The results of in vitro bacterial genetic mutation assay are summarized in Table 1. In all bacterial strains exposed to different doses of EAHE mycelium (5, 2.5, 1.25, 0.625, and 0.3125 mg/plate) with the presence and absence of S9-Mix metabolic activators, the revertant colonies

showed no dose dependency and were similar to those of negative control. These findings suggest that EAHE mycelium displayed no mutagenicity, especially in Salmonella typhimurium strains TA98, TA100, TA102, TA1535, and TA1597. Since the Ames test cannot detect chromosome aberrations induced by chemicals [35], it has been recommended to use in vitro tests as a minimum requirement selleck chemicals llc for mutagenicity testing [36]. According to the guidelines OECD 473 [31], the highest dose used in the in vitro chromosome aberration test should be a concentration above the limit of solubility to avoid false positive results. As the amount of precipitation recorded for EAHE was at 5 mg/ml, dose levels of 2.5, 1.25, and 0.625 mg/ml were selected and exposed to the CHO-K1 cells (BCRC 60006) in the presence and absence of a metabolic activation system derived from rat liver Selleck AZD9291 S9 mix [30]. The cell proliferation of CHO-K1 in the 3 h treatment with the presence and absence of S9 activation was inhibited by <7.7% and <21.4%, respectively. Incubation of these cells under the same condition for 20 h in the absence of S9 activation

resulted in <34.3% decreases of cell growth (data not shown). As the highest concentration showed a significant reduction in the degree of confluency, such doses were then used for chromosome observation. The validity of the tests was observed in the incidence of cells having aberrant chromosomes, which was 0% to 1% and 6.5% to 12.5% in negative groups and positive C-X-C chemokine receptor type 7 (CXCR-7) groups, respectively ( Table 2). Neither 3 h nor 20 h EAHE mycelium treatments induced higher frequency of aberrations that were significantly different from negative controls (p > 0.05, Chi-square test) (Table 2). In summary, these data indicate that exposure to EAHE mycelium does not result in genetic damage in cultured

mammalian cells under the test conditions. The uptake of EAHE mycelium that resulted in chromosomal damage was further investigated by using the in vivo erythrocyte micronucleus test in ICR mice since the in vivo assay takes into account whole animal processes, such as absorption, distribution, metabolism, and excretion. Our earlier study on acute oral toxicity indicated that acute oral LD50 of EAHE mycelium was greater than 5 g/kg (data not shown). Hence, doses of 1.25 g/kg (low dose), 2.5 g/kg (mid dose) and 5 g/kg (high dose) were selected for this study, whereas distilled water and cyclophosphamide were served as negative and positive controls, respectively. During the 72-hr post-treatment, EAHE at all tested doses (1.25, 2.5, and 5 g/kg) did not induce any symptoms of toxicity, morbidity, or mortality in all mice (n = 25).

We evaluated the in vivo myotoxicity of Bothrops snake venoms using two different protocols. First we assessed the activity of creatine kinase (CK) in plasma, which increases in cases of muscle damage. Mice received perimuscular injections of venom, as described above. Two hours after the injection of venom alone or associated with treatments, the animals were lightly anesthetized and ROCK inhibitor blood was collected by orbital puncture. The determination of plasma CK activity was performed as previously described ( Melo and Suarez-Kurtz, 1988b; Melo et al., 1993 and Melo et al., 1994), and

expressed as units per liter of plasma (U/L). We also determined the EDL muscle CK content in the same groups of mice at 24 and 72 h after the injections, which is expected to decrease in cases of muscle damage. Animals were sacrificed under anesthesia, then the EDL muscles were removed, weighed, minced and homogenized in 2 mL PSS + 0.1% albumin and the CK content was determined in the homogenate as described previously ( Melo and Ownby, 1996; Tomaz et al., 2008). The results

were expressed as units per gram see more of muscle tissue (U/g). Inflammation was assessed by multiple parameters. The local edema induced by the venom, and the protection by the treatments, were evaluated using a caliper rule. The diameters of mice legs were measured before and 1 h after the perimuscular venom injections (as described above) and the results are shown as mm of increase in the leg diameter click here (Melo et al., 2010). Blood was collected by orbital puncture under ether anesthesia 24 h after the injections, and treated with Turk’s solution (19:1 v/v) for leukocyte count in a Neubauer chamber. The results are shown as leukocytes per mm3 (×103 cells/mm3). The same animals were

killed under anesthesia and the EDL muscles were removed, weighed, minced and homogenized in 2.0 mL PSS and then centrifuged at 20,000 rpm. We then removed 1.8 mL of the supernatant, resuspended the cell pellet and treated a 20 μL sample with 380 μL of Turk’s solution. The leukocyte count was performed in Neubauer chamber and the results expressed in leukocytes per gram of muscle tissue (×106 cells/g). To determine the myeloperoxidase (MPO) activity in the muscles, EDL muscles were removed, weighed, minced and homogenized in 1.0 mL of 0.5% hexadecyltrimethyl-ammonium bromide (HTAB) in potassium phosphate buffer 50 mM, pH 6.0 (Bradley et al., 1982). After centrifugation at 10,000 rpm for 5 min, 100 μL samples of the supernatant were mixed with potassium phosphate buffer 50 mM containing 1.0 mM O-dianisidine dihydrochloride and 0.001% H2O2. Absorbance was measured at 460 nm taking 4 readings at 60 s intervals. Each MPO unit activity was defined as that degrading 1 μmol of H2O2 per minute at 25 °C and considering that 1 μmol H2O2 gives a change in absorbance of 1.13 × 10−2 nm min−1 (Posadas et al., 2004). The results were expressed as units per gram of muscle tissue (U/g).

Subgroup Lan had smaller percentage (23.5%) of resistant lines than other heterotic subgroups. None of the lines in groups LRC and SPT was resistant to CLS. Resistance to CLS in other heterotic subgroups was rare with the highest percentage of 11.8% in subgroup PB. The lines in subgroup PB contained the highest frequency of resistant

lines against GLS (47.1%). Lines CN165, 81565, Qi 319, Dan 9046, and 141, which belong to subgroup PA or PB, were resistant to GLS. Another 5 lines (i.e., HP-3, TS005, TS499, CA23, and CA24) without known information on heterotic subgroups also were resistant to GLS. The percentages of lines resistant to CLS were small in other heterotic subgroups and no resistant HIF inhibitor line was observed in subgroups Lan and SPT. Similarly, resistance to southern rust occurred in fewer than one fourth of the lines in each heterotic subgroup, except for subgroup PB (52.9%). Most lines in each BGB324 price heterotic subgroup were resistant to common rust, but not to other diseases, with frequencies ranging from 65.0% to 93.8% (Fig. 2). Among the six heterotic subgroups, PB lines showed the higher

resistance than other subgroups to the foliar diseases tested, especially to CLS, GLS, and southern rust. Of the 12 lines with resistance to 4 or 5 diseases, 6 belonged to subgroup PB (Fig. 3). Foliar diseases are epidemic not only in China, but also in a wide range of corn production regions in the world, for example, NCLB in Brazil [33] and the U.S. [34] and [35]; SCLB in the U.S. [36]; GLS in sub-Saharan Africa [37], Kenya [38], and the U.S. [39]; common rust in Kenya [40] and the U.S. [40] and [41]; and southern rust in the

U.S. [41] and [42]. These diseases have caused severe economic losses worldwide. Variation in reaction to different foliar diseases in maize was detected in major parental lines currently used in commercial hybrids in China. A small number of lines displayed a highly resistant reaction to each disease. The majority of lines in the resistant categories oxyclozanide had disease severity rating score of 3 (R) or 5 (MR). In particular, none of the lines was highly resistant to NCLB, SCLB, CLS, and GLS. Resistance of a line against 4 to 5 foliar diseases occurred in 7.9% of the lines tested. Based on their pedigrees, most of them were derived from the U.S. germplasm. Lines belonging to different heterotic subgroups exhibited variation in their reactions to the diseases examined. Lines in subgroup PB contained greater percentages of lines resistant to various diseases, especially to GLS, CLS, and southern rust. Six of the twelve lines with resistance to 4 or 5 diseases belong to subgroup PB. Lines in subgroup SPT displayed a high frequency of resistance to SCLB. Subgroup SPT consists of some important inbred lines, such as Chang 7-2. This line was resistant to NCLB, SCLB, GLS, and common rust, but susceptible to CLS and southern rust.

, 2001, Girisk and Kemparaju, 2007 and Matsushita and Okabi, 2001). Other peptides that have been isolated are the oxyopinins from the wolf spider Oxyopes kitabensis, which form pores in lipid membranes ( Belokoneva et al., 2003 and Corzo et al., 2002) and, considering the anti-tumor action of other pore-forming peptides,

oxyopinins could also be considered as good candidates for anti-cancer therapy ( Duke et al., 1994 and Shaposhnikova et al., 1997). It is known that many toxins rely on the influx of ions through the plasma membrane in order to act as anti-cancer agents ( Tu et al., 2008), and many peptides isolated from spider venoms act MAPK inhibitor blocking ion channels, such as ω-ACTX-1- and ω-ACTX-2-type toxins from funnel-web spiders, which selectively block insect calcium channels ( Tedford et al., 2004), and Protoxins

I and II from Thrixopelma pruriens, that act on Na+ channels. These are just a few examples of the great number of toxins found in spider venoms that KU-60019 supplier have not yet been the subject of anti-cancer research and that could represent an advance in this science field. Among the studies that report the effects of spider venom using in vivo and in vitro tumor models, a paper published by Gao et al. (2005b) is notable, in which the authors verified the effects of the venom of Macrothele raven (Araneae, Hexathelidae) upon the proliferation and cytotoxicity of human cervical carcinoma cells (HeLa). Spider venom at doses of 40, 20, and 10 mg/l significantly decreased cell proliferation in HeLa cells, in a dose- and time-dependent manner; furthermore, these same Isoconazole doses significantly increased cytotoxicity as determined by LDH release from the cells. There was an arrest in cell cycle and activation

of caspase-3 in treated cells, leading to apoptosis. The authors also investigated the in vivo effect of the venom, using nude mice subcutaneously injected with HeLa cells. In the groups injected with various concentrations of spider venom by the tail vein, the size of the tumor inside the skin was significantly smaller than in untreated mice. A similar study was performed using the same venom on the human breast carcinoma cell line MCF-7 (Gao et al., 2007). Through the [3H]-methyl thymidine incorporation assay it was shown that the venom affected cell viability in a dose- and time-dependent manner. The venom, at doses of 10, 20, and 40 μg/ml, lead these cells to death both by necrosis and apoptosis, which could be verified by flow cytometry that also showed cell cycle arrest in the G2/M and G0/G1 phases. In vivo, the venom, at doses of 1.6, 1.8, and 2.0 μg/g, reduced tumor size compared to control in mice after 21 days of treatment.

The intuition behind the reserve size based growth rate is that an ecosystem supplies a number of different functions which are spatially distributed, for instance spawning and nursery grounds, juvenile and feeding areas, as well as hiding places. The larger the un-fished areas, the more of these

functions become protected, and the more they supply growth related services that increase the intrinsic growth. Thus, before fishing Enzalutamide solubility dmso starts on a virgin stock, the intrinsic growth rate is at its high virgin level r. When fishing is introduced, habitat deteriorates, reducing the intrinsic growth rate to r(0). The implementation of an MPA allows habitat to recover and thus the intrinsic growth rate of this part of the stock׳s distribution area increases towards its virgin maximum. The fact that effort does not affect the intrinsic growth rate directly – r(0) being a parameter – can be explained at least in two ways [30]. First, even though the same areas and habitats repeatedly are fished upon, the destructive habitat effects may occur upon the first fishing contact. Increased effort in the same area does therefore not decrease habitat any further. Second, r(0) is the reduced

intrinsic growth rate when the open-access fishery has reached its bioeconomic click here equilibrium. In this case the habitat may only be reduced further if economic and technical parameters change. The habitat destruction with change from r   to r  (0), and the restoration capacity of an MPA, give us a new Eq. (2) with r˜(m) and γ˜(m), while Eq. (3) remains unchanged, Calpain γ˜(m)=σr˜(m)>γ.Applying this gives a new precautionary effort level: equation(7a) E˜ε=1−ε+m(1−ε)+(γ−γ˜(m))γ˜(m)/m(1−ε)−1.when there is a negative habitat effect of fishing, the precautionary effort curves in Fig. 1 shift to the right, though still emanating at E˜ε=1−ε,   since E˜ε is now smaller than E  ε and with an asymptote at m=γ˜(m)/(1−ε), which also shifts to the right. From this, comparing (7a) to (7), it can be seen that the habitat effect of fishing implies that the upper limit to effort, to assure a precautionary

stock level, is reduced for any MPA size, i.e. due to the habitat effect, the stock can sustain a lower effort level before it is reduced to it׳s critical level ε, but this effort level increases with the MPA size, as for the curves in Fig. 1. One of the possible objectives of fisheries management, though usually not favored by economists, is maximizing sustainable yield in order to secure enough protein for people. In a single species context this implies securing maximum sustainable yield (MSY). Can this be achieved with an MPA in combination with an outside open-access harvest zone? For given parameter values the answer is yes in the case post-MPA growth equals pre-MPA growth as described in Eqs. (3) and (4). 5 This is illustrated in Fig.

, 2003). It has been reported that ASTA has a high antioxidant

activity: 10 times higher than other carotenoids such as lutein, canthaxantin, and β-carotene and 100 times higher than α-tocopherol (Goto et al., 2001 and Naguib, 2000). This potent antioxidant activity has been observed to modulate biological functions ranging from lipid peroxidation to tissue protection against light damage (McNulty et al., 2007 and Santocono et al., 2006). At the same time, ASTA displays interesting anti-inflammatory effects OSI-906 cell line by preserving redox-sensitive (and essential) structures of human lymphocytes, although the applied dose apparently hinders lymphocyte proliferation (Bolin et al., 2010). As fatty acids are potent inducers of oxidative stress and as reported by many authors that ASTA has an important and prominent antioxidant activity, we propose Epigenetics inhibitor to evaluate the oxidative

stress caused by a mixture of fatty acids previously used by our group, and the possible ASTA protective role of oxidative stress induced by the FA mixture. Astaxanthin (ASTA) and most of other chemicals were purchased from Sigma–Aldrich Chemical Company (St. Louis, MO, USA), excepting the RPMI-1640 culture medium, pluronic acid, Vybrant MTT Cell Proliferation kit and acetoxymethylester (Fura-2 AM) which were from Life Technologies (California, USA). Common reagents for buffers (e.g. PBS) and regular laboratory solutions were obtained from Labsynth (Diadema, SP, Brazil). The Ethical Committee of the Universidade Cruzeiro do Sul (protocol number 030/07) approved the experimental procedure of this study. Around 30 healthy adult women and men (mean age 27.0 ± 9.0) were included in the present study. All subjects did not present systemic or topical therapeutic regimen at least for the last 2 months. Subjects with a smoking history, alcohol habits, obesity or any other

systemic diseases were excluded of the study (based on an anamnesis protocol). Lymphocytes were obtained through the collection of human peripheral blood by venipuncture procedure in vacuum/siliconized tubes containing 0.1 mM EDTA. Peripheral blood 3-oxoacyl-(acyl-carrier-protein) reductase lymphocytes were isolated under sterile conditions by using a density gradient present in the reagent Histopaque 1077 (Sigma–Aldrich) according to the manufacturer’s instructions. After centrifugation, lymphocytes were counted in a neubauer chamber using Trypan blue (1%). Lymphocytes (1 × 106/mL) were cultured in 5 mL of RPMI 1640 supplemented as described above. The cells were treated with 0.3 mM of the fatty acid mixture added or not of 2 μM of ASTA solubilized in DMSO and cultured at 5% CO2 for up to 24 h at 37 °C. After this period, the cells were collected, centrifuged and stored at −80 °C. To perform the assays of enzymes activities and oxidative damages in biomolecules, cells were defrosted and immediately used.

By default, selleck products attractors had limited life-time due to relatively strong cellular adaptation, which caused the attractor activations to terminate several hundred milliseconds after the onset. To estimate attractor’s life-time we defined the term of attractor dwell time, Tdwell, computed using the spike data as the interval between the attractor activation and deactivation events. The activation was identified as a transition period from the state of distributed firing activity within each hypercolumn

to the state where at least 50% of all spikes from pyramidal cells in each hypercolumn originated only from a single minicolumn. This transition was tracked with a 100-ms sliding window shifted by 10 ms. Analogously, the transition from such a unimodal to a more uniform distribution of spiking events within a hypercolumn was

defined as an attractor deactivation. In the model the attractor dwell time was directly dependent upon the parameter setup of the cellular adaptation (Lundqvist et al., 2006). Persistent attractor dynamics, on the other hand, could be enforced by reducing adaptation to ~15% of the reference level (Table 1) in the finite dwell time regime (Lundqvist et al., 2010). This was used on two occasions, i.e. when we investigated the origin of a theta cycle and tested gamma-band synchrony. Additionally to the coding attractor states, the network had a non-coding ground state (Amit and Brunel, 1997 and Djurfeldt et Staurosporine nmr Docetaxel order al., 2008) with all excitatory cells in the network spiking at a very low rate (~0.2 s−1). This ground state could be stable, quasi-stable or completely unstable, depending on excitation levels (including both contribution from recurrent connections and background noise excitation). High excitation tended to destabilize this state. If other parameters were fixed, in particular background noise excitation, the conductance of recurrent excitation could be increased by ~60% before the ground state destabilized. In the simulations with partially cued memories (the pattern completion paradigm), the ground state was thus

always stable. Additionally in this setting, the coding attractors had finite life-time so that external stimuli could cause a brief activation of a specific cell assembly at the cost of this otherwise stable ground state. In the memory replay paradigm, the addition of augmentation in the excitatory recurrent connections led to a temporary increase of excitation within a particular coding cell assembly following a prior activation triggered by stimulation. This temporary ~50–60% conductance boost (Wang et al., 2006) in recurrent excitatory connections of the specific attractor destabilized the ground state. This caused the network to spontaneously reactivate the augmented assembly and then, owing to the attractors’ finite life-times, fall back to the ground state.

We therefore used a recently described method to identify specific intervention features likely to be associated successfully or unsuccessfully with the outcome of interest [31]. Interventions were analyzed based on their success in producing a significant change (p-value ≤ 0.05) in outcomes, in the hypothesized direction [31]. Outcome measures of interest were HbA1c levels, anthropometrics, physical activity, and diet outcomes. Studies that reported at least one of the four outcomes were included in the analysis. selleck chemicals These four outcomes were selected based on what most studies investigated, although instruments measuring these outcomes varied across studies. For instance, anthropometrics

consisted of various measures including body mass index, thigh skinfold, body weight, tricep skinfold, waist-to-hip ratio, total body fat, percent body fat, trunk fat, and fat-free mass. Diet was assessed with a desirable change in any of the following: total kilocalorie intake, dietary risk score, mean vegetable consumption, fruit consumption, consumption of five fruits and vegetables per day, fried food consumption, healthy

eating plan adherence, fat-related this website dietary habits, dietary fat intake, dietary cholesterol intake, kilocalories from saturated fat, and percent kilocalories from fat. When a study used several instruments to measure an outcome (e.g., diet), at least 60% (an arbitrary cut-off) of the measures must have reported significant positive Tangeritin results

to be considered a success for that outcome. Only post-test outcome data were used for all analysis. A rate difference determines which intervention feature has a positive or negative association with an outcome [31]. A rate difference was estimated for each intervention feature identified in the review using the following steps. First, a success rate was calculated for both the intervention with and without the feature. The success rate for the intervention feature (SRWF) is the number of studies reporting on the intervention having the feature of interest associated with a positive participant outcome, divided by all the studies reporting on intervention with the feature regardless of outcome; the specific formula used was: number of studies with feature with positive outcome/all studies with feature. Second, a success rate without a feature (SRWoF) is the number of studies reporting on the intervention without the feature of interest with a positive participant outcome, divided by all the studies without the feature regardless of outcome; the formula was: number of studies without feature with positive outcome/all studies without the feature. Third, rate differences were calculated for each intervention feature, by subtracting the success rate with feature (SRWF) from the success rate without the feature (SRWoF).

, 1994; Chow et al., 2003). There is evidence that intoxication with cyanotoxins may lead to oxidative stress and lesion

in some organs, such as liver, kidney and lungs (Moreno et al., 2005; Carvalho et al., 2010). In mice liver there are also reports of cylindrospermopsin-induced depletion of glutathione, a tripeptide that plays an important I-BET-762 mw role in the detoxification of many xenobiotics and participates in cellular defense against oxidative damage (Runnegar et al., 1994; Humpage et al., 2005). In the present study, the latter could also contribute to the toxicity induced by cylindrospermopsin, once depleted glutathione content would result in a less important removal of reactive oxygen species. Generally, as a result of initial oxidative

stress, there is an activation of the antioxidant defense system in order to minimize the tissue damage. In this line, we analyzed antioxidant enzymes involved in the balance of redox status (SOD and CAT) as well as a marker of oxidative damage (lipid peroxidation) in samples of lung tissue of mice (Fig. 3). SOD catalyzes superoxide anion dismutation to molecular oxygen and hydrogen peroxide. The latter is detoxified by CAT activity and both Tyrosine Kinase Inhibitor Library high throughput enzymes can be triggered after a poisoning event with microcystins (Pandey et al., Carnitine dehydrogenase 2003). The present study identified a crescent increase in SOD activity until 8 h after exposure to cylindrospermopsin, thus confirming that the native toxin could increase superoxide anion production. SOD activity was reduced after the initial

effect until returning to control levels in 96 h, in line with the notion that SOD is the first defense line against ROS (Foronjy et al., 2006). Additionally, SOD activity could have diminished as a consequence of the decreasing amount of toxin in the lung as time progressed (Fig. 4). On the other hand, CAT activity was similar to control until 24 h after cylindrospermopsin exposure and significantly decreased afterwards. These data corroborate those aforementioned. Since CAT takes part in catalyzing hydrogen peroxide, its performance depends on SOD substrate, i.e., hydrogen peroxide. Moreover, the reduction in CAT activity in CYN48 and CYN96 is in agreement with the increase in MPO in these groups (Fig. 3). MPO also uses hydrogen peroxide as a substrate, whose affinity is higher for MPO than for CAT. Hydrogen peroxide is a stable ROS, so in inflammatory conditions such as increased PMN influx it could react more with MPO after 24 h, leading to the production of another ROS, the hypochlorous acid, which also contributes to oxidative stress.

001 and p = 0.046 respectively) but the femur length exhibited

no difference (p > 0.05). In the oim group, no significant differences were found for the three parameters (p > 0.05 for all). Vibration treatment had a significant effect on the cortical morphology parameters (CSA, CtTh, Imax, Imin) in the femur and tibia of both wild type and oim animals when all the position within the tibia diaphysis were considered (percentage of total length (%TL)). In the wild type group, vibration treatment increased the cross section area (p = 0.026) and the mean cortical thickness (p < 0.001) in the tibia and increased CSA (p = 0.016); Imin (p = 0.014) and CtTh (p = 0.001) in the femur. In the oim Ivacaftor mice group, Dapagliflozin datasheet all cortical parameters showed significant increases between vibrated and sham mice for the femur (CSA: p < 0.001,

Imin: p = 0.008, Imax: p = 0.012, CtTh: p < 0.001) and for the tibia (CSA: p < 0.001, Imin: p = 0.012; Imax: p = 0.019, CtTh: p = 0.001). In the Fig. 3, the differences observed for CSA and CtTh between the vibrated and sham mice are displayed for each of the positions along the tibia (Figs. 3a and b) and femur (Figs. 3c and d). In the femur of the oim vibrated mice, mean CtTh exhibited a significant increase for the central portion of the diaphysis (30-70%TL) while the wild mice exhibited a significant increase of CSA at 60%TL (p = 0.045). In the tibia, oim vibrated mice exhibited a significant increase of CtTh and CSA at the proximal end of the diaphysis (50-80%TL) while wild type vibrated mice Chloroambucil show

a significant increase of the mean cortical thickness at various positions (30, 50 and 60% TL). In the proximal tibial trabecular bone, a significant difference was observed between vibrated and sham groups. Bone surface and bone volume fraction were significantly increased in the vibrated group (p = 0.03 and p = 0.017 respectively) but not the trabecular thickness and spacing (p > 0.05). When genotype group were analysed separately, the wild type group exhibited no significant difference between vibrated and sham mice for all trabecular parameters (p > 0.05) (Figs. 4a and b). However, the oim vibrated mice exhibited a significant increase of the tibia bone volume fraction (p = 0.019) ( Fig. 4b). In the femur distal metaphysis, no significant differences between vibrated and sham mice were found for the trabecular bone morphology parameters in either wild type or oim groups (BS, BVTV, TbTh or TbSp, p > 0.05 in all condition, Figs. 4c and d). In the wild type group, the vibration treatment had a significant impact on the femur bending stiffness and yield load (p = 0.034 and p = 0.035 respectively) but the other parameters (ultimate load, total work to fracture, ultimate stress, Young’s modulus and yield stress) were not significantly different.