We have also been able to inactivate specific loci on several oth

We have also been able to inactivate specific loci on several other, globally successful plasmids including

those carrying the carbapenemases bla KPC and bla NDM-1, illustrating the utility of our approach and its broad applicability to the study of plasmid gene function (manuscripts in preparation). Recent advances in sequencing have identified AR-13324 various ‘successful’ plasmids such as those found associated with the globally disseminated strain E. coli ST131 [7] or those carrying other prominent resistance genes such as bla CMY-2 or bla NDM-1. Investigating the factors key to their dissemination could also be examined using a similar approach [28, 29]. A better understanding of the biological relevance of plasmid ‘backbone’ genes in the successful survival and spread of antibiotic resistance plasmids will be of paramount importance if we are to prevent future persistence and further spread of both plasmid vectors and the antibiotic resistance genes that they carry. Methods Bacterial strains and plasmid extraction Wild-type plasmid pCT [Genbank: FN868832] was isolated from a veterinary E. coli strain C159/11 [15, 16]. Wild-type pCT and recombinant pCT DNA was extracted using a QIAprep Spin Miniprep Kit (Qiagen, Germany) and a QIAGEN Large selleck chemicals llc Construct Kit (Qiagen, Germany) according to the manufacturers’ instructions.

All plasmids were transformed into E. coli DH5α electro-competent cells (Bioline, UK) (1.25 kV, 25 μF, 200Ω, in chilled 2 mm electroporation cuvettes) and transformants selected by growing on agar containing 8 mg/L of cefotaxime (Sigma-Aldrich, USA) or 50 mg/L of kanamycin (Sigma-Aldrich, USA) when the aph cassette is used for gene inactivation. Inactivation

of the six selected pCT genes To inactivate the six selected pCT genes, pCT was transformed into the E. coli strain, SW102 which carried a chromosomal Lambda-Red Recombinase [23]. Where transformation of the Atazanavir plasmid into this strain is difficult, conjugation by filter mating was done by selecting the transconjugants on media containing 50 mg/L of tetracycline and 8 mg/L of cefotaxime. The hybrid primers used to inactivate the selected pCT genes were designed to have 20 bp identity to the aph cassette on pKD4 [30] and 40 bp sequence identity to the target genes (Table 2). Recombination of Selleck PF 2341066 amplimers encoding the aph gene with each pCT gene was carried out as previously described [18]. Recombination was confirmed in each case by PCR and sequencing across the mutated DNA region (Table 2). The recombinant plasmid was then extracted and electroporated into DH5α or conjugated into another host strain to avoid further recombination from occurring and for further study.

As such strains could potentially be

As such strains could potentially be defeated by using bacteriocins we need more knowledge about bacteriocin resistance phenomena in enterococci. In this work we have performed transcriptional analyses by genomic microarray to study the effects on class IIa bacteriocin resistance in E. faecalis V583, a vancomycin-resistant clinical isolate [19, 20]. Our data confirm the important role of the mannose PTS in bacteriocin sensitivity and provide new insight into its role in global gene regulation in this organism. Methods Bacterial strains and growth conditions BAY 63-2521 solubility dmso Enterococci were routinely grown at 37°C in M17

(Oxoid) supplemented with 0.5% glucose (GM17) or brain heart infusion (BHI) (Bacto™ BHI, Difco Laboratories, Becton, Dickinson and Company). Growth was monitored using a Bioscreen C instrument (Oy Growth Curves Ab Ltd.), at 37°C. Bacteriocin assay Pediocin PA-1 was obtained from Pediococcus acidilactici Pac 1.0 [21] grown for 24 hours in MRS (Oxoid) at 30°C. The culture supernatant was heated to 70°C for 15 min, and applied to a column of SP-sepharose (Amersham Pharmacia Biotech). The column was washed with sodium ARS-1620 purchase phosphate buffer (10 mM, pH 5) before the concentrated bacteriocin was eluted with 1 M NaCl. Bacteriocin activity was measured with

a 96-well microtiter-plate assay [22]. Stationary phase cultures diluted 100 times in MRS were used as indicators. The plates were incubated for 16 hours at 37°C, and growth was measured spectrophotometrically at 620 nm. One bacteriocin unit (BU) was defined as the amount of bacteriocin that inhibited growth of the indicator strain E. Acesulfame Potassium faecalis V583 by 50% under these conditions. Isolation of resistant mutants Aliquots from a culture of E. faecalis V583 grown in GM17 to an Captisol supplier optical density at 600 nm of 1.0 were spread onto GM17 agar plates containing 10 BU/ml pediocin PA-1. After incubation

overnight at 37°C, the spontaneously pediocin PA-1 resistant mutant MOP1 was picked. Mutant MOP5 was obtained by inoculating MOP1 in lactic broth [23] supplemented with 800 BU/ml pediocin PA-1. After growth over night the mutant was colony purified on GM17 agar. Mutant MOP2 was resistant to 2-deoxyglucose (2-DG), 2-DG is known to enter the bacteria via mannose PTS [24]. One μl of an E. faecalis culture grown overnight at 37°C in M17 broth supplemented with 0.2% fructose was spread onto M17 agar (Oxoid) plates containing 10 mM 2-DG (Sigma) and 0.2% fructose. After incubation for 24 hours, the mutant was isolated. To construct a strain with an inactivated mpt, a 355 basepair fragment of gene mptD was PCR amplified using primers mptDi-F and mptDi-R and the template was DNA from V583 (Table 1).

With the increase of the mass ratio to 1:7 5, Ag particles furthe

As the mass ratio is increased to 1:15, the size of Ag particles is remarkably increased along with partial particles deposited together to form bigger spheres with a diameter of approximately 1 μm (Figure 4e). With the increase of the mass ratio to 1:7.5, Ag particles further aggregate but still disperse well (Figure 4f). Finally, with the mass ratio of 2:1, the morphology of those Ag particles becomes bigger and irregular (Figure 4g). Figure 3 AFM images of graphene oxide. (a) AFM image

and (b) the height profile of the image. Figure 4 SEM images of surface morphologies of different films. (a) Graphene oxide films, (b) graphene films (reduced by ascorbic acid), and (c to g) graphene-Ag composite films (the amount of AgNO3 is from 2 to 300 mg in each film). EDX is used to qualitatively determine the variation of relative ratio of each element. The results in Figure 5 and Table 1 show that this website the atomic ratios of C/O of the graphene films and graphene-Ag composite films are various from 2.2 to 2.5, lower than those in a previous study [11]. Compared with the graphene oxide films (the atomic ratio of C/O is approximately 1.5), the increased E7080 atomic ratio of C/O of the composite films means that

the selleck reduction progress has occurred. Simultaneously, the weight percentages of the Ag element may influence the reaction in some way. When the amount of AgNO3 reaches to 300 mg, the atomic ratio of C/O is far lower, indicating that the reduction process may be affected

when the amount of AgNO3 is excessive. As for EDX results, the appropriate amount of AgNO3 is around 5 to 10 mg. Figure 5 EDX spectra of graphene and composite films. (a) Graphene films and (b) graphene-Ag composite films; the mass ratio of AgNO3/graphene oxide is 2:1. Table 1 Elements of all films measured by EDX AgNO3 (mg) Weight (%) Atomic (%) Atomic ratio (C/O)   C O Ag C O Ag   GO 50.03 44.03   58.11 39.17   1.48 0 65.57 34.43   71.72 28.28   2.54 2 61.54 37.83 0.63 68.37 31.55 0.08 2.17 5 64.85 34.26 0.89 71.52 28.37 0.11 2.52 10 63.46 34.42 2.12 70.88 28.86 0.26 2.46 20 59.06 35.09 5.85 68.63 30.61 0.76 2.24 300 51.86 40.87 7.27 62.22 36.81 0.97 1.69 0 stands for the graphene film reduced for 5 h. The XRD patterns also support the results from SEM and EDX. Only when the amount of AgNO3 is 300 mg, the final weight percentage of Ag is more than 7%, so the crystal structure Ketotifen and ordering of Ag particles can be characterized by XRD. As shown in Figure 6 (i), the characteristic peaks at 38.02°, 44.24°, and 64.56° correspond with the (111), (200), and (220) planes of the cubic Ag crystal (JCPDS no. 04–0783), respectively, which indicates that the metallic Ag particles are formed after being reduced.

0 (Table 4) The PCR cycling

0 (Table 4). The PCR cycling eFT-508 manufacturer conditions for amplifying EV71 vp1s, EV71 vp4s and CA16 vp4s consisted of 4 min at 94°C, followed by 35 cycles of 94°C 30 s, 52°C 30 s, 72°C 1 min, and then 72°C for 7 min. The steps for amplifying EV71 vp4s were the same as those for amplifying the other 3 protein genes except for annealing temperatures at 55°C for 30 s. Agarose gel electrophoresis and EasyPure Quick Gel Extraction Kit (Trans Gen Biotech, China) were used to purify those amplified products.

The purified products were ligated to pGEM-T cloning vector (Promega, USA) for transformation into competent DH5α cells. Positive clones were identified by White-Blue colony selection and sequencing (Invitrogen Co). Table A769662 4 Primers used for cloning and sequencing primers sequences fragments (bp) EV71-VP1-1F 5′-TGAAGTTRTGYAAGGATGC-3′   EV71-VP1-1R 5′-CCACTCTAAAATTRCCCAC-3′ 993 EV71-VP4-1F 5′-CTACTTTGGGTGTCCGTGTT-3′   EV71-VP4-1R 5′-GGGAACTTCCAGTACCATCC-3′ 655 CA16-VP1-1F 5′-ACTATGCAAGGACACWGAG -3′   CA16-VP1-1R 5′- check details CAGTGGTGGAAGAGACTAAA-3′ 1076

CA16-VP4-1F 5′- GGCTGCTTATGGTGACAA-3′   CA16-VP4-1R 5′- CATGGGAGCTATGGTGAC-3′ 1090 F referred as forward primer and R referred as reverse primer. Olopatadine Expression and Purification of VP1s and VP4s The pET-30a vector with an N-terminal His·Tag/thrombin/S·Tag™/-enterokinase configuration plus an optional C-terminal His·Tag sequence with endonuclease sites of BamH׀and Xho׀and the pGEX-4T-1 vector with an N-terminal GST (glutathione S-transferase) ·Tag/thrombin configuration with endonuclease sites of EcoR׀

and Xho׀were used for expressing VP1s and VP4s, respectively. The virus isolates selected for expression were s67 (for VP4 of EV71), s108 (for VP1 of EV71), s390 (for VP1 of CA16) and s401 (for VP4 of CA16). The genes were purified with agarose gel electrophoresis and EasyPure Quick Gel Extraction Kit after being amplified by PCR with corresponding primers (Table 5). The cycling condition for amplifying VP1s of EV71 and CA16 consists of 95°C for 4 min, followed by 35 cycles of 95°C 30 s, 55°C 30 s, 72°C 1 min, and then 72°C for 7 min. The steps for amplifying VP4 of EV71 and CA16 were the same as those for amplifying the VP1s, except that the annealing temperatures were 50°C and 57°C respectively.

Curr Med Chem 2009, 16: 1688–1703 PubMedCrossRef 19 Katoh Y, Kat

Curr Med Chem 2009, 16: 1688–1703.PubMedCrossRef 19. Katoh Y, Katoh M: Comparative gemomics on PROM1 gene encoding stem cell marker CD133. Int J Mol Med 2007, 19: 967–970.PubMed 20. Mehra N, Penning M, Maas J, Beerepoot LV, van Daal N, van Gils CH, Giles RH, Voest EE: Progenitor marker CD133 mRNA is elevated in peripheral blood of cancer patients with bone metastases. Clin Cancer Res 2006, 12: 4859–4866.PubMedCrossRef 21. Lin EH, Hassan M, Li Y, Zhao H, Nooka A, Sorenson E, Xie K, Champlin R, Wu X, Li D: Elevated circulating endothelial progenitor marker CD133 messenger RNA levels predict colon cancer recurrence. Cancer 2007, 110: 534–542.PubMedCrossRef Competing interests The authors Etomoxir declare that


have no competing interests. Authors’ contributions PZ contributed in study design, definition of intellectual content, literature research, experimental studies, data acquisition, data analysis, statistical analysis and manuscript preparation. JGW and SHW contributed in literature research, study design and data analysis. PZ, JGW, XQL contributed in pathological and immunohistochemical observations. PZ, JGW, RQL contributed in RT-PCR analysis. STW contributed in technique supports in laboratory. XCN, JWY, and BJJ contributed in clinical managements. BJJ and JWY contributed in grants for this study, guarantor of integrity of the entire study, study concepts, study design and manuscript review. All authors read and approved the final manuscript for publication.”
“Background Breast cancer selleck screening library is a major public health issue, with more than one million new cases observed around the world in 2002 [1].

The pathogenesis of breast cancer is quite complex. Lifetime exposure to estrogen is reported to be associated with women’s risk for breast cancer and the EPZ015666 biological actions of estrogens are mediated primarily by ERα which belongs to the nuclear receptor superfamily, a family of ligand-regulated transcription factors [2–4]. ERα, which promotes cell growth, metastasis and also mediates resistance to apoptosis, plays a key role in progression of breast cancer [5, 6]. HBO1 (histone acetyltransferase binding to ORC1), also named MYST2, belongs to the MYST family which is characterized by a highly conserved Carnitine palmitoyltransferase II C2HC zinc finger and a putative histone acetyltransferase domain. The role of HBO1 in cancer remains unclear, although its expression has been reported in testicular germ cell tumors, breast adenocarcinomas, and ovarian serous carcinomas [7]. Recent investigations have revealed that over-expression of HBO1 dramatically enhances the anchorage-independent growth of both MCF7 and SKBR3 breast cancer cells [8]. Furthermore, it also functions as a transcriptional coactivator for hormone receptors including ERα and PR [9], leading to consideration of this protein as a carcinogenetic factor.

YHS and XPH performed the experiments and were involed in draftin

YHS and XPH performed the experiments and were involed in drafting the article. All authors have read and approved the final manuscript.”
“Introduction Lung cancer is one of the leading causes of cancer-related mortality both in China and throughout the world [1, 2]. Non-small cell lung cancer (NSCLC) accounts for75-80% of all lung cancer [3]. Standard therapeutic strategies such as surgery, chemotherapy, or radiotherapy have

reached a plateau [1]. Significant advances in the research of the biology and molecular mechanisms of cancer have allowed the development of new molecularly targeted agents for the treatment of NSCLC [4–8]. One such target is the epidermal growth factor receptor Idasanutlin clinical trial (EGFR), a 170-kDa trans-membrane glycoprotein and member of erbB family. Small molecule tyrosine kinase inhibitors (TKI), such as gefitinib and erlotinib, disrupt EGFR kinase activity by binding the adenosine triphosphate pocket within the catalytic region of the tyrosine kinase domain [9]. Currently, both

gefitinib and erlotinib are used for treatment of patients with advanced NSCLC. TKI clinical trials have shown that these agents have dramatic effect on the subset of NSCLC patients with somatic mutations in the tyrosine kinase domain of the EGFR gene, whereas the presence of KRAS mutations seems to be correlated with primary resistance to these agents [10–15]. So it is necessary to identify the mutation status of KRAS and EGFR for selection GSK2118436 of patients who are more likely to benefit from TKI. Although almost 70% of patients with NSCLC present with locally advanced or metastatic disease at the

time of diagnosis [16, 17], KRAS and EGFR mutation status is most commonly assessed only in the primary tumor tissue based on the assumption that primary and metastases are Nirogacestat in vivo pathologically concordant. Etofibrate However, it has been known that lung cancers are often heterogeneous at the molecular level even within the same tumor and many key molecular alterations may occur during metastatic progression [18–20]. It is still unclear whether KRAS and EGFR mutation status in primary tumors is reflected in their corresponding metastases in Chinese patients with NSCLC, although several recent relevant studies in western countries have been performed and published [21–26]. In the present study, we investigate KRAS and EGFR mutation status using PCR-based sequencing analyses in 80 primary tumor samples and their corresponding local lymph node metastases from Chinese patients with NSCLC. The goal is to determine whether KRAS and EGFR mutation profile is stable during the metastatic progress and to investigate the clinical usefulness of mutational analyses in primary tumor versus in metastases for planning EGFR-targeted therapies for the treatment of patients with NSCLC.

Biochim Biophys Acta 1972, 261:284–289 PubMed 39 Tsai CM, Frasch

Biochim Biophys Acta 1972, 261:284–289.PubMed 39. Tsai CM, Frasch CE: A sensitive silver stain for detecting lipopolysaccharides in polyacrylamide gels. Anal Biochem 1982, 119:115–119.PubMedCrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions LP has given an important contribution

to the elaboration of paper. CdL, SB, AL, LODL and MRC gave important contributions in the order to design of the paper and to draft of manuscript. GG and AlL have cooperated for technical assistance. GDR and MM have studied histopathology features. FR and LR conceived the study participating to its scientific design. Ralimetinib in vivo All authors read and approved the final manuscript.”
“Background Mycoplasma synoviae is

an economically important pathogen of poultry, causing synovitis, chronic respiratory tract disease, and retarded growth in chickens and turkeys [1, 2]. M. synoviae is a member of the genus Mycoplasma of the class Mollicutes, a group of wall-less Gram-positive bacteria with genomes ranging from 1358 kb to as little as 580 kb [3]. The genome sequence of M. synoviae strain WVU 1853 has been determined and comparative analysis with M. gallisepticum, another major avian pathogen, provided evidence ATM Kinase Inhibitor manufacturer for horizontal gene transfer between the two species, though belonging to two distinct phylogenetic groups [4, 5]. Among the genes that could have arisen by horizontal gene transfer are those encoding for haemagglutinins. In avian mycoplasmas, genes encoding for these immunogenic and surface exposed proteins are the subject of considerable antigenic variability [6]. By alternating the composition of their surface proteins, mycoplasmas are thought to colonize more efficiently mucosal surfaces and become more virulent [7,

8]. Haemagglutinins account among the most important surface proteins involved in Tau-protein kinase colonization and virulence of avian mycoplasmas [6, 9]. In M. synoviae, haemagglutinins are encoded by related sequences of a selleck compound multigene family referred to as vlhA genes [10–12]. The haemagglutinins of M. gallisepticum (pMGA) and M. imitans are also encoded by multigene families related to vlhA [13, 14]. Both organization and control of expression of vlhA genes are quite different between M. gallisepticum and M. synoviae. In the former species, vlhA genes are located in five distinct genomic regions and each gene appears to be translationally competent [14, 15]. By contrast, in M. synoviae, all vlhA sequences are confined to a restricted genomic region with a unique copy being expressed in a single strain [16, 17] The uniquely expressed vlhA gene of M. synoviae yields a product that is cleaved post-translationally into a N-terminal lipoprotein (MSPB) and a C-terminal haemagglutinin protein (MSPA) [11]. Cleavage was found to occur immediately after amino acid residue 344 [17].

find m

Following M. genitalium exposure, ectocervical ECs secreted significant levels of IL-6 and IL-8 (p < 0.05 vs. PBS control). Endocervical ECs responded to M. genitalium with the most number of secreted cytokines that included IL-6, IL-8, G-CSF, GM-CSF and MCP-1 (p < 0.05 vs. PBS control). Using IL-8 secretion at 48 h PI as a comparator for all cell types, endocervical ECs were more responsive than vaginal or ectocervical cells when the fold increase of cytokine secretion by infected cells was calculated and compared to cells

that received only PBS (ANOVA; p < 0.01, data not shown). A similar pattern of cytokine elaboration was observed following inoculation of M. genitalium at a MOI of 1 (data not shown). Cytokines that were not significantly induced by M. genitalium G37 or M2300 in any genital ATM Kinase Inhibitor in vivo EC type included IL1-b, IL-2, IL-4, IL-5, IL-7, IL-9, IL-10, IL-12(p40), IL-12(p70), IL-13, IL-15, IL-17, MIP1-a, MIP1-b,

Basic FGF, Eotaxin, IP-10, PDGF-BB and VEG-F. The pattern of cytokines elaborated from cervical selleck screening library ECs was consistent with monocyte and macrophage recruitment and thus we next evaluated the responses of primary human MDM to M. genitalium exposure and determined whether these cells were capable of M. genitalium phagocytosis and killing. Table 1 Cytokine elaboration from human genital epithelial cells following M. genitalium G37 exposure a .   Vaginal (V19I, V12I, V11I) Ectocervical (3ECI) Endocervical (sA2EN)  

MOI 10 PBS MOI 10 PBS MOI 10 PBS IL-6 127 ± 13.1* 69 ± 1.7 63.7 ± 1.8* 21.3 ± 2.4 348 ± 13* 196 ± 15 IL-8 1458 ± 117* 785 ± 11.3 3304 ± 300* 722 ± 98 5e7 ± 1347* 6e4 ± 367 G-CSF 261 ± 46 227 ± 37 548 ± 143 779 ± 122 155 ± 6.2* 93 ± 21 GM-CSF 24 ± 1.8* 8 ± 3.1 16 ± 2.6 10 ± 1.0 160 ± 9.4* 45 ± 12 MCP-1 5.8 ± 1.4 7 ± 2.1 11.4 ± 1.3 10 ± 3.1 7.2 ± 1.1* 0.46 ± 0.02 a Human vaginal (n = 3 donors), ectocervical or endocervical ECs were inoculated with M. genitalium G37 (MOI 10). An equal volume of the PBS vehicle was added Cobimetinib cell line and processed in parallel as a control. Culture supernatants were collected 48 h PI to quantify secreted cytokines. Values are expressed as the mean ± SEM pg/mL from triplicate wells. Cytokine elaboration pattern and magnitudes induced following exposure to AR-13324 strain M2300 were not significantly different than G37. PBS values are presented to indicate basal cytokine elaboration from each cell type. ND, not detected. *, p < 0.05 vs. PBS control using Student’s t-test. Phagocytosis of M. genitalium by human monocyte-derived macrophages To determine the susceptibility of M. genitalium to macrophage phagocytosis, human MDM were exposed to log-phase M. genitalium strains G37 or M2300 (MOI 100) and processed at selected time points for TEM. Within 5 min of inoculation, M. genitalium appeared dark staining with a dense content of ribosomes and no signs of membrane degeneration (Figure 4A). As early as 30 min PI, M.

PubMed 23 Wilkinson DJ, Hossain T, Hill DS, Phillips BE, Crossla

PubMed 23. Wilkinson DJ, Hossain T, Hill DS, Phillips BE, Crossland H, Williams J, Loughna P, Churchward-Venne TA, Breen L, Phillips SM, et al.: Effects of Leucine and its metabolite, beta-hydroxy-beta-methylbutyrate (HMB) on human skeletal muscle

protein metabolism. J Physiol 2013, 591:2911–2923.PubMed 24. Manders RJ, Little JP, Forbes SC, Candow DG: Insulinotropic and LY2606368 clinical trial muscle protein synthetic effects of branched-chain amino acids: potential therapy for type 2 diabetes I-BET151 in vitro and sarcopenia. Nutrients 2012, 4:1664–1678.PubMedCrossRef 25. Newsholme P, Brennan L, Rubi B, Maechler P: New insights into amino acid metabolism, beta-cell function and diabetes. Clin Sci (Lond) 2005, 108:185–194.CrossRef 26. Sener A, Malaisse WJ: L-leucine and a nonmetabolized analogue activate pancreatic islet

glutamate dehydrogenase. Nature 1980, 288:187–189.PubMedCrossRef 27. Panten U, Kriegstein E, Poser W, Schonborn J, Hasselblatt A: Effects of L-leucine and alpha-ketoisocaproic acid upon insulin secretion and metabolism of isolated pancreatic islets. FEBS Lett 1972, 20:225–228.PubMedCrossRef Competing interests Ivo Pischel and Hartwig Sievers are employees of PhytoLab GmbH & Co. KG, Germany and were involved in the study design, but not in any data generation or processing. OpunDia™ is applied for patents by Finzelberg GmbH & Co. KG, Germany, e. g. US 2010323045 (A1) – Extract Formulation of Opuntia ficus Indica (Priorities: US20080741562 20081106; EP20070120081 20071106; US20070002058P 20071106; WO2008EP65048 20081106). Authors’ ZD1839 research buy AZD9291 mw contributions PH, IP and HS were responsible for the concept of this project and for the study design. KVP, and MR were responsible for the acquisition and the analysis of the data. PH, KVP and LD were responsible for

the interpretation of the data. PH and LD wrote the first version of the manuscript which was edited by the other authors. The final version was approved by all authors.”
“Background In the past decade significant progress has been made in unravelling the mechanisms that regulate the complex pathways that couple gene expression to protein synthesis. Emerging from these studies has been the influence of amino acids, most predominately leucine, on protein synthesis. Leucine, over and above being a necessary amino acid in protein synthesis, also potentiates the activity of the key kinases regulating translation initiation. Far from being the only determinate of protein synthesis, leucine along with energy status, mechano-sensing, ionic and hormonal mediators all converge to dictate the rate of protein synthesis. Insulin also plays an important role in protein synthesis, as a potent stimulator of PI-3K/Akt/mTOR axis, coupling growth with nutritional availability. In a recent review by Stark et al. [1] published in the Journal of the International Society of Sports Nutrition, it was stated that fast-acting carbohydrates (e.g.

Nature 1980, 286:309

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