References of "Critical Care Medicine"
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See detailSerum markers of sepsis in burn patients: it takes more to convince!
ROUSSEAU, Anne-Françoise ULg; LAYIOS, Nathalie ULg

in Critical Care Medicine (2015), 43(3), 100-1

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See detailConnection between cardiac vascular permeability, myocardial oedema and inflammation during sepsis: role of the alpha1AMPK isoform
Castanares-Zapatero, Diego; Bouleti, C; Sommereyns, C et al

in Critical Care Medicine (2013), 41(12), 411-22

Objective: Since AMP-activated protein kinase (AMPK) both controls cytoskeletonorganization in endothelial cells (ECs) and exerts anti-inflammatory effects, we here postulated that it could influence ... [more ▼]

Objective: Since AMP-activated protein kinase (AMPK) both controls cytoskeletonorganization in endothelial cells (ECs) and exerts anti-inflammatory effects, we here postulated that it could influence vascular permeability and inflammation, thereby counteracting cardiac wall oedema during sepsis. Design: Controlled animal study Settings: University research laboratory Subjects: C57BL/6J, α1AMPK-/- and α1AMPK+/+ mice Intervention: Sepsis was triggered in vivo using a sub-lethal injection of lipopolysaccharide (LPS, O55B5, 10 mg.kg-1), inducing systolic left ventricular (LV) dysfunction. LV function, oedema, vascular permeability and inflammation were assessed in vivo in both wild type (WT) mice (α1AMPK+/+) and α1AMPK-deficient mice (α1AMPK-/-). 5-Aminoimidazole-4-carboxamide riboside (AICAr) served to study the impact of AMPK activation on vascular permeability in vivo. The integrity of EC monolayers was also examined in vitro after LPS challenge in the presence of AICAr and/or after α1AMPK silencing. Measurements and main results: α1AMPK-deficiency dramatically impaired tolerance to LPS challenge. Indeed, α1AMPK-/- exhibited heightened cardiac vascular permeability after LPS challenge compared to α1AMPK+/+. Consequently, an increase in LV mass corresponding to exaggerated wall oedema occurred in α1AMPK-/-, without any further decrease in systolic function. Mechanistically, the LPS-induced α1AMPK-/- cardiac phenotype could not be attributed to major changes in the systemic inflammatory response, but was due to an increased disruption of interendothelial tight junctions. Accordingly, AMPK activation by AICAr counteracted LPS-induced hyperpermeability in WT mice in vivo as well as in ECs in vitro. This effect was associated with a potent protection of ZO-1 linear border pattern in ECs. Conclusions: Our results demonstrate, for the first time the involvement of a signalling pathway in the control of LV wall oedema during sepsis. AMPK exerts a protective action through the preservation of interendothelial tight junctions. Interestingly, exaggerated LV wall oedema was not coupled with aggravated systolic dysfunction. However, it could contribute to diastolic dysfunction in septic patients. [less ▲]

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See detailThe authors reply
DAMAS, Pierre ULg; LAYIOS, Nathalie ULg

in Critical Care Medicine (2013), 41(2), 19

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See detailThe authors reply
LAYIOS, Nathalie ULg; DAMAS, Pierre ULg

in Critical Care Medicine (2013), 41(3), 28

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See detailProcalcitonin usefulness for the initiation of antibiotic treatment in intensive care unit patients.
LAYIOS, Nathalie ULg; LAMBERMONT, Bernard ULg; CANIVET, Jean-Luc ULg et al

in Critical Care Medicine (2012), 40(8), 2304-9

OBJECTIVES: : To test the usefulness of procalcitonin serum level for the reduction of antibiotic consumption in intensive care unit patients. DESIGN: : Single-center, prospective, randomized controlled ... [more ▼]

OBJECTIVES: : To test the usefulness of procalcitonin serum level for the reduction of antibiotic consumption in intensive care unit patients. DESIGN: : Single-center, prospective, randomized controlled study. SETTING: : Five intensive care units from a tertiary teaching hospital. PATIENTS: : All consecutive adult patients hospitalized for > 48 hrs in the intensive care unit during a 9-month period. INTERVENTIONS: : Procalcitonin serum level was obtained for all consecutive patients suspected of developing infection either on admission or during intensive care unit stay. The use of antibiotics was more or less strongly discouraged or recommended according to the Muller classification. Patients were randomized into two groups: one using the procalcitonin results (procalcitonin group) and one being blinded to the procalcitonin results (control group). The primary end point was the reduction of antibiotic use expressed as a proportion of treatment days and of daily defined dose per 100 intensive care unit days using a procalcitonin-guided approach. Secondary end points included: a posteriori assessment of the accuracy of the infectious diagnosis when using procalcitonin in the intensive care unit and of the diagnostic concordance between the intensive care unit physician and the infectious-disease specialist. MEASUREMENTS AND MAIN RESULTS: : There were 258 patients in the procalcitonin group and 251 patients in the control group. A significantly higher amount of withheld treatment was observed in the procalcitonin group of patients classified by the intensive care unit clinicians as having possible infection. This, however, did not result in a reduction of antibiotic consumption. The treatment days represented 62.6 +/- 34.4% and 57.7 +/- 34.4% of the intensive care unit stays in the procalcitonin and control groups, respectively (p = .11). According to the infectious-disease specialist, 33.8% of the cases in which no infection was confirmed, had a procalcitonin value >1microg/L and 14.9% of the cases with confirmed infection had procalcitonin levels <0.25 microg/L. The ability of procalcitonin to differentiate between certain or probable infection and possible or no infection, upon initiation of antibiotic treatment was low, as confirmed by the receiving operating curve analysis (area under the curve = 0.69). Finally, procalcitonin did not help improve concordance between the diagnostic confidence of the infectious-disease specialist and the ICU physician. CONCLUSIONS: : Procalcitonin measuring for the initiation of antimicrobials did not appear to be helpful in a strategy aiming at decreasing the antibiotic consumption in intensive care unit patients. [less ▲]

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See detailCirculating microRNAs after cardiac arrest.
Stammet, Pascal ULg; Goretti, Emeline; Vausort, Melanie et al

in Critical care medicine (2012), 40(12), 3209-14

OBJECTIVE: Prediction of clinical outcome after cardiac arrest is clinically important. While the potential of circulating microRNAs as biomarkers of acute coronary syndromes is an active field of ... [more ▼]

OBJECTIVE: Prediction of clinical outcome after cardiac arrest is clinically important. While the potential of circulating microRNAs as biomarkers of acute coronary syndromes is an active field of investigation, it is unknown whether microRNAs are associated with outcome in cardiac arrest patients. DESIGN: Prospective, single-center proof-of-concept study. SETTING: Eighteen-bed adult general intensive care unit of an academic tertiary care hospital in Luxembourg. PATIENTS: Twenty-eight patients with cardiac arrest treated by therapeutic hypothermia after cardiac resuscitation were enrolled. MEASUREMENTS AND MAIN RESULTS: Blood samples were obtained at 48 hrs after cardiac arrest for the determination of microRNA levels and neuron-specific enolase. Neurological outcome was determined by the cerebral performance category at discharge from the intensive care unit and at 6-month follow-up. Analysis of microRNA arrays and quantitative assessment by polymerase chain reaction identified two microRNAs, miR-122 and miR-21, overexpressed in patients with poor neurological outcome (cerebral performance category 3-5, n = 14) compared to patients with favorable neurological outcome (cerebral performance category 1-2, n = 14) (48-fold and three-fold, respectively). In vitro experiments showed that both miR-122 and miR-21 are produced by neuronal cells, indicating that the elevation of circulating levels of these microRNAs after cardiac arrest may reflect brain damage. miR-122 and miR-21 predicted neurological outcome with areas under the receiver operating characteristic curve of 0.73 and 0.77, respectively. Patients within the highest third of miR-122 or miR-21 values had elevated mortality rate (p = .02). Neuron-specific enolase was an accurate predictor of neurological outcome (areas under the receiver operating characteristic curve = 0.98) and mortality (p < .001). MicroRNA levels were not associated with myocardial damage or activation of inflammation. CONCLUSIONS: As compared to neuron-specific enolase, circulating microRNAs are modest but significant predictors of neurological outcome and mortality in this small group of patients with cardiac arrest. This motivates assessing the prognostic value of microRNAs in larger cohorts of cardiac arrest patients. [less ▲]

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See detailEfficiency of a French-language triage algorithm in the Emergency Department
JOBE, Jérôme ULg; Ghuysen, Alexandre ULg; GERARD, P et al

in Critical Care Medicine (2011), 15(suppl 1), 455

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See detailPolymorphisms in innate immunity genes predispose to bacteremia and death in the medical intensive care unit
Henckaerts, L.; Nielsen, K. R.; Steffensen, R. et al

in Critical Care Medicine (2009), 37(1), 192-2011-3

OBJECTIVE: Critically ill patients are at risk of sepsis, organ failure, and death. Studying the impact of genetic determinants may improve our understanding of the pathophysiology and allow ... [more ▼]

OBJECTIVE: Critically ill patients are at risk of sepsis, organ failure, and death. Studying the impact of genetic determinants may improve our understanding of the pathophysiology and allow identification of patients who would benefit from specific treatments. Our aim was to study the influence of single nucleotide polymorphisms in selected genes involved in innate immunity on the development of bacteremia or risk of death in patients admitted to a medical intensive care unit. DESIGN, SETTING, AND PATIENTS: DNA was available from 774 medical intensive care unit patients. We selected 31 single nucleotide polymorphisms in 14 genes involved in host innate immune defense. Serum levels of MASP2 and chemotactic capacity, phagocytosis, and killing capacity of monocytes at admission were quantified. Univariate Kaplan-Meier estimates with log-rank analysis and multivariate logistic regression were performed. Bootstrap resampling technique and ten-fold cross-validation were used to assess replication stability, prognostic importance of the variables, and repeatability of the final regression model. MAIN RESULTS: Patients with at least one NOD2 variant were shown to have a reduced phagocytosis by monocytes (p = 0.03) and a higher risk of bacteremia than wild-type patients (p = 0.02). The NOD2/TLR4 combination was associated with bacteremia using survival analyses (time to bacteremia development, log-rank p < 0.0001), univariate regression (p = 0.0003), and multivariate regression analysis (odds ratio [OR] 4.26, 95% confidence interval [CI] 1.85-9.81; p = 0.0006). Similarly, the same combination was associated with hospital mortality using survival analysis (log-rank p = 0.03), univariate regression (p = 0.02), and multivariate regression analysis (OR 2.27, 95% CI 1.09-4.74; p = 0.03). Also variants in the MASP2 gene were significantly associated with hospital mortality (survival analysis log-rank-p = 0.003; univariate regression p = 0.02; multivariate regression analysis OR 2.35, 95% CI 1.38-3.99; p = 0.002). CONCLUSIONS: Functional polymorphisms in genes involved in innate immunity predispose to severe infections and death, and may become part of a risk model, allowing identification of patients at risk, who could benefit from early introduction of specific preventive or therapeutic interventions. [less ▲]

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See detailClinical Experience with Tight Glucose Control by Intensive Insulin Therapy
Preiser, Jean-Charles ULg; Devos, P.

in Critical Care Medicine (2007), 35(9 Suppl), 503-7

OBJECTIVE: To describe the current status and the clinical data related to the effects of tight glucose control by intensive insulin therapy in critically ill patients. DESIGN: Review article. SETTING ... [more ▼]

OBJECTIVE: To describe the current status and the clinical data related to the effects of tight glucose control by intensive insulin therapy in critically ill patients. DESIGN: Review article. SETTING: University hospital. PATIENTS: Medical and surgical critically ill patients in whom a correlation between blood glucose and outcome variables were searched. INTERVENTIONS: Tight glucose control by intensive insulin therapy. MEASUREMENTS AND MAIN RESULTS: In contrast to the decreases in mortality and to low severity of adverse effects reported when insulin rate was titrated to keep blood glucose between 80 and 110 mg/dL, the benefits were not confirmed in multicenter prospective studies. Retrospective data found an association between a mean blood glucose level of <140-150 mg/dL and improved outcome. Currently unanswered issues include the optimal target for blood glucose, the effects of high blood glucose variability, the risks and hazards of hypoglycemia, and the potential influence of the underlying disorder on the effects of tight glucose control. CONCLUSIONS: Recommendations regarding the practical aspects of tight glucose control by intensive insulin therapy cannot be presently issued. An intermediate target level for blood glucose of 140-180 mg/dL seems to be associated with the lowest risk-to-benefit ratio. [less ▲]

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See detailLevosimendan: Right for the right ventricle?
Lambermont, Bernard ULg; Ghuysen, Alexandre ULg; Harstein, Gary et al

in Critical Care Medicine (2007), 35(8), 1995-1996

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See detailThe RIFLE criteria: are the foundations robust?
Delanaye, Pierre ULg; Krzesinski, Jean-Marie ULg; Cavalier, Etienne ULg et al

in Critical Care Medicine (2007), 35(11), 26692669-70

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See detailMethylene blue: An old-timer or a compound ready for revival?
Donati, A.; Preiser, Jean-Charles ULg

in Critical Care Medicine (2006), 34(11), 2862-2863

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See detailSingle-beat evaluation of right ventricular contractility - Reply
Lambermont, Bernard ULg; Segers, P.; D'Orio, Vincenzo ULg

in Critical Care Medicine (2005), 33(4), 918-918

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See detailHeme oxygenase: A new piece in the glutamine puzzle
Preiser, Jean-Charles ULg; Coeffier, M.

in Critical Care Medicine (2005), 33(2), 457-458

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See detailThe use of protocols for nutritional support is definitely needed in the intensive care unit
Preiser, Jean-Charles ULg; Ledoux, Didier ULg

in Critical Care Medicine (2004), 32(11), 2354-2355

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See detailComparison between single-beat and multiple-beat methods for estimation of right ventricular contractility.
Lambermont, Bernard ULg; Segers, Patrick; Ghuysen, Alexandre ULg et al

in Critical Care Medicine (2004), 32(9), 1886-90

OBJECTIVE: It was investigated whether pharmacologically induced changes in right ventricular contractility can be detected by a so-called "single-beat" method that does not require preload reduction ... [more ▼]

OBJECTIVE: It was investigated whether pharmacologically induced changes in right ventricular contractility can be detected by a so-called "single-beat" method that does not require preload reduction. DESIGN: Prospective animal research. SETTING: Laboratory at a large university medical center. SUBJECTS: Eight anesthetized pigs. INTERVENTIONS: End-systolic elastance values obtained by a recently proposed single-beat method (Eessb) were compared with those obtained using the reference multiple-beat method (Eesmb). MEASUREMENTS AND MAIN RESULTS: Administration of dobutamine increased Eesmb from 1.6 +/- 0.3 to 3.8 +/- 0.5 mm Hg/mL (p =.001), whereas there was only a trend toward an increase in Eessb from 1.5 +/- 0.2 to 1.7 +/- 0.4 mm Hg/mL. Esmolol decreased Eesmb from 1.7 +/- 0.3 to 1.1 +/- 0.2 mm Hg/mL (p =.006), whereas there was only a trend for a decrease in Eessb from 1.5 +/- 0.2 to 1.3 +/- 0.1. CONCLUSIONS: The present method using single-beat estimation to assess right ventricular contractility does not work as expected, since it failed to detect either increases or decreases in right ventricular contractility induced by pharmacologic interventions. [less ▲]

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See detailIntrahepatic synthesis of tumor necrosis factor-alpha related to cardiac surgery is inhibited by interleukin-10 via the Janus kinase (Jak)/signal transducers and activator of transcription (STAT) pathway.
Qing, Ma; Nimmesgern, Ariane; Heinrich, Peter C et al

in Critical Care Medicine (2003), 31(12), 2769-75

SUMMARY: OBJECTIVES To identify the signaling pathways involved in the anti-inflammatory shift of the cytokine balance due to hypothermia during cardiopulmonary bypass. DESIGN Experimental animal study ... [more ▼]

SUMMARY: OBJECTIVES To identify the signaling pathways involved in the anti-inflammatory shift of the cytokine balance due to hypothermia during cardiopulmonary bypass. DESIGN Experimental animal study. SETTING Department of experimental surgery of a university hospital. SUBJECTS Young pigs. INTERVENTIONS Animals underwent normothermic (37 degrees C) or hypothermic (28 degrees C) cardiopulmonary bypass (n = 6 each). Samples of liver tissue were taken before and 6 hrs after cardiopulmonary bypass. MEASUREMENTS AND MAIN RESULTS Intrahepatic expression of tumor necrosis factor-alpha, interleukin-10, inducible nitric oxide synthase, and suppressor of cytokine signaling-3 was detected by reverse transcriptase polymerase chain reaction and/or Western blotting. Concentrations of the inhibitory protein of nuclear factor-kappaB, IkappaB, and of the signal transducer and activator of transcription (STAT)-3 were measured by Western blotting. The DNA-binding activity of nuclear factor-kappaB and STAT-3 was assessed by electrophoretic mobility shift and supershift assays. Liver cell necrosis and apoptosis were assessed by histology and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling assay, respectively. Pigs operated on in hypothermia showed significantly higher intrahepatic concentrations of interleukin-10 and lower concentrations of tumor necrosis factor-alpha than the others. They also showed a lower percentage of hepatic cell necrosis but not of apoptosis. This anti-inflammatory reaction observed in the hypothermic group was associated with a higher expression of suppressor of cytokine signaling-3 and with increased activation of STAT-3. Activation of nuclear factor-kappaB and expression of inducible nitric oxide synthase, however, were not significantly different between both groups. CONCLUSION Our results show that hypothermia during cardiopulmonary bypass up-regulates interleukin-10 via STAT-3 activation, which in turn leads to the attenuation of tumor necrosis factor-alpha expression and to hepatic protection. [less ▲]

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See detailGlutamine, a life-saving nutrient, but why?
Preiser, Jean-Charles ULg; Wernerman, J.

in Critical Care Medicine (2003), 31(10), 2555-2556

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