BackgroundSystemic immune inflammation is a key mediator in the progression of coronary artery disease (CAD), concerning various metabolic and lipid changes. In this study, the relationship between the inflammatory index and metabolic profile in patients with CAD was investigated to provide deep insights into metabolic disturbances related to inflammation.MethodsWidely targeted plasma metabolomic and lipidomic profiling was performed in 1,234 patients with CAD. Laboratory circulating inflammatory markers were mainly used to define general systemic immune and low-grade inflammatory states. Multivariable-adjusted linear regression was adopted to assess the associations between 860 metabolites and 7 inflammatory markers. Least absolute shrinkage and selection operator (LASSO) logistic-based classifiers and multivariable logistic regression were applied to identify biomarkers of inflammatory states and develop models for discriminating an advanced inflammatory state.ResultsMultiple metabolites and lipid species were linearly associated with the seven inflammatory markers [false discovery rate (FDR) <0.05]. LASSO and multivariable-adjusted logistic regression analysis identified significant associations between 45 metabolites and systemic immune-inflammation index, 46 metabolites and neutrophil–lymphocyte ratio states, 32 metabolites and low-grade inflammation score, and 26 metabolites and high-sensitivity C-reactive protein states (P < 0.05). Glycerophospholipid metabolism and arginine and proline metabolism were determined as key altered metabolic pathways for systemic immune and low-grade inflammatory states. Predictive models based solely on metabolite combinations showed feasibility (area under the curve: 0.81 to 0.88) for discriminating the four parameters that represent inflammatory states and were successfully validated using a validation cohort. The inflammation-associated metabolite, namely, β-pseudouridine, was related to carotid and coronary arteriosclerosis indicators (P < 0.05).ConclusionsThis study provides further information on the relationship between plasma metabolite profiles and inflammatory states represented by various inflammatory markers in CAD. These metabolic markers provide potential insights into pathological changes during CAD progression and may aid in the development of therapeutic targets.
An enzyme-linked immunosorbent assay (ELISA) was developed to screen for the presence of botulinal toxin types A, B, and E in inoculated food studies. A commercially available trivalent antitoxin (Connaught Laboratories, Ontario) was used as a capture antibody and biotinylated for use as a secondary antibody. An avidin-alkaline phosphatase conjugate coupled with an enzymebased amplification system resulted in a high degree of sensitivity. Detection levels of purified neurotoxins in gelatin phosphate buffer were 9 LD50 for type A and <1 intraperitoneal mouse LD50 for types B and E, respectively. Toxin produced by two-type F strains (proteolytic and nonproteolytic) was detected in a liquid laboratory medium. In a comparative study of over 490 samples of ground turkey meat inoculated with C. botulinum types E and nonproteolytic B, the ELISA gave no false negatives and 91 false positives. False positives were thought to be due to the presence of inactivated toxin or toxin levels insufficient to cause mouse death. Statistical analysis of these data showed an ELISA sensitivity of 100%, specificity of 70.6%, and an efficiency of 81.4% when compared to the mouse bioassay for detection of botulinal toxins types B and E. Coffee intermediates inoculated with proteolytic Clostridium botulinum types A and B caused nonspecific death in mice but were negative for presence of toxin by ELISA.
The effect of sodium lactate and storage temperature on toxigenesis by proteolytic (Pr) and nonproteolytic (Np) Clostridium botulinum spores inoculated in processed ‘sous‐vide’‐type beef, chicken breast and salmon was explored. Three g samples of beef and salmon homogenates with 0, 2.4 and 4.8% (w/w) lactate and of chicken with 0, 1.8 and 3.6% (w/w) lactate were placed in 24‐well tissue culture plates. The samples were inoculated with 104 spores of pools of Pr (4A + 2B + 2F strains) or Np (4B + 4E strains), vacuum‐packaged in barrier bags, and stored at 16 and 30°C for Pr and at 4, 8, 12 and 30°C for Np for up to 90 d. Lactate at 2.4% in beef and 1.8% in chicken delayed toxigenesis by Np for 40 d at 12°C and by Pr for 28 d at 16°C. Delaying toxigenesis for similar periods of time in salmon required 4.8% lactate and 12°C for Np, and 2.4% lactate and 16°C for Pr. Increasing levels of lactate and decreasing temperature significantly delayed toxigenesis of Cl. botulinum in the ‘sous‐vide’ products.
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