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      Year in review 2006: Critical Care – multiple organ failure, sepsis, and shock

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          Abstract

          In 2006, Critical Care provided important and clinically relevant research data in the field of multiple organ failure, sepsis, and shock. This review summarizes the results of the experimental studies and clinical trials and discusses them in the context of the relevant scientific and clinical background.

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          Most cited references47

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          Opposing effects of ERK and JNK-p38 MAP kinases on apoptosis.

          Apoptosis plays an important role during neuronal development, and defects in apoptosis may underlie various neurodegenerative disorders. To characterize molecular mechanisms that regulate neuronal apoptosis, the contributions to cell death of mitogen-activated protein (MAP) kinase family members, including ERK (extracellular signal-regulated kinase), JNK (c-JUN NH2-terminal protein kinase), and p38, were examined after withdrawal of nerve growth factor (NGF) from rat PC-12 pheochromocytoma cells. NGF withdrawal led to sustained activation of the JNK and p38 enzymes and inhibition of ERKs. The effects of dominant-interfering or constitutively activated forms of various components of the JNK-p38 and ERK signaling pathways demonstrated that activation of JNK and p38 and concurrent inhibition of ERK are critical for induction of apoptosis in these cells. Therefore, the dynamic balance between growth factor-activated ERK and stress-activated JNK-p38 pathways may be important in determining whether a cell survives or undergoes apoptosis.
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            Implementation of a bundle of quality indicators for the early management of severe sepsis and septic shock is associated with decreased mortality.

            The purpose of this study was to examine the outcome implications of implementing a severe sepsis bundle in an emergency department as a quality indicator set with feedback to modify physician behavior related to the early management of severe sepsis and septic shock. Two-year prospective observational cohort. Academic tertiary care facility. Patients were 330 patients presenting to the emergency department who met criteria for severe sepsis or septic shock. Five quality indicators comprised the bundle for severe sepsis management in the emergency department: a) initiate central venous pressure (CVP)/central venous oxygen saturation (Scvo2) monitoring within 2 hrs; b) give broad-spectrum antibiotics within 4 hrs; c) complete early goal-directed therapy at 6 hrs; d) give corticosteroid if the patient is on vasopressor or if adrenal insufficiency is suspected; and e) monitor for lactate clearance. Patients had a mean age of 63.8 +/- 18.5 yrs, Acute Physiology and Chronic Health Evaluation II score 29.6 +/- 10.6, emergency department length of stay 8.5 +/- 4.4 hrs, hospital length of stay 11.3 +/- 12.9 days, and in-hospital mortality 35.2%. Bundle compliance increased from zero to 51.2% at the end of the study period. During the emergency department stay, patients with the bundle completed received more CVP/Scvo2 monitoring (100.0 vs. 64.8%, p < .01), more antibiotics (100.0 vs. 89.7%, p = .04), and more corticosteroid (29.9 vs. 16.2%, p = .01) compared with patients with the bundle not completed. In a multivariate regression analysis including the five quality indicators, completion of early goal-directed therapy was significantly associated with decreased mortality (odds ratio, 0.36; 95% confidence interval, 0.17-0.79; p = .01). In-hospital mortality was less in patients with the bundle completed compared with patients with the bundle not completed (20.8 vs. 39.5%, p < .01). Implementation of a severe sepsis bundle using a quality improvement feedback to modify physician behavior in the emergency department setting was feasible and was associated with decreased in-hospital mortality.
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              Signalling from adenosine receptors to mitogen-activated protein kinases.

              The purine nucleoside adenosine acts via four distinct adenosine receptor subtypes: the adenosine A(1), A(2A), A(2B), and A(3) receptor. They are all G protein-coupled receptors (GPCR) coupling to classical second messenger pathways such as modulation of cAMP production or the phospholipase C (PLC) pathway. In addition, they couple to mitogen-activated protein kinases (MAPK), which could give them a role in cell growth, survival, death and differentiation. Although each of the adenosine receptors can activate one or more of the MAPKs, the mechanisms appear to differ substantially, both between receptor subtypes in the same cell type and between the same receptor in different cell types.
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                Author and article information

                Journal
                Crit Care
                Critical Care
                BioMed Central
                1364-8535
                1466-609X
                2007
                24 August 2007
                : 11
                : 4
                : 221
                Affiliations
                [1 ]Anesteziologicko-resuscitacni klinika, Fakultni nemocnice u sv. Anny, Pekarska 53, 656 00 Brno, Czech Republic
                [2 ]Sektion Anästhesiologische Pathophysiologie und Verfahrensentwicklung, Klinik für Anästhesiologie, Universität Ulm, Parkstrasse 11, D – 89073 Ulm, Germany
                Article
                cc5938
                10.1186/cc5938
                2206506
                17764584
                7e7bb22c-4b54-45fd-a728-45ebcc4418eb
                Copyright © 2007 BioMed Central Ltd
                History
                Categories
                Review

                Emergency medicine & Trauma
                Emergency medicine & Trauma

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