Patient- and surgery-related characteristics (n = 120).

<p><i>SD</i> = <i>standard deviation</i></p><p><i>IQR</i> = <i>interquartile range</i></p><p>Patient- and surgery-related characteristics (n = 120).</p

Time course of biomarkers as related to the absence or presence of cardiopulmonary bypass.

<p>All inflammatory markers investigated showed a steeper rise in patients subjected to cardiopulmonary bypass without reaching statistical significance. (p>0.05 for interaction for all biomarkers, determined by a linear mixed effects regression model).</p

Association of PSP, CRP and WBC levels with age (A), gender (B) and diabetes (C).

<p>Shown are values at baseline (preoperative values). The groups were compared by one-way ANOVA. Asterisks indicate significant differences (*p<0.05; **p<0.01).</p

Time course of biomarkers as related to the surgical technique employed.

<p>PSP levels showed a significantly steeper rise in the postoperative course of patients subjected to sternotomy compared to those receiving minimally invasive surgery (p<0.05 for interaction, determined by a linear mixed effects regression model). There was no significant difference in the postoperative levels of CRP and WBC between the two cohorts of patients.</p

Time course of biomarkers (A-C) following cardiac surgery.

<p>All inflammatory markers investigated showed a statistically significant rise in the course of postoperative day 1–3 (p<0.05, determined by a linear mixed effects regression model).</p

Receiver operating characteristics curve to predict infection for PSP (A), CRP (B) and WBC (C) at postoperative 1–3.

<p>A cutoff of 48.1 ng/ml for PSP levels at postoperative day 2 reveals a sensitivity of 64% and a specificity of 70%. PLR (positive likelihood ratio) = 2.1. NLR (negative likelihood ratio) = 0.51.</p

Discriminatory power of biomarkers for postoperative infection.

<p>PSP levels showed a significantly stronger postoperative rise at day 1–3 in patients receiving a diagnosis of infection during their hospital stay as opposed to patients exhibiting an uneventful course. (p<0.05 for interaction, determined by a linear mixed effects regression model). Other biomarkers (CRP and WBC) failed to differentiate infection from postoperative inflammatory power.</p

Additional file 1: of A hospital-wide evaluation of delirium prevalence and outcomes in acute care patients - a cohort study

Components of the delirium management protocol. (PDF 101 kb

Clinical characteristics of septic patients subjected to targeted metabolomic analysis of bile acids.

<p>APACHE II, Acute Physiology and Chronic Health Evaluation II; SAPS II, Simplified Acute Physiology Score; SOFA, Sequential Organ Failure Assessment.</p

Polymicrobial sepsis causes deranged bile acid conjugation and transport.

<p>At 15 h after sepsis induction, plasma, liver tissue, and bile were subjected to targeted metabolomics. Expression of BAAT, facilitating conjugation to taurine and glycine, was quantified by immunoblotting. (A) The plot depicts median log₂ fold changes of unconjugated as well as glycine- and taurine-conjugated bile acid in plasma, liver, and bile, comparing septic to sham-operated rats (<i>n</i> = 12 per group, *<i>p</i><0.05 or **<i>p</i><0.01 compared to sham). (B) Conjugation index as a surrogate for the observed conjugation defect reflected by the ratio of unconjugated bile acids CA and CDCA to the corresponding taurine (TCA and taurochenodeoxycholic acid) and glycine (GCA and glycochenodeoxycholic acid) conjugates in plasma, liver and bile (ratio given as log₂ fold change, <i>n</i> = 12 per group). (C and D) Representative immunoblots of BAAT 15 h after sepsis induction in cytosolic (c) as well as peroxisomal (p) fractions, with corresponding densitometric analysis (<i>n</i> = 5 for sham, <i>n</i> = 8 for sepsis; BAAT (c): *<i>p</i> = 0.002; BAAT (p): *<i>p</i> = 0.006 compared to sham). Densitomentric values are normalised to β-actin. DCA, deoxycholic acid; GDCA, glycodeoxycholic acid; GCDCA, glycochenodeoxycholic acid; GLCA, glycolithocholic acid; GLCAS, glycolithocholic acid sulphate; GUDCA, glycoursodeoxycholic acid; TCDCA, taurochenodeoxycholic acid; TLCA, taurolithocholic acid; TLCAS, taurolithocholic acid sulphate; TUDCA, tauroursodeoxycholic acid; UDCA, ursodeoxycholic acid.</p