This confirms that any difference in the dispersal assay is

caused by effects of NO and NOS on active dispersal of vegetative biofilm cells and not on germination of spores. Interestingly, the addition of exogenously supplied NO with the chemical NO donor SNAP to the nos mutant and L-NAME-inhibited wild-type cells did not restore dispersal to wild-type levels. We used NO microsensors to measure whether R406 the Selleck P5091 extracellular NO concentrations established by the NO donor during the dispersal assay were sufficient to complement for the loss of NOS synthesis. We found that addition of 300 μM SNAP to the dispersal drop resulted in an NO concentration between 150 to 200 nM (Figure 6). NO was consumed within the biofilm resulting in NO concentrations around the lower detection limit (~ 30 nM). Apparent NO consumption did not depend on the ability of B. subtilis to synthesize NO with NOS. NO concentrations

within SCH727965 biofilms not exposed to the NO donor were also around the lower detection limit and could not be quantified with confidence. Thus, we could not discern if similar extracellular concentrations of NO were present during the different treatments in the biofilm microenvironment. Figure 6 Nitric oxide microprofiles measured during the dispersal assay. The y-axis shows the biofilm depth with 0 (dashed line) denoting the surface of the biofilm. Positive values are inside the spot colony biofilm and negative values are above the biofilm in the MSgg medium drop. MSgg medium was supplemented with 300 μM of the NO donor SNAP (closed symbols) or supplied without supplementation of SNAP (open symbols). Wild-type B. subtilis

3610 was incubated with a drop of MSgg (A) without further supplementation and (B) further supplemented with 100 μM NOS inhibitor L-NAME. (C) shows B. subtilis 3610 Δnos supplied with MSgg without further supplementation. Error bars depict the standard deviation (N = 10) between repeated measurements at the same position in the sample reflecting the precision of the measurement. Taken together the results show that the addition of the NO donor during the dispersal experiment potentially provided a sufficient flux of extracellular NO to complement the deficiency for NO synthesis. The apparent failure of complementation suggests that NOS-derived NO is not an intercellular signalling molecule for the maintenance of these cells in the biofilm. Rather, it mediates its effect on dispersal at defined intracellular concentrations, which cannot be restored by the exogenous addition of NO. Defined intracellular NO concentrations would be particularly important if NOS-mediated signalling proceeds via redox-based modifications of enzymes [3] or when it is used for biosynthesis of other signalling molecules [8]. Our results suggest that one of these two mechanisms might act within B. subtilis cells to facilitate the maintenance of cells in the biofilm. Kolodkin-Gal et al. [29] described the disassembly of B.

Animals were randomly allocated into two groups to receive either Cr (n = 8; 5 g/kg/d) or placebo (Pl; n = 7; distillated water). The groups have similar body mass (Cr = 324.7 ± 41.9 vs.

Pl = 325.2 ± 21.6; p = 0.97). Cr monohydrate was administered by gavage for nine weeks. Forty-eight hours after the intervention, arterial blood C188-9 pressure and heart rate were invasively measured using a catheter inserted into the femoral artery [14]. Thereafter, animals were killed by decapitation. Plasma, heart, carotid artery, plantaris, and extensor digitorum longus (EDL) muscles were isolated, weighted and deep frozen at -80°C for further analyses. Cardiomyocyte width and cardiac collagen deposition were also assessed by histological analyses, as measures of cardiac remodeling selleck [15]. Additionally, lipid hydroperoxidation (an important marker of oxidative stress) was determined in the plasma, heart, carotid artery, and skeletal muscles. These aforementioned methods have been described in details below. Hemodynamic parameters After an intra-peritoneal anesthetic injection (80 mg/kg ketamine and 12 mg/kg xylazine, i.p.), a catheter filled with 0.06 mL of saline was inserted into the femoral artery of rats. Twenty four hours after the catheter insertion, the arterial cannula was connected to a strain-gauge transducer (Blood Pressure XDCR; Kent Scientific, Torrington, CT, USA), and arterial pressure

see more signals were recorded over a 30 min period in conscious rats by a microcomputer equipped Prostatic acid phosphatase with an analog-to-digital converter board (WinDaq, 2 kHz, DATAQ, Springfield, OH, USA). The recorded data were analyzed on a beat-to-beat basis to quantify systolic, diastolic and mean arterial pressure, as well as heart rate. Histological

analyses Cardiac chambers were fixed by immersion in 4% buffered formalin and embedded in paraffin for routine histologic processing. Sections (4 μm) were stained with hematoxylin and eosin for examination by light microscopy. Only nucleated cardiac myocytes from areas of transversely cut muscle fibers were included in the analysis. Quantification of left ventricular fibrosis was achieved by Sirius red staining. Cardiac myocyte width and ventricular fibrosis were measured in the LV free wall with a computer assisted morphometric system (Leica Quantimet 500, Cambridge, UK). Lipid hydroperoxidation measurement Lipid hydroperoxidation was assessed since this oxidative stress marker has been implicated in the pathogenesis of a number of cardiovascular diseases, including arterial hypertension [16, 17]. Lipid hydroperoxides were evaluated by the ferrous oxidation-xylenol orange technique (FOX2) [18]. Plasma, Heart, Carotid Artery, Plantar and EDL samples were homogenized in phosphate-buffered saline (PBS; 100 mmol/L, pH 7.4) and immediately centrifuged at 12.000 g for 20 min at 4°C.

In summary, polyP has numerous and varied biological functions

in bacteria that have been discovered mainly by studying its deficiency. To better understand the function of polyP we used broad-host-range constitutive and regulated vectors to deplete cellular polyP and found new functional and structural changes. In addition, it is generally accepted that energy supply of the cells could be severely compromised in the absence of polyP. We confirmed this evidence by using differential proteomic studies and suggested that during polyP scarcity energy metabolism and particularly nucleoside triphosphate (NTP) formation were affected, generating a general stress condition. We propose that bacterial cells prevail by increasing the flux of energy-generating metabolic pathways such as tricarboxilic acid (TCA) Staurosporine clinical trial cycle and β-oxidation and by reducing energy-consuming ones such as active transporters and amino acid biosynthesis. Methods Bacterial strains and growth

conditions Pseudomonas sp. B4 wt, control (pMLS7) and polyP-deficient (pS7PPX1) recombinant strains were previously obtained [21] and grown aerobically BIBW2992 research buy at 37°C on Luria-Bertani (LB) rich medium supplemented with trimetropim (50 μg/ml). When required, LB plates (1,5% (w/v) of Bacto-agar) were used for obtaining cells from the colonies after 48 h of growth. Optical and Electron Selleckchem ACY-1215 Microscopy Unstained cells from the different cultures were routinely examined for the presence of polyP granules Mannose-binding protein-associated serine protease by transmission electron microscopy [43]. Cells were mixed and dispersed in distilled water and added onto carbon-coated nickel grids. The drops

containing the microorganisms were drained off with filter paper and air dried during 30-50 s. Electron microscopy was performed with a Philips Tecnai 12 electron microscope using 80 kV accelerating voltage (Electron Microscopy Laboratory, Pontificia Universidad Católica de Chile). Optical microscopy was routinely performed in an Olympus BX50 microscope (Olympus Corporation, Japan). LPS analysis Culture samples were adjusted to an optical density at 600 nm of 2.0 in a final volume of 100 μl. Then, proteinase K-digested whole-cell lysates were prepared as described previously [44], and LPS was separated on 14% acrylamide gels using a Tricine-sodium dodecyl sulfate (SDS) buffer system [45]. Gel loadings were normalized so that each sample represented the same number of cells. Gels were silver stained by a modification of the procedure of Tsai and Frasch [46, 47]. Samples preparation and 2D-PAGE Cells (200 mg) were harvested by centrifugatio n (7,000 × g for 15 min at 25°C) from liquid cultures or were collected with an inoculation loop from agar plates. Pellets were washed four times in sonication buffer (40 mM Tris pH 8.15; 1 mM PMSF).

qPCR for BoNT Type-Specific PXD101 Detection The qPCR assay consisted of seven separate reactions, each specific for one of the seven neurotoxin gene types. For absolute quantification, template standards for each of the neurotoxin gene types were run alongside

the DNA samples for each of the seven qPCRs. qPCR conditions were as follows: 95°C for 5 minutes, then 45 cycles of 95°C for 15 seconds and 60°C for 1 minute. PCR reaction mixture contained PCR Buffer, 3.5 uM MgCl2, 200 nM dNTPs, 500 nM forward or reverse primer, 200 nM Fam/BHQ1-labeled probe, 3 nM BD636 reference dye, 0.25 U Taq Polymerase (Invitrogen Corp, Carlsbad, CA). 5 μL of purified DNA or plasmid standard was used in each 25 μL PCR reaction. Based on cycle of threshold (Ct) values with known copy numbers of plasmid in each reaction, a standard curve is generated that will be used to calculate the values of unknown samples. Acknowledgements We would like to thank Dr. David Kulesh from USAMRIID for his expert technical advice and the use of equipment. We would also https://www.selleckchem.com/products/shp099-dihydrochloride.html like to

thank Dr. Nir Dover for extracting and providing fecal DNA from the California patient with infant botulism. We also thank Alma Boritz for contributing a healthy infant stool sample. The opinions, interpretations and recommendations are those of the author and are not necessarily those of the US Army. References 1. Metabolism inhibitor Montecucco C: Clostridial neurotoxins: the molecular pathogenesis of tetanus and botulism. Current Topics of Microbial immunology 1995, 195:1–278. 2. Gill DM: Bacterial Regorafenib chemical structure toxins: a table of lethal amounts. Microbiol Rev 1982,46(1):86–94.PubMed 3. Montecucco C, Molgo J: Botulinal neurotoxins: revival of an old killer. Curr Opin Pharmacol 2005,5(3):274–279.PubMedCrossRef 4. Arnon SS, Schechter R, Inglesby TV, Henderson DA, Bartlett JG, Ascher MS, Eitzen E, Fine AD, Hauer J, Layton M, et al.: Botulinum toxin as a biological weapon: medical and public health management. Jama 2001,285(8):1059–1070.PubMedCrossRef 5. Centers for Disease Control C: Centers for Disease Control and Prevention: Botulism

in the United States, 1899–1996. Handbook for Epidemiologists, Clinicians, and Laboratory Workers, Atlanta, GA. Centers for Disease Control and Prevention; 1998. 6. Koepke RJS, Arnon SS: Global Occurrence of Infant Botulism, 1976–2006. Pediatrics 2008, in press. 7. Akbulut D, Dennis J, Gent M, Grant KA, Hope V, Ohai C, McLauchlin J, Mithani V, Mpamugo O, Ncube F, et al.: Wound botulism in injectors of drugs: upsurge in cases in England during 2004. Euro Surveill 2005,10(9):172–174.PubMed 8. Artin I, Bjorkman P, Cronqvist J, Radstrom P, Holst E: First case of type E wound botulism diagnosed using real-time PCR. J Clin Microbiol 2007,45(11):3589–3594.PubMedCrossRef 9. Sobel J: Botulism. Clin Infect Dis 2005,41(8):1167–1173.PubMedCrossRef 10. Hall JD, McCroskey LM, Pincomb BJ, Hatheway CL: Isolation of an organism resembling Clostridium barati which produces type F botulinal toxin from an infant with botulism.

9% in open versus 0% in laparoscopic adnexal surgery. Only in appendectomies there was no difference between the two techniques [153]. There is some class I evidence in obstetrics supporting the theory that suturing the peritoneum increases this website the risk of adhesions [154]. It is therefore prudent to avoid peritoneal closure during laparotomies. Mechanical barriers In theory, inert materials that LY3023414 prevent contact between the damaged serosal surfaces for the first few critical days allow separate healing of the injured surfaces and may help in the prevention

of adhesion formation. Various bioabsorbable films or gels, solid membranes, or fluid barrier agents have been tested experimentally and in clinical trials. Hyaluronic acid/carboxymethylcellulose (Seprafilm) is the most extensively tested adhesion prevention agent in general surgery. Its safety with regard to systemic or specific complications has been established in many studies, including a safety study of 1,791 patients with abdominal or pelvic surgery, however there are concerns about a higher incidence of anastomotic leaks in cases in which the film is placed directly around the anastomosis [155]. Several prospective randomized controlled trials showed efficacy in reducing the incidence and extent of postoperative adhesions. In a prospective, randomized,

multicenter, double-blind study of 175 evaluable patients with colectomy and ileoanal pouch procedure, compared Seprafilm with controls, The Seprafilm group Selleck VS-4718 had significantly fewer and less severe adhesions and well as of reduced extent [156]. A further prospective multicenter study, randomized 71 patients undergoing Hartmann’s resection into a Seprafilm and a control group: although the

incidence of adhesions did not differ significantly between the study groups, the Seprafilm group showed a significant reduction of the severity of adhesions [157]. Cohen et al, in a prospective multicenter trial, randomized 120 patients with colectomy and ileal pouch surgeries into a Seprafilm and a control group [158]. The outcomes included incidence and severity of adhesions and were assessed laparoscopically by a blinded observer at a second surgery 8 to 12 weeks later for ileostomy closure. Treatment with Seprafilm significantly reduced the incidence and severity of adhesions. Teicoplanin Kumar et al in a recent Cochrane collective review of 6 randomized trials with nongynecologic surgical patients found that Seprafilm significantly reduced the incidence of adhesions (OR, .15; 95% CI, .05-.43; P < .001) and the extent of adhesion (mean difference, –25.9%; 95% CI, –40.56 to –11.26; P < .001) [159]. Although there is satisfactory class I evidence that Seprafilm significantly reduces the incidence and severity of postoperative adhesions, there is fairly limited work on the effect of this adhesion reduction on the incidence of SBO.

In S. aureus, methicillin resistance is conferred by an acquired, β-lactam-insensitive penicillin-binding protein (PBP), PBP2a [1–4]. PBP2a is encoded by mecA, which is divergently transcribed from its cognate regulators, mecR1 (sensor/signal transducer) and mecI (repressor).

If mecR1-mecI are absent or truncated, transcriptional control of mecA is taken over by the structurally similar blaZ (penicillinase) regulatory elements blaR1/blaI, if present. In the absence of both regulatory loci, mecA is constitutively transcribed [5, 6]. In the presence of β-lactams, the transmembrane sensor/signal transducers BlaR1/MecR1, undergo a conformational change, followed by autoproteolytic cleavage of the n-terminal cytoplasmic domain, leading to the activation of the cytoplasmic peptidase Tariquidar and subsequent dissociation of the repressor

due to proteolytic degradation [7–9]. However, the signal transduction cascade of this regulatory system has still not been completely elucidated. CX-6258 mw Oxacillin resistance levels conferred by mecA are strain specific and can vary greatly, with oxacillin minimal inhibitory concentrations (MICs) of different strains ranging from phenotypically susceptible levels, as low as 1 μg/ml up to extremely high values of > 500 μg/ml. Methicillin resistance is also generally expressed heterogeneously. Heterogeneously

resistant MRSA, when exposed to β-lactam antibiotics, segregate highly resistant subpopulations, which are much more resistant than the majority of the cells [10]. The frequency Linifanib (ABT-869) of highly resistant subclones generated is often well above the spontaneous mutation frequency, and once selected high level resistance often remains stable, even in the absence of selective pressure. There is currently no satisfactory genetic model which explains how these higher resistance levels are triggered or selected and exactly what factors are functionally responsible for the increased resistance in clinical isolates. Methicillin resistance levels are known to not directly correlate with mecA transcription or levels of PBP2a mTOR signaling pathway produced [11, 12]. However, resistance levels can be manipulated by environmental conditions, such as temperature, pH, osmolarity, and medium composition [13, 14]. It has been shown experimentally, that in addition to mecA, methicillin resistance depends on the correct interplay of a multitude of genomic factors, termed fem/aux factors, including genes involved in peptidoglycan precursor formation, composition and turnover; teichoic acid synthesis; and genes of unknown or poorly characterised functions [15–18].

90 1.181-3.057 <0.01 Low GCS in ED 0.883 0.845-0.924 <0.0001 Creatinine in ED 1.003 1.000-1.005 0.03 Discharge to ALF 0.315 0.214-0.463 <0.0001 GCS–Glasgow coma scale; ED–emergency department; ALF–assisted living Citarinostat datasheet facility. Discussion The major finding of this study is that in the Emricasan in vivo elderly population following severe trauma, long term survival can be predicted based on the pre-hospital parameters of age, mechanism of injury, and GCS on admission. In contrast, parameters in hospital care, including blood transfusion, requirement for ICU admission,

surgical procedures and complications did not predict long term survival in this elderly group. There is a paucity of data describing the long term outcome of the injured geriatric patient, accordingly, this was a primary objective of our study. Contrary to what is often assumed, we have demonstrated that long term survival subsequent to a severe trauma in the elderly population is not uncommon, for we noted that almost two-thirds of elderly patients who were discharged from the hospital were alive at a mean follow up of over 4 years. Previous reports have analyzed the course and in-hospital outcome of elderly patients following Selleckchem LY2090314 trauma [4, 11, 12]. A mature trauma system performance could be assessed by the percent of severely injured patients who are discharged

from the trauma center. For example, Florida trauma system analysis over a 15 year period showed significant increase in both the number of elderly injured and the severity of injury [13]. Others [14] stressed the importance of triage of the severely injured elderly patients to designated trauma centers. This resulted in significantly higher overall discharge when compared to non-trauma centers. Not surprisingly, and in concert with others [4, 15] our Dolichyl-phosphate-mannose-protein mannosyltransferase data demonstrated that chronological

age is a predictor of post-discharge mortality. The post-discharge survival of patients ≥ 80 years is significantly worse compared to their younger counterparts. These intuitive findings could not be explained by the ISS, which was not different between the age groups. Although age related co-morbidities likely contribute to long term survival, we were surprised to note that age, rather than co-morbidities and ISS, was an independent predictor of death, particularly in the ≥80 age group. It has been noted that in the elderly population, multi-system trauma from falls predominant with increasing age, with a corresponding decreasing frequency of motor vehicular and pedestrian related injuries [5]. Similarly, we noted that falls were the most common mechanism of injury and were associated with poor long term outcome. It has been suggested that a senior’s propensity to fall may indicate poor functional capacity and higher mortality risk in this population [16]. Various studies confirm that pre-existing co-morbidities significantly increase the risk of mortality following blunt trauma in geriatric patients [17–20].

In patients with recurrent or metastatic disease the prognosis is poor, with a median survival time of less than one year [7]. Undesirable complications

of chemoradiotherapy for NPC can be severe and can limit patient compliance [8]. A blood test that could identify pre-symptomatic, earlier-stage NPC would help to increase patient survival and reduce treatment-related toxicity; a blood test that could predict patient response to therapy could increase compliance with treatment regimens. In this report, selleck compound we used blood samples to identify gene expression signatures for NPC and to predict patient response to treatment. Such a test would significantly improve the medical management of this disease. Methods Patients and blood samples Blood samples were collected from patients with NPC STA-9090 order recruited at Mount Miriam Cancer

click here Hospital (Penang, Malaysia). Consent forms were obtained from all study participants according to protocols approved by the hospital’s Research Ethics Board. We performed gene profiling and microarray analysis on 66 samples taken from patients with tumours confirmed as NPC by hospital pathologists, and for 33 controls (Table 1), collected between November 2006 and April 2010. Table 1 Clinical characteristics of the patient cohorts for microarray hybridization Characteristics NPC Control P value* Control & 447 Other P value* (NPC vs Control)   (NPC vs Control & 447 Other) No. 66 33   480   Age – Median (Range) 51 (24–74) 31 (19–74) <0·01 55 (19–86) 0.32 Malay 12 (18·2) 2 (6·1) 0·13 n/a n/a Chinese 45 (68·2) 30 (90·9) 0·01 n/a n/a Indonesian 8 (12·1) 0 (0·0) 0·05 n/a n/a Indian 0 (0·0) 1 (3·0) 0·33 n/a n/a Unknown 1 (1·5) 0 (0·0) 1·00 n/a n/a Male 49 Vasopressin Receptor (74·2) 20 (60·6) 0·17 242 (57.1) 0.01 Female 17 (25·8) 13 (39·4) 0·17 182 (42.9) 0.01 not available       56   * P values for age and BMI were calculated using the Mann–Whitney test, P values for ethnicity, sex and medical conditions were calculated using Fisher’s exact test. To obtain a gene signature specific to NPC, we included 447 expression

profiles of samples with other conditions (27 bladder cancer; 10 breast cancer; 17 cervical cancer; 16 endometrical cancer; 40 ovarian cancer; 91 prostate cancer; 47 Crohn’s disease; 43 osteoarthritis; 38 rheumatoid arthritis; 85 cardiovascular disease; 20 schizophrenia; 13 miscellaneous other conditions). Blood collection, RNA isolation and RNA quality control Peripheral whole blood (2×10 ml) was collected from patients in EDTA Vacutainer tubes (Becton Dickinson, New Jersey, USA), and RNA was isolated as described previously [10]. Isolated RNA was checked using 2100 Bioanalyzer RNA 6000 Nano Chip (Agilent Technologies, California, USA). Samples were excluded for subsequent microarray analysis that did not meet the following quality criteria: RIN > = 7·0; 28S:18S rRNA > =1·0. RNA quantity was determined by absorbance at 260 nm in a DU640 Spectrophotometer (Beckman-Coulter, California, USA).

Thus, we conjectured that the nanolayer effect might be the only important factor among these three mechanisms affecting the SHC of the nanofluid. Accordingly, a theoretical model considering the nanolayer effect on the SHC was proposed. Since the solid-like nanolayer formed on the surface of NP is at a thermodynamic state between solid salt and molten salt [26], the value of the SHC of the nanolayer should lay between those of the solid salt (1.04 kJ/kg-K) and the molten salt (1.59 kJ/kg-K). In other words, the nanolayer selleckchem has

a lower SHC than that of the molten salt. Further, the thermal properties of the nanolayer (e.g., thermal conductivity and SHC) could vary with different combinations of NPs and base fluids, since the structure of the nanolayer is dependent on the interaction of molecules [28]. In addition, Lin et al. [25] also found selleck compound that the nanolayer structure is size-dependent, resulting in a size-dependent thermal conductivity. As a result, the SHC of the nanolayer is dependent on the size of the NP and the combinations of the NPs and base fluids. To the best of our knowledge, there is no experimental and theoretical data available for the SHC of the nanolayer for the molten salt-based alumina nanofluid. Thus, in this proposed model, the SHC of the nanolayer (c p,layer)

for a given NP size is first obtained from the experimental result of the SHC of the nanofluid at a certain particle concentration (i.e., c p,m): (2) where the subscript layer is denoted as nanolayer; W is weight; and W nf = W np + W f. In the model, it is assumed that the Progesterone measured SHC of the nanofluid (c p,m) is a result of the superposition of the SHCs of the nanolayer (c p,layer), the

NP (c p,np), and the Selleck MK-0457 solvent (c p,f) as in contrast to the existing model (Equation 1). Thus, the SHC of the nanolayer (c p,layer) for the given NP size could be obtained from Equation 2: (3) Once the SHC of the nanolayer was known, the SHC of the nanofluid (c p,nf) at any NP concentration (having a mass fraction α’ = W np ’/W nf ’) for the given NP size could be obtained as follows: (4) where W np ’, W layer ’, and W nf ’ are the weights of NP, nanolayer, and nanofluid at such NP concentration, respectively. Meanwhile, the weight of solvent (W f) is kept as a constant for various particle concentrations. Substituting c p,layer from Equation 3 into Equation 4, one can obtain the SHC of the nanofluid for the given NP size at such NP mass fraction (α’ = W np ’/W nf ’) as follows: (5) where α ( = W np/W nf) is the NP mass fraction in determining SHC of the nanolayer in Equations 2 and 3 and the SHC of the solvent (c p,f) was obtained from the DSC measurements (c p,f = 1.59 kJ/kg-K). It is worth noting that the SHCs of the NPs and nanolayer are not required for the theoretical prediction using Equation 5, of which the effects on the SHC of the nanofluid are implicitly included in the term c p,m in Equation 5.

Conclusions Full GSK458 Trauma activations involving attending surgeons were quicker at transferring seriously head-injured patients to CT. Patients with FTA were younger, higher ISS, lower scene GCS, and more often intubated in the pre-hospital setting. Discerning the reasons for delays to CT should be used to refine protocols aimed at minimizing unnecessary delays and maximizing workforce efficiency. Acknowledgements The authors thank Dr David Zygun, MD FRCPC, University of Alberta, Dr Kevin Stevenson University of Saskatchewan, Viesha A. Ciura University of Calgary, Kimberley Musselwhite, MN RN, Alberta Health Services,

Christine Vis Alberta LY294002 chemical structure Health Services for their assistance for this study. References 1. Committee on Trauma of the American College of Surgeons: Resources for optimal care of the injured. Chicago, IL: Committee on Trauma of the American College of Surgeons; 2006. 2. Davis T, Dinh M, Roncal

S, Byrne C, Petchell J, Leonard E, et al.: Prospective evaluation of a two-tiered trauma activation protocol in an Australian major trauma referral hospital. Injury 2010,41(5):470–474.PubMedCrossRef 3. Kouzminova N, Shatney C, Palm E, McCullough M, Sherck J: The efficacy of a two-tiered trauma activation system at a level I trauma center. J Trauma 2009,67(4):829–833.PubMedCrossRef 4. Norwood SH, McAuley CE, Berne JD, Vallina VL, Creath RG, McLarty J: A prehospital glasgow coma scale FHPI clinical trial score < or = 14 accurately predicts the need for full trauma team activation and patient hospitalization

after motor vehicle collisions. J Trauma 2002,53(3):503–507.PubMedCrossRef 5. Lehmann RK, Arthurs ZM, Cuadrado DG, Casey LE, Beekley AC, Martin MJ: Trauma mafosfamide team activation: simplified criteria safely reduces overtriage. Am J Surg 2007,193(5):630–634. discussion 4–5PubMedCrossRef 6. Tinkoff GH, O’Connor RE: Validation of new trauma triage rules for trauma attending response to the emergency department. J Trauma 2002,52(6):1153–1158. discussion 8–9PubMedCrossRef 7. Cook CH, Muscarella P, Praba AC, Melvin WS, Martin LC: Reducing overtriage without compromising outcomes in trauma patients. Arch Surg 2001,136(7):752–756.PubMedCrossRef 8. Cherry RA, King TS, Carney DE, Bryant P, Cooney RN: Trauma team activation and the impact on mortality. J Trauma 2007,63(2):326–330.PubMedCrossRef 9. Region AHSC: Trauma Services Annual Reports. Calgary: Calgary Regional Trauma Services; 2010. [cited 2010 Feb 26 2010]; Available from: http://​www.​calgaryhealthreg​ion.​ca/​programs/​trauma/​reports.​htm 10. Fung Kon Jin PH, van Geene AR, Linnau KF, Jurkovich GJ, Goslings JC, Ponsen KJ: Time factors associated with CT scan usage in trauma patients. Eur J Radiol 2009,72(1):134–138.PubMedCrossRef 11. Grossman MD, Portner M, Hoey BA, Stehly CD, Schwab CW, Stotzfus J: Emergency traumatologists as partners in trauma care: the future is now. J Am Coll Surg 2009, 208:503–509.PubMedCrossRef 12. Shackford S: How then shall we change? J Trauma 2006,60(1):1–7.