However, for objectives Dabrafenib datasheet relevant to bodybuilding,

the current evidence indicates that the global macronutrient composition of the diet is likely the most important nutritional variable related to chronic training adaptations. Figure 1 below provides a BMS345541 Continuum of importance with bodybuilding-specific context for nutrient timing. Figure 1 Continuum of nutrient & supplement timing importance. Meal frequency Previous optimal meal frequency studies have lacked structured resistance training protocols. Moreover, there are no studies that specifically examined meal frequency in bodybuilders, let alone during contest preparation conditions. Despite this limitation, the available research has consistently learn more refuted the popular belief that a grazing pattern (smaller, more frequent meals) raises energy expenditure compared to a gorging pattern (larger, less frequent meals). Disparate feeding patterns ranging from two to seven meals per day have been compared in tightly controlled studies using metabolic chambers, and no significant differences in 24-hour thermogenesis have

been detected [100, 101]. It should be noted that irregular feeding patterns across the week, as opposed to maintaining a stable daily frequency, has been shown to decrease post-prandial thermogenesis [102] and adversely affect insulin sensitivity and blood lipid profile [103]. However, relevance of the latter findings might be limited to sedentary populations, since regular exercise is well-established in its ability to improve insulin sensitivity and blood lipids. Bodybuilders typically employ a higher meal frequency in an attempt to optimize fat loss and muscle preservation. However, the majority of chronic experimental studies have failed

to show that different meal frequencies have different influences on bodyweight or body composition [104–108]. Of particular interest is the research examining the latter, since the preservation of muscle mass during fat loss is a paramount concern in the pre-contest phase. A recent review by Varady [109] examined 11 daily caloric restriction (CR) studies and 7 intermittent calorie restriction (ICR) studies. Ribonucleotide reductase CR involved a linear consumption of 15-60% of baseline needs every day, while ICR alternated ad libitum ‘feed’ days with ‘fast’ days involving partial or total food intake restriction. It was concluded that although both types have similar effects on total bodyweight reduction, ICR has thus far been more effective for retaining lean mass. Three of the ICR studies showed no significant decrease in LBM, while all of the CR studies showed decreased LBM. However, the majority of the ICR trials used bioelectrical impedance analysis (BIA) to measure body composition, while the majority of CR studies used dual X-ray absorptiometry (DXA) or magnetic resonance imaging (MRI).

DppV, a member of the dipeptidyl-peptidase family in A. fumigatus, is identical to one of the principal antigens used in the diagnosis of IA. Moreover, DppV can generate protection responses, and improve the survival rate of Aspergillus-infected mice [28]. DppV can also bind with collagen or other human proteins and degrade them, which can damage the host. Recombinant DppV has shown a great potential in the serodiagnosis of IA in immunocompromised and immunocompetent patients [35]. NAD-dependent malate dehydrogenase, a key enzyme in glycometabolism that catalyze the reversible conversion

between malate and oxaloacetate, was reported recently as an allergen of A. selleck kinase inhibitor fumigatus and A. versicolor [29]. Malate dehydrogenase was also shown to be a Paracoccidioides MM-102 solubility dmso brasileinsis immunogenic protein [36] as well as a Candida albicans immunogen [32]. Aspartyl aminopeptidase, an enzyme that specifically degrades only amino-terminal acidic amino acids from peptides, was recently reported as an antigen of A. fumigatus [30] . TR of A. fumigatus has been described as an extracellular antigenic protein by two recent studies [30, 31]. In one former

study, the secreted fraction of two geographically different strains (190/96 and DAYA) of A. fumigatus were used to identify new immunogenic molecules reacting with pooled ABPA patient sera (IgG and IgE). TR was only detected on 2DE immunoblots of the secreted proteome of the DAYA strain probed with the IgE antibody fraction from pooled ABPA Pictilisib price Amobarbital patients sera [31]. This result suggested that TR might not be a good biomarker for ABPA. In another study, the immunosecretome of A. fumigatus was detected using pooled patient sera (total n = 22 patients [ABPA, n = 11; aspergilloma, n = 5; IA, n = 6]). The immunoreactive intensity of TR was lower than most other proteins [30]. A possible explanation is that the anti-TR antibody titers were not high in pooled sera because most cases included in the study were not IA. Although

investigators in other laboratories recently noted the antigenic nature of TR [30, 31], no study has found shown diagnostic value for TR in non-neutropenic patients with IA. We showed that TR (spot no. 2A-2 M) had the strongest immunoreactivity with patient sera. TR, a component of the gliotoxin biosynthetic cluster, provides self protection to A. fumigatus against gliotoxin [37, 38]. This protein has been described as an extracellular protein of A. fumigatus by Singh and Kumar [30, 31]. However, Schrettl et al. showed that GliT is preferentially localized in the cytoplasm and nuclei by a GFP-GliT construct [38]. To predict whether or not GliT is actively secreted into the culture supernatant, we used two bioinformatic tools (SignalP and WoLF PSORT) to analyze its localization. Our results support the findings of Singh and Kumar [30, 31].

Original magnifications, × 10. (C) Quantification of results in B. *** P < 0.001 for Student's t-test versus Mock + pSRα group, whereas **P < 0.01 for Student's t-test versus HSV-1

+ pSRα group. 3.3. Both overexpression of PTEN and activation of GSK-3β pathway also inhibit HSV-1-induced KSHV reactivation From Figure 2, we observed that expression of PTEN (negative regulator of PI3K/AKT pathway) was low in HSV-1-infected BCBL-1 cells, therefore, we asked whether overexpression of PTEN could influence HSV-1-induced KSHV replication. To address this issue, the PTEN cDNA construct was transfected to the cells. Western blot analysis demonstrated that overexpression of PTEN not only decreased phosphorylated Nec-1s cell line AKT and GSK-3β (data not shown), but also reduced HSV-1-induced KSHV Rta and vIL-6 proteins expression (Figure 5A). To further determine whether overexpression of PTEN could reduce the release of KSHV progeny virions induced by HSV-1, experiments were designed to detect the copy number of KSHV progeny virions. The results of real-time DNA-PCR demonstrated that the copy number of KSHV virions in the supernatant from PTEN-transfected and HSV-1 infected BCBL-1 cells was significantly decreased when compared

to those from pcDNA-transfected and HSV-1 infected BCBL-1 cells (Figure 5B). Figure 5 Overexpression of PTEN and activation of GSK-3β inhibit HSV-1-induced KSHV reactivation. (A) Western blot analysis was used to detect the expression of KSHV Rta, vIL-6 and the level of the transfected PTEN in PTEN or SU5402 control vector transfected and HSV-1 infected BCBL-1 cells as indicated. (B) Real-time DNA-PCR was used to detect the copy number of KSHV progeny virions in the supernatant of PTEN or control vector transfected and HSV-1 infected BCBL-1 cells as indicated. ** p < 0.01 and ## p < 0.01 for Student's t-test versus Mock + pcDNA and HSV-1 + pcDNA groups, respectively. (C) Western blot analysis was used to detect the expression of KSHV Rta, vIL-6 and the level of the transfected GSK-3β-S9A

in GSK-3β-S9A or control vector transfected and HSV-1 infected BCBL-1 cells as indicated. Because HSV-1 infection of BCBL-1 cells increased phosphorylated GSK-3β (Figure 2) and transfection of PI3K-DN decreased Astemizole HSV-1-induced phosphorylation of GSK-3β (Figure 3C), we reasoned that inactivated GSK-3β might promote HSV-1-induced KSHV replication. To test this hypothesis, the GSK-3β Sotrastaurin purchase mutant plasmid GSK-3β-S9A, which exhibits constitutively active GSK-3β, was transfected to BCBL-1 cells. As expected, the expression of KSHV Rta and vIL-6 proteins in GSK-3β-S9A-transfected and HSV-1 infected BCBL-1 cells was markedly reduced compared to pcDNA-transfected and HSV-1 infected BCBL-1 cells (Figure 5C). Taken together, these data suggest that PTEN/PI3K/AKT/GSK-3β pathway may play an important role in HSV-1-induced KSHV reactivation. 3.4.

Approved standard, 9th ed. Wayne, PA: CLSI document M7-A7; 2012. 51. Hobert O: PCR fusion-based approach to create reporter gene constructs for expression analysis in transgenic C. elegans . Biotechniques 2002, 32:728–730.PubMed 52. May

R, Völksch B, Kampmann G: Antagonistic activities of epiphytic bacteria from soybean leaves against Pseudomonas syringae pv. glycinea in vitro and in planta. Microb Ecol 1997, 34:118–124.PubMedCrossRef 53. Schenk A, Weingart H, SHP099 ic50 Ullrich MS: Extraction Abemaciclib solubility dmso of high-quality bacterial RNA from infected leaf tissue for bacterial in planta gene expression analysis by multiplexed fluorescent Northern hybridization. Mol Plant Pathol 2008, 9:227–235.PubMedCrossRef 54. McGhee GC, Jones AL: Complete nucleotide sequence of ubiquitous plasmid pEA29 from Erwinia amylovora strain Ea88: gene organization and intraspecies variation. Appl Environ Microbiol 2000, 66:4897–4907.PubMedCentralPubMedCrossRef 55. Takle GW, Toth IK, Brurberg MB: Evaluation of reference genes for real-time RT-PCR expression studies selleck in the plant pathogen Pectobacterium atrosepticum . BMC Plant Biol 2007, 7:50.PubMedCentralPubMedCrossRef 56. Hornik K: R: A language and environment for statistical computing. Vienna, Austria: R Foundation for

Statistical Computing; 2013. 57. Rutherford K, Parkhill J, Crook J, Horsnell T, Rice P, Rajandream MA, Barrell B: Artemis: sequence visualization and annotation. Bioinformatics 2000, 16:944–945.PubMedCrossRef Competing interests The authors declared that they have no competing interests. Authors’ contributions DP carried out the molecular work, participated in the bioinformatical analysis and drafted the manuscript. HW conceived of the study, participated in its design and coordination and helped to draft the manuscript. All authors read and approved the final manuscript.”
“Background Development of resistance to beta-lactam antibiotics in Streptococcus pneumoniae involves alterations

in the target proteins, the penicillin-binding Mirabegron proteins (PBPs) which result in decreased affinity to beta-lactams. In order to identify individual mutations in S. pneumoniae that are related to the resistance phenotype, a series of independent mutant families has been selected in the laboratory using stepwise increasing concentrations of antibiotics [1]. Two beta-lactams were chosen for selection: piperacillin, which induces rapid lysis in the bacteria, and cefotaxime which does not interact with PBP2b and leads to a tolerant response [2]. Point mutations in pbp2b from piperacillin-resistant mutants and in pbp2x from cefotaxime resistant mutants have been described [3–5]. Surprisingly, a decrease in antibiotic susceptibility in some mutants correlated with a mutation in non-PBP genes [6].

Even after zinc administration was discontinued, tumor growth was slower than in control animals (figure 2). Importantly, at the dosage delivered to the animals, we did not observe any evidence of biotoxicity during the treatment protocol and no animal death was recorded. Further, a blinded pathologist performed a full post-mortum histological analysis of tissues and uncovered no evidence of tissue toxicity in the animals enrolled in the zinc treatment protocol (data not shown). Liver changes reported by others

at the LD50 level were not seen with our substantially lower dosage even with the chronic administration schedule. Survival of Animals following treatment of prostate cancer xenografts with zinc As a final measure of the potential PI3K inhibitor usefulness of zinc as a component check details of prostate cancer chemotherapeutics, we assayed the ability of the intra-tumoral zinc injection protocol to extend the life of animals in our prostate cancer xenograft model. Because they are growing subcutaneously rather than orthotopically xenograft tumors may grow to significant size without causing animal death. For humane reasons, a scoring system was established to assess animal welfare and animals

not able to meet two requirements were euthanized. The scoring system consisted of the following: 1. Maintenance of PLX-4720 cost Normal weight (Weight loss > 12%); 2. Normal ambulation; 3. Normal grooming; 4. Normal feeding. Importantly, the decision to remove an animal from the protocol due to extreme tumor burden was made by an animal care technician unaware of the treatment group of the particular animal at the time of the SPTLC1 decision. Thus, humane removal of an animal from the protocol was recorded as a death event, and with these data we evaluated survival. As seen in figure 5, intra-tumoral injection of zinc acetate significantly extended the lifespan

of animals in this xenograft model of prostate cancer. Dramatically, although the treatment protocol extended for only two weeks, the enhanced survival of animals in the zinc treatment group was persistent for several weeks beyond (figure 5). In the control group, all animals had succumbed to the debilitating effects of the growing tumor within eight weeks of the beginning of the treatment protocol. However, in the same time period, 80% of those treated with zinc acetate injections remained alive (figure 5). This dramatic result was significant (p = 0.002) by Kaplan-Meier Survival Analysis and revealed the intra-tumoral injection can halt the growth of prostate cancer in vivo with marked in gains in survival. Figure 5 Effect of Intra-Tumoral Zinc Injection on Survival. Prostate cancer cell xenografts were placed into SCID mice and allowed to grow to a size of 200 mm3. Every 48 hours for 14 days, mice were then anesthetized and injected with 200 μL of either saline or 3 mM zinc acetate.

Once all samples are processed, the sample set is analyzed through the qPCR readout portion of the assay. These samples are also analyzed using the appropriate gene-specific qPCR assay as a comparison. The MIC as determined by the molecular AST analyses were compared to the MIC as determined from the predicate macrobroth analysis to determine the agreement between these methods. check details A brief description of the mechanism

of the ETGA assay is as follows; the ETGA reaction solution bead mill tube is formulated to facilitate microbe-derived DNA polymerase-mediated extension of a primer-template oligonucleotide substrate. Upon bead milling, microbe cell wall lysis allows contact between active microbe derived DNA polymerases and the primer-template substrate. A successful DNA polymerase primer-template extension event of the substrate’s primer oligonucleotide provides a new primer binding site for a subsequent qPCR detection reaction. Thus, DNA polymerase extension activity enables and triggers a downstream qPCR

detection reaction. The subsequent qPCR detection signal is directly proportional to the amount of substrate extended, which is proportional of the amount of microbial DNA polymerase extension activity present, and this is proportional to the amount of viable SB431542 concentration proliferating bacteria present from culture. Complete details regarding the ETGA

assay have been previously described [21] a hyperlink is provided [http://​nar.​oxfordjournals.​org/​content/​40/​14/​e109.​full.​pdf+html?​sid=​ea56a354-4e91-4515-aec8-ccdc5acfb438]. ETGA and gene-specific qPCR analysis of the time course samples Stored samples were allowed to thaw at room temperature, briefly vortexed, and spun down at 12,000×g for one minute. ETGA readout by qPCR was performed by Selleckchem LY3023414 adding 4 μL of each sample into a reaction well containing 27.2 μL of qPCR reaction mix which has been previously described [21]. For the parallel-run of corresponding gsPCR for either S. aureus or E. coli samples, single reactions were run composed of 3 μL bead mill lysate added to 28 μL of the appropriate qPCR reaction mix into a reaction well. The Edoxaban gene targets for the S. aureus and E. coli-specific qPCR assays are nuc and uidA respectively. The primer and probe sequences for these assays have been previously reported [21]. All qPCR analysis was performed on a Roche LightCycler 480 II system (Roche Applied Science, Indianapolis, IN). Cycle values were plotted against time of incubation. The values produced by the overnight samples were plotted as the measured Ct minus 10 to account for the 1000-fold dilution compared to the earlier samples. This assumes that each 10-fold dilution equates to a 3.33 cycle decrease in signal based on an efficient qPCR reaction.

There was no systematic schedule for INR monitoring after the administration of reversal agents, and repeat doses of VX-770 in vitro coagulation factors were administered at the treating provider’s discretion based on the follow-up INR after the first dose. There was no systematic screening for thromboembolic events; patients were assessed for any potential thromboembolic complications as was deemed clinically appropriate. Data were

compared between the two groups to determine if differences were statistically significant for the above-mentioned demographic, coagulation, and outcome parameters, with the primary efficacy end-point being achievement of goal INR less than or equal to 1.5, and the primary safety end-point being number of thromboembolic events. Statistical tests utilized include the Wilcoxon Rank Sum test to compare continuous data, reported as median [IQR], and

Chi Square selleck or Fisher exact test for categorical data, reported as n, %. A p value less than or equal to 0.05 was considered statistically significant. Results Based on inclusion and exclusion criteria, 74 PCC3 patients and 32 LDrFVIIa patients were included in the final analysis (Figure 1). There were no significant differences between the groups with regards to age, gender, or indication for anticoagulation with warfarin (Table 1). There Fedratinib solubility dmso was also no difference in the indication for emergent reversal (Table 2), except for more patients who presented with subdural hematoma received LDrFVIIa. The groups were similar with regards to the percentage of patients receiving vitamin K (77.0% PCC3 vs. 68.8% LDrFVIIa, p = 0.37) or FFP (66.2% PCC3 vs. 65.6% LDrFVIIa p = 0.95), and the number FFP units administered (2[0-4] PCC3 vs. 2[0-4] LDrFVIIa, p = 0.75) (Table 3). The initial dose of PCC3 was 1540[1429-1978] units or 19.9 [18.6-20.8] units/kg, and

the dose of LDrFVIIa was 1000[1000-1000] mcg or 11.5 [10.1-15.0] mcg/kg. Table 4 details the INR response comparing the two coagulation factors. Baseline INRs were equivalent for the two groups prior to the first dose of either PCC3 or LDrFVIIa (3.1[2.3-4.1] PCC3 vs. 2.8[2.2-3.6] LDrFVIIa, p = 0.52). After Astemizole one dose of coagulation factor, 71.9% of patients in the LDrFVIIa group achieved goal INR of 1.5 or less compared to 33.8% in the PCC3 group (p = 0.001). The time between pre and post coagulation factor INRs was similar (3:53[2:32-7:17]) in PCC3 group and 4:30[2:21-6:25] in LDrFVIIa group, p = 0.78). The percent change in INR was higher after administration of LDrFVIIa compared to PCC3 (54.1% [47.3%-62.7%] for the LDrFVIIa group vs. 38.8% [30.7%-56.0%] for the PCC3 group, p = 0.002). Table 1 Baseline demographic characteristics of the study patients Characteristics PCC3 (n = 74) LD rFVIIa (n = 32) p Demographics       Age (years)* 73 [62.3-81.0] 67 [59.5-79.3] 0.32 M:F 43:31 22:10 0.

Mean biofilm thickness provides a measure of the spatial size of the biofilm. Maximum thickness: the maximum thickness over a given location, ignoring pores and voids inside the biofilm. Roughness selleck chemicals llc coefficient: a measure of variation in biofilm thickness across the field of view, an indicator

of biofilm heterogeneity. The percentage of adhering cells (% Coverage) was calculated using ImageJ NIH image processing software [72]. Atomic Force Microscopy Imaging and force measurements to characterise the nanomechanical properties of Shewanella algae cells were performed by AFM. In these studies every treated polystyrene disc containing the immobilised bacteria was attached to a steel sample puck by means of an adhesive tape. Combretastatin A4 research buy When measuring in liquid, 50 μL of FSW were added onto the disc prior to be placed into the AFM liquid cell. For measurements performed in air, polystyrene discs were carefully rinsed and dried in N2 atmosphere before

using. Tapping Mode: S. algae cells were imaged by AFM operating in tapping mode in air using a Multimode microscope and a Nanoscope V control unit from Bruker at a scan rate of 1.0–1.2 Hz. To this end, etched silicon tips (RTESP, 271–311 kHz, and 40–80 N/m) were used. Peak Force Tapping and force-distance analysis: Quantitative mapping were performed in FSW at room temperature using a Nanoscope V controller (Bruker). Images were

acquired in AFM contact and Peak Force Tapping Mode [73] (Peak Force-Quantitative Nanomechanics, PF-QNM). AFM probes used in these studies were silicon AZD1480 datasheet nitride probes (NP-C, Bruker) with a nominal tip radius of 20–60 nm. The spring constant of cantilevers were measured using the thermal tuning method [74], and its values ranged 0.14-0.26 N/m. Mica surfaces were selected as rigid substrates for deflection sensitivity calibration. Note that in PF-QNM measurements AFM tips were carefully calibrated before every experience as described elsewhere [74–77]. Experimental results were acquired for single bacteria or little groups of them from the PF-QNM images, excluding thus contributions due to bacteria/EPS-free substrate. Data proceeding from at least 115 units from two Immune system independent cultures were collected for each medium. Adhesion force and Young’s modulus values distribution has been expressed as histograms. Force-distance (FD) curves were collected using low loading forces (F < 20 nN) in order to protect both the AFM tip and the bacterial cells [59]. Data processing was carried out using the commercial Nanoscope Analysis (Bruker), WSxM (Nanotec) [78] and Gwyddeon (GNU) softwares. Statistics The effects of culture medium, incubation temperature and their interaction on the dependent variables (total cell density and biofilm formation) were assessed by a two-way ANOVA.

If MRI is not feasible because of metallic implants like e.g. pacemaker or vessel clips, functional lateral x-rays in traction, extension and flexion or dynamic fluoroscopy can be performed by the experienced physician to visualize instability by e.g. intervertebral space widening [56, 58]. In addition to these signs of instability in the cervical spine, further injuries give way for diagnosis of instable thoracic and lumbar spine trauma. Fractures, especially serial fractures of the transverse process and

ribs account for instable, type C rotational injury. Patients with associated sternal fractures following hyperflexion injury in e.g. restrained motor vehicle passengers might suffer from discoligamentous posterior column injury (assigned type B) of the upper thoracic spine. In EPZ-6438 price contrast, retroperitoneal bleeding as shown in contrast medium selleckchem CT-Scan is often associated with instable anterior spine injury from hyperextension to the thoracolumbar region. McLain and Benson reported that anterior vertebral body height loss of more than 50%, sagittal angulation of more than 25°, three-column injury, primary neurologic deficit and serial vertebral fracture are associated with instable spine injuries [28]. Classification and need to surgical stabilization Due to a similar vertebral structure, injuries to the

subaxial spinal column are classified according to Magerl et al. [72]. Various reports address this classification and the reader is kindly referred to these articles. In brief, based on Flavopiridol (Alvocidib) the two column concept of Whitesides from 1977 [73], injuries are classified by the injuring mechanical force applied to the spine and the consecutive fracture pattern of the vertebral column (see Figure 2). Regarding the given recommendations in this section, the reader should be aware that these can only rely on a hand full of RCTs and low-quality studies that have been published so far [74–80], as well as on third opinion and the article author’s personal experience. Controversial discussion regarding

all questions on where, how and when to perform surgery or even use conservative treatment strategies has been going on and will endure as long as no high-quality trials are published [79, 81–83], as it was brought up in a recent Cochrane review on thoracolumbar fractures [84], being able to enter only one poor-quality study into their review article which precluded firm conclusions. Figure 2 Classification of spinal injury and treatment recommendation in the polytraumatized patient. Classification of Magerl et al. (1993) [72] based on the two column concept of Whitesides (1977)[73]. The mechanism of applied forces to the spine generates specific fractures. Pure axial compression VS-4718 results in type A fractures. Distraction leads to type B and rotational momentum with compression or distraction results in type C fractures. Type A1 and A2 (except for A2.3) are regarded as stable. Whereas burst fractures, especially higher rated A3.

Park et al found no correlation between either ∝ angle or MA to PT and PTT [16] while Cotton et al (using Rapid TEG) reported

a correlation between ∝ angle and MA with platelet, PT and PTT. In this study G was failed to correlate with any traditional lab tests [17]. Johansson et al reported that all the TEG® parameters improved after the administration of predefined transfusion packages [18]. Watters et al reported that MA parameters were higher in patients after splenectomy [19]. Using the platelet mapping sequence in the TEG®, Nekludov found that bleeding patients have reduced platelet response to arachdonic acid [20]. In ROTEM® studies Rugeri found that CA15-EXTEM® correlated with PT, CA15-INTEM® with platelets

and PTT, and CA10-FIBTEM® with fibrinogen [21]. Levrat et al noted that in EXTEM® CA10, MCF and CLI60 correlated well with the euglobulin lysis time, which they used as the gold standard I-BET-762 in vivo to selleck chemicals detect fibrinolysis [22]. Davenport et al reported that CA5 could be an early indicator of coagulopathy in trauma and CT, CA and MCF improved after transfusion [23, 24]. In summary, the single apparent similarity between TEG® and ROTEM® parameters when used to diagnose coagulopathy in trauma is between TEG® MA and ROTEM® MCF and their similar association to platelet count and PTT. Results of the 2 studies on the use of TEG® and ROTEM® in guiding transfusion in trauma In a retrospective study, Kashuk et al suggested that using TEG® parameters such as r to guide transfusion may lead to a reduction in plasma transfusion [25]. Schochl AZD9291 chemical structure et al reported that ROTEM®-based protocols are useful to guide transfusion of fibrinogen concentrates and prothrombin complex that in turn reduce the need for transfusion of red blood cells and platelets [26]. As summarized in Table 2, no similarity between TEG® and ROTEM® can be Carnitine dehydrogenase made from these studies. Results of the 11 studies on the use of TEG® and ROTEM® and outcome in trauma Plotkin

et al in a retrospective study on TEG® reported that low MA correlated with increased transfusion requirement [14]. For ROTEM®, 2 studies by Leeman et al and Doran et al reported the same finding with MCF (INTEM®), the later study also showed that reduced MCF (EXTEM®) is useful to guide transfusion [27, 28]. Park developed a prognostic scoring system for trauma patients using inflammatory and coagulation parameters, in which of all TEG® parameters only MA was an independent predictor of mortality [29]. Carroll also detected a significant correlation between TEG® platelet mapping and transfusion requirements, and a correlation between r and MA values with mortality [30]. Kashuk in both a “before and after” and a prospective observational study found that TEG® G values were associated with survival [31]. Similarly Pezold in a retrospective TEG® study found that low G values were associated with both increased transfusion requirements and mortality [32].