Aqueous solubility values were derived by rearranging the dose number (Dn) equation ( Amidon et al., 1995) into Eq. (2), and employing the Dn values as reported by Benet et al. (2011), only for the compounds for which the authors reported the experimental aqueous solubility. The dose employed for the

estimation of the solubility as function of the Dn was 30 mg. The reason for selecting this dose was based on an exploratory study initially performed for buspirone, where administered the dose for the CR formulation was 30 mg ( Sakr and Andheria, 2001a and Sakr and Andheria, 2001b). The aforementioned procedure allowed us to evaluate the impact of SCH 900776 mouse solubility, regardless of the selected dose. equation(2) Solubility=Dose/250mlDn Human jejunal effective permeability was obtained from the report by Lennernas (2007).

Peff values were converted to apparent passive permeability in Caco-2 cell monolayers (Papp,Caco-2 (10−6 cm/s)) employing the relationship reported by Sun and co-workers (Eq. (3)) ( Darwich et al., 2010 and Sun et al., 2002). This conversion was performed to account for the passive component of the intestinal permeability described within Peff, whereas the active component was explicitly accounted by the simulations of the learn more P-gp-mediated efflux (described below). equation(3) Papp,Caco-2=10LogPeff+0.54410.7224 The use of the aforementioned correlation entails some limitations mainly due to the limited number of compounds on which it is based (n = 13), the observed mild correlation (r2 = 0.85), and the associated wide prediction intervals. Thus, a note of caution is recommended before its application. Nevertheless,

for the work performed herein, once the Papp,Caco-2 range was obtained using the aforementioned correlation, the Papp,Caco-2 values were converted back to Peff in the ADAM model, using the same equation. This was done in order to estimate the absorption rate constant (ka,i) in each of segments of the ADAM model ( Jamei et al., 2009c). Enzyme kinetic parameters, i.e., intrinsic metabolic clearance (CLint), Vmax and Km, for CYP3A4-mediated metabolism in human liver Modulators microsomes (HLM) were obtained from the review by Bu for 113 compounds ( Bu, 2006). Reported Vmax and Km values were employed directly as no Fossariinae correlation was observed between them. The CYP3A4-mediated intrinsic metabolic clearance was calculated from the ratio between the Vmax and Km, assuming linear conditions (Vmax/Km). Vmax and Km values were limited, when possible, to those that in combination generated CLint,CYP3A4 values within the CLint,CYP3A4 range reported by Bu (2006). Transporter kinetic parameters, i.e., Jmax and Km, for the P-gp-mediated efflux in Caco-2 cell monolayers were obtained from the work of Troutman and Thakker (2003) for 8 different P-gp substrates.

The location of antibody binding sites (epitopes) or escape from binding can also be inferred from correlating the antibody cross-reactivity of viruses to their capsid sequence similarities [11]. Epitopes can also be predicted, in the absence of antibody recognition data, using different epitope

prediction programmes using viral crystal structure [12]. However, there are no reports for analysis of epitopes or vaccine strain selection studies using serotype A isolates originating from East Africa. #Libraries randurls[1|1|,|CHEM1|]# Most FMD outbreaks in East Africa have been caused by serotype O, followed by serotype A and SAT-2 [13], [14] and [15]. The serotype A viruses are present in all areas of the world where FMD has been reported and are diverse both antigenically and genetically. More than 32 subtypes [16] and 26 genotypes of serotype A FMDV have been reported [17]. Control of FMD mainly depends on the availability DNA Damage inhibitor of matching vaccines that can be selected based on three criteria: epidemiological information, phylogeny of the gene sequence for evolutionary

analysis and serological cross-reactivity of bovine post-vaccinal serum (bvs) with circulating viruses [18] and [19]. Mono-, bi- and quadri-valent vaccines are currently in use in East African countries for FMD control [20], [21] and [22]. These vaccines are mainly produced in vaccine production plants located in Ethiopia and Kenya using relatively historic viruses

and regular vaccine matching tests to select the best vaccine for use in the region are rarely carried out. Hence, the existing vaccines may not provide optimal protection against recently circulating FMD viruses. This study was, therefore, designed to characterise recently circulating FMD viruses in the region both antigenically and genetically and recommend matching vaccine strains nearly for use in FMD control program in East African countries. Fifty-six serotype A viruses from Africa submitted to the World Reference Laboratory for FMD (WRLFMD) at Pirbright were used in this study. These viruses were from five East African countries, Ethiopia (n = 8), Eritrea (n = 9), Sudan (n = 6), Kenya (n = 6), Tanzania (n = 7) and from three neighbouring countries: Democratic Republic of Congo (COD, n = 5), Egypt (n = 10) and Libya (n = 5). These samples are known to have been derived from cattle epithelial tissues except eight viruses from Egypt and one virus from Kenya where the host species is not known (Supplementary Table 1). All the samples were initially grown in primary bovine thyroid cells (BTY) with subsequent passage in either BHK-21 or IB-RS2 cells. The virus stocks were prepared by infecting cell monolayers and stored at −70 °C until use. Viruses are named according to a three letter code for the country of origin followed by the isolate number and the year of isolation, e.g. A-COD-02-2011.

Transcripts of IFNs, Mx, ISG15, Viperin, IFIT5 (also named ISG58), RIG-I, TLR7, TLR3 in cDNA from organs or leucocytes were analyzed by qPCR using 7500 Fast Real-Time PCR System (Applied Biosystems) as described previously [15]. Relative quantifications of gene transcripts were Selleck FRAX597 performed by the Pfaffl method [18], using Elongation Factor 1αB (EF1αB) as reference

gene [19]. Frozen organs were weighed and transferred to 2 ml microtubes and tissue lysis buffer (Tissue Extraction Reagent I, Invitrogen) was added (100 mg tissue in 100 μl lysis buffer). Homogenization was performed with Precellys beads and homogenizer (Precellys®24, Bertin Technologies) at 5900 rpm for 20 s. After centrifugation for 5 min at 10,000 × g at 4 °C, protein concentration in the supernatants was measured with BCA protein assay kit (Pierce, Thermo Science). Supernatants (10 μg protein per well) were subjected to LDS-electrophoresis on a 4–12% NuPAGE Bis-Tris Gel (Invitrogen). Blotting, antibody incubations and development of blots were done as described previously [9]. Organs were fixed in 4% paraformaldehyde in PBS for 24 h at 4 °C and embedded in paraffin wax by routine procedures. Tissue sections (4 μm) were cut and mounted onto poly-l-lysine coated slides, dried and cleared with HistoClear solution

(National Diagnostics). After rehydration, slides were boiled in 10 mM sodium citrate buffer (pH 6.0) for 30 min followed by incubation in 1% hydrogen peroxide for 15 min. The slides were blocked with 5% nonfat dried milk powder (AppliChem) Capmatinib for 2 h and subsequently incubated with anti-Mx antibody (1:500) for 16 h at 4 °C and with HRP-conjugated antibody (1:2000, goat anti-rabbit IgG, Invitrogen) for 1 h. Red color showing Mx staining was developed

by incubation with 100 μl AEC Substrate Chromogen (Dako) for 10 min and the sections were then counterstained with Mayer’s hematoxylin (Sigma). Statistical analyses were performed using GraphPad Prism vision 6.01 for Windows. Gene transcripts in organs or leukocytes the were compared using an unpaired Student’s t-test and considered as statistically significant at p ≤ 0.05. The differences in mortality and survival rate were compared using chi square test and considered as statistically significant at p ≤ 0.01. As expected i.m. injection of expression plasmids for IFNa1, IFNb and IFNc into Atlantic salmon presmolts resulted in strong expression of the respective IFNs in the muscle tissue (Fig. 1A). Consequently, all three IFN plasmids caused strong induction of the antiviral genes Mx, Viperin, ISG15 and IFIT5 at the muscle injection site (Fig. 1B). This is most likely due to release of IFN from muscle cells that have taken up plasmid, since transfection of the IFN expression plasmids into Libraries HEK293 cells resulted in secretion of functional IFNs [8]. IFNa1 plasmid seemed to have a somewhat stronger effect compared to the IFNb and IFNc plasmids, which had similar effects. Interestingly, i.m.

The average anti-human VEGF antibody titers corresponding to each blood extraction during the experiment is depicted in Fig. 7. In the weekly schedule group, all vaccinated monkeys responded with anti-VEGF-specific IgG antibodies (1:3000) following the first dose and average titers reached 1:6000 after the eighth dose of the induction phase. A reduction in antibody titer was observed in the sample taken 67 days after the eighth dose. Average titers experience a boost to 1:8000 after monthly immunization

was re-initiated on day 126. These values dropped inhibitors progressively to near first dose titer 94 days after the third and last maintenance phase vaccination. GSK1120212 solubility dmso Monkeys receiving CIGB-247 biweekly also responded producing VEGF-specific IgG antibodies following the first dose, and average titer values fluctuated between 1:2500 and 1:3800 during all the induction phase. Titers were boosted to an average of 1:5800 after the first dose of the maintenance phase and declined in a fashion similar to that seen for the weekly scheme. The addition of montanide to the biweekly scheme had two effects. Firstly, whereas average

titer values were in a similar range as those reported above, these fluctuated less during the induction phase and did not seem to drop. Secondly, titers rose over Selleck Olaparib those produced by the biweekly immunization without montanide during maintenance phase and peaked to 1:7300, almost reaching the levels produced by the weekly scheme. Anti-VEGF antibody titer declination after the last immunization was similar to what was described already for the other two schemes. The ability of serum to block the interaction of KDR-Fc with human VEGF was estimated using the same inhibition ELISA system reported for rats and rabbits, with a change in the final detection reagents Endonuclease (due to the human-like Fc of monkey antibodies). The best serum dilution for this test was 1:500. Fig. 8 depicts the average inhibition values

(three repetitions of each sample) produced by dilutions of the sera of individual monkeys of each scheme, taken after the fourth, sixth and eighth vaccinations. Sera from all the vaccinated monkeys showed some inhibition of VEGF/KDR-Fc interaction after the fourth dose, with a majority showing inhibition peaks after the sixth dose. Animals immunized under the weekly and biweekly plus montanide schedules exhibited significantly higher inhibition values than those detected after the biweekly vaccination (p < 0.05, One way ANOVA, Bonferroni post-test). IgG antibodies were purified from sera of individual monkeys from the weekly scheme at peak titer (day 189), and tested at specific IgG concentrations in the same ELISA inhibition system. Fig. 9 shows that purified antibodies have better specific inhibition activity in the test.

La posologie sera adaptée progressivement selon l’efficacité antalgique : soit intégration des interdoses d’opioïde LI, à la dose d’opioïde LP, si Libraries utilisation par le patient de quatre interdoses ou plus par jour, avec une répartition de la dose des 24 heures en deux prises (matin et soir) ; soit maintien de la prescription si le patient est soulagé avec moins de quatre interdoses d’opioïde LI par jour (encadré 4). Si la posologie d’opioïde LP est augmentée, les interdoses d’opioïde LI (destinés à traiter les accès douloureux) seront ajustées en conséquence (1/10 de la dose journalière). En cas de

douleurs mal soulagées, le malade peut prendre une interdose toutes les heures, sans dépasser quatre prises successives en 4 heures, avant d’en référer au médecin. Si le malade n’est pas soulagé après ces quatre prises successives, une réévaluation, éventuellement KPT-330 purchase en hospitalisation, est nécessaire (recommandation, accord d’experts) [9] and [10]. Choisir de préférence la même molécule que celle utilisée pour le traitement de fond : – Sévrédol, Actiskénan, Oramorph (si morphine LP) ; Pour les douleurs par excès de nociception liées au cancer, un traitement

antalgique efficace se définit par une douleur de fond absente ou d’intensité faible, un sommeil respecté, moins de quatre accès douloureux par jour, avec une efficacité des traitements, prévus pour les accès douloureux, supérieure à 50 %, des activités habituelles qui, même VRT752271 solubility dmso si elles sont restreintes par l’évolution du cancer, restent possibles et peu limitées par la douleur, des effets indésirables mineurs ou absents [2]. Les Tableau I, Tableau II, Tableau III and Tableau IV résument les principaux médicaments antalgiques disponibles Nous disposons actuellement en France de cinq formes galéniques de citrate de fentanyl

transmuqueux pour traiter les ADP (tableau V). Leur mode d’utilisation est bien décrit dans les publications récentes de 2012 [11] and [12]. Il est nécessaire de réaliser une titration en commençant par la plus faible dose disponible (pour la forme galénique (-)-p-Bromotetramisole Oxalate prescrite). Il n’existe pas de corrélation entre la dose de fentanyl transmuqueux efficace et celle du traitement opioïde de fond (AMM). Si la douleur est insuffisamment soulagée, il convient de ré-administrer une dose supplémentaire, 10 à 30 minutes après (selon la molécule de fentanyl) [11]. Une fois que la dose efficace de citrate fentanyl transmuqueux a été déterminée (accès douloureux traité par une seule unité bien tolérée), les malades l’utiliseront pour traiter les ADP ultérieurs (AMM). La survenue de plus de quatre ADP par jour, pendant plusieurs jours consécutifs, doit conduire à une adaptation du traitement de fond, après réévaluation de la douleur et de son mécanisme physiopathologique (AMM) [11] and [12].

Due to an ageing population, the number of the most common upper limb fractures – proximal humeral fractures and distal radius fractures – are expected to increase by about 10% every five years to 2036 (Sanders et al 1999). Following an upper limb fracture, patients are often referred to physiotherapy for rehabilitation to reduce pain, improve range of movement and strength, and to regain function (AIHW 2008). Even though the aims of physiotherapy are clear, the interventions used during the rehabilitation phase can vary greatly. These interventions can include thermal modalities, ultrasound,

electrical stimulation, continuous passive movement, electromyographic biofeedback, soft tissue mobilisation, mobilising and strengthening exercises, application of resting or dynamic splints, advice, and education find more (Bertoft et al 1984, Clifford, 1980, Lundberg et al 1979, Michlovitz et al 2001). Exercise is a common intervention after upper limb fracture. For example, Michlovitz et al (2001) found that exercise was prescribed to at least 90% of patients receiving rehabilitation after distal radius fracture. The application Obeticholic Acid ic50 of exercise is also consistent with the third key principle of fracture management – movement (Adams and Hamblen, 1995).

Previous research has identified that therapeutic exercise is beneficial across a broad range of health conditions (Taylor et al 2007). However, previous systematic reviews of trials of upper limb fracture management have not focused on the effect of exercise (Handoll et al 2003, Handoll et al 2006). In addition, clinical practice

guidelines for the treatment of distal radius fractures Libraries concluded that there was weak evidence to support the use of a home exercise program (Lichtman et al 2010). New trials of physiotherapy rehabilitation have been published since the two reviews were completed in 2003 and 2006. Physiotherapists need current evidence about the effectiveness of treatment techniques to help them make clinical decisions about patient care and to allocate limited therapy resources for people with upper limb fractures. Therefore, the specific research question for this systematic review was: What is the effect of exercise on reducing nearly impairment and increasing activity in the rehabilitation of people with upper limb fractures? Relevant randomised and quasi-randomised controlled trials were identified using a search strategy (See Appendix 1 on the eAddenda for full search strategy) from the earliest date possible until January 2011 in the following electronic databases: CINAHL, MEDLINE, Embase, AMED, SPORT Discus, PubMed, PEDro and the Cochrane Central Register of Controlled Trials. To ensure all relevant studies were captured, manual reference list checks and citation tracking of included studies using Web of Science were performed. One reviewer examined the study titles and abstracts to determine if they satisfied the inclusion criteria.

Serum samples collected at week 4 were examined by pseudo-neutralization assay. For separate inoculation experiments, mice (n = 4 per group) were immunized intramuscularly with Trivalent-1, Separate 16, Separate 18, Separate 58 and corresponding monovalent

vaccines, respectively. Trivalent-1 vaccine and monovalent vaccines were inoculated at one site, while “Separate” selleck vaccines were inoculated at two sites. “Separate 16” indicated that HPV 16 L1 VLPs were injected at left leg separately, while HPV 18 L1 VLPs and HPV 58 L1 VLPs were mixed and injected at right leg. “Separate 18” meant that HPV 18 L1 VLPs were injected at left leg, while other two types at right leg. “Separate 58” also had similar meaning. Serum samples were collected at week 4 and 6 and detected by pseudo-neutralization assay. Production of pseudoviruses were produced according to previous studies [34], [35] and [36]. To be specific, 293TT cells (provided by Prof. John Schiller) were co-transfected with L1, L2 expression vectors (p16SHELL and p18SHELL, provided by Prof. John Schiller; p58SHELL, provided VX-809 in vitro by Prof. Tadahito Kanda) and reporting plasmid (pEGFP-N1, Clonetech). Cells were harvested 48 h after transfection, lysed with cell lysis buffer [0.5% Brij58 (Sigma–Aldrich), 0.2% Benzonase (Merck), 0.2% Plasmid Safe ATP-Dependent DNase (EPICENTRE

Biotechnologies) DPBS-Mg solution], and incubated at 37 °C for 24 h. The cell lysate was extracted with 5 M NaCl solution, and then examined for the titers. The titers of pseudoviruses were defined as the dilution factors at TCID50 (tissue culture infective dose). 2000 TCID50/50 μl pseudoviruses were determined as the inoculating dose for neutralization assay. 293TT cells were incubated at 37 °C in 96-well plate at a density of 1.5 × 104 cells per well for 6 h. Sera were diluted according to a 5-fold dilution. Pseudoviruses were diluted to 2000 TCID50/50 μl. 60 μl pseudoviruses Modulators diluent and 60 μl serially diluted sera were mixed thoroughly and incubated at 4 °C for 1 h in a dilution plate. The negative

control was prepared by mixing of 60 μl pseudoviruses diluent and 60 μl culture media. 100 μl of mixture per well were added to the cell culture plate and incubated at 37 °C no for 72 h. Cells were digested with trypsinase and transferred to cell sorting tube. The fluorescent cells were detected by FACS (fluorescence activated cell sorting). The percent infection inhibition was calculated with following formula: Percent infection inhibition (%)=1−the proportion of fluorescent cells in the sera incubated samplethe proportion of fluorescent cells in the negative control sample×100 The endpoint titers were calculated as the base 10 logarithm of the highest sera dilution with percent infection inhibition higher than 50%.

This in turn makes AZD9291 cell line it possible to identify the factors associated with the selective expansion of certain clones in vivo. We found that the chief determinants of clonal abundance were the transcriptional orientation of the provirus

and its position (upstream or downstream), relative to the nearest host transcriptional start site. Proviruses integrated within a host gene were significantly more frequent in clones of high abundance in vivo than in those with low abundance, but only when integrated in the same transcriptional sense as the host gene. Because of the known mitogenic properties of Tax, we postulated that Tax-expressing clones would reach a higher mean abundance than non-expressing clones in the circulation. But again the results confounded expectation: the frequency of Tax expression was significantly greater in low-abundance clones (Fig. 2) [80]. Although it was unexpected, this result is consistent with the observations noted above that orientation of the provirus in the same transcriptional sense as the flanking host gene is associated with silencing Crenolanib mw of Tax expression [80] and with high clone abundance [72] and [80]. Since the proviral load is higher in HAM/TSP patients than in asymptomatic HTLV-1 carriers, and oligoclonal proliferation is frequently detected more easily in samples

from patients with HAM/TSP [54], it was natural to infer that oligoclonal proliferation was stronger in HAM/TSP and therefore that it might contribute to the pathogenesis of the inflammatory disease. However, this inference could not be formally tested in the absence of an objective measure of oligoclonality. What is required is a measure of the non-uniformity or entropy of the clone frequency distribution. A widely used entropic index, the Shannon index, the is of very limited usefulness here because this index is correlated with the sample size, which can be very large in high-throughput

sequencing. We therefore defined [72] the oligoclonality index (OCI), an application of the Gini index (Fig. 3). An OCI of 1 indicates perfect monoclonality, whereas an index of 0 indicates that each clone has the same frequency. This index allows a rigorous quantitative comparison of the degree of oligoclonality between disease states. We found that, contrary to expectation, there is no significant difference in oligoclonality (as measured by OCI) between patients with HAM/TSP and asymptomatic carriers [72]; The OCI in patients with malignant disease, ATLL, is significantly higher, as expected. Further, the degree of oligoclonality (OCI) does not correlate with the proviral load in patients with non-malignant infection [72]. Rather, the proviral load correlated with the total number of distinct clones, and this number is significantly greater in patients with HAM/TSP than in asymptomatic carriers.

The strength

of the contribution of image value (R2val) was quantified as (SSval/SStotal). For each trial after reversal, we then averaged the contribution of image value (R2val) obtained for each cell over all cells in a subgroup. We normalized the population average by dividing by the maximum average R2val. We then fitted the neural data from each subgroup with a Weibull function (Equation 1). Results were similar and statistically significant for both monkeys, so the data were combined. In several instances, check details we fit neural data with a sigmoid curve using a Weibull function: equation(1) f(x)=u+(l−u)exp(−xα)β,which modeled the data as a function of trial number after reversal (Figure 5) or time during the trial (Figures 8E and 8F). The u and l parameters

adjust the upper and lower asymptotes of the fit curve, respectively, and the β parameter adjusts the shape of the curve. The α parameter can be considered to be a scale-adjusted rise latency: it is equivalent to the value of x (trial number) for which f(x) reaches a certain percentage of its maximum value. This value depends upon the upper and lower limits of the fit. Specifically, when x is equal to α, the function reaches a level defined by: equation(2) f(x)≈0.63∗u+0.37∗l.f(x)≈0.63∗u+0.37∗l. We could determine whether the α parameter was significantly different for two data sets by fitting the data twice: once with all parameters free, and once with the α parameter

constrained to be the same for the two data sets. An F-test was used to determine whether separate Idelalisib α parameters explained the data better than a single α parameter—i.e., whether one fit reaches its scale-adjusted threshold significantly earlier than the other. We also examined whether the 95% confidence bounds for the out α parameters overlap. In some cases, we report the difference between the α parameters to quantify the separation between two curves. To evaluate the detailed time course of changes in neural activity and behavior after reversal, we performed a sliding ANOVA analysis. For every value-coding cell, we divided each trial into 200 ms bins that were slid across the trial in 20 ms steps, and obtained the spike count for each bin. Then, for the data from each bin, we calculated the two-way ANOVA using the last six trials of each type before reversal, and a group of six trials of each type after reversal, slid in one-trial steps. Again, the total variance obtained from each iteration of the ANOVA (SStotal) was partitioned into image value (SSval), image identity (SSid), interaction (SSint) and error (SSerr) terms. The strength of the contribution of image value (R2val) was quantified as (SSval/SS). The proportion of total explainable variance (SSexp) was calculated as (1 − SSerr/SStotal).

, 2009; Grützner et al., 2010; Jokisch and Jensen, 2007; Palva et al., 2010; Roux et al., 2012) (Figure 2). So far, electrophysiological studies in schizophrenia and ASD have largely focused on obtaining amplitude estimates of spectral power at the sensor level. While the fluctuation of gamma-band power is an important variable that reflects changes in the E/I balance, it nonetheless provides only limited insights into the dynamics of extended cortical circuits. This is demonstrated, for example,

by the fact that local cortical circuits of schizophrenia patients may not have an intrinsic deficit to generate high-frequency oscillations. It is therefore conceivable that power fluctuations reflect only the tip of the iceberg of aberrant learn more network dynamics and that the pathognomonic factors are only revealed by considering the integration of local oscillators into coherently organized global brain states. This perspective is consistent with a long-standing hypothesis in schizophrenia research that clinical symptoms and cognitive deficits are the result of a buy ISRIB disconnection syndrome that emphasizes abnormal interactions between brain regions (Bleuler, 1911; Friston, 1998; Wernicke, 1906). Thus, future studies should employ novel measures that allow for the testing of time- and frequency-sensitive neuronal interactions

between cortical regions. Preliminary results obtained with scalp-recorded EEG data have highlighted alterations in long-range synchronization at beta- and gamma-band frequencies (Spencer et al., 2003; Uhlhaas et al., 2006). However, because of the methodological problems and low spatial resolution of these approaches, we suggest that this promising approach should be complemented by source reconstruction of EEG and MEG data, which allows better insights into the dynamics and organization of extended functional networks (Palva and Palva, 2012). Additional problems remain that

deserve careful consideration when interpreting the EEG/MEG data for clinical and nonclinical applications. One issue is the contribution of eye-movement-related artifacts, the saccadic spike potentials (SSPs), which are produced by saccades and mircosaccades these and mimic gamma oscillations in bandpass-filtered EEG and MEG recordings (Carl et al., 2012; Yuval-Greenberg et al., 2008). Similarly, muscle artifacts can constitute another nonneuronal source of high-frequency activity that, if not carefully removed, can simulate power modulations in the gamma-band range (Whitham et al., 2007). Finally, an important issue concerns the detection of an oscillatory process versus the possibility of spectral changes due to spiking activity. Recent studies that have examined the involvement of high (>60 Hz) gamma-band activity in cortical processes in MEG (Grützner et al., 2010; Vidal et al., 2006) and intracranial electroencephalographic (iEEG) recordings in humans (Canolty et al., 2006; Crone et al.