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  • 1
    Language: German
    In: Orthopädie und Unfallchirurgie Mitteilungen und Nachrichten, 2014, Vol.03(04), pp.445-446
    Keywords: DGU
    ISSN: 2193-5254
    E-ISSN: 2193-5262
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  • 2
    In: PLoS ONE, 2014, Vol.9(12)
    Description: The increasing incidence of implant-associated infections induced by Staphylococcus aureus (SA) in combination with growing resistance to conventional antibiotics requires novel therapeutic strategies. In the current study we present the first application of the biofilm-penetrating antimicrobial peptide lysostaphin in the context of bone infections. In a standardized implant-associated bone infection model in mice beta-irradiated lysostaphin-coated titanium plates were compared with uncoated plates. Coating of the implant was established with a poly(D,L)-lactide matrix (PDLLA) comprising lysostaphin formulated in a stabilizing and protecting solution (SPS). All mice were osteotomized and infected with a defined count of SA. Fractures were fixed with lysostaphin-coated locking plates. Plates uncoated or PDLLA-coated served as controls. All mice underwent debridement and lavage on Days 7, 14, 28 to determine the bacterial load and local immune reaction. Fracture healing was quantified by conventional radiography. On Day 7 bacterial growth in the lavages of mice with lysostaphin-coated plates showed a significantly lower count to the control groups. Moreover, in the lysostaphin-coated plate groups complete fracture healing were observed on Day 28. The fracture consolidation was accompanied by a diminished local immune reaction. However, control groups developed an osteitis with lysis or destruction of the bone and an evident local immune response. The presented approach of terminally sterilized lysostaphin-coated implants appears to be a promising therapeutic approach for low grade infection or as prophylactic strategy in high risk fracture care e.g. after severe open fractures.
    Keywords: Research Article ; Medicine And Health Sciences ; Physical Sciences ; Research And Analysis Methods
    E-ISSN: 1932-6203
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  • 3
    Language: English
    In: Critical Care, Jan 13, 2011, Vol.15, p.R20
    Description: Introduction Deregulated apoptosis and overshooting neutrophil functions contribute to immune and organ dysfunction in sepsis and multiple organ failure (MOF). In the present study, we determined the role of soluble Fas (sFas) in the regulation of posttraumatic neutrophil extrinsic apoptosis and the development of sepsis. Methods Forty-seven major trauma patients, 18 with and 29 without sepsis development during the first 10 days after trauma, were enrolled in this prospective study. Seventeen healthy volunteers served as controls. Blood samples from severely injured patients were analyzed at day 1, day 5 and day 9 after major trauma. sFas levels, plasma levels of neutrophil elastase (PMNE) and levels of interleukin (IL)-6 were quantified by enzyme-linked immunosorbent assay and related to patients' Sequential Organ Failure Assessment (SOFA) score and Multiple Organ Dysfunction Score (MODS). Neutrophil apoptosis was determined by propidium iodide staining of fragmented DNA and flow cytometry. sFas-mediated effects on neutrophil apoptosis were investigated in cells cultured with agonistic anti-Fas antibodies in the presence of recombinant sFas, sFas-depleted serum or untreated serum from septic patients. Results Serum levels of sFas in patients who later developed sepsis were significantly increased at day 5 (P [less than] 0.01) and day 9 (P [less than] 0.05) after trauma compared with patients with uneventful recovery. Apoptosis of patient neutrophils was significantly decreased during the observation period compared with control cells. Moreover, Fas-mediated apoptosis of control neutrophils was efficiently inhibited by recombinant sFas and serum from septic patients. Depletion of sFas from septic patient sera diminished the antiapoptotic effects. In septic patients, sFas levels were positively correlated with SOFA at day 1 (r = 0.7, P [less than] 0.001), day 5 (r = 0.62, P [less than] 0.01) and day 9 (r = 0.58, P [less than] 0.01) and with PMNE and leukocyte counts (r = 0.49, P [less than] 0.05 for both) as well as MODS at day 5 (r = 0.56, P [less than] 0.01) after trauma. Conclusions Increased sFas in patients with sepsis development impairs neutrophil extrinsic apoptosis and shows a positive correlation with the organ dysfunction scores and PMNE. Therefore, sFas might be a therapeutic target to prevent posttrauma hyperinflammation and sepsis.
    Keywords: Apoptosis -- Physiological Aspects ; Apoptosis -- Genetic Aspects ; Apoptosis -- Research ; Injuries -- Complications And Side Effects ; Injuries -- Patient Outcomes ; Injuries -- Research ; Multiple Organ Failure -- Risk Factors ; Multiple Organ Failure -- Development And Progression ; Multiple Organ Failure -- Genetic Aspects ; Multiple Organ Failure -- Research ; Sepsis -- Risk Factors ; Sepsis -- Development And Progression ; Sepsis -- Genetic Aspects ; Sepsis -- Research
    ISSN: 1364-8535
    Source: Cengage Learning, Inc.
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  • 4
    Language: English
    In: Critical Care, Jan 13, 2011, Vol.15, p.R20
    Description: Introduction Deregulated apoptosis and overshooting neutrophil functions contribute to immune and organ dysfunction in sepsis and multiple organ failure (MOF). In the present study, we determined the role of soluble Fas (sFas) in the regulation of posttraumatic neutrophil extrinsic apoptosis and the development of sepsis. Methods Forty-seven major trauma patients, 18 with and 29 without sepsis development during the first 10 days after trauma, were enrolled in this prospective study. Seventeen healthy volunteers served as controls. Blood samples from severely injured patients were analyzed at day 1, day 5 and day 9 after major trauma. sFas levels, plasma levels of neutrophil elastase (PMNE) and levels of interleukin (IL)-6 were quantified by enzyme-linked immunosorbent assay and related to patients' Sequential Organ Failure Assessment (SOFA) score and Multiple Organ Dysfunction Score (MODS). Neutrophil apoptosis was determined by propidium iodide staining of fragmented DNA and flow cytometry. sFas-mediated effects on neutrophil apoptosis were investigated in cells cultured with agonistic anti-Fas antibodies in the presence of recombinant sFas, sFas-depleted serum or untreated serum from septic patients. Results Serum levels of sFas in patients who later developed sepsis were significantly increased at day 5 (P [less than] 0.01) and day 9 (P [less than] 0.05) after trauma compared with patients with uneventful recovery. Apoptosis of patient neutrophils was significantly decreased during the observation period compared with control cells. Moreover, Fas-mediated apoptosis of control neutrophils was efficiently inhibited by recombinant sFas and serum from septic patients. Depletion of sFas from septic patient sera diminished the antiapoptotic effects. In septic patients, sFas levels were positively correlated with SOFA at day 1 (r = 0.7, P [less than] 0.001), day 5 (r = 0.62, P [less than] 0.01) and day 9 (r = 0.58, P [less than] 0.01) and with PMNE and leukocyte counts (r = 0.49, P [less than] 0.05 for both) as well as MODS at day 5 (r = 0.56, P [less than] 0.01) after trauma. Conclusions Increased sFas in patients with sepsis development impairs neutrophil extrinsic apoptosis and shows a positive correlation with the organ dysfunction scores and PMNE. Therefore, sFas might be a therapeutic target to prevent posttrauma hyperinflammation and sepsis.
    Keywords: Apoptosis -- Physiological Aspects ; Apoptosis -- Genetic Aspects ; Apoptosis -- Research ; Injuries -- Complications And Side Effects ; Injuries -- Patient Outcomes ; Injuries -- Research ; Multiple Organ Failure -- Risk Factors ; Multiple Organ Failure -- Development And Progression ; Multiple Organ Failure -- Genetic Aspects ; Multiple Organ Failure -- Research ; Sepsis -- Risk Factors ; Sepsis -- Development And Progression ; Sepsis -- Genetic Aspects ; Sepsis -- Research
    ISSN: 1364-8535
    Source: Cengage Learning, Inc.
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  • 5
    Language: English
    In: PLoS ONE, 01 January 2016, Vol.11(5), p.e0155870
    Description: Skeletal muscle injury causes a local sterile inflammatory response. In parallel, a state of immunosuppression develops distal to the site of tissue damage. Granulocytes and monocytes that are rapidly recruited to the site of injury contribute to tissue regeneration. In this study we used a mouse model of traumatic skeletal muscle injury to investigate the previously unknown role of dendritic cells (DCs) that accumulate in injured tissue. We injected the model antigen ovalbumin (OVA) into the skeletal muscle of injured or sham-treated mice to address the ability of these DCs in antigen uptake, migration, and specific T cell activation in the draining popliteal lymph node (pLN). Immature DC-like cells appeared in the skeletal muscle by 4 days after injury and subsequently acquired a mature phenotype, as indicated by increased expression of the costimulatory molecules CD40 and CD86. After the injection of OVA into the muscle, OVA-loaded DCs migrated into the pLN. The migration of DC-like cells from the injured muscle was enhanced in the presence of the microbial stimulus lipopolysaccharide at the site of antigen uptake and triggered an increased OVA-specific T helper cell type 1 (Th1) response in the pLN. Naïve OVA-loaded DCs were superior in Th1-like priming in the pLN when adoptively transferred into the skeletal muscle of injured mice, a finding indicating the relevance of the microenvironment in the regenerating skeletal muscle for increased Th1-like priming. These findings suggest that DC-like cells that accumulate in the regenerating muscle initiate a protective immune response upon microbial challenge and thereby overcome injury-induced immunosuppression.
    Keywords: Sciences (General)
    E-ISSN: 1932-6203
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  • 6
    Language: English
    In: Intensive Care Medicine, 2004, Vol.30(1), pp.96-102
    Description: Primary events such as severe injury and elective surgery cause a deterioration of the immune response measurable by reduction of expression of HLA-DR on monocytes or ex vivo LPS-induced TNFalpha production. The further influence of secondary surgery after severe injury on the immune response remains unresolved. Prospective observation study. Surgical intensive care unit of an university hospital. Sixteen severely injured patients with an ISS 〉25 points. On day 1 after trauma and immediately before secondary surgery, mean fluorescence intensity (MFI) of HLA-DR expression on monocytes and TNFalpha ex vivo synthesis was significantly reduced compared to healthy donors. Overall, surgical intervention during the second week after trauma caused no further reduction of HLA-DR expression on monocytes and of the ex vivo TNFalpha-synthesis. However, major surgery such as intramedullary nailing or pelvic osteosynthesis caused reduction of the HLA-DR expression and TNFalpha-synthesis, whereas, minor surgical interventions such as osteosynthesis on peripheral joints exhibited no significant effects on the immune response. Surgical intervention performed to clear septic foci normalised immune response by elevating HLA-DR expression on monocytes and ex vivo TNFalpha synthesis. Severe injury caused elevated serum IL-10 levels, whereas secondary surgery did not induce a further increase in serum IL-10 levels. This study shows that initial trauma as well as major secondary surgery causes a suppression of immune functions, whereas minor secondary surgery does not cause significant immune disturbance.
    Keywords: Trauma ; HLA-DR ; Surgery ; Immune response ; TNFα
    ISSN: 0342-4642
    E-ISSN: 1432-1238
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  • 7
    In: The Journal of Trauma and Acute Care Surgery, 2012, Vol.72(4), pp.936-942
    Description: BACKGROUND:: Recent findings have emphasized the need for early and aggressive coagulation support in bleeding trauma patients. This study aimed to examine whether blood component transfusion and hemostatic drug administration during acute trauma care have changed in daily practice during the recent years. METHODS:: The multicenter trauma registry of the German Society for Trauma was retrospectively analyzed for primarily admitted patients older than 16 years with an Injury Severity Score ≥16 who had received at least five red blood cell (RBC) units between emergency room arrival and intensive care unit admission. Administration of fresh frozen plasma and platelet units has been documented since 2002, and use of hemostatic drugs since 2005. RESULTS:: From 2002 until 2009 (n = 2,813), the fresh frozen plasma:RBC ratio increased from 0.65 to 0.75 (p = 0.02) and the platelet:RBC ratio from 0.04 to 0.09 (p 〈 0.0001). A constant increase was also observed regarding the overall use of hemostatic drugs (n = 1,811; 2005–2009) as these were administered to 43.4% of the patients in 2005 and to 60.7% in 2009 (p 〈 0.0001). Especially, the administration of fibrinogen concentrate (2005: 17.0%, 2009: 45.6%; p 〈 0.0001) and recombinant factor VIIa (2005: 1.9%, 2009: 6.3%; p = 0.04) showed a marked increase. However, mortality rates remained unchanged during the 8-year study period. CONCLUSIONS:: The therapy of bleeding trauma patients has changed in Germany during the recent years toward more aggressive coagulation support. This development continues although grades of evidence are still low regarding most of the changes reported in our study. Randomized controlled trials are needed with respect to blood component therapy using predefined ratios and to the administration of hemostatic drugs commonly used for the severely injured. LEVEL OF EVIDENCE:: III, therapeutic study.
    Keywords: Blood Component Transfusion -- Trends ; Exsanguination -- Therapy ; Hemostatics -- Therapeutic Use ; Trauma Centers -- Trends ; Wounds and Injuries -- Therapy;
    ISSN: 0022-5282
    ISSN: 21630755
    E-ISSN: 21630763
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  • 8
    In: Critical Care Medicine, 2009, Vol.37(10), pp.2849-2850
    Keywords: Intensive Care Units ; Monitoring, Physiologic ; Bacterial Infections -- Immunology ; Cross Infection -- Immunology ; HLA-Dr Antigens -- Blood ; Monocytes -- Immunology ; Shock, Septic -- Immunology ; Systemic Inflammatory Response Syndrome -- Immunology;
    ISSN: 0090-3493
    E-ISSN: 15300293
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  • 9
    Language: English
    In: Injury, Oct, 2014, Vol.45, p.S64-S69
    Description: To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.injury.2014.08.020 Byline: Thomas Paffrath, Rolf Lefering, Sascha Flohe Abstract: Multiple injured patients, polytrauma or severely injured patients are terms used as synonyms in international literature describing injured patients with a high risk of mortality and cost consuming therapeutic demands. In order to advance the definition of these terms, we analysed a large trauma registry. In detail, we compared critically ill trauma patients first specified on a pure anatomical base according to the ISS or NISS, second in the original "polytrauma definition" with two body regions affected and finally all of them combined with a physiological component. Author Affiliation: (a) Department of Orthopaedic and Trauma Surgery, University Witten/Herdecke, Cologne-Merheim Medical Center (CMMC), Cologne, Germany (b) Institute for Research in Operative Medicine (IFOM), University Witten/Herdecke, Cologne, Germany (c) Department of Trauma and Hand Surgery, University Hospital Duesseldorf, Duesseldorf, Germany (d) Committee on Emergency Medicine, Intensive Care and Trauma Management (Sektion NIS) of the German Trauma Society (DGU), Germany
    Keywords: Mortality
    ISSN: 0020-1383
    Source: Cengage Learning, Inc.
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  • 10
    Language: English
    In: Critical care (London, England), 2011, Vol.15(1), pp.R20
    Description: Deregulated apoptosis and overshooting neutrophil functions contribute to immune and organ dysfunction in sepsis and multiple organ failure (MOF). In the present study, we determined the role of soluble Fas (sFas) in the regulation of posttraumatic neutrophil extrinsic apoptosis and the development of sepsis. Forty-seven major trauma patients, 18 with and 29 without sepsis development during the first 10 days after trauma, were enrolled in this prospective study. Seventeen healthy volunteers served as controls. Blood samples from severely injured patients were analyzed at day 1, day 5 and day 9 after major trauma. sFas levels, plasma levels of neutrophil elastase (PMNE) and levels of interleukin (IL)-6 were quantified by enzyme-linked immunosorbent assay and related to patients' Sequential Organ Failure Assessment (SOFA) score and Multiple Organ Dysfunction Score (MODS). Neutrophil apoptosis was determined by propidium iodide staining of fragmented DNA and flow cytometry. sFas-mediated effects on neutrophil apoptosis were investigated in cells cultured with agonistic anti-Fas antibodies in the presence of recombinant sFas, sFas-depleted serum or untreated serum from septic patients. Serum levels of sFas in patients who later developed sepsis were significantly increased at day 5 (P 〈 0.01) and day 9 (P 〈 0.05) after trauma compared with patients with uneventful recovery. Apoptosis of patient neutrophils was significantly decreased during the observation period compared with control cells. Moreover, Fas-mediated apoptosis of control neutrophils was efficiently inhibited by recombinant sFas and serum from septic patients. Depletion of sFas from septic patient sera diminished the antiapoptotic effects. In septic patients, sFas levels were positively correlated with SOFA at day 1 (r = 0.7, P 〈 0.001), day 5 (r = 0.62, P 〈 0.01) and day 9 (r = 0.58, P 〈 0.01) and with PMNE and leukocyte counts (r = 0.49, P 〈 0.05 for both) as well as MODS at day 5 (r = 0.56, P 〈 0.01) after trauma. Increased sFas in patients with sepsis development impairs neutrophil extrinsic apoptosis and shows a positive correlation with the organ dysfunction scores and PMNE. Therefore, sFas might be a therapeutic target to prevent posttrauma hyperinflammation and sepsis.
    Keywords: Apoptosis -- Physiology ; Fas Ligand Protein -- Blood ; Neutrophils -- Physiology ; Sepsis -- Etiology ; Wounds and Injuries -- Blood
    ISSN: 13648535
    E-ISSN: 1466-609X
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