***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Background Timely risk stratification is the key strategy to improve prognosis of patients with sepsis . Previous study has proposed to develop a powerful risk assessment rule by the combination of Acute Physiology and Chronic Health Evaluation II ( APACHE II ) score and plasma soluble urokinase plasminogen activator receptor ( suPAR ) . That reaffirmation of suPAR as a prognostic marker in Chinese patients with severe sepsis is the aim of the study . Methods A total of 137 consecutive Chinese patients with sepsis were enrolled in a prospect i ve study cohort . Demographic and clinical characteristics , conventional risk factors and important laboratory data were prospect ively recorded . Sequential plasma suPAR concentrations  were measured by an enzymeimmunoabsorbent assay on days 1 , 3 , and 7 after admission to the intensive care unit ( ICU ) . Receiver operating characteristic ( ROC ) curves and Cox regression analysis were used to examine the performance of suPAR in developing a rule for risk stratification . Results The results showed that plasma suPAR concentrations remained relatively stable within survivors and non-survivors during the first week of disease course . Regression analysis indicated that APACHE II ≥15 and suPAR ≥10.82 ng/mL were independently associated with unfavorable outcome . With the above cutoffs of APACHE II and suPAR , strata of disease severity were determined . The mortality of each stratum differed significantly from the others . Conclusions Combination of APACHE II score and suPAR may supply the powerful prognostic utility for the mortality of sepsis In systemic inflammation and sepsis , endothelial activation and microvascular dysfunction are characteristic features that promote multiorgan failure . As symmetric dimethylarginine ( SDMA ) impacts vascular tension and integrity via modulating nitric oxide ( NO ) pathways , we investigated circulating SDMA in critical illness and sepsis . 247 critically ill patients ( 160 with sepsis , 87 without sepsis ) were studied prospect ively upon admission to the medical intensive care unit ( ICU ) and on day 7 , in comparison to 84 healthy controls .  SDMA serum levels were significantly elevated in critically ill patients at admission to ICU compared to controls and remained stably elevated during the first week of ICU treatment . The highest SDMA levels were found in patients with sepsis . SDMA levels closely correlated with disease severity scores , biomarkers of inflammation , and organ failure ( renal , hepatic , and circulatory ) . We identified SDMA serum concentrations at admission as an independent prognostic biomarker in critically ill patients not only for short-term mortality at the ICU but also for unfavourable long-term survival . Thus , the significant increase of circulating  SDMA  in critically ill patients indicates a potential pathogenic involvement in endothelial dysfunction during sepsis and may be useful for mortality risk stratification at the ICU ABSTRACT Systemic inflammation often leads to complications in critically ill patients . Activation of the receptor for advanced glycation end-products ( RAGE ) generates inflammatory cytokines , proteases , and oxidative stress and may link inflammation to subsequent organ damage . Furthermore , hyperglycemia-induced oxidative stress increases RAGE lig and s and RAGE expression . We hypothesized that preventing hyperglycemia during critical illness reduces the risk of excessively enhanced RAGE signaling , which could relate to clinical outcomes and risk of death . In 405 long-stay surgical intensive care unit patients r and omized to intensive or conventional insulin treatment  , serum concentrations of  soluble RAGE ( decoy receptor ) and the RAGE lig and s high-mobility group box 1 ( HMGB1 ) and S100A12 were measured on admission , day 7 , and last day . These were compared with levels in 71 matched control subjects and with C-reactive protein ( CRP ) as a routinely monitored inflammation marker . On admission , soluble RAGE , HMGB1 , S100A12 , and CRP were higher in patients than in controls . The HMGB1 , S100A12 , and CRP remained elevated throughout intensive care unit stay , whereas soluble RAGE decreased to levels lower than in controls by day 7 . Unexpectedly , insulin treatment did not affect the circulating levels of these markers . In univariable analysis , elevated levels of soluble RAGE on admission were associated with adverse outcome , including circulatory failure , kidney failure , liver dysfunction , and mortality . The associations with circulatory and kidney failure remained significant in multivariable logistic regression analysis corrected for baseline risk factors . Critical illness affects components of RAGE signaling , unaffected by insulin treatment . Elevated on-admission soluble RAGE was associated with adverse outcomes BACKGROUND Endothelial injury is recognized to trigger organ failures during the first 48h of septic shock . We evaluate endothelial biomarkers at ICU admission in their ability to predict severity , outcome , and organ failures in septic shock patients . METHODS This prospect i ve observational pilot study was conducted in a medical intensive care unit of a university hospital . Plasma levels of endothelial biomarkers as angiopoietin-2 , sE-selectin or endocan were measured at ICU admission of 20 patients presenting with septic shock .  Clinical and biological data were recorded at inclusion and each day during the first week . RESULTS Significant correlations were found between angiopoietin-2 and severity scores at Day 1 : SAPS2 ( r(2)=0.620 ; p=0.004 ) and LOD score ( r(2)=0.681 ; p=0.001 ) . The angiopoietin-2 level was significantly higher in patients presenting with organ failure such as hemodynamic , renal or hepatic failure . It correlated with catecholamine infusion dose and was higher in non survivors compared with survivors ( 33.5 [ 28.9 - 51.4 ] vs. 12.4 [6.4 - 14.7]ng/ml ; p=0.001 ) . In contrast , in that population presenting with septic shock , endocan level at inclusion was not related to any organ failure at inclusion or Day 1 but appeared lower in patients presenting with respiratory failure at Day 3 compared to those who do not ( 1.9 [ 0.99 - 3.1 ] vs 5.2 [3.1 - 17.2]ng/ml ; p=0.032 ) . The endocan level at inclusion was correlated with the decrease in PaO2/FiO2 ratio at Day 2 ( r(2)=0.628 ; p=0.0004 ) and Day 3 ( r(2)=0.645 ; p=0.005 ) . Endocan level < 2.54ng/ml at admission is predictive of a respiratory failure presence at Day 3 . CONCLUSION In septic shock patients , angiopoietine-2 is related with clinical severity during the first 24h but only endocan is able to predict the presence of respiratory failure at Day 3 Introduction The endothelial specific angiopoietin (Ang)-Tie2 lig and -receptor system has been identified as a non-redundant mediator of endothelial activation in experimental sepsis . Binding of circulating Ang-1 to the Tie2 receptor protects the vasculature from inflammation and leakage , whereas binding of Ang-2 antagonises Tie2 signalling and disrupts endothelial barrier function . Here , we examine whether circulating Ang-1 and /or Ang-2 independently predict mortality in a cohort of critically ill medical patients . Methods Circulating vascular endothelial growth factor ( VEGF ) , Ang-1 and Ang-2 were prospect ively measured in sera from 29 healthy controls and 43 medical ICU patients by immunoradiometric assay ( IRMA ) and ELISA , respectively . Survival after 30 days was the primary outcome studied . Results Median serum Ang-2 concentrations were increasingly higher across the following groups : healthy controls , patients without sepsis , patients with sepsis and patients with septic shock . In contrast , Ang-1 and VEGF concentrations were significantly lower in all patient groups compared with healthy controls . Ang-2 correlated with partial pressure of oxygen in arterial blood (PaO2)/fraction of inspired oxygen ( FiO2 ) , tissue hypoxia , Sequential Organ Failure Assessment ( SOFA ) and Physiology and Chronic Health Evaluation II ( APACHE II ) score . Multivariate Cox regression analyses confirmed a strong independent prognostic impact of high Ang-2 as a novel marker of 30-day survival . Conclusions A marked imbalance of the Ang-Tie system in favour of Ang-2 is present in critically ill medical patients . Our findings highlight the independent prognostic impact of circulating Ang-2 in critical illness . Ang-2 may be used as a readily available powerful predictor of outcome and may open new perspectives to individualise treatment in the ICU Introduction High-mobility group box-1 protein ( HMGB1 ) has been known as a chromosomal protein for many years . HMGB1 has recently been shown to be a proinflammatory cytokine with a role in the immunopathogenesis of sepsis . Lipopolysaccharide-binding protein ( LBP ) has a central role in the innate immune response when the host is challenged by bacterial pathogens . Procalcitonin ( PCT ) has been suggested as a marker of severe bacterial infections and sepsis . The aim of the present study was to investigate levels of HMGB1 , LBP and PCT in a well-characterised sepsis cohort . The study plan included analysis of the levels of the inflammatory markers in relation to the severity of infection , to the prognosis and to the ability to identify patients with bacteraemia . Methods Patients suspected of having severe infections and admitted to a department of internal medicine were included in a prospect i ve manner . Demographic data , comorbidity , routine biochemistry , microbiological data , infection focus , severity score and mortality on day 28 were recorded . Plasma and serum were sample d within 24 hours after admission .  Levels of all studied markers ( HMGB1 , LBP , PCT , IL-6 , C-reactive protein , white blood cell count and neutrophils ) were measured with commercially available laboratory techniques . Results A total of 185 adult patients were included in the study ; 154 patients fulfilled our definition of infection .  Levels of HMGB1 , LBP and PCT were higher in infected patients compared with a healthy control group ( P < 0.0001 ) . Levels of HMGB1 , LBP and PCT were higher in the severe sepsis group compared with the sepsis group ( P < 0.01 ) . No differences were observed in levels of the inflammatory markers in fatal cases compared with survivors . Levels of all studied markers were higher in bacteraemic patients compared with nonbacteraemic patients ( P < 0.05 ) . PCT performed best in a receiver – operator curve analysis discriminating between bacteraemic and nonbacteraemic patients ( P < 0.05 ) . HMGB1 correlated to LBP , IL-6 , C-reactive protein , white blood cell count and neutrophils ( P < 0.001 ) . LBP correlated to PCT , IL-6 and C-reactive protein ( P < 0.001 ) . Conclusion Levels of HMGB1 , PCT and LBP were higher in infected patients compared with those in healthy controls , and levels were higher in severe sepsis patients compared with those in sepsis patients . Levels of all studied inflammatory markers ( HMGB1 , LBP , PCT , IL-6 ) and infection markers ( C-reactive protein , white blood cell count , neutrophils ) were elevated among bacteraemic patients . PCT performed best as a diagnostic test marker for bacteraemia Purpose Sepsis is a major health burden worldwide . Pre clinical investigations in animals and retrospective studies in patients have suggested that inhibition of platelets may improve the outcome of sepsis . In this study we investigated whether chronic antiplatelet therapy impacts on the presentation and outcome of sepsis , and the host response . Methods We performed a prospect i ve observational study in 972 patients admitted with sepsis to the mixed intensive care units ( ICUs ) of two hospitals in the Netherl and s between January 2011 and July 2013 . Of them , 267 patients ( 27.5 % ) were on antiplatelet therapy (  95.9 % acetylsalicylic acid )  before admission . To account for differential likelihoods of receiving antiplatelet therapy , a propensity score was constructed , including variables associated with use of antiplatelet therapy . Cox proportional hazards regression was used to estimate the association of antiplatelet therapy with mortality . Results Antiplatelet therapy was not associated with sepsis severity at presentation , the primary source of infection , causative pathogens , the development of organ failure or shock during ICU stay , or mortality up to 90 days after admission , in either unmatched or propensity-matched analyses . Antiplatelet therapy did not modify the values of 19 biomarkers providing insight into hallmark host responses to sepsis , including activation of the coagulation system , the vascular endothelium , the cytokine network , and renal function , during the first 4 days after ICU admission . Conclusions Pre-existing antiplatelet therapy is not associated with alterations in the presentation or outcome of sepsis , or the host response Purpose : Sclerostin is a negative regulator of bone metabolism and associated with chronic morbidities . We investigated circulating sclerostin in critically ill patients . Methods : A total of 264 patients ( 170 with sepsis ) were studied prospect ively upon admission to the medical intensive care unit ( ICU ) and on day 7 . Patients ' survival was followed for up to 
    Output:
    
Conclusions Ang-1 , Ang-2 , and suPAR provide beneficial prognostic information about mortality in adult patients with sepsis .