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Materials and methods For this purpose, we generated an endotoxinic model with glucose administration.

The slightly higher AUC of the model with glucose (0.9181 vs. 0.9169) and the joint model (Additional file 1: Table A1) suggests some advantage for glucose.

As shown in Table  1 the mean Brier score of the model with glucose (2216x10-5) and cholesterol (2232x10-5) were similar, and no statistically significant difference could be found (p-value 0.287).

The model with glucose had a slightly better predictive capacity (BS: 2216x10-5 vs. 2232x10-5; AUC: 0.9181 vs. 0.9169, IDI: 0.009 with p-value 0.026) and could well discriminate the overall risk of persons with high and low concentrations.

The addition of Prx4 to the DESIR clinical model with glucose minimally improved the C-statistic (change of +0.003; p = 0.33), but led to an IDI of 0.003 (p = 0.04) and a continuous NRI of 0.15 (p = 0.01) in men.

The external validation using the NHANES III data, confirmed the overall pattern (Table  1): The results with glucose and cholesterol are comparable and also suggest slightly better predictive performance of the model with glucose (Brier score: 7662x10-5 vs. 7744x10-5 with p-value 0.245; AUC: 0.8766 vs. 0.8737; IDI 0.029 with p-value < 0.001).

Similar(54)

The glucose influence on xylose consumption of the selected strain was investigated by model SSCF with glucose or hydrolysate feed.

Gene expression profiling in a pancreatic beta cell model treated with glucose and cAMP has shown that the majority of genes regulated in sustained treated cells were not regulated by transient (1 h) treatment, indicating that beta cells can produce drastically different transcriptional outputs in response to different durations of metabolic stimuli [ 2].

We therefore investigated whether an in-vivo septic animal model with labelled glucose would provide useful data about glucose and energy metabolism and whether the same tracer set up could be used to reliably estimate the turnover of individual proteins.

In both the larger model and the model with fasting glucose, low hemoglobin was associated with increased risk (OR 1.43, 95% CI 1.09-1.86 for large model and OR 1.60, (95% CI 1.07-2.40) for the model with fasting glucose (Table  3)).

At each point, an algorithm based on a uniform model (with personal glucose calibration) was used to calculate the three blood parameters.

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