Association Between Buprenorphine Dose and the Urine "Norbuprenorphine" to "Creatinine" Ratio: Revised.

Background: Utilizing a 1-year chart review as the data, Furo et al. conducted a research study on an association between buprenorphine dose and the urine "norbuprenorphine" to "creatinine" ratio and found significant differences in the ratio among 8-, 12-, and 16-mg/day groups with an analysis of variance (ANOVA) test. This study expands the data for a 2-year chart review and is intended to delineate an association between buprenorphine dose and the urine "norbuprenorphine" to "creatinine" ratio with a higher statistical power.

Trauma-induced lung injury is associated with infiltration of activated TLR expressing myeloid cells.

Introduction: Traumatic injury with hemorrhage (TH) induces an inflammatory response in the lung resulting in lung injury involving activation of immune cells including myeloid cells (i.e., monocytes, granulocytes and macrophages), in part through TLRs.

Shock index and pulse pressure as triggers for massive transfusion.

Background: Hemorrhage is the most common cause of preventable death in trauma patients. These mortalities might be prevented with prehospital transfusion. We sought to characterize injured patients requiring massive transfusion to determine the potential impact of a prehospital whole blood transfusion program.

The composition of T-cell subsets are altered in the burn wound early after injury.

Background: Burn-induced inflammation leads to impaired immune responses resulting in increased morbidity and mortality. T-cells are central in the immune response and circulating CD4 and CD8 T-cells have been used to evaluate immune status; however, the role of these T-cell subsets in the burn wound is unknown.

Methods: Male C57BL/6 mice were subjected to a major 3rd degree scald burn or sham treatment.

Damage-associated molecular patterns (DAMPs) released after burn are associated with inflammation and monocyte activation.

Burns are associated with activation of the innate immunity that can contribute to complications. Damage-associated molecular patterns (DAMPs) released after tissue injury play a critical role in the activation of the innate immunity, which appears to be mediated via toll-like receptors (TLRs). Previous findings have shown that TLRs and TLR-mediated responses are up-regulated after burn.

Toll-like receptor responses are suppressed in trauma ICU patients.

Background: Inflammation and activation of the innate immune system are often associated with traumatic injury and may involve alterations in toll-like receptor (TLR)-mediated responses.

Methods: A prospective observational study was designed and conducted. Twenty-one severely injured (ISS = 16-41) trauma intensive care unit (ICU) patients and six healthy volunteers that served as controls were enrolled.

The Role of Communication During Trauma Activations: Investigating the Need for Team and Leader Communication Training.

Objective: Fatal errors due to miscommunication among members of trauma teams are 2 to 4 times more likely to occur than in other medical teams, yet most trauma team members do not receive communication effectiveness training. A needs assessment was conducted to examine trauma team members' miscommunication experiences and research scientists' evaluations of live trauma activations. The purpose of this study is to demonstrate that communication training is necessary and highlight specific team communication competencies that trauma teams should learn to improve communication during activations.

Dermal γδ T-Cells Can Be Activated by Mitochondrial Damage-Associated Molecular Patterns.

Background: Gamma delta T-cells have been shown to be important to the early immunoinflammatory response to injury, independent of infection. This unique T-cell population acts to regulate cell trafficking and the release of cytokines and growth factors. We propose this sterile inflammatory response is in part associated with damage associated molecular patterns (DAMPs) generated by major injury, such as burn, and mediated via toll-like receptors (TLRs).

The association between the Th-17 immune response and pulmonary complications in a trauma ICU population.

Background: The overall immunopathology of the T-helper cell (Th)-17 immune response has been implicated in various inflammatory diseases including pulmonary inflammation; however its potential role in acute respiratory distress syndrome (ARDS) is not defined. This study aimed to evaluate the Th-17 response in bronchoalveolar lavage fluid (BALF) and blood and from trauma patients with pulmonary complications.

Methods: A total of 21 severely injured intensive care unit (ICU) subjects, who were mechanically ventilated and undergoing bronchoscopy, were enrolled.

Gamma delta T cells regulate inflammatory cell infiltration of the lung after trauma-hemorrhage.

Trauma-hemorrhage (TH) promotes acute lung injury (ALI) and other pulmonary-related complications in part through an exaggerated inflammatory response. Studies have implicated γδ T cells in the development of inflammatory complications after major injury; however, it is unknown whether γδ T cells play a role in the development of ALI after TH. To study this, C57BL/6 wild-type (WT) and δ TCR mice were subjected to TH or sham treatment.

Gamma delta T cells regulate wound myeloid cell activity after burn.

Major burns induce immune complications, which are associated with myeloid cell activation by ill-defined mechanisms. Although γδ T cells have been shown to be important in postinjury inflammation and wound healing, their role in the regulation of myeloid cells remains unknown. To study this, wild-type (WT) and γδ T cell-deficient (δTCR) mice were subjected to major burn (25% total body surface area, third degree) or sham treatment.

Activated skin γδ T-cells regulate T-cell infiltration of the wound site after burn.

Burn induces an immunopathological response involving multiple immune cell types that includes γδ T-cells. Nonetheless, the role of γδ T-cells at the wound site after burn is not clearly defined. Wild type and γδ T-cell receptor deficient (δ TCR(-/-)) mice were subjected to a major burn or sham procedure.

Burn wound γδ T-cells support a Th2 and Th17 immune response.

Major burn triggers immune dysfunction, which is associated with wound healing complications. Gamma-δ T-cells have been shown to be important in postburn inflammation and wound healing; however, their cytokine phenotype at the burn wound site is unknown. C57BL/6 male mice were subjected to a major burn (25% TBSA, third degree) or sham treatment.

Effect of inhaled tacrolimus on ischemia reperfusion injury in rat lung transplant model.

Objective: Systemic tacrolimus therapy has been shown to protect against lung ischemia-reperfusion injury in animal models. We sought to investigate on a functional and cellular level if inhaled nanoparticle tacrolimus administered to the donor lung before procurement could similarly attenuate ischemia-reperfusion injury after lung transplant.

Methods: An isogenic orthotopic rat model of single left lung transplant was used.

Mitochondrial damage-associated molecular patterns activate γδ T-cells.

Gamma delta T-cells have been shown to be important in the early immunoinflammatory response to injury, which can be independent of infection. This sterile inflammatory response is believed to be, in part, associated with danger-associated molecular patterns (DAMPs). Mitochondrial DAMPs (MTDs) have been shown to be important in trauma-induced neutrophil activation, but it is unknown whether MTDs activate other innate immune cells, such as γδ T-cells.

Gamma delta (γδ) T-cells are critical in the up-regulation of inducible nitric oxide synthase at the burn wound site.

Background: The high incidence of morbidity and mortality following major burn can in part be attributed to immune derangements and wound healing complications. Inflammation plays an important role in wound healing, of which inducible nitric oxide synthase (iNOS) derived nitric oxide is a central mediator. T-cells of the γδ TCR lineage have also been shown to be important in healing of the burn wound site.

Aging and the pathogenic response to burn.

Aging is an important and critical factor that contributes to the clinical outcome of burn patients. The very young and the elderly are more likely to succumb after major burn as compared to their adult counterparts. With the aging population, improved understanding of the mechanisms underlying age-associated complications after burns becomes even more demanding.

Burn enhances toll-like receptor induced responses by circulating leukocytes.

Burn and toll-like receptors (TLR) are associated with innate immune system activation, but the impact of burn on TLR-induced inflammation responses by circulating leukocytes is unknown. To study this, C57BL/6 mice were subjected to burn (3(rd) degree, 25% TBSA) or sham procedure and 1-7 days later blood was collected. Whole blood cell suspensions were incubated for 24 hr in the presence of zymosan (TLR-2 agonist) or LPS (TLR-4 agonist).

Burn-induced alterations in toll-like receptor-mediated responses by bronchoalveolar lavage cells.

Unlabelled: Burn is associated with profound inflammation and activation of the innate immune system in multiple organ beds, including the lung. Similarly, toll-like receptors (TLR) are associated with innate immune activation. Nonetheless, it is unclear what impact burn has on TLR-induced inflammatory responses in the lung.

Modulation of dendritic cell differentiation in the bone marrow mediates sustained immunosuppression after polymicrobial sepsis.

Murine polymicrobial sepsis is associated with a sustained reduction of dendritic cell (DC) numbers in lymphoid organs and with a dysfunction of DC that is considered to mediate the chronic susceptibility of post-septic mice to secondary infections. We investigated whether polymicrobial sepsis triggered an altered de novo formation and/or differentiation of DC in the bone marrow. BrdU labeling experiments indicated that polymicrobial sepsis did not affect the formation of splenic DC.

Increased expression of cardiac IL-17 after burn.

Background: Cardiac dysfunction is a common complication associated with major burns. While recent findings have linked the Th-17 T-cell response to the development of autoimmune myocarditis, the role of IL-17 and the Th-17 T-cell response in the development of post-burn cardiac dysfunction remains unknown.

Methods: Male C57BL/6 mice were subjected to a major burn (3rd degree, 25% TBSA) or sham treatment.

Diversity of interferon gamma and granulocyte-macrophage colony-stimulating factor in restoring immune dysfunction of dendritic cells and macrophages during polymicrobial sepsis.

The development of immunosuppression during polymicrobial sepsis is associated with the failure of dendritic cells (DC) to promote the polarization of T helper (Th) cells toward a protective Th1 type. The aim of the study was to test potential immunomodulatory approaches to restore the capacity of splenic DC to secrete interleukin (IL) 12 that represents the key cytokine in Th1 cell polarization. Murine polymicrobial sepsis was induced by cecal ligation and puncture (CLP).

Toll-like receptor 2 and 4 expression after severe injury is not involved in the dysregulation of the innate immune system.

Background: Severe injury after trauma is associated with a diminished production of different proinflammatory cytokines after stimulation with bacterial cell wall components. The cellular mechanisms, leading to a decreased responsiveness especially of monocytes after multiple injuries have not yet been elucidated in detail. The expression of Toll-like receptors (TLR) on leukocytes is essential for recognition of bacterial components.

Haemorrhagic shock in mice--intracellular signalling and immunomodulation of peritoneal macrophages' LPS response.

Haemorrhagic shock leads to decreased proinflammatory cytokine response which is associated with an increased susceptibility to bacterial infections. In the present study, the effect of GM-CSF on lipopolysaccharide (LPS)-induced TNF-alpha release and MAPkinase activation was analysed on the background of a possible immunostimulating activity of this substance. Male BALB/c mice were bled to a mean arterial blood pressure of 50 mmHg for 45 min followed by resuscitation.