Therefore, the overall detected gold content reduces. Figure 4 EDX test showing the Au-Si percentage within different laser cycling. (A) 2 cycles. (B) 3 cycles. (C) 4 cycles. (D) 5 cycles. Figure 5 Gold nanoparticle variation with number of cycles and dwell time. 1 ms (red), 0.75 ms (green), and 0.50 ms (purple). Light reflectance The nanofibrous structure can significantly influence optical properties, which can differ considerably with those of the bulk materials. This type of structure enhances

optical absorption due to surface plasmon excitation in the metal nanoparticle [10]. The micro-nanoscale surface roughness of the treated substrate could also increase light absorption SYN-117 ic50 due to the multiple reflections selleck chemical in Tanespimycin nmr micro-cavities and the variation of light incident angles. Metal surfaces with roughness on the scale of the optical wavelength are found to have a strong coupling of the incident light and become discolored as a result of selective surface plasmon absorption.In order to investigate the samples’ enhanced absorption behavior in the visible region, a spectroradiometer

was employed with a broad wavelength range of 250 to 1,200 nm. The measured integrating reflectance spectra are illustrated in Figure 6, where the red curve represents the reflectance of the unirradiated gold-silicon sample showing a high reflective intensity around 4,000 a.u. Figure 6 Measured integrating reflectance spectra. (A) 0.25 ms, (B) 0.50 ms, and (C) 1.00 ms. The dark red curve represents the untreated sample, while

the olive green, purple, light blue, and orange curves represent the reflection spectrum of the fibrous nanostructure layer with 2, 3, 4, and 5 cycles over visible wavelength, respectively, at different dwell times. The fibrous nanostructure increases the surface area by more than an order of magnitude which causes the radiation to pass through a longer distance before being reflected back. Therefore, a photon incident on a structured surface is likely to undergo more than one reflection before leaving the surface. Comparing the reflection spectrum to that of pure silicon nanofibers obtained from a previous experiment repeated on silicon wafer [20], we can conclude that the fibrous structure is the main attribute for light enhancement. 3-mercaptopyruvate sulfurtransferase The embedded gold particles will further enhance such multi-reflection, by increasing the intensity of reflection. This is evident from Figure 6A. At 2 scanning cycles and 0.25 ms of dwell time, the quantity of nanofiber is the lowest, but the percentage content of gold reaches the highest. Therefore, the enhancement effect is the most noticeable. It was observed that the reflectance decreased as the scanning cycle increased. As the scanning cycle increased, more fibrous nanostructures were generated and the thickness of the deposition increased, hence more effective in reflecting illumination.

To cope with DNA CBL0137 ic50 alkylation damage, cells have evolved genes that encode proteins with alkylation-specific DNA repair activities. It is notable that these repair systems are conserved from bacteria to humans [6]. In Escherichia coli, cells exposed to a low concentration SIS3 mouse of an alkylating agent, such as N-methyl-N’-nitro-N-nitrosoguanidine (MNNG) or methyl methanesulfonate (MMS), show a remarkable increase in resistance to both the lethal and mutagenic effects of subsequent high-level challenge treatments with the

same or other alkylating agents [7, 8]. This increased resistance has been known as “”adaptive response”" to alkylation damage in DNA. To date, four Navitoclax price genes have been identified as components of this response, ada, alkA, alkB and aidB. The ada gene encodes

the Ada protein, which has the dual function of a transcriptional regulator for the genes involved in the adaptive response, and a methyltransferase that demethylates two methylated bases (O6meG and O4meT) and methylphosphotriesters produced by methylating agents in the sugar phosphate backbone [6, 9]. When methylated at Cys-69, Ada is converted to a potent activator for the transcription of the ada and alkA, alkB and aidB genes by binding to a consensus sequence referred to as an “”Ada box”" present in the promoter. The alkA gene encodes a glycosylase that repairs several different methylated bases, and the alkB gene, which forms a small operon with the ada gene, is required for error-free replication of methylated single-stranded DNA [10]. The aidB gene encodes the protein that appears to detoxify nitrosoguanines and to reduce the level of methylation by alkylating agents. Early studies

have shown that the expression of the ada-alkB operon, alkA and aidB genes is positively controlled by Ada protein, after it interacts with methylated DNA [11–14]. In contrast, Ada protein also plays a pivotal role in the negative modulation of its own synthesis, and consequently, in the down-regulation of the adaptive response. The carboxyl-terminus of Ada protein appears to be necessary for this negative regulatory function; thus, Ada protein can act as both a positive AMP deaminase and a negative regulator for the adaptive response of E. coli to alkylating agents [13]. The transcriptional activity of E. coli Ada protein is also directly regulated by posttranslational covalent modification; however, the regulatory components and pathways controlling the adaptive response have not been well studied. Recent advances in functional genomics studies have facilitated understanding of global metabolic and regulatory alterations caused by genotypic and/or environmental changes. DNA microarray has proven to be a successful tool for monitoring genome-wide expression profiles at the mRNA level.

Figure 6 M-values of specific genes throughout the time-course following acidic pH shift in S. meliloti 1021 wild type strain (closed squares) and sigma factor rpoH1 mutant (open squares). Graphics A and B exemplify RpoH1-independent up and downregulation, respectively, whereas graphics D and E show RpoH1-dependently regulated genes. click here C and F account for complex RpoH1-dependent find more downregulation in the later time points following acidic shift. Identification of S. meliloti genes that are regulated in an RpoH1-dependent manner following an acidic pH shift Genes classified as RpoH1-dependent did not present significant differential

expression after pH shift in the rpoH1 mutant arrays, having shown otherwise a threefold differential expression for at least one time point in the wild type arrays. They comprise as many as 101 genes of the S. meliloti genome whose transcription

after pH shift seems to be dependent on selleck products rpoH1 expression (Additional file 4). A number of protein turnover and chaperone genes were upregulated in the wild type arrays, such as the ones coding for the heat shock proteins IbpA, GrpE and GroEL5 (Figure 6D), as the ones coding for the Clp proteases, which are involved in the degradation of misfolded proteins [25]. No differential expression whatsoever was observed for those genes in the rpoH1 mutant arrays, characterizing thus an RpoH1-dependent expression of stress-response genes upon acid pH shift (Figure 5B, Additional file 6). Genes involved in translation, like tufA and tufB, rplC rplD and rplS, were downregulated, characterizing a seemingly RpoH1-dependent inhibition of translational activity in S. meliloti

cells under pH stress. Genes cheW3 and mcpT (Figure 6E), coding Lonafarnib price for proteins involved in chemotaxis, were also downregulated only in the wild type arrays. Identification of S. meliloti genes that are regulated in a complex manner following an acidic pH shift RpoH1 is also involved in the downregulation of specific transiently expressed genes. Interestingly, three genes from wild type cluster C were not grouped in cluster I as transiently upregulated in the rpoH1 mutant arrays. Those are the genes dctA, coding for a dicarboxylate transport protein, ndvA, coding for a beta glucan export protein, and the gene smc01505, which codes for the RpoE2 anti-sigma factor. These genes seem to have an RpoH1-independent upregulation, but an RpoH1-dependent downregulation as of 20 minutes following pH shift. In the wild type arrays, their expression is transient, but in the rpoH1 mutant arrays they remained upregulated throughout the entire time period analyzed (Figure 6C, F).

ACS Nano 2011, 5:5717–5728.CrossRef

Competing interests The authors declare that they have no competing interests. Authors’ contributions LDJ, SXL, DXY, and GHQ buy S3I-201 designed this work. GMX, ZML, and ZYT performed hemocompatibility experiments and observations. GMX, GDS, and LRY performed XPS, FTIR, SEM, and TEM measurements. GMX collected and analyzed data and wrote the manuscript. GHQ and WRX supported blood experiments. LDJ, SXL, and LRY revised the manuscript. All authors read and approved the final manuscript.”
“Background Of the popular nanomaterials, quantum dots (QDs) and graphene have promising applications in various fields; however, the cytotoxicty of these nanomaterials is also largely concerned [1, 2]. To date, a few studies have revealed that QDs and graphene posed harm to a spectrum of organisms and cells [3–6]. Blood cells are a large group of cells that play SIS3 critical roles in many physiological and pathological processes. Of the blood cells, erythrocytes are responsible for carrying oxygen, carbon dioxide, and other wastes; whereas, macrophages are part of the immune system responsible for inflammation and the clearance of pathogens [7]. Erythropoiesis is a highly dynamic process that produces numerous new red blood cells (RBCs), which requires a large amount of iron [8, 9]. Senescent erythrocytes undergo phagocytosis by macrophages, and iron is released into the circulation

for erythropoiesis upon erythropoietic demand [10]. Thus, erythrocytes and macrophages are essentially involved in governing the balance of erythropoiesis and iron recycling in the

body. Thus far, limited work has been performed in blood cells in evaluating MG-132 concentration the biosafety of QDs and graphene. Previous studies have documented that QDs could transport through the plasma membrane of RBCs, exerting potential impairment tuclazepam on the survival or function of RBCs [11]. Our own studies have demonstrated that QDs engulfed by macrophages in spleen could cause impairment to macrophages, which triggered the accumulation of aged RBCs in spleen with splenomegaly [12]. A few other studies have also suggested that graphene or graphene oxide (GO) might impose toxicity to RBCs through hemolysis and incur cell death and cytoskeleton destruction to macrophages [13–16]. To date, the cytotoxicity and related mechanisms of QDs and graphene still remain inconclusive for blood cells due to limited data. To this end, in the current study, we embarked on the cytotoxicity of QDs with different surface modifications to macrophages and GO to erythroid cells. Overall, we demonstrated significant adverse effects of QDs on macrophages and GO on erythrocytes. Methods Nanomaterials QDs with the same core Cd/Te coated with Sn/S and the same diameter (approximately 4 nm) modified with polyethylene glycol (PEG) (QD-PEG), PEG-conjugated amine (QD-PEG-NH2), or PEG-conjugated carboxyl groups (QD-PEG-COOH) were purchased from Wuhan Jiayuan Quantum Dots Co., Ltd. (Wuhan, China) [12, 17].

This is necessary

because the amount of oleic acid affects MNC formation. Steric repulsion among the hydrocarbon tails of oleic acid on individual MNPs impacts assembly capability of individual MNPs. To modify the amount of oleic acid on the MNPs, the MNPs were dissolved in n-hexane Fludarabine and PRIMA-1MET ethanol was added to the solution to remove part of the oleic acid coating. Finally, three samples of PMNPs were successfully obtained from the precipitates [25, 26], each coated with different oleic acid amounts: 19 (low PMNPs, LMNPs), 33 (medium PMNPs, MMNPs), and 46 (high PMNPs, HMNPs) wt.% (Figure 2b). To investigate the effect of primary ligand on MNCs, the interactions of oleic acid molecules on the surface of MNPs were analyzed through derivative weight curves of the three samples of PMNPs (Figure 2c). These PMNPs showed three derivative peaks positioned between 25°C and 550°C [28–30]. The first peak positioned at approximately 250°C (Figure 2c, i) was due to the removal of free oleic acid molecules surrounding the MNPs (Figure 2d,

i), consistent with the derivative peak of pure oleic acid (Additional file 1: Figure S2). The second peak positioned at approximately 350°C (Figure 2c, ii), which was close to the boiling temperature of oleic acid, indicated bilayered oleic acid molecules with hydrophobic interactions between hydrocarbon tails (Figure 2d, ii). The third peak at approximately 450°C (Figure 2c, iii) corresponded to oleic acid molecules covalently bound to MNPs (Figure 2d, iii). The characteristic peaks of the oleic acid-MNP conjugates from asymmetric and symmetric COO− stretches of oleic

acid (1,630 www.selleckchem.com/products/iwr-1-endo.html and 1,532 cm−1) were confirmed by FT-IR spectroscopy (Additional file 1: Figure S3 and Table S1) and were categorized as a chelating bidentate complex: peak separation as Etofibrate 98 cm−1 = 1,630 to 1,532 cm−1 (Additional file 1: Table S2) [30, 31]. The derivative weight curve of an iron-oleate precursor used for MNP synthesis also agreed with the derivative peaks of PMNPs (Additional file 1: Figure S4). From these results, it was determined that LMNPs contained mostly surface-bound oleic acid molecules showing a sharp peak approximately 450°C (Figure 2c, red line). Increased oleic acid in MMNPs formed a surface bilayer, which showed as an additional derivative peak at approximately 350°C (Figure 2c, blue line). The appearance of a sharp peak at approximately 250°C in HMNPs represented excess free oleic acid molecules (Figure 2c, black line). Therefore, we expected that (1) LMNPs were more likely to agglomerate and form large dense MNCs, (2) MMNPs would undergo less self-assembly and form smaller MNCs compared with LMNPs, and (3) excess free oleic acid in HMNPs would disrupt the assembly of individual MNPs to form MNCs. Following primary-ligand modulation, PMNPs were then emulsified with the nanoemulsion method, using polysorbate 80 as a secondary ligand to fabricate MNCs.

1, 3, 6, 19 and 21, who were infected by 2 genotypes, still have a major one across both gastric niches, and that was also true in 2 (no. 14, 27) patients having 3, and 1 (no. 17) patient having 4 genotypes represented in their infections. – indicating that the patients have non-dominant babA and babB click here genotype in the isolates of antrum or corpus. The patients’ number was according to our previous study [22]. Among those 12 patients infected with more than one genotype (Table 2), GSI-IX the frequency of the major dominant genotype, A B combined with AB AB, in the antrum

was higher compared with that in the corpus (75% [9/12] vs. 16.2% [2/12], p = 0.012, odds ratio: 15). However, 6 of 12 patients lacked a dominant genotype in their corpus isolates. Sequence analysis and comparison At locus A, each patient’s antrum and corpus isolates had specific substitutions

BKM120 molecular weight of amino acids in the region of BabA (Figure 2 and Table 3). However, there was no obvious difference between the antrum and corpus isolates in the sequencing region, except from patient no. 27 (amino acid 134 and 198). We also found 5 different nonsynonymous substitutions at amino acid 161 in 6 patients’ isolates, as compared with strain J99. The same scenario (sequence specificity in individual patients’ strains but not between the antrum and corpus isolates) was in the babB sequences. Figure 1 PCR banding patterns of babAB genotypes. (A) Primer pairs used for gene detection at locus A and B. The forward primers, HypDF1 and S18F1, located in the upstream region of babA or babB, are paired with BabAR1 or

BabBR1 cAMP primers to determine whether the gene at locus A and B is babA or babB. (B) PCR banding patterns of genotype A B, AB B, A AB and AB AB. The AB B genotype showed two bacterial populations in the single-colony isolate, the dominant as babA and the minor as babB, at locus A. The strain with A AB genotype represented a dominant population of babB and a minor population of babA at locus B. The combination of AB B and A AB was defined as an AB AB genotype. Lane M1, a 100 bp molecular marker; lane M2, l HindIII marker. The size of PCR products at locus A and B was 2.1-2.6 kb and 1.0-1.5 kb, respectively. Table 3 The amino acid substitutions in BabA encoded by babA at locus A   The location of amino acid substitutions Case No.

For simple Selleckchem CX-4945 anodization, we observe a large ring, whereas the FT of double-anodized alumina shows a less thick and more prominent circle. If a thick ring is typical of a non-spatial organisation and varying inter-pore distances, we verify with the thin ring that a uniform inter-pore distance without any preferred orientation in the organisation is obtained for double-anodized alumina. This confirms the presence of grains with a hexagonal array randomly

orientated. On the FT of the SEM image from the nanoimprinted sample, a hexagonal array of fine dots is seen. This confirms the regularity of the arrays in two directions irrespective of grain size. These samples and the analysis of the SEM images show good versatility and improved control of the array in the case of nanoimprint anodization, making AAO a promising template. In addition,

original structures with a mixed growth of NIL-guided pores and generation of naturally guided pores have been developed. The nanoimprint process is used to pre-texture the aluminium surface with pores in a triangular array of period a. When the anodization voltage is adapted to an array of period , pores will be created in the holes made with the nanoimprint process, and it will force the creation of new pores in the middle of three imprinted ones. Samples MM-102 with excellent regularity were obtained on surfaces of 4 cm2, as seen in Figure 2e. The shape of these newly created pores, called ‘induced pores’, can be tuned from a triangular to a selleck chemicals cylindrical section by changing the acid used and the anodization conditions, whereas

‘imprinted’ ones always present a rounded shape. This technique not only allows to propose original structures but also to get rid of the limitation due to the complexity to produce templates of small period with the standard high-resolution lithography technique, here, electron-beam lithography. This also proves the ability of this technique to eventually restore any missing pore in the initial pattern. A mould of isosceles triangular lattice (230 × 230 × 200 nm3) was also used instead ALOX15 of the classical equilateral triangle. During oxidation, the isosceles lattice is preserved as depicted in Figure 2f. However, we observe pores enlarging in the direction of the apex, leading to an oval/polygonal pore section. A possible hypothesis to explain this phenomenon is the confinement of the barrier layer in the small direction of the triangle, leading to an impossibility of etching the Al2O3 in this direction [38]. Finally, we show here that the quality of AAO template is widely improved compared to simple or double anodization processes, in terms of homogeneity of the array and pores, in term of size as well as in originality with arrays of oval pore section or double array of cylindrical/triangular pore shape [39].

It exerts its effects based on an increase in tumor oxygen levels, thereby circumventing restrictions due to the blood brain barrier [14, 28–30] Shaw et al [14] conducted a phase II, buy SB525334 open-label, multicenter study of efaproxaril plus WBRT in 57 patients with brain metastases. The results were retrospectively

compared to the RTOG RPA brain metastases database; the average survival time for the efaproxaril treated patients was 6.4 months compared to 4.1 months for the database (P <.0174). Motexafin-gadolinium (MGd) is a metalloporphyrin redox modulator that demonstrates selective tumor localization and catalyzes the oxidation of a number of intracellular metabolites, such as ascorbate, glutathione, and nicotinamide adenine dinucleotide phosphate, thereby generating reactive oxygen species, and depleting the pools of reducing agents necessary to repair cytotoxic damage [31]. Preliminary studies in patients with brain metastases treated with MGd and WBRT demonstrated radiological responses in 68% to 72% of patients [31]. Thalidomide inhibits the angiogenic activity of bFGF (FGF2), a peptide with pleiotropic

activities that performs on various cell types, including endothelial cells, following interaction with heparan-sulfate proteoglycans and tyrosine kinase FGF receptors [32–34]. FGF2 Immunology inhibitor seems to stimulate both tumor cell growth and PDGFR inhibitor angiogenesis through paracrine mechanisms [33]. Thalidomide can improve blood flow through tumor neovasculature, resulting in improved oxygenation and decreased interstitial fluid pressures [34]. Improved tumor oxygenation during WBRT would improve the therapeutical ratio for the

use of radiation for tumors with hypoxic cells. Thalidomide was being given as salvage therapy for recurrent gliomas, and a Phase II trial documented that cranial radiation therapy could be delivered with concomitant thalidomide administration without unusual toxicity [35]. The presence of hypoxia in solid tumors has been acknowledged for over 50 years. Hypoxic cells are more resistant to standard chemotherapy and radiotherapy, in addition to being more invasive and metastatic, resistant to apoptosis, and genetically unstable [36]. Thus, it is not surprising that Megestrol Acetate hypoxia has been considered an attractive target for the development of new anti-cancer therapies, including pro-drugs activated by hypoxia, hypoxia-specific gene therapy, targeting the hypoxia-inducible factor 1 transcription factor, and recombinant anaerobic bacteria [38]. The potential to improve local control and survival by hypoxia modification was demonstrated by a meta-analysis of 83 clinical trials [38] and a number of therapeutical strategies have also been established to overcome tumor hypoxia by improving oxygen supply either by oxygen or carbogen breathing or by increasing the hemoglobin level and oxygen delivery [39, 40]. Unfortunately, our data, including 7 RCTs with 1.

1 M phosphate buffer (pH 7.2) for 2 h at 4°C, and then post-fixed in 1% osmium tetroxide at 4°C for 2 h. The https://www.selleckchem.com/products/azd4547.html specimens were dehydrated with a series of ethanol solutions (30%-100%) and treated with hexamethyldisilazane Caspase inhibitor twice for 15 min. The specimens were mounted on metal stubs, coated with a thin layer platinum under argon using a sputter-coater (SCD 005; BAL-TEC, Bannockburn, IL, USA), and then visualized by field emission-scanning electron microscopy (FE-SEM) (Supra 55VP; Carl Zeiss, Oberkochen, Germany) at the accelerating voltage of 2 kV at the National Instrumentation Center for Environmental Management (NICEM; Seoul, Korea). Images were captured

in TIFF format. Confocal microscopy To determine membrane

integrity, bacterial cells were stained with membrane-permeant and -impermeant fluorescent CT99021 dyes according to the manufacturer’s instructions (Live/Dead BacLight Bacterial Viability Kit; Molecular Probes, Eugene, OR, USA) followed by confocal microscopy. Hp cells from BB agar plates were inoculated (OD600, 0.01 or 0.1) into BB-NBCS media and grown under various gas conditions. Aliquots were taken at 12 or 36 h, stained with SYTO 9 and propidium iodide (PI) for 15 min, and washed twice with phosphate buffered saline (PBS). Cells were then spread on slide glasses, covered with mounting medium and cover slips, and visualized by confocal microscopy (Leica TCS SP5; Leica Microsystems GmbH, Wetzlar, Germany). SYTO 9 is a green fluorescent membrane-permeant dye that labels all bacteria by staining nucleic acid, whereas PI is a Akt inhibitor red fluorescent membrane-impermeant dye that labels only bacteria with damaged membranes. High performance liquid chromatography analysis of organic acid metabolites The concentrations of fermentation products in the Hp culture media were determined by high

performance liquid chromatography (HPLC) using the HP1100 system (Hewlett Packard, Palo Alto, CA, USA) at NICEM. Hp cells grown on agar plates were collected, washed, and inoculated into 20 ml of fresh media (OD600, 0.1). Cells were cultured under various gas conditions for 36 h, and the culture medium was collected and divided into two aliquots (one of which was spiked with 15 mM pyruvate as internal control for quantification), which were processed simultaneously. The culture medium was extracted twice with phenol/chloroform to remove proteins and then passed through a 0.45-μm syringe filter. The samples were injected into an ion exchange column (Aminex HPX-87H, 300 × 7.8 mm; Bio-Rad, Richmond, CA, USA), and eluted at 40°C with 0.01 N H2SO4 at a flow rate of 0.5 ml/min. Organic acids were analyzed with a refractive index detector HP1100 (Hewlett Packard). Solutions containing glucose and organic acids including acetate, formate, propionate, lactate, pyruvate, succinate, and butyrate were used as standards.

36 ± 0.18 * 1.61 ± 0.25 † 1.44 ± 0.23 HDL- C (mmol/l) 0.85 ± 0.15 * 1.05 ± 0.23   1.00 ± 0.21 HDL- C (mmol/l 0.51 ± 0.08   0.56 ± 0.07 † 0.46

± 0.01 LDL-C (mmol/l) 2.74 ± 0.57   2.80 ± 0.85 † 2.27 ± 0.47 Lp (a) (mmol/l) 0.29 ± 0.32   0.31 ± 0.27   0.24 ± 0.25 TC (mmol/l) 4.37 ± 0.76   4.66 ± 0.97   3.99 ± 0.57 TG (mmol/l) 1.02 ± 0.56   0.87 ± 0.39   0.76 ± 0.23 logTG (mg/dl) 1.90 ± 0.23   1.85 ± 0.19   1.81 ± 0.13 Apo A- (mg/dl) 134.4 ± 18.8   149.6 ± 18.0 † 133.6 ± 17.5 Apo A-I (mg/dl) 30.3 ± 5.7   31.2 ± 4.8 † 26.9 ± 3.5 Apo B (mg/dl) 76.9 ± 15.9 † 78.1 ± 22.6   63.8 ± 12.7 LCAT activity (nmol/ml/h/37 83.3 ± 19.9 † 87.2 ± 20.1 † 65.5 ± 15.0 Values are the mean ± SD. this website Abbreviations; HDL-C, high-density lipoprotein

cholesterol; LDL-C, low-density lipoprotein cholesterol; Lp, lipoprotein; Apo, apolipoprotein; LCAT activity,lecitin:cholesterol. acyltransferase. *p < 0.05 LY3009104 cost RG7112 concentration vs Backs. †p < 0.05 vs Controls. The hematological parameters are shown in Table 5. The forwards had significantly higher mean Ht, MCV, and lower MCHC than the control group. The backs had significantly higher transferring, TIBC, Ht, MCV, and significantly lower haptoglobin than the control group. Four forwards (22%), five backs (31%), and three controls (12%) had hemolysis (data not shown). None of the rugby players or controls had anemia. None of the rugby players had iron depletion, while one of the controls did. Table 5 Hematological parameters of rugby players and controls   Forward   Backs   Controls   (n=18)   (n=16)   (n=26) Ferritin (ng/ml) 73.4 ± 28.8   47.7 ± 17.6   72.0 ± 37.3 Transferrin (mg/dl) 262.8 ± 33.5

  269.1 ± 28.5 † 243.8 ± 31.6 Serum iron (?g/dl) 17.6 ± 7.5   19.3 ± 5.9   19.3 ± 5.9 TIBC (?g/dl) 61.8 ± 7.4   63.6 ± 6.3 † 57.7 ± 7.0 UIBC (?g/dl) 44.2 ± 9.9   44.2 Nutlin-3 ± 7.8   38.4 ± 9.4 Red blood cell (×10000/?l) 503.3 ± 23.2   514.6 ± 19.0   515.7 ± 28.3 Hemoglobin (g/dl) 15.4 ± 0.8   15.8 ± 0.6   16.0 ± 0.9 Hematocrit (%) 50.7 ± 2.5 † 51.9 ± 2.3 † 48.6 ± 2.8 MCV (fl) 100.8 ± 4.3 † 100.9 ± 3.5 † 94.3 ± 3.0 MCH (pg) 30.7 ± 1.5   30.7 ± 0.8   31.0 ± 0.9 MCHC (%) 30.5 ± 0.8 † 30.4 ± 0.7 † 32.9 ± 0.6 Platelet (×10000/?l) 26.0 ± 4.0 * 21.8 ± 2.7   24.5 ± 3.8 Haptoglobin (mg/dl) 65.8 ± 36.9   51.9 ± 24.0 † 85.2 ± 41.5 Tf% 28.6 ± 12.2   30.5 ± 9.3   34.0 ± 11.1 Values are the mean ± SD. Abbreviations; TIBC, total iron binding capacity; UIBC, unsaturated iron binding capacity; MCV= mean corpuscular volume, MCH, mean conpuscular hemoglobin; MCHC, mean corpuscular hemoglobin concentration; Tf%, saturated transferrin. *p < 0.05 vs Backs. †p < 0.05 vs Controls. Discussion Nutrient intake Lundy et al. [24] reported on the nutrient intake of Australian rugby players, in which the mean daily energy intakes of the forwards and backs were 4309±947 and 4142±822 kcal, respectively.