Framingham Heart Study 73 Mt

Total Page:16

File Type:pdf, Size:1020Kb

Framingham Heart Study 73 Mt Framingham Heart Study 73 Mt. Wayte Avenue Framingham, MA 01702 Laboratory data - method manual dataset name= l_urmtbl_ex06_1_0742s Analyte(s) measured Urine Panel (Metabolomics and CKD) Units none (Integrated LC-MS peak areas) Laboratory information Laboratory name Broad Institute of MIT and Harvard Location 7 Cambridge Center, Cambridge, MA 02142 Contact name Contact email Other contacts Contact email Sample information Offspring exam 6, This was a nested case control study of 386 individuals. All participants were free of CKD at baseline. Half developed CKD at follow- up (exam 8); cases and controls were age-sex Cohort / Exam number matched Sample type Urine Number of samples N=386; case-control [Incident CKD between exams 6 and 8] Methodology Method Type LC-MS: CHM or HILIC Assay characteristics Number of measurements (single/duplicate/other design) 10% in duplicate; randomly chosen Inter-assay CV See worksheet Intra- Inter-assay CVs Intra-assay CV See worksheet Intra- Inter-assay CVs Run dates Sept - Dec 2012 Framingham Heart Study Offspring exam 6 - Urine panel Fox/Broad Intra- and Inter-assay CVs 2/4/2013 Variable Method Intra-assay CV N Inter-assay CV N 2-aminoadipate CMH 9.8 15 10.5 23 3-hydroxykynurenate CMH 10.6 15 13.7 23 3-phosphoglycerate CMH 8.2 15 10.5 23 alpha-glycerophosphate CMH 7.2 15 7.0 23 4-pyridoxate CMH 10.9 15 17.9 23 aconitate CMH 12.6 15 9.3 23 adenine CMH 9.4 15 14.0 23 adipate CMH 10.5 15 12.5 23 AMP CMH 21.7 15 18.4 23 ADP CMH 23.2 14 22.2 21 cAMP CMH 8.2 15 6.9 23 citrate CMH 7.7 15 6.8 23 isocitrate CMH 9.4 15 12.5 23 CMP CMH 13.2 14 17.5 20 cystathionine CMH 8.7 14 7.5 22 cytidine CMH 8.2 15 6.9 23 erythrose-4-phosphate CMH 10.2 15 12.0 23 F1P/F6P/G1P/G6P CMH 16.9 15 13.0 23 fructose/glucose/galactose CMH 5.9 15 5.0 23 fumarate/maleate/alpha-ketoisovalerate CMH 12.8 15 18.7 23 glucuronate CMH 11.5 15 11.5 23 guanine CMH 9.6 15 11.5 23 guanosine CMH 7.6 14 11.2 23 hippurate CMH 5 15 6.2 23 homocystine CMH 24 14 23.5 22 homovanillate CMH 11 15 11.3 23 hypoxanthine CMH 6.9 15 8.6 23 inosine CMH 8 15 9.0 23 kynurenine CMH 11.2 15 14.2 23 lactate CMH 13 15 15.8 23 lactose CMH 8.9 15 8.0 23 malate CMH 7.9 15 9.4 23 orotate CMH 14.4 15 15.5 23 oxalate CMH 8.8 15 14.0 23 pantothenate CMH 10.8 15 11.1 23 phosphotyrosine CMH 18.1 15 17.8 21 propionate CMH 20.8 14 20.3 23 quinolinate CMH 11.5 15 15.2 23 salicylurate CMH 24.1 15 34.3 22 sorbitol CMH 5.1 15 3.6 23 succinate CMH 7.3 15 10.4 23 methylmalonate CMH 12.5 15 17.6 23 sucrose CMH 7.8 15 6.1 23 thymine CMH 8.7 15 7.5 23 uracil CMH 6.5 15 6.3 23 urate CMH 5.6 15 5.4 23 uridine CMH 6.8 15 5.2 23 xanthine CMH 10.4 15 12.8 23 xanthurenate CMH 9.1 15 11.1 23 cholate CMH 22.1 13 25.8 20 glycocholate CMH 10.5 15 7.3 23 taurocholate CMH 15.8 15 21.1 23 glycodeoxycholate/glycochenodeoxycholate CMH 9.4 15 10.4 23 taurodeoxycholate/taurochenodeoxycholate CMH 15 15 32.7 23 suberate CMH 9.6 15 10.2 23 hydroxyphenylacetate CMH 8.9 15 9.2 23 indoxylsulfate CMH 9.7 15 7.6 23 indole-3-propionate CMH 9.3 15 10.1 23 gentistate CMH 9.6 15 7.6 23 3-methyladipate-pimelate CMH 10.8 15 9.0 23 FMN CMH 28.9 15 38.9 23 Framingham Heart Study Offspring exam 6 - Urine panel Fox/Broad Intra- and Inter-assay CVs 2/4/2013 VMA CMH 10.2 15 7.8 23 alpha-hydroxybutyrate CMH 7.8 15 14.2 23 beta-hydroxybutyrate CMH 10.1 15 12.8 23 2-hydroxyglutarate CMH 9.7 15 12.6 23 inositol CMH 9.7 15 9.2 23 4-hydroxybenzaldehyde CMH 20.5 14 20.8 22 phosphocreatine CMH 22.1 3 30.5 7 benzoate CMH 30.4 6 27.9 10 indolelactate CMH 27.7 10 28.2 10 homogentisate CMH 18.6 12 24.2 15 PEP CMH 27.9 13 29.5 17 glycine HILIC 5.7 16 5.5 22 alanine HILIC 4.7 16 6.1 22 serine HILIC 3.7 16 6.2 22 threonine HILIC 5.6 16 7.2 22 methionine HILIC 9.1 13 14.8 22 glutamate HILIC 5.4 16 6.3 22 asparagine HILIC 4.5 16 4.9 22 glutamine HILIC 3.4 16 4.6 22 histidine HILIC 7.4 16 6.6 22 arginine HILIC 6.3 16 6.2 22 lysine HILIC 7.2 16 6.4 22 valine HILIC 2.5 16 4.6 22 leucine HILIC 3.4 16 5.1 22 isoleucine HILIC 5.7 16 6.2 22 phenylalanine HILIC 4 16 4.6 22 tyrosine HILIC 5 16 5.4 22 tryptophan HILIC 3.7 16 5.8 22 proline HILIC 4.6 16 5.4 22 cis/trans-hydroxyproline HILIC 4.2 16 5.6 22 ornithine HILIC 13.3 16 12.0 22 citrulline HILIC 5.3 16 6.7 22 taurine HILIC 3.6 16 3.5 22 5-hydroxytryptophan HILIC 12.2 15 20.1 21 5-HIAA HILIC 6.9 16 7.2 22 serotonin HILIC 7.5 16 8.9 22 GABA HILIC 10.4 16 10.5 22 acetylglycine HILIC 11.2 15 13.1 22 dimethylglycine HILIC 2.8 16 5.9 22 argininosuccinate HILIC 14.6 16 11.9 22 ADMA HILIC 3.7 16 2.7 22 SDMA HILIC 4 16 6.0 22 NMMA HILIC 5.1 16 9.8 22 allantoin HILIC 3.4 16 4.9 22 aminoisobutyric acid HILIC 3.3 16 4.6 22 anthranilic acid HILIC 5.3 16 6.6 22 kynurenic acid HILIC 7.1 16 5.3 22 1-methylhistamine HILIC 4.2 16 4.4 22 5-adenosylhomocysteine HILIC 10 15 8.4 22 carnosine HILIC 6.4 16 8.2 22 histamine HILIC 14 16 14.3 22 3-hydroxyanthranilic acid HILIC 12.2 16 20.0 22 N-carbamoyl-beta-alanine HILIC 5.6 16 5.8 22 thiamine HILIC 4.5 16 11.2 22 niacinamide HILIC 7.1 16 7.5 22 betaine HILIC 2.1 16 2.6 22 choline HILIC 2.1 16 3.4 22 alpha-glycerophosphocholine HILIC 4.5 16 7.2 22 acetylcholine HILIC 3.1 16 5.4 22 creatine HILIC 2.4 16 3.3 22 creatinine HILIC 1.3 16 1.6 22 trimethylamine-N-oxide HILIC 2 16 2.1 22 Framingham Heart Study Offspring exam 6 - Urine panel Fox/Broad Intra- and Inter-assay CVs 2/4/2013 glycerol HILIC 14.9 16 11.6 22 glucose HILIC 7.2 16 11.2 21 adenosine HILIC 5 16 8.1 22 cytosine HILIC 4.8 16 13.1 22 thymidine HILIC 6.8 16 7.4 22 xanthosine HILIC 5.8 16 4.2 22 2-deoxyadenosine HILIC 9.4 16 6.2 22 2-deoxycytidine HILIC 13 16 13.8 22 cotinine HILIC 23.1 16 26.4 22 mevalonic acid HILIC 5 16 6.2 22 pipecolic acid HILIC 10.6 16 11.2 22 5-aminolevulinic acid HILIC 9.3 16 12.5 22 pyroglutamic acid HILIC 5 16 4.9 22 1-methylnicotinamide HILIC 2.6 16 4.4 22 butyrobetaine HILIC 2.4 16 4.2 22 putrescine HILIC 17.3 12 24.6 17 methionine sulfoxide HILIC 4.4 16 3.2 22 sarcosine HILIC 13.9 16 15.7 22 beta-alanine HILIC 5.9 16 7.9 22 anserine HILIC 6.9 16 6.9 22 carnitine HILIC 2.5 16 3.9 22 acetylcarnitine HILIC 3.5 16 3.3 22 propionylcarnitine HILIC 2.4 16 3.2 22 malonylcarnitine HILIC 3 16 5.0 22 butyrylcarnitine/isobutyrylcarnitine HILIC 3.3 16 4.7 22 valerylcarnitine/isovalerylcarnitine/2-methylbutyroylcarnitine HILIC 4.6 16 7.6 22 heptanoylcarnitine HILIC 2.3 16 6.1 22 octanoylcarnitine HILIC 4.3 16 6.2 22 nonanoylcarnitine HILIC 5.7 16 7.5 22 decanoylcarnitine HILIC 11.6 16 14.0 22 lauroylcarnitine HILIC 11.7 16 17.7 22.
Recommended publications
  • Altered Metabolome of Lipids and Amino Acids Species: a Source of Early Signature Biomarkers of T2DM
    Journal of Clinical Medicine Review Altered Metabolome of Lipids and Amino Acids Species: A Source of Early Signature Biomarkers of T2DM Ahsan Hameed 1 , Patrycja Mojsak 1, Angelika Buczynska 2 , Hafiz Ansar Rasul Suleria 3 , Adam Kretowski 1,2 and Michal Ciborowski 1,* 1 Clinical Research Center, Medical University of Bialystok, Jana Kili´nskiegoStreet 1, 15-089 Bialystok, Poland; [email protected] (A.H.); [email protected] (P.M.); [email protected] (A.K.) 2 Department of Endocrinology, Diabetology and Internal Medicine, Medical University of Bialystok, 15-089 Bialystok, Poland; [email protected] 3 School of Agriculture and Food System, The University of Melbourne, Parkville, VIC 3010, Australia; hafi[email protected] * Correspondence: [email protected] Received: 27 June 2020; Accepted: 14 July 2020; Published: 16 July 2020 Abstract: Diabetes mellitus, a disease of modern civilization, is considered the major mainstay of mortalities around the globe. A great number of biochemical changes have been proposed to occur at metabolic levels between perturbed glucose, amino acid, and lipid metabolism to finally diagnoe diabetes mellitus. This window period, which varies from person to person, provides us with a unique opportunity for early detection, delaying, deferral and even prevention of diabetes. The early detection of hyperglycemia and dyslipidemia is based upon the detection and identification of biomarkers originating from perturbed glucose, amino acid, and lipid metabolism. The emerging “OMICS” technologies, such as metabolomics coupled with statistical and bioinformatics tools, proved to be quite useful to study changes in physiological and biochemical processes at the metabolic level prior to an eventual diagnosis of DM.
    [Show full text]
  • Analysis of the Effects of Three Commercially Available Supplements on Performance, Exercise Induced Changes and Bio-Markers in Recreationally Trained Young Males
    Analysis of the effects of three commercially available supplements on performance, exercise induced changes and bio-markers in recreationally trained young males Robert Cooper A thesis is submitted in partial fulfilment of the requirements of the University of Greenwich for the Degree of Doctor of Philosophy This research programme was carried out in collaboration with GlaxoSmithKline Maxinutrition division December 2013 School of Science University of Greenwich, Medway Campus Chatham Maritime, Kent ME4 4TB, UK i DECLARATION “I certify that this work has not been accepted in substance for any degree, and is not concurrently being submitted for any degree other than that of Doctor of Philosophy being studied at the University of Greenwich. I also declare that this work is the result of my own investigations except where otherwise identified by references and that I have not plagiarised the work of others”. Signed Date Mr Robert Cooper (Candidate) …………………………………………………………………………………………………………………………… PhD Supervisors Signed Date Dr Fernando Naclerio (1st supervisor) Signed Date Dr Mark Goss-Sampson (2nd supervisor) ii ACKNOWLEDGEMENTS Thank you to my supervisory team, Dr Fernando Naclerio, Dr Mark Goss Sampson and Dr Judith Allgrove for their support and guidance throughout my PhD. Particular thanks to Dr Fernando Naclerio for his tireless efforts, guidance and support in developing the research and my own research and communication skills. Thank you to Dr Eneko Larumbe Zabala for the statistics support. I would like to take this opportunity to thank my wonderful mother and sister who continue to give me the support and drive to succeed. Also on a personal level thank you to my amazing fiancée, Jennie Swift.
    [Show full text]
  • Open Full Page
    [CANCER RESEARCH 46, 3768-3774, August 1986] 31PNuclear Magnetic Resonance Study of a Human Colon Adenocarcinoma Cultured Cell Line1 Franck Desmoulin, Jean-Philippe Galons, Paul Cantoni, Jacques Marvaldi, and Patrick J. Cozzone2 Laboratoire de Biologie Physicochimique, Institut de Chimie Biologique, Universitéd'Aix-Marseille, Place Victor Hugo 13003 Marseille (France) ABSTRACT Saccharomyces cerevisiae (14-16). Investigation of mammalian cell lines has received only scant appraisal because of several •"Pnuclear magnetic resonance (NMR) spectroscopy has been used to technical difficulties. Work has been limited to a few cell types, monitor the energy metabolism in a human colon adenocarcinoma cell essentially HeLa cells (17, 18), Ehrlich ascites tumor cells (19), line (HT 29). NMR spectra were recorded at 80.9 MHz on approximately 2.5 x 10" cells continuously perfused with culture medium within a 20- and normal and transformed fibroblasts (20, 21). In addition, a detailed analysis of the metabolite content of radiation-induced iiini NMR sample tube. Typical NMR spectra display a series of well-resolved resonances fibrosarcoma cells by using multinuclear NMR has been re assigned to nucleoside triphosphates (mainly adenosine S'-triphosphate), cently published (22). uridine diphosphohexose derivatives (uridine 5'-diphosphate-A/-acetyl- A major difficulty to overcome in the study of perfused cells glucosamine, uridine 5/-diphosphate-Ar-acetylgalactosamine, uridine 5'- is the preservation of physiological conditions in the NMR diphosphate-glucose), intra- and extracellular inorganic phosphate, and sample tube where the accumulation of metabolite by-products phosphomonoesters (mainly phosphorylcholine and glucose 6-phos- and the required bubbling of gas may affect the viability of the phate).
    [Show full text]
  • Identification of the Specific Spoilage Organism in Farmed Sturgeon
    foods Article Identification of the Specific Spoilage Organism in Farmed Sturgeon (Acipenser baerii) Fillets and Its Associated Quality and Flavour Change during Ice Storage Zhichao Zhang 1,2,†, Ruiyun Wu 1,† , Meng Gui 3, Zhijie Jiang 4 and Pinglan Li 1,* 1 Beijing Laboratory for Food Quality and Safety, College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083, China; [email protected] (Z.Z.); [email protected] (R.W.) 2 Jiangxi Institute of Food Inspection and Testing, Nanchang 330001, China 3 Beijing Fisheries Research Institute, Beijing 100083, China; [email protected] 4 NMPA Key Laboratory for Research and Evaluation of Generic Drugs, Beijing Institute for Drug Control, Beijing 102206, China; [email protected] * Correspondence: [email protected]; Tel.: +86-10-6273-8678 † The authors contributed equally to this work. Abstract: Hybrid sturgeon, a popular commercial fish, plays important role in the aquaculture in China, while its spoilage during storage significantly limits the commercial value. In this study, the specific spoilage organisms (SSOs) from ice stored-sturgeon fillet were isolated and identified by analyzing their spoilage related on sensory change, microbial growth, and biochemical properties, including total volatile base nitrogen (TVBN), thiobarbituric acid reactive substances (TBARS), and proteolytic degradation. In addition, the effect of the SSOs on the change of volatile flavor compounds was evaluated by solid phase microextraction (SPME) and gas chromatography-mass spectrometry (GC-MS). The results showed that the Pseudomonas fluorescens, Pseudomonas mandelii, Citation: Zhang, Z.; Wu, R.; Gui, M.; and Shewanella putrefaciens were the main SSOs in the ice stored-sturgeon fillet, and significantly affect Jiang, Z.; Li, P.
    [Show full text]
  • The Effect of Short-Term Combination of Hmb (Beta
    Brazilian Journal of Biomotricity ISSN: 1981-6324 [email protected] Universidade Iguaçu Brasil Faramarzi, Mohammad; Nuri, Reza; Banitalebi, Ebrahim THE EFFECT OF SHORT -TERM COMBINATION OF HMB (BETA-HYDROXY-BETA- METHYLBUTYRATE) AND CREATINE SUPPLEMENTATION ON ANAEROBIC PERFORMANCE AND MUSCLE INJURY MARKERS IN SOCCER PLAYERS Brazilian Journal of Biomotricity, vol. 3, núm. 4, diciembre, 2009, pp. 366-375 Universidade Iguaçu Itaperuna, Brasil Available in: http://www.redalyc.org/articulo.oa?id=93012717009 How to cite Complete issue Scientific Information System More information about this article Network of Scientific Journals from Latin America, the Caribbean, Spain and Portugal Journal's homepage in redalyc.org Non-profit academic project, developed under the open access initiative Faramarzi et al.: Combination of HMB and Creatine supplementation www.brjb.com.br ORIGINAL PAPER THE EFFECT OF SHORT –TERM COMBINATION OF HMB (BETA- HYDROXY-BETA-METHYLBUTYRATE) AND CREATINE SUPPLEMENTATION ON ANAEROBIC PERFORMANCE AND MUSCLE INJURY MARKERS IN SOCCER PLAYERS Mohammad Faramarzi, Reza Nuri, and Ebrahim Banitalebi Department of Physical Education and Sport Sciences, Faculty of Human Sciences, University of Shahrekord, Iran Corresponding author: Mohammad Faramarzi (PhD) Assistant Professor in Exercise Physiology Department of Physical Education and Sport Sciences, Faculty of Human Sciences, University of Shahrekord, Iran Phone: 0098- 381- 4424411 Cell: 0098- 9133040196 Fax: 0098- 381- 4424411 Email: [email protected] Submitted for publication: Nov 2009 Accepted for publication: Dec 2009 ABSTRACT FARAMARZI, M.; NURI, R.; BANITALEBI, E. The effect of short –term combination of HMB (beta-hydroxy- beta-methylbutyrate) and creatine supplementation on anaerobic performance and muscle injury markers in soccer players. Brazilian Journal of Biomotricity, v.
    [Show full text]
  • Protective Effect of the Energy Precursor Creatine Against Toxicity of Glutamate and ␤-Amyloid in Rat Hippocampal Neurons
    Journal of Neurochemistry Lippincott Williams & Wilkins, Inc., Philadelphia © 2000 International Society for Neurochemistry Protective Effect of the Energy Precursor Creatine Against Toxicity of Glutamate and ␤-Amyloid in Rat Hippocampal Neurons Gregory J. Brewer and *Theo W. Wallimann Departments of Medical Microbiology/Immunology and Neurology, Southern Illinois University School of Medicine, Springfield, Illinois, U.S.A.; and *Institute for Cell Biology, Swiss Federal Institute of Technology, Zurich, Switzerland Abstract: The loss of ATP, which is needed for ionic (Manos et al., 1991; Molloy et al., 1992) and in vivo homeostasis, is an early event in the neurotoxicity of (Hemmer et al., 1994; Kaldis et al., 1996), CK isozyme glutamate and ␤-amyloid (A␤). We hypothesize that cells BB catalyzes the reversible conversion of PCr and ADP supplemented with the precursor creatine make more to ATP and Cr to manage different aspects of high- phosphocreatine (PCr) and create larger energy reserves energy demands in the brain (Hemmer and Wallimann, with consequent neuroprotection against stressors. In serum-free cultures, glutamate at 0.5–1 mM was toxic to 1993; Chen et al., 1995). On the other hand, mitochon- embryonic hippocampal neurons. Creatine at Ͼ0.1 mM drial CK catalyzes the reversible conversion of Cr and greatly reduced glutamate toxicity. Creatine (1 mM) could ATP to ADP and PCr to generate energy reserves in the be added as late as 2 h after glutamate to achieve pro- cytoplasm (Wyss et al., 1992). PCr reserves are depleted tection at 24 h. In association with neurotoxic protection even more rapidly than ATP during ischemia (Passon- by creatine during the first 4 h, PCr levels remained neau and Lowry, 1971) owing to their conversion to ATP constant, and PCr/ATP ratios increased.
    [Show full text]
  • List of Supplementary Materials
    List of Supplementary Materials: Supplemental Experimental Procedures Supplemental Figures Supplemental Table Supplemental Experimental Procedures Cell proliferation and death assays Cells were placed in 96-well plates at 2x103 cells/well in 100 l of growth medium and then incubated for 48 hours in each treatment condition. Cell proliferation was examined with Cell Count Reagent SF (Nacalai Tesque) according to the manufacturer’s instructions. The absorbance of the treated and untreated cells was measured with a microplate reader (Thermo Scientific) at 450 nm. Cell death was assessed by trypan blue exclusion (Nacalai Tesque). Western blotting Cultured cells or snap-frozen tissue samples were lysed and homogenized with a Lysis buffer AM1 and phosphatase inhibitor and protease inhibitor cocktail (Active Motif). Equal amounts of protein extracts were separated by electrophoresis on 4-12% NuPAGE Bis-Tris Mini Gels (Invitrogen) and then transferred to a nitrocellulose membrane (GE Healthcare) with the XCell II Blot Module (Invitrogen). The membrane was blocked for 1 hour in Tris- buffered saline containing 0.1% Tween20 and 5% nonfat milk and then probed with various primary antibodies, followed by secondary antibodies conjugated to horseradish peroxidase (HRP). The immunoreactivity was revealed with Super Signal West Pico Chemiluminescent Substrate or the West Femto Trial Kit (Thermo Scientific). TUNEL staining Cells were placed in 6-well chamber slides at 1x105 cells/well in 5 ml of growth medium and then incubated for 48 hours in each treatment condition. Apoptotic cells were evaluated with the In Situ Cell Death Detection Kit, Fluorescein and following the manufacturer’s protocol (Roche). Nuclei were stained blue by 4′, 6-diamidino-2-phenylindole (DAPI) (Invitrogen).
    [Show full text]
  • Phenotype Microarrays™
    Phenotype MicroArrays™ PM1 MicroPlate™ Carbon Sources A1 A2 A3 A4 A5 A6 A7 A8 A9 A10 A11 A12 Negative Control L-Arabinose N-Acetyl -D- D-Saccharic Acid Succinic Acid D-Galactose L-Aspartic Acid L-Proline D-Alanine D-Trehalose D-Mannose Dulcitol Glucosamine B1 B2 B3 B4 B5 B6 B7 B8 B9 B10 B11 B12 D-Serine D-Sorbitol Glycerol L-Fucose D-Glucuronic D-Gluconic Acid D,L -α-Glycerol- D-Xylose L-Lactic Acid Formic Acid D-Mannitol L-Glutamic Acid Acid Phosphate C1 C2 C3 C4 C5 C6 C7 C8 C9 C10 C11 C12 D-Glucose-6- D-Galactonic D,L-Malic Acid D-Ribose Tween 20 L-Rhamnose D-Fructose Acetic Acid -D-Glucose Maltose D-Melibiose Thymidine α Phosphate Acid- -Lactone γ D-1 D2 D3 D4 D5 D6 D7 D8 D9 D10 D11 D12 L-Asparagine D-Aspartic Acid D-Glucosaminic 1,2-Propanediol Tween 40 -Keto-Glutaric -Keto-Butyric -Methyl-D- -D-Lactose Lactulose Sucrose Uridine α α α α Acid Acid Acid Galactoside E1 E2 E3 E4 E5 E6 E7 E8 E9 E10 E11 E12 L-Glutamine m-Tartaric Acid D-Glucose-1- D-Fructose-6- Tween 80 -Hydroxy -Hydroxy -Methyl-D- Adonitol Maltotriose 2-Deoxy Adenosine α α ß Phosphate Phosphate Glutaric Acid- Butyric Acid Glucoside Adenosine γ- Lactone F1 F2 F3 F4 F5 F6 F7 F8 F9 F10 F11 F12 Glycyl -L-Aspartic Citric Acid myo-Inositol D-Threonine Fumaric Acid Bromo Succinic Propionic Acid Mucic Acid Glycolic Acid Glyoxylic Acid D-Cellobiose Inosine Acid Acid G1 G2 G3 G4 G5 G6 G7 G8 G9 G10 G11 G12 Glycyl-L- Tricarballylic L-Serine L-Threonine L-Alanine L-Alanyl-Glycine Acetoacetic Acid N-Acetyl- -D- Mono Methyl Methyl Pyruvate D-Malic Acid L-Malic Acid ß Glutamic Acid Acid
    [Show full text]
  • United States Patent Office 3,506,642
    United States Patent Office Patented Apr.3,506,642 14, 1970 2 3,506,642 inversely proportional to the cationic content of the salt. wv vs. However, the stability of these acid salts also decreases STABLE ORATE HEPARNOID with decreasing cationic content so that the formulation Teow Y. Koh and Kekhusroo R. Bharucha, Toronto, On- is necessarily a compromise between stability and tario, Canada, assignors to Canada Packers Limited, 5 heparinic activity. Toronto, Ontario, Canada No Drawing. Filed July 3, 1967, Ser. No. 650,621 SUMMARY OF THE INVENTION Int. C. C08b. 19/03, 19/08 O We have now discovered that heparinic acid forms U.S. C. 260-209 19 Claims salts or complexes (hereinafter collectively designated as 10 heparinoid complexes) with a number of weakly basic or amphoteric organic compounds to provide products ABSTRACT OF THE DISCLOSURE which are not only quite stable but which when orally This invention relates to new stable, orally active administered result in systemic anticoagulant effect of heparinoid complexes, prepared by reacting heparinic high order. o acid or other acid heparinoids with non-toxic organic 15 The expression "oral administration,” as used herein, compounds having weakly basic or amphoteric properties means administration by mouth and includes introduc and characterized by a base strength pKb in the range tion of therapeutic compositions containing the new of from about 7.0 to 12.5 or by an isoelectric point pI heparinoid complexes into the sublingual or buccal below about 9.7, to methods for preparing and using regions for absorption therefrom as well as the ad these new heparinoid complexes, and to therapeutic com- 20 ministration in the form of enteric-coated compositions positions containing them.
    [Show full text]
  • Effect of Guanidinoacetic Acid Supplementation on Nitrogen Retention and Methionine Methyl Group Flux in Growing Steers Fed Corn-Based Diets
    Efficacy of guanidinoacetic acid supplementation to growing cattle and relative bioavailability of guanidinoacetic acid delivered ruminally or abomasally by Hannah Fae Speer B.S., Fort Hays State University, 2015 A THESIS submitted in partial fulfillment of the requirements for the degree MASTER OF SCIENCE Department of Animal Sciences and Industry College of Agriculture KANSAS STATE UNIVERSITY Manhattan, Kansas 2019 Approved by: Major Professor Evan C. Titgemeyer Copyright © Hannah Speer 2019. Abstract Two experiments were conducted to assess the value of guanidinoacetic acid (GAA) as a feed additive for growing cattle. The first experiment utilized 7 ruminally cannulated Holstein steers (280 ± 14 kg) in a 5 × 5 Latin square design and evaluated relative bioavailability of GAA. Treatments were continuous ruminal or abomasal infusion of 0, 10, or 20 g/d GAA, and blood and urine samples were collected on the final day of each period for analysis of creatine, creatinine, and GAA concentrations. Plasma and urinary creatine concentrations were used as the primary response criteria to calculate ruminal bypass value of GAA by slope-ratio methodology; values were 47% and 49%, respectively. In Exp. 2, effects of GAA supplementation on N retention and methionine (Met) methyl group flux in steers fed corn-based diets were determined utilizing 6 ruminally cannulated Holstein steers (256 ± 14 kg) in a 6 × 6 Latin square design. Factorial treatments were 2 levels of Met (0 or 5 g/d) and 3 levels of GAA (0, 7.5, or 15 g/d) delivered by continuous abomasal infusion. Periods were 10 d in length and included 3 d for total fecal and urine collections; blood samples were collected and Met flux was measured on the final day of each period.
    [Show full text]
  • Effect of the Combination of Creatine Monohydrate Plus HMB
    nutrients Review Effect of the Combination of Creatine Monohydrate Plus HMB Supplementation on Sports Performance, Body Composition, Markers of Muscle Damage and Hormone Status: A Systematic Review Julen Fernández-Landa 1 , Julio Calleja-González 1, Patxi León-Guereño 2 , Alberto Caballero-García 3, Alfredo Córdova 4 and Juan Mielgo-Ayuso 4,* 1 Laboratory of Human Performance, Department of Physical Education and Sport, Faculty of Education, Sport Section, University of the Basque Country, 01007 Vitoria, Spain; [email protected] (J.F.-L.); [email protected] (J.C.-G.) 2 Faculty of Psychology and Education, University of Deusto, Campus of Donostia-San Sebastián, 20012 San Sebastián, Spain; [email protected] 3 Department of Anatomy and Radiology, Faculty of Health Sciences, University of Valladolid. Campus de Soria, 42003 Soria, Spain; [email protected] 4 Department of Biochemistry, Molecular Biology and Physiology, Faculty of Health Sciences, University of Valladolid, 42003 Soria, Spain; [email protected] * Correspondence: [email protected]; Tel.: +34-975-129-187 Received: 13 September 2019; Accepted: 18 October 2019; Published: 20 October 2019 Abstract: Although there are many studies showing the isolated effect of creatine monohydrate (CrM) and β-hydroxy β-methylbutyrate (HMB), it is not clear what effect they have when they are combined. The main purpose of this systematic review was to determine the efficacy of mixing CrM plus HMB in comparison with their isolated effects on sports performance, body composition, exercise induced markers of muscle damage, and anabolic-catabolic hormones. This systematic review was carried out in accordance with PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) statement guidelines and the PICOS model, for the definition of the inclusion criteria.
    [Show full text]
  • Metabolite Identification in Fecal Microbiota Transplantation Mouse Livers and Combined Proteomics with Chronic Unpredictive
    Li et al. Translational Psychiatry (2018) 8:34 DOI 10.1038/s41398-017-0078-2 Translational Psychiatry ARTICLE Open Access Metabolite identification in fecal microbiota transplantation mouse livers and combined proteomics with chronic unpredictive mild stress mouse livers Bo Li1,2,3,KenanGuo4,LiZeng1,2, Benhua Zeng4,RanHuo1,2,3, Yuanyuan Luo1,2,5, Haiyang Wang1,2,MeixueDong1,2, Peng Zheng1,2,6, Chanjuan Zhou1,2,JianjunChen1,2,YiyunLiu1,2,ZhaoLiu1,2,LiangFang5,HongWei2 and Peng Xie2,3,5,6,7 Abstract Major depressive disorder (MDD) is a common mood disorder. Gut microbiota may be involved in the pathogenesis of depression via the microbe–gut–brain axis. Liver is vulnerable to exposure of bacterial products translocated from the gut via the portal vein and may be involved in the axis. In this study, germ-free mice underwent fecal microbiota transplantation from MDD patients and healthy controls. Behavioral tests verified the depression model. Metabolomics using gas chromatography–mass spectrometry, nuclear magnetic resonance, and liquid chromatography–mass spectrometry determined the influence of microbes on liver metabolism. With multivariate statistical analysis, 191 metabolites were distinguishable in MDD mice from control (CON) mice. Compared with CON mice, MDD mice showed lower levels for 106 metabolites and higher levels for 85 metabolites. These metabolites are associated with 1234567890():,; 1234567890():,; lipid and energy metabolism and oxidative stress. Combined analyses of significantly changed proteins in livers from another depression model induced by chronic unpredictive mild stress returned a high score for the Lipid Metabolism, Free Radical Scavenging, and Molecule Transports network, and canonical pathways were involved in energy metabolism and tryptophan degradation.
    [Show full text]