Database : MEDLINE
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  1 / 3671 MEDLINE  
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PMID:29175453
Author:Zhang Y; Lickteig AJ; Csanaky IL; Klaassen CD
Address:School of Pharmaceutical Science and Technology, Tianjin University, Tianjin 300072, PR China. Electronic address: youcai.zhang@tju.edu.cn.
Title:Activation of PPARα decreases bile acids in livers of female mice while maintaining bile flow and biliary bile acid excretion.
Source:Toxicol Appl Pharmacol; 338:112-123, 2018 01 01.
ISSN:1096-0333
Country of publication:United States
Language:eng
Abstract:Fibrates are hypolipidemic drugs that act as activators of peroxisome proliferator-activated receptor α (PPARα). In both humans and rodents, females were reported to be less responsive to fibrates than males. Previous studies on fibrates and PPARα usually involved male mice, but little has been done in females. The present study aimed to provide the first comprehensive analysis of the effects of clofibrate (CLOF) and PPARα on bile acid (BA) homeostasis in female mice. Study in WT male mice showed that a 4-day CLOF treatment increased liver weight, bile flow, and biliary BA excretion, but decreased total BAs in both serum and liver. In contrast, WT female mice were less susceptible to these CLOF-mediated responses observed in males. In WT female mice, CLOF decreased total BAs in the liver, but had little effect on the mRNAs of hepatic BA-related genes. Next, a comparative analysis between WT and PPARα-null female mice showed that lack of PPARα in female mice decreased total BAs in serum, but had little effect on total BAs in liver or bile. However, lack of PPARα in female mice increased mRNAs of BA synthetic enzymes (Cyp7a1, Cyp8b1, Cyp27a1, and Cyp7b1) and transporters (Ntcp, Oatp1a1, Oatp1b2, and Mrp3). Furthermore, the increase of Cyp7a1 in PPARα-null female mice was associated with an increase in liver Fxr-Shp-Lrh-1 signaling. In conclusion, female mice are resistant to CLOF-mediated effects on BA metabolism observed in males, which could be attributed to PPARα-mediated suppression in females on genes involved in BA synthesis and transport.
Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
Name of substance:0 (Bile Acids and Salts); 0 (PPAR alpha); 97C5T2UQ7J (Cholesterol); EC 1.14.14.23 (Cholesterol 7-alpha-Hydroxylase); EC 1.14.14.23 (Cyp7a1 protein, mouse); HPN91K7FU3 (Clofibrate)


  2 / 3671 MEDLINE  
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PMID:28714084
Author:Ji Z; LeBaron MJ
Address:Toxicology and Environmental Research and Consulting, The Dow Chemical Company, Midland, Michigan, 48674.
Title:Applying the erythrocyte Pig-a assay concept to rat epididymal sperm for germ cell mutagenicity evaluation.
Source:Environ Mol Mutagen; 58(7):485-493, 2017 Aug.
ISSN:1098-2280
Country of publication:United States
Language:eng
Abstract:The Pig-a assay, a recently developed in vivo somatic gene mutation assay, is based on the identification of mutant erythrocytes that have an altered repertoire of glycosylphosphatidylinositol (GPI)-anchored cell surface markers. We hypothesized that the erythrocyte Pig-a assay concept could be applied to rat cauda epididymal spermatozoa (sperm) for germ cell mutagenicity evaluation. We used GPI-anchored CD59 as the Pig-a mutation marker and examined the frequency of CD59-negative sperm using flow cytometry. A reconstruction experiment that spiked un-labeled sperm (mutant-mimic) into labeled sperm at specific ratios yielded good agreement between the detected and expected frequencies of mutant-mimic sperm, demonstrating the analytical ability for CD59-negative sperm detection. Furthermore, this methodology was assessed in F344/DuCrl rats administered N-ethyl-N-nitrosourea (ENU), a prototypical mutagen, or clofibrate, a lipid-lowering drug. Rats treated with 1, 10, or 20 mg/kg body weight/day (mkd) ENU via daily oral garage for five consecutive days showed a dose-dependent increase in the frequency of CD59-negative sperm on study day 63 (i.e., 58 days after the last ENU dose). This ENU dosing regimen also increased the frequency of CD59-negative erythrocytes. In rats treated with 300 mkd clofibrate via daily oral garage for consecutive 28 days, no treatment-related changes were detected in the frequency of CD59-negative sperm on study day 85 (i.e., 57 days after the last dose) or in the frequency of CD59-negative erythrocytes on study day 29. In conclusion, these data suggest that the epidiymal sperm Pig-a assay in rats is a promising method for evaluating germ cell mutagenicity. Environ. Mol. Mutagen. 58:485-493, 2017. © 2017 Wiley Periodicals, Inc.
Publication type:JOURNAL ARTICLE
Name of substance:0 (CD59 Antigens); 0 (Glycosylphosphatidylinositols); 0 (Membrane Proteins); 0 (Mutagens); 0 (phosphatidylinositol glycan-class A protein); HPN91K7FU3 (Clofibrate); P8M1T4190R (Ethylnitrosourea)


  3 / 3671 MEDLINE  
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PMID:28389698
Author:Venkatachalam AB; Parmar MB; Wright JM
Address:Department of Biology, Dalhousie University, 1355 Oxford Street, PO BOX 15000, Halifax, NS, B3H 4R2, Canada.
Title:Evolution of the duplicated intracellular lipid-binding protein genes of teleost fishes.
Source:Mol Genet Genomics; 292(4):699-727, 2017 Aug.
ISSN:1617-4623
Country of publication:Germany
Language:eng
Abstract:Increasing organismal complexity during the evolution of life has been attributed to the duplication of genes and entire genomes. More recently, theoretical models have been proposed that postulate the fate of duplicated genes, among them the duplication-degeneration-complementation (DDC) model. In the DDC model, the common fate of a duplicated gene is lost from the genome owing to nonfunctionalization. Duplicated genes are retained in the genome either by subfunctionalization, where the functions of the ancestral gene are sub-divided between the sister duplicate genes, or by neofunctionalization, where one of the duplicate genes acquires a new function. Both processes occur either by loss or gain of regulatory elements in the promoters of duplicated genes. Here, we review the genomic organization, evolution, and transcriptional regulation of the multigene family of intracellular lipid-binding protein (iLBP) genes from teleost fishes. Teleost fishes possess many copies of iLBP genes owing to a whole genome duplication (WGD) early in the teleost fish radiation. Moreover, the retention of duplicated iLBP genes is substantially higher than the retention of all other genes duplicated in the teleost genome. The fatty acid-binding protein genes, a subfamily of the iLBP multigene family in zebrafish, are differentially regulated by peroxisome proliferator-activated receptor (PPAR) isoforms, which may account for the retention of iLBP genes in the zebrafish genome by the process of subfunctionalization of cis-acting regulatory elements in iLBP gene promoters.
Publication type:JOURNAL ARTICLE; REVIEW
Name of substance:0 (Fatty Acid-Binding Proteins); 0 (PPAR alpha); 0 (PPAR gamma); 0 (Retinol-Binding Proteins); HPN91K7FU3 (Clofibrate)


  4 / 3671 MEDLINE  
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PMID:28248971
Author:Kochem M; Breslin PA
Address:Rutgers University Department of Nutritional Sciences, New Brunswick, NJ, United States of America.
Title:Clofibrate inhibits the umami-savory taste of glutamate.
Source:PLoS One; 12(3):e0172534, 2017.
ISSN:1932-6203
Country of publication:United States
Language:eng
Abstract:In humans, umami taste can increase the palatability of foods rich in the amino acids glutamate and aspartate and the 5'-ribonucleotides IMP and GMP. Umami taste is transduced, in part, by T1R1-T1R3, a heteromeric G-protein coupled receptor. Umami perception is inhibited by sodium lactisole, which binds to the T1R3 subunit in vitro. Lactisole is structurally similar to the fibrate drugs. Clofibric acid, a lipid lowering drug, also binds the T1R3 subunit in vitro. The purpose of this study was to determine whether clofibric acid inhibits the umami taste of glutamate in human subjects. Ten participants rated the umami taste intensity elicited by 20 mM monosodium glutamate (MSG) mixed with varying concentrations of clofibric acid (0 to 16 mM). In addition, fourteen participants rated the effect of 1.4 mM clofibric acid on umami enhancement by 5' ribonucleotides. Participants were instructed to rate perceived intensity using a general Labeled Magnitude Scale (gLMS). Each participant was tested in triplicate. Clofibric acid inhibited umami taste intensity from 20 mM MSG in a dose dependent manner. Whereas MSG neat elicited "moderate" umami taste intensity, the addition of 16 mM clofibric acid elicited only "weak" umami intensity on average, and in some subjects no umami taste was elicited. We further show that 1.4 mM clofibric acid suppressed umami enhancement from GMP, but not from IMP. This study provides in vivo evidence that clofibric acid inhibits glutamate taste perception, presumably via T1R1-T1R3 inhibition, and lends further evidence that the T1R1-T1R3 receptor is the principal umami receptor in humans. T1R receptors are expressed extra-orally throughout the alimentary tract and in regulatory organs and are known to influence glucose and lipid metabolism. Whether clofibric acid as a lipid-lowering drug affects human metabolism, in part, through T1R inhibition warrants further examination.
Publication type:CLINICAL TRIAL; JOURNAL ARTICLE
Name of substance:0 (Receptors, G-Protein-Coupled); 0 (taste receptors, type 1); 3KX376GY7L (Glutamic Acid); HPN91K7FU3 (Clofibrate)


  5 / 3671 MEDLINE  
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PMID:27742692
Author:Kochem M; Breslin PA
Address:Department of Nutritional Sciences, Rutgers University, 65 Dudley Road, New Brunswick, NJ 08901, USA and.
Title:Lipid-Lowering Pharmaceutical Clofibrate Inhibits Human Sweet Taste.
Source:Chem Senses; 42(1):79-83, 2017 Jan.
ISSN:1464-3553
Country of publication:England
Language:eng
Abstract:T1R2-T1R3 is a heteromeric receptor that binds sugars, high potency sweeteners, and sweet taste blockers. In rodents, T1R2-T1R3 is largely responsible for transducing sweet taste perception. T1R2-T1R3 is also expressed in non-taste tissues, and a growing body of evidence suggests that it helps regulate glucose and lipid metabolism. It was previously shown that clofibric acid, a blood lipid-lowering drug, binds T1R2-T1R3 and inhibits its activity in vitro The purpose of this study was to determine whether clofibric acid inhibits sweetness perception in humans and is, therefore, a T1R2-T1R3 antagonist in vivo Fourteen participants rated the sweetness intensity of 4 sweeteners (sucrose, sucralose, Na cyclamate, acesulfame K) across a broad range of concentrations. Each sweetener was prepared in solution neat and in mixture with either clofibric acid or lactisole. Clofibric acid inhibited sweetness of every sweetener. Consistent with competitive binding, inhibition by clofibric acid was diminished with increasing sweetener concentration. This study provides in vivo evidence that the lipid-lowering drug clofibric acid inhibits sweetness perception and is, therefore, a T1R carbohydrate receptor inhibitor. Our results are consistent with previous in vitro findings. Given that T1R2-T1R3 may in part regulate glucose and lipid metabolism, future studies should investigate the metabolic effects of T1R inhibition.
Publication type:JOURNAL ARTICLE
Name of substance:0 (Receptors, G-Protein-Coupled); 0 (Sweetening Agents); HPN91K7FU3 (Clofibrate)


  6 / 3671 MEDLINE  
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PMID:27193034
Author:More VR; Campos CR; Evans RA; Oliver KD; Chan GN; Miller DS; Cannon RE
Address:Signal Transduction Laboratory, National Institute of Environmental Health Sciences (NIEHS), National Institute of Health, Research Triangle Park, NC, USA.
Title:PPAR-α, a lipid-sensing transcription factor, regulates blood-brain barrier efflux transporter expression.
Source:J Cereb Blood Flow Metab; 37(4):1199-1212, 2017 Apr.
ISSN:1559-7016
Country of publication:United States
Language:eng
Abstract:Lipid sensor peroxisome proliferator-activated receptor alpha (PPAR- α) is the master regulator of lipid metabolism. Dietary release of endogenous free fatty acids, fibrates, and certain persistent environmental pollutants, e.g. perfluoroalkyl fire-fighting foam components, are peroxisome proliferator-activated receptor alpha ligands. Here, we define a role for peroxisome proliferator-activated receptor alpha in regulating the expression of three ATP-driven drug efflux transporters at the rat and mouse blood-brain barriers: P-glycoprotein (Abcb1), breast cancer resistance protein (Bcrp/Abcg2), and multidrug resistance-associated protein 2 (Mrp2/Abcc2). Exposing isolated rat brain capillaries to linoleic acid, clofibrate, or PKAs increased the transport activity and protein expression of the three ABC transporters. These effects were blocked by the PPAR- α antagonist, GW6471. Dosing rats with 20 mg/kg or 200 mg/kg of clofibrate decreased the brain accumulation of the P-glycoprotein substrate, verapamil, by 50% (in situ brain perfusion; effects blocked by GW6471) and increased P-glycoprotein expression and activity in capillaries ex vivo. Fasting C57Bl/6 wild-type mice for 24 h increased both serum lipids and brain capillary P-glycoprotein transport activity. Fasting did not alter P-glycoprotein activity in PPAR- α knockout mice. These results indicate that hyperlipidemia, lipid-lowering fibrates and exposure to certain fire-fighting foam components activate blood-brain barrier peroxisome proliferator-activated receptor alpha, increase drug efflux transporter expression and reduce drug delivery to the brain.
Publication type:JOURNAL ARTICLE
Name of substance:0 (ATP Binding Cassette Transporter, Sub-Family G, Member 2); 0 (ATP-Binding Cassette, Sub-Family B, Member 1); 0 (Alkanesulfonic Acids); 0 (Fluorocarbons); 0 (GW 6471); 0 (Multidrug Resistance-Associated Proteins); 0 (Oxazoles); 0 (PPAR alpha); 42HK56048U (Tyrosine); 4AF605U6JN (multidrug resistance-associated protein 2); 9H2MAI21CL (perfluorooctane sulfonic acid); 9KJL21T0QJ (Linoleic Acid); HPN91K7FU3 (Clofibrate)


  7 / 3671 MEDLINE  
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PMID:27354598
Author:Schmeel LC; Schmeel FC; Schmidt-Wolf IG
Address:Department of Radiology and Radiation Oncology, University Hospital Bonn, Bonn, Germany Center for Integrated Oncology (CIO), Medical Clinic and Polyclinic III, University Hospital Bonn, Bonn, Germany.
Title:Clofibrate Demonstrates Efficacy in In Vitro Treatment of Lymphoma and Multiple Myeloma.
Source:Anticancer Res; 36(7):3395-400, 2016 Jul.
ISSN:1791-7530
Country of publication:Greece
Language:eng
Abstract:BACKGROUND/AIM: Multiple myeloma (MM), a hematological malignancy of monoclonal B-lymphocytes, remains largely incurable and novel treatments are urgently required. Aberrant activation of wingless-related integration site (WNT)/ß-catenin signaling has been demonstrated in both lymphoma and MM, rendering its signaling molecules attractive for the development of new targeted-therapies. Clofibrate has proven anticarcinogenic effects attributed to peroxisome proliferator-activated receptor alpha (PPARα) agonism, also affecting WNT-associated signaling molecules. MATERIALS AND METHODS: The antitumor apoptotic effect of clofibrate at doses ranging from 0.1-600 µM was investigated on four human and one murine myeloma cell lines, as well as in two human lymphoma cell lines, using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium-bromide assay. RESULTS: Clofibrate significantly reduced cell viability in all tested myeloma and lymphoma cell lines in a dose-dependent manner, while healthy cells were hardly affected. CONCLUSION: Given the known safety profile and induction of apoptosis at low effective doses, our data warrant further investigation of clofibrate as a novel therapy agent in MM.
Publication type:JOURNAL ARTICLE
Name of substance:HPN91K7FU3 (Clofibrate)


  8 / 3671 MEDLINE  
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PMID:27110876
Author:Ibarra-Lara L; Del Valle-Mondragón L; Soria-Castro E; Torres-Narváez JC; Pérez-Severiano F; Sánchez-Aguilar M; Ramírez-Ortega M; Cervantes-Pérez LG; Pastelín-Hernández GS; Oidor-Chan VH; Zarco-Olvera G; Sánchez-Mendoza A
Address:Department of Pharmacology, National Institute of Cardiology Ignacio Chávez, Mexico City, Mexico.
Title:Peroxisome proliferator-activated receptor-α stimulation by clofibrate favors an antioxidant and vasodilator environment in a stressed left ventricle.
Source:Pharmacol Rep; 68(4):692-702, 2016 Aug.
ISSN:1734-1140
Country of publication:Poland
Language:eng
Abstract:BACKGROUND: Arterial high blood pressure is a risk factor for target organ damage; the most susceptible organs are the arteries, brain, kidneys, and heart. The damage mechanisms include oxidative stress and renin-angiotensin system (RAS) overactivity. Therefore, our aim was to study whether clofibrate-induced peroxisome proliferator-activated receptor-alpha (PPAR-α) stimulation is able to prevent alterations in cardiac functioning derived from RAS overstimulation in the left ventricle of rats with hypertension secondary to aortic coarctation and to improve antioxidant defenses. METHODS: Male Wistar rats were assigned to Control (Sham)- or aortic coarctation-surgery and further divided to receive (1 or 21 days) vehicle, clofibrate (100mg/kg), captopril (20mg/kg), or clofibrate+captopril. The left ventricle was obtained to measure: angiotensin II and -(1-7), AT1 and AT2 receptors, angiotensin converting enzyme (ACE)-1 and -2, and MAS receptor; the activity and expression of superoxide dismutase, catalase, endothelial nitric oxide synthase, the production of reactive oxygen species (ROS) and peroxidated lipids; as well as ex vivo cardiac functioning. RESULTS: Clofibrate decreased angiotensin II, AT1 receptor and ACE expression, and raised angiotensin-(1-7), AT2 receptor, ACE-2 expression, superoxide dismutase and endothelial nitric oxide synthase participation. These effects promoted lower coronary vascular resistance and improved mechanical work compared to aortic coarctated vehicle-treated rats. CONCLUSIONS: Clofibrate-induced PPAR-α stimulation changes the angiotensin II receptor profile, favors the ACE2/angiotensin-(1-7)/AT2 receptor axis decreasing the vasoconstrictor environment, activates the antioxidant defense, and facilitates endothelial nitric oxide synthase activity favoring vasodilation. This may represent a protection for the stressed heart.
Publication type:JOURNAL ARTICLE
Name of substance:0 (Antioxidants); 0 (PPAR alpha); 0 (Peptide Fragments); 0 (Proto-Oncogene Proteins); 0 (Reactive Oxygen Species); 0 (Receptor, Angiotensin, Type 1); 0 (Receptor, Angiotensin, Type 2); 0 (Receptors, G-Protein-Coupled); 0 (proto-oncogene proteins c-mas-1); 11128-99-7 (Angiotensin II); 9041-90-1 (Angiotensin I); 9G64RSX1XD (Captopril); EC 1.11.1.6 (Catalase); EC 1.14.13.39 (Nitric Oxide Synthase Type III); EC 1.15.1.1 (Superoxide Dismutase); EC 3.4.15.1 (Peptidyl-Dipeptidase A); EC 3.4.17.- (angiotensin converting enzyme 2); HPN91K7FU3 (Clofibrate); IJ3FUK8MOF (angiotensin I (1-7))


  9 / 3671 MEDLINE  
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PMID:27050838
Author:Ibarra-Lara Mde L; Sánchez-Aguilar M; Soria E; Torres-Narváez JC; Del Valle-Mondragón L; Cervantes-Pérez LG; Pérez-Severiano F; Ramírez-Ortega Mdel C; Pastelín-Hernández G; Oidor-Chan VH; Sánchez-Mendoza A
Address:a Department of Pharmacology, National Institute of Cardiology Ignacio Chávez, Juan Badiano No. 1, Col. Sección XVI, Tlalpan, 14080 Mexico City, México.
Title:Peroxisome proliferator-activated receptors (PPAR) downregulate the expression of pro-inflammatory molecules in an experimental model of myocardial infarction.
Source:Can J Physiol Pharmacol; 94(6):634-42, 2016 Jun.
ISSN:1205-7541
Country of publication:Canada
Language:eng
Abstract:Myocardial infarction (MI) has been associated with an inflammatory response and a rise in TNF-α, interleukin (IL)-1ß, and IL-6. Peroxisome proliferator-activated receptors (PPARs) promote a decreased expression of inflammatory molecules. We aimed to study whether PPAR stimulation by clofibrate decreases inflammation and reduces infarct size in rats with MI. Male Wistar rats were randomized into 3 groups: control, MI + vehicle, and MI + clofibrate (100 mg/kg). Treatment was administered for 3 consecutive days, previous to 2 h of MI. MI induced an increase in protein expression, mRNA content, and enzymatic activity of inducible nitric oxide synthase (iNOS). Additionally, MI incited an increased expression of matrix metalloproteinase (MMP)-2 and MMP-9, intercellular adhesion molecule (ICAM)-1, and IL-6. MI also elevated the nuclear content of nuclear factor-κB (NF-κB) and decreased IκB, both in myocyte nuclei and cytosol. Clofibrate treatment prevented MI-induced changes in iNOS, MMP-2 and MMP-9, ICAM-1, IL-6, NF-κB, and IκB. Infarct size was smaller in clofibrate-treated rats compared to MI-vehicle animals. In silico analysis exhibited 3 motifs shared by genes from renin-angiotensin system, PPARα, iNOS, MMP-2 and MMP-9, ICAM-1, and VCAM-1, suggesting a cross regulation. In conclusion, PPARα-stimulation prevents overexpression of pro-inflammatory molecules and preserves viability in an experimental model of acute MI.
Publication type:JOURNAL ARTICLE
Name of substance:0 (Inflammation Mediators); 0 (PPAR alpha); HPN91K7FU3 (Clofibrate)


  10 / 3671 MEDLINE  
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PMID:27020044
Author:Bodié K; Buck WR; Pieh J; Liguori MJ; Popp A
Address:Abbvie Deutschland GmbH & Co. KG, Preclinical Safety, D-67061 Ludwigshafen, Germany. Electronic address: karen.bodie@abbvie.com.
Title:Biomarker evaluation of skeletal muscle toxicity following clofibrate administration in rats.
Source:Exp Toxicol Pathol; 68(5):289-99, 2016 May.
ISSN:1618-1433
Country of publication:Germany
Language:eng
Abstract:The use of sensitive biomarkers to monitor skeletal muscle toxicity in preclinical toxicity studies is important for the risk assessment in humans during the development of a novel compound. Skeletal muscle toxicity in Sprague Dawley Rats was induced with clofibrate at different dose levels for 7 days to compare standard clinical pathology assays with novel skeletal muscle and cardiac muscle biomarkers, gene expression and histopathological changes. The standard clinical pathology assays aspartate aminotransferase (AST), alanine aminotransferase (ALT), and creatine kinase (CK) enzyme activity were compared to novel biomarkers fatty acid binding protein 3 (Fabp3), myosin light chain 3 (Myl3), muscular isoform of CK immunoreactivity (three isoforms CKBB, CKMM, CKMB), parvalbumin (Prv), skeletal troponin I (sTnI), cardiac troponin T (cTnT), cardiac troponin I (cTnI), CKMM, and myoglobin (Myo). The biomarker elevations were correlated to histopathological findings detected in several muscles and gene expression changes. Clofibrate predominantly induced skeletal muscle toxicity of type I fibers of low magnitude. Useful biomarkers for skeletal muscle toxicity were AST, Fabp3, Myl3, (CKMB) and sTnI. Measurements of CK enzyme activity by a standard clinical assay were not useful for monitoring clofibrate-induced skeletal muscle toxicity in the rat at the doses used in this study.
Publication type:JOURNAL ARTICLE
Name of substance:0 (Biomarkers); 0 (FABP3 protein, rat); 0 (Fatty Acid Binding Protein 3); 0 (Fatty Acid-Binding Proteins); 0 (Hypolipidemic Agents); 0 (Myoglobin); 0 (Myosin Light Chains); 0 (Parvalbumins); 0 (Troponin C); 0 (Troponin I); EC 2.6.1.1 (Aspartate Aminotransferases); EC 2.6.1.2 (Alanine Transaminase); EC 2.7.3.2 (Creatine Kinase); HPN91K7FU3 (Clofibrate)



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