true false 3040606019 Lipoprotein associated phospholipase A2 ... 1-alkyl-2-acetylglycerophosphocholine esterase (substance). Code System Preferred Concept Name. 1-alkyl-2- ... acetylglycerophosphocholine esterase (substance). Concept Status. Published. Concept Status Date. 03/01/2020. ...
Y1 - 2016/10/1. N2 - Objective The objective of this paper is to elucidate the not yet known plasma molecule candidates ... TF mRNA was markedly induced by oxidized LDL/β2GPI complexes with either WBCAL-1 (monoclonal aCL/β2GPI) or purified IgG from ... TF mRNA was markedly induced by oxidized LDL/β2GPI complexes with either WBCAL-1 (monoclonal aCL/β2GPI) or purified IgG from ... TF mRNA was markedly induced by oxidized LDL/β2GPI complexes with either WBCAL-1 (monoclonal aCL/β2GPI) or purified IgG from ...
Low Density Lipoprotein Receptor-Related Protein Associated Protein 1 ELISA Kits * LPS-Responsive Vesicle Trafficking, Beach ... 1-alkyl-2-acetylglycerophosphocholine esterase , 2-acetyl-1-alkylglycerophosphocholine esterase , LDL-PLA(2) , LDL-associated ... phospholipase A2 , PAF 2-acylhydrolase , PAF acetylhydrolase , gVIIA-PLA2 , group-VIIA phospholipase A2 , lipoprotein- ...
96-Strip-Wells / $795 +1 FREE 8GB USB. 5x96-Strip-Wells / $2,890 +3 FREE 8GB USB. 10x96-Strip-Wells / $5,465 +6 FREE 8GB USB. ... 24-Strip-Wells (LIMIT 1) / $250 +1 FREE 8GB USB. 48-Strip-Wells / $550 +1 FREE 8GB USB. ... Catalytic activity: 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine + H2O = 1-alkyl-sn-glycero-3-phosphocholine + acetate. ... Has a specificity for substrates with a short residue at the sn-2 position. It is inactive against long-chain phospholipids.. ...
Y1 - 2010/12/1. N2 - OBJECTIVE - To determine the predictors of progression of calcified atherosclerosis and the effect of ... However, the albumin-to-creatinine ratio (ACR) (P = 0.02) and lipoprotein-associated phospholipase A2 (Lp-PLA2) (P=0.01) ... CONCLUSIONS - In patients with long-standing type 2 diabetes, baseline CAC, Lp-PLA2, and ACR predicted progression of CAC. ... CONCLUSIONS - In patients with long-standing type 2 diabetes, baseline CAC, Lp-PLA2, and ACR predicted progression of CAC. ...
2. Ventricular Tachycardia 05/2010 - 12/2003. Drug/Important Bio-Agent (IBA). 140. glucuronyl glucosamine glycan sulfate ( ... 2. Chest Pain (Chest Pains) 10/2013 - 09/2010. 2. Peripheral Vascular Diseases (Peripheral Vascular Disease) 02/2013 - 12/2012 ... 1/2015. Stent thrombosis in early-generation drug-eluting stents versus newer-generation everolimus-eluting stent assorted by ... 1/2015. The EXCEL and NOBLE trials: similarities, contrasts and future perspectives for left main revascularisation.. ...
Cholesterol Esterase D8.811.277.352.100.150 D8.811.277.352.100.700. (Replaced for 2008 by Sterol Esterase). Chorea C10.228. ... Fura-2 D3.383.312.225.250. gamma-Endorphin D6.472.699.631.525.475.505 D6.472.699.631.525.600.505. gamma-Lipotropin D6.472. ... 1-Deoxynojirimycin D9.477.500.33 D3.132.14. D9.546.412.500.33. 3,5-Cyclic-GMP Phosphodiesterase D8.811.277.352.640.125 D8.811 ... Replaced for 2008 by Shiga Toxin 1). Shiga-Like Toxin II D8.811.277.450.430.700.750.750.124. D12.776.97.275.879. (Replaced for ...
  • 8 In the Integrated Biomarkers and Imaging Study-2 (IBIS-2 study) in CHD patients, darapladib, compared with placebo over 12 months, halted progression of the secondary endpoint of coronary artery plaque necrotic core, as determined by intravascular ultrasound virtual histology. (acc.org)
  • The determination of new and specific blood biomarkers of vascular inflammation associated with obesity-related metabolic syndrome (MetS) and diabetes such as lipoprotein-associated phospholipase A 2 (Lp-PLA 2 ) could be useful to identify subject with high risk of cardiovascular events. (unicatt.it)
  • We evaluated additive predictive value of two commercially available biomarkers: C-reactive protein and lipoprotein-associated phospholipase A 2 to determine if they added to risk prediction by the Framingham Stroke Risk Score or by traditional risk factors, which included lipids and other variables not included in the Framingham Stroke Risk Score. (elsevier.com)
  • The concordance of findings from Mendelian randomization and clinical trials suggests that for these 2 drugs, and for other novel biomarkers in future, validation of potential therapeutic targets by genetic studies (such as Mendelian randomization) before embarking on costly phase III randomized controlled trials could increase efficiency and offset the high risk of drug development, thereby facilitating discovery of new therapeutics and mitigating against the exuberant costs of drug development. (ox.ac.uk)
  • There are multiple enzymes with this function: Lipoprotein-associated phospholipase A2 Platelet-activating factor acetylhydrolase 2, cytoplasmic Platelet-activating factor acetylhydrolase 1b: regulatory subunit 1, catalytic subunit 2, catalytic subunit 3 This enzyme belongs to the family of hydrolases, specifically those acting on carboxylic ester bonds. (wikipedia.org)
  • Lipoprotein-associated phospholipase A(2) activity. (nih.gov)
  • Vulnerable 1 and ruptured atherosclerotic plaques, are characterized by inflammation and high expression of lipoprotein-associated phospholipase A 2 (Lp-PLA 2 ). (acc.org)
  • However, the albumin-to-creatinine ratio (ACR) (P = 0.02) and lipoprotein-associated phospholipase A 2 (Lp-PLA 2 ) (P=0.01) predicted progression of CAC, and these results were not altered by adjustment for age and other traditional risk factors. (elsevier.com)
  • Mass levels of lipoprotein-associated phospholipase A(2) (Lp-PLA(2)), a leukocyte-derived enzyme involved in the metabolism of low-density lipoprotein to pro-inflammatory mediators, are associated with prognosis after stroke. (nih.gov)
  • Increased lipoprotein-associated phospholipase A(2) (Lp-PLA(2)) activity is associated with increased risk of cardiac events, but it is not known whether Lp-PLA(2) is a causative agent. (nih.gov)
  • The study aimed to disclose the changes of inflammatory factors including serum intracellular adhesion molecule-1 (ICAM-1), chitinase-3-like protein 1 (YKL-40), and lipoprotein-associated phospholipase A2 (Lp-PLA2) in patients with ACS and its clinical significance. (bvsalud.org)
  • Lipoprotein-associated phospholipase A2 (Lp-PLA 2 ) is a crucial enzyme in atherosclerosis as a potential drug target. (elsevier.com)
  • Conclusions: C-reactive protein and lipoprotein-associated phospholipase A 2 can improve prediction of certain subtypes of ischemic stroke in older women, over the Framingham stroke risk model and traditional risk factors, and may help to guide surveillance and treatment of women at risk. (elsevier.com)
  • Lipoprotein- associated phospholipase A 2 (Lp-PLA 2 ) is a proinflammatory enzyme secreted by macrophages. (umn.edu)
  • Of the 19 markers studied, lipoprotein-associated phospholipase A(2), vitamin B(6), interleukin 6, and soluble thrombomodulin added the most to the AUC (range, 0.006-0.011). (unboundmedicine.com)
  • Lipoprotein-associated phospholipase A(2) and risk of coronary disease, stroke, and mortality: collaborative analysis of 32 prospective studies. (ox.ac.uk)
  • BACKGROUND: Lipoprotein-associated phospholipase A(2) (Lp-PLA(2)), an inflammatory enzyme expressed in atherosclerotic plaques, is a therapeutic target being assessed in trials of vascular disease prevention. (ox.ac.uk)
  • We further show that this response, including invadopodia formation in association with confining matrix fibrils, requires an intact connection between the nucleus and the centrosome via the linker of nucleoskeleton and cytoskeleton (LINC) complex protein nesprin-2 and dynein adaptor Lis1. (mblwhoilibrary.org)
  • We assessed Lp-PLA 2 and C-reactive protein (CRP) levels along with traditional risk factors to examine their relation to ischemic stroke. (umn.edu)
  • Pretreatment of rats with the protein synthesis inhibitor cycloheximide (2 mg/kg) at 1, 3 or 5 h prior to perfusion of rat hindlegs did not influence the amount of t-PA released by platelet-activating factor (20 nM) or bradykinin (1 μM). (tudelft.nl)
  • The affinity of the paired antibodies, PLA1 and PLA5, both reached 1×10⁻⁸. (bvsalud.org)
  • sPLA2 [odds ratio 1.23 for 1 standard deviation (SD) increase, p = 0.007], but not Lp-PLA2 (p = 0.26), activity was related to carotid atherosclerosis and to the amount of stenosis by WBMRA (p = 0.006) following adjustment for multiple risk factors. (acc.org)
  • OBJECTIVE - To determine the predictors of progression of calcified atherosclerosis and the effect of intensive glycemic control on this process in patients with type 2 diabetes. (elsevier.com)
  • RESEARCH DESIGN AND METHODS - As part of the Risk Factors, Atherosclerosis, and Clinical Events in Diabetes (RACED) substudy of the Veterans Affairs Diabetes Trial (VADT), 197 and 189 individuals with type 2 diabetes received baseline and follow-up computed tomographic scans for measurement of coronary and abdominal artery calcium, respectively. (elsevier.com)
  • Here we show that selective inhibition of Lp-PLA(2) with darapladib reduced development of advanced coronary atherosclerosis in diabetic and hypercholesterolemic swine. (nih.gov)
  • Atherosclerosis , 199 (1), 110-115. (elsevier.com)
  • Darapladib is a potent and reversible oral inhibitor of Lp-PLA 2 . (acc.org)
  • 6 Darapladib has been shown to reduce levels of Lp-PLA 2 in atherosclerotic plaque, the necrotic core. (acc.org)
  • 7 Darapladib has also been shown to reduce Lp-PLA 2 activity in human carotid plaque. (acc.org)
  • During 3.7 years median follow-up the primary endpoint occurred in 9.7% patients in the darapladib group and 10.4% patients in the placebo group: hazard ratio (HR) 0.94, 95% confidence interval (CI) (0.85, 1.03), p=0.20 (Figure 1). (acc.org)
  • Major coronary events occurred in 9.3% patients in the darapladib versus 10.3% in the placebo group: HR 0.90, 95% CI (0.82, 1.00), nominal p=0.045 (Figure 2). (acc.org)
  • Darapladib markedly inhibited plasma and lesion Lp-PLA(2) activity and reduced lesion lysophosphatidylcholine content. (nih.gov)
  • Plasma glucose, cholesterol and Lp-PLA 2 activity increase upon DM-HC induction, but only Lp-PLA 2 activity is influenced by darapladib. (nih.gov)
  • Four weeks later, pigs were assigned to either a control or a treated group, and 10 mg kg −1 darapladib was orally administered daily to the treated group. (nih.gov)
  • We determined the binding pose of Darapladib to Lp-PLA 2 through docking study. (elsevier.com)
  • Darapladib formed two hydrogen bonding interactions with the side chain of Tyr160 and Gln352 and several pi-pi interactions with aromatic and aliphatic hydrophobic residues of Lp-PLA 2 . (elsevier.com)
  • In enzymology, a 1-alkyl-2-acetylglycerophosphocholine esterase (EC 3.1.1.47) is an enzyme that catalyzes the chemical reaction 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine + H2O ⇌ {\displaystyle \rightleftharpoons } 1-alkyl-sn-glycero-3-phosphocholine + acetate Thus, the two substrates of this enzyme are 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine and H2O, whereas its two products are 1-alkyl-sn-glycero-3-phosphocholine and acetate. (wikipedia.org)
  • Gene Ontology (GO) annotations related to this gene include hydrolase activity and 1-alkyl-2-acetylglycerophosphocholine esterase activity . (genecards.org)
  • Recent evidence from our laboratory has revealed that cytoplasmic dynein coimmunoprecipitates with LIS-1 in bovine brain cytosol, supporting a role in the dynein pathway in vertebrates. (umassmed.edu)
  • Preparation and crystal structure of the recombinant alpha(1)/alpha(2) catalytic heterodimer of bovine brain platelet-activating factor acetylhydrolase Ib. (cbrc.jp)
  • Serum levels of ICAM-1, YKL-40, and Lp-PLA2 of different groups were determined by enzyme-linked immunosorbent assay. (bvsalud.org)
  • The serum levels of ICAM-1, YKL-40, and Lp-PLA2 were correlated with different clinical types of CHD, but not well correlated the severity and extent of artery stenosis, suggesting that ICAM-1, YKL-40, and Lp-PLA2 might be involved in occurrence of instability of atherosclerotic plaque, and might reflect the severity of CHD mostly through reflecting the plaque stability. (bvsalud.org)
  • 2,3 In the Lp-PLA 2 studies collaboration meta-analysis of individual records from 79036 participants in 32 prospective studies, there was a continuous association between Lp-PLA 2 activity and the risk of coronary heart disease (CHD) with a relative risk, per 1 standard deviation increase in Lp-PLA 2 activity, of 1.10 (95% CI 1.05-1.16) adjusted for conventional risk factors. (acc.org)
  • p = 0.90), activity predicted death or recurrent MI during 1-year follow-up. (acc.org)
  • Lp-PLA(2) mass correlates only moderately with levels of Lp-PLA(2) activity. (nih.gov)
  • The relationship of Lp-PLA(2) activity to risk of stroke recurrence is unknown. (nih.gov)
  • We hypothesized that Lp-PLA(2) activity levels would predict risk of recurrence. (nih.gov)
  • Levels of Lp-PLA(2) activity were assessed in 467 patients, and categorized by quartile. (nih.gov)
  • Compared to the lowest quartile of Lp-PLA(2) activity, those in the highest had an increased risk of recurrent stroke (adjusted HR 2.54, 95% CI 1.01-6.39). (nih.gov)
  • Stroke patients with Lp-PLA(2) activity levels in the highest quartile, compared to those in the lowest quartile, had an increased risk of recurrence after first ischemic stroke. (nih.gov)
  • Further studies are warranted to determine whether this biomarker has clinical utility in determining high-risk populations of stroke survivors, and whether anti-inflammatory strategies that reduce levels of activity of Lp-PLA(2) reduce the risk of stroke recurrence. (nih.gov)
  • Distribution of Lp-PLA 2 activity levels in the cohort. (nih.gov)
  • Plasma glucose ( a ), cholesterol ( b ) and Lp-PLA 2 activity ( c ) levels were monitored throughout the 28-week study period. (nih.gov)
  • Data shown are means ± s.e.m. for glucose and cholesterol and means ± s.d. for Lp-PLA 2 activity. (nih.gov)
  • We investigated associations of circulating Lp-PLA(2) mass and activity with risk of coronary heart disease, stroke, and mortality under different circumstances. (ox.ac.uk)
  • FINDINGS: Lp-PLA(2) activity and mass were associated with each other (r=0.51, 95% CI 0.47-0.56) and proatherogenic lipids. (ox.ac.uk)
  • We noted roughly log-linear associations of Lp-PLA(2) activity and mass with risk of coronary heart disease and vascular death. (ox.ac.uk)
  • INTERPRETATION: Lp-PLA(2) activity and mass each show continuous associations with risk of coronary heart disease, similar in magnitude to that with non-HDL cholesterol or systolic blood pressure in this population. (ox.ac.uk)
  • Associations of Lp-PLA(2) mass and activity are not exclusive to vascular outcomes, and the vascular associations depend at least partly on lipids. (ox.ac.uk)
  • 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine + H(2)O = 1-alkyl-sn-glycero-3-phosphocholine + acetate. (cbrc.jp)
  • These data show that selective inhibition of Lp-PLA(2) inhibits progression to advanced coronary atherosclerotic lesions and confirms a crucial role of vascular inflammation independent from hypercholesterolemia in the development of lesions implicated in the pathogenesis of myocardial infarction and stroke. (nih.gov)
  • As is the case with diacylglycerols, glycerophosphocholines can have many different combinations of fatty acids of varying lengths and saturation attached at the SN-1 and SN-2 positions. (hmdb.ca)
  • In this review, we will argue the evolving role of Lp-PLA 2 in predicting cardiovascular events in metabolic disease patients. (unicatt.it)
  • LIS-1 is homologous to the fungal genes NudF and PAC1, which are involved in cytoplasmic dynein mediated nuclear transport, but it is also almost identical to a subunit of PAF acetylhydrolase, an enzyme which inactivates the lipid mediator platelet activating factor. (umassmed.edu)
  • Together, these results suggest a role for LIS-1 in cytoplasmic dynein functions involving microtubule plus-ends. (umassmed.edu)
  • doi: 10.1016/s0896-6273(00)00147-1. (nih.gov)
  • Has a marked selectivity for phospholipids with short acyl chains at the sn-2 position. (uniprot.org)
  • Contributes to the biosynthesis of N-acyl ethanolamines, including the endocannabinoid anandamide by hydrolyzing the sn-1 and sn-2 acyl chains from N-acyl phosphatidylethanolamine (NAPE) generating glycerophospho-N-acyl ethanolamine (GP-NAE), an intermediate for N-acyl ethanolamine biosynthesis. (genecards.org)
  • CONCLUSIONS - In patients with long-standing type 2 diabetes, baseline CAC, Lp-PLA 2 , and ACR predicted progression of CAC. (elsevier.com)
  • PLA2G7 alters the action of PAF (platelet-activating factor) by hydrolyzing the sn-2 ester bond to yield the biologically inactive lyso-PAF. (prospecbio.com)
  • PLA2G7 has specificity for substrates with a short residue at the sn-2 position. (prospecbio.com)
  • The systematic name of this enzyme class is 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine acetohydrolase. (wikipedia.org)
  • Recent evidence has implicated the human LIS-1 gene in Miller-Dieker lissencephaly and isolated lissencephaly sequence. (umassmed.edu)
  • PA1B2_HUMAN ] Inactivates PAF by removing the acetyl group at the sn-2 position. (proteopedia.org)
  • Furthermore, they suggest that mutations in LIS-1 may produce a lissencephalic phenotype either by interfering with the movement of neuronal nuclei within extending processes, or by interference with the division cycle of neuronal progenitor cells in the ventricular and subventricular zones of the developing nervous system. (umassmed.edu)
  • Additionally genetic studies have shown that the presence of the V279F null allele within the gene encoding Lp-PLA 2 is associated with decreased CHD. (acc.org)
  • Results: Mean Lp-PLA 2 and CRP levels adjusted for sex, race, and age were higher in the 194 stroke cases than the 766 noncases, whereas low-density lipoprotein cholesterol (LDL-C) level was not significantly different. (umn.edu)