From the Margins: A Literary Perspective

Box plot of selected variables using RF classification. (PPTX 104 kb

Additional file 3: of Integration of metabolomics, lipidomics and clinical data using a machine learning method

List of lipidomics, metabolomics and clinical chemistry data set. (XLSX 897 kb

Additional file 1: Figure S1. of 1H NMR spectroscopy-based metabolomics analysis for the diagnosis of symptomatic E. coli-associated urinary tract infection (UTI)

Representative 1H NMR spectra of E.Coli-pos urine sample. 1 TSP; 2 lactate; 3 alanine; 4 acetate; 5 citrate; 6 dimethylamine; 7 trimethylamine; 8 creatinine; 9 histidine; 10 choline; 11 TMA N-Oxide; 12 taurine; 13 glycine; 14 urea; 15 phenylalanine;16 hippurate; 17 formate. (TIFF 156 kb

Additional file 3: of Nitrate enhances skeletal muscle fatty acid oxidation via a nitric oxide-cGMP-PPAR-mediated mechanism

Supporting data. (XLSX 45.3 kb

Additional file 2: Figure S2. of Nitrate enhances skeletal muscle fatty acid oxidation via a nitric oxide-cGMP-PPAR-mediated mechanism

Ucp3, Acadl and Cpt1b expression in C2C12 myoblasts cultured and differentiated over 6 days in the presence of 500 μM nitrate. Data are represented as mean ± SEM, n = 3 repeats per condition. *** P ≤0.001. (PDF 24 kb

Additional file 1: Figure S1. of Nitrate enhances skeletal muscle fatty acid oxidation via a nitric oxide-cGMP-PPAR-mediated mechanism

Muscle differentiation marker expression in C2C12 myoblasts cultured and differentiated over 6 days in the presence of 0, 50 and 500 μM nitrate, and (A) in the presence and absence of sGCi (1H-[1,2,4] oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), 1 μM) and (B) in the presence and absence of PGKi (KT5823, 1 μM). Data are represented as mean ± SEM, n = 4 repeats per condition. (PDF 52 kb

Additional file 1: of Mechanistic insights revealed by lipid profiling in monogenic insulin resistance syndromes

Supplementary Table S1 and Figures S1 and S2. (DOCX 102 kb

Additional file 1: of Hepatic steatosis risk is partly driven by increased de novo lipogenesis following carbohydrate consumption

contains all the additional supplementary data in the form of a Word document. (DOCX 1130 kb

Assessment of left ventricular tissue mitochondrial bioenergetics in patients with stable coronary artery disease

Recurrent myocardial ischemia can lead to left ventricular (LV) dysfunction in patients with coronary artery disease (CAD). In this observational cohort study, we assessed for chronic metabolomic and transcriptomic adaptations within LV myocardium of patients undergoing coronary artery bypass grafting. During surgery, paired transmural LV biopsies were acquired on the beating heart from regions with and without evidence of inducible ischemia on preoperative stress perfusion cardiovascular magnetic resonance. From 33 patients, 63 biopsies were acquired, compared to analysis of LV samples from 11 donor hearts. The global myocardial adenosine triphosphate (ATP):adenosine diphosphate (ADP) ratio was reduced in patients with CAD as compared to donor LV tissue, with increased expression of oxidative phosphorylation (OXPHOS) genes encoding the electron transport chain complexes across multiple cell types. Paired analyses of biopsies obtained from LV segments with or without inducible ischemia revealed no significant difference in the ATP:ADP ratio, broader metabolic profile or expression of ventricular cardiomyocyte genes implicated in OXPHOS. Differential metabolite analysis suggested dysregulation of several intermediates in patients with reduced LV ejection fraction, including succinate. Overall, our results suggest that viable myocardium in patients with stable CAD has global alterations in bioenergetic and transcriptional profile without large regional differences between areas with or without inducible ischemia.</p