A samples were depleted for high Macitentan abundant proteins, trypsin digested and

A samples were depleted for high abundant proteins, trypsin digested and labelled with iTRAQ 8plex system. The tryptic peptides were separated by SCX chromatography and analysed with LC-MS. The collected data processed and submitted to mascot search engine with selection of swissprot database and 1 FDR. The results from mascot were further analysed by isobaric Q. Results: The proteome profile unable us to indentify total 64 and 61 differentially expressed proteins in CAP and HAP survival patients, while, 68 and 75 protein were identified in CAP and HAP non survival patients. Total 26 proteins were common in survival patients, whereas 38 and 35 proteins were specific for CAP and HAP, respectively. Total 33 proteins were common in non survival patients, whereas 35 and 42 proteins were specific for CAP and HAP, respectively. On the comparison of proteins across all groups, 21 proteins were common; 12 and 10 proteins were specific to CAP and HAP survival, while, 13 and 16 protein were unique to CAP and HAP non survival groups. These proteins are key molecules for various biological functions including inflammatory <a href="PubMed”>https://www.ncbi.nlm.nih.gov/pubmed/8486289″>PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/8486289 response as well as signalling cascade like acute phase response etc. The further analysis and validation is in progress. Conclusions: This study provides the first molecular level evidence of differential response in septic patients secondary to CAP and HAP. The results show higher numbers of unique proteins to corresponding groups. Underlying diseases, previous therapeutic interventions and different etiology may underscore the differences observed at a protein level. P029 Monocyte HLA-DR expression in community-acquired bacteremic sepsis – dynamics <a href="PubMed”>https://www.ncbi.nlm.nih.gov/pubmed/16474207″>PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/16474207 associated to aetiology and prediction of secondary sepsis SC Cajander1, G Rasmussen1, E Tina1, B S erquist1, J K lman1, K Str in2 1 Faculty of Medicine and Health ebro University, ebro, Sweden; 2 Department of Infectious Diseases, Karolinska University Hospital, Stockholm, Sweden Critical Care 2016, 20(Suppl 2):PP027 Copeptin predicts 10-year all-cause mortality in community patients J. Odermatt1, R Bolliger1, L Hersberger1, M Ottiger1, M Christ-Crain2, B Mueller1, P Schuetz1 1 Kantonsspital Aarau, Aarau, Switzerland, 2University Hospital Basel, Basel, Switzerland Critical Care 2016, 20(Suppl 2):P027 Introduction: We evaluated associations of copeptin levels with 10 year mortality in otherwise healthy patients visiting their general practitioner (GP) for a respiratory infection included in a previous trial (1). Copeptin, the C-terminal part of the arginine vasopressin precursor peptide, is secreted in response to stress and correlates with adverse clinical outcomes in the acute-care hospital setting (2, 3). There are no comprehensive data regarding its prognostic value in the community. Methods: This is a secondary analysis including data from 359 patients included in the PARTI trial. Copeptin was measured in batch-analysis on admission and after 7 days. We calculated cox regression models and area under the receiver operating characteristic curve (AUC) to assess an association of copeptin with mortality. Mortality data were collected through phone interviews 10 years after trial inclusion. Results: After a median follow-up of 10.0 (interquartile range (IQR) 9.5-10.3) years, mortality was 9.8 . Median admission copeptin levels were significantly elevated in non-survivors compared to survivors (13.8 pmol/l, IQR 5.9-27.8; vs. 6.3 pmol/l, IQR 4.1-11.5; p < 0.001), Admission copept.