Cell number, also monitored over 14 days of treatment, was not affected by any of the compounds (data not shown). On day 1, none VX-809 of the selected compounds did induce significant changes in any of the investigated endpoints and thus were not included in the following illustration of results.

CsA was daily administered at concentrations of 0.3, 1 and 3 μM for 14 days. On day 1, 3, 7, 10 and 14, samples were investigated for the selected endpoints. Morphological investigations revealed that the 3 μM CsA exposure resulted into accumulation of vacuoles within the cytoplasm associated with minimal loss of hepatic morphology on day 3 (Fig. 4D). An increased number of vacuoles and disruption of canalicular network was observed after 14 days (Fig. 4P). The presence of vacuoles was visible already at the lower concentrations from day 7 (Fig. 4G, J, N, O). Further biochemical investigations are shown in Fig. 5A. The intracellular ATP levels were not affected within the Alpelisib manufacturer first days of culture, but decreased only after 14 days of treatment with CsA at the concentrations of 1 μM (*p < 0.05) and 3 μM (**p < 0.01) Accordingly, LDH levels increased

at day 14 at both 1 μM (*p < 0.05) and 3 μM CsA concentrations (**p < 0.01). In contrast, CsA affected the Mrp2-mediated canalicular transport already after 3 days of exposure at 3 μM (****p < 0.0001). The inhibition occurred in a time- and concentration-fashion and resulted in a 54% spot average intensity decrease at 0.3 μM (****p < 0.0001) and 76% decrease at 1 μM CsA on day 14. Images click here confirmed that partial inhibition of Mrp2-mediated canalicular transport occurred already after 3 days at 3 μM dose ( Suppl. Fig. 3D). This resulted into a reduced quantification of fluorescent signal, as displayed by the cyan spots overlaying with the DCF ( Suppl. Fig. 3H). As a consequence

of the reduced export of DCF, a clear retention of the dye within the cytoplasm was observed; such effect was exacerbated after 14 days of treatment ( Suppl. Fig. 3N–P). The effect of CsA on lipid metabolism was evaluated by reagents staining respectively neutral lipids and phospholipids. As shown in Fig. 5A, the accumulation of neutral lipids was detected already after 3 days of treatment (3 μM, **p < 0.01). The size of intracellular vacuoles increased over the time of treatment ( Suppl. Fig. 4). On contrast, CsA exposure did not affect the amount of phospholipids. Exposure to AMD did not affect intracellular ATP levels, but affected LDH levels at late stages of treatment (day 10 and 14) at the highest drug concentration only (5 μM, *p < 0.05) ( Fig. 5B). AMD treatment was associated with increase of phospholipids content already after 3 days at a concentration of 5 μM (*p < 0.05), resulting in significant changes after 14 days at concentrations of 2.5 μM (*p < 0.05) as well as a at 5 μM (***p < 0.001) (Images taken at day 3 and 14 ( Suppl. Fig.

, 2006). In a review by Nel et al. (2006) a question, “Do nanomaterials properties necessitate a new toxicological science?” was raised. It was argued that the main characteristic of nanomaterials is their size in the transitional zone between individual

atoms or molecules and the corresponding bulk materials. This can modify the physicochemical properties of the material as well as create the opportunity for increased uptake and interaction with biological tissues (Chithrani et al., 2006 and Sonavane et al., 2008). This combination of effects can generate adverse biological responses in living cells see more otherwise not seen with the same material in larger (bulk) form (Nel et al., 2006). The increase in surface area determines the potential number of reactive groups on the particle surface. Table 1 summarizes the observed biological effects vis-à-vis physicochemical properties and the types of nanomaterials. Shape of the nanoparticles has been shown to have a pronounced effect on the biological activity. It is reported that silver nanoparticles undergo shape-dependent interaction with E. coli ( Pal et al., 2007); Chithrani et al. (2006) reported better uptake of spherical gold nanoparticles than gold nanorods in HeLa cells. In case of anatase TiO2 nanomaterial, it was shown that alteration to a fiber structure of greater Entinostat concentration than 15 μm created a highly toxic particle that initiated an inflammatory response by alveolar macrophages

and that length may be an important determinant of nanomaterial biocompatibility ( Hamilton et al., 2009). Another study by Journeay et al. (2008) demonstrated that water-soluble rosette nanotube structures display low pulmonary toxicity due to their biologically inspired design and self-assembled architecture. In a review on widely used metal oxide and carbon nanomaterials,

Landsiedel et al. (2010) emphasized that physico-chemical characterization Ribonucleotide reductase of nanomaterials and their interaction with biological media are essential for reliable studies. In a study with 1.5 nm sized gold nanoparticles it was observed that surface charge was a major determinant of their action on cellular processes; the charged NPs inducing cell death through apoptosis and neutral NPs leading to necrosis in HaCaT cells ( Schaeublin et al., 2011). Considering the physicochemical properties of various nanomaterials and their interactions with the biological environment, Maynard et al. (2011) state that the challenges presented by simple nanoscale materials such as TiO2, ZnO, Ag, carbon nanotubes, and CeO2 are now beginning to be appreciated. But these simple materials are merely the vanguard of a new era of complex materials, where novel and dynamic functionality is engineered into multifaceted substances. Further, according to Maynard et al. (2011), if we are to meet the challenge of ensuring the safe use of this new generation of substances, it is time to move beyond “nano” toxicology and toward a new toxicology of sophisticated materials.

We categorized our cohort of patients into two groups according to the detection of TAMM asymmetry: “normal and symmetric” (NS), “normal and asymmetric” (NA). A significant TAMM asymmetry (NA Group) was observed

in 13/31 patients (41.9%). Silent ischemic lesions were detected in 6/13 (46.2%) NA and 7/18 (38.9%) NS patients. No significant difference was found in silent stroke rate (Chi square test with continuity correction, χ2 = 0.598), lesion number (t-student test, p = 0.09) and lesion burden (t-student test, p = 0.22) between the two groups ( Table 1). According to this study, TAMM asymmetry does not seem to be a significant predictor of silent cerebral ischemia as evaluated by brain MRI; in particular, it PLX-4720 research buy does not have a prognostic value in terms of silent stroke rate, lesion number and lesion burden. Furthermore, this study confirms the high prevalence of brain ischemic lesions (>40%) in so-called selleck kinase inhibitor “normals” and underlines the importance of stroke prevention even when TCD findings are within a normal range. The lack of association between TAMM asymmetry detected by TCD and MRI findings

might be related to the pathogenesis of ischemic stroke in sickle cell disease. Even though an increase in TAMM velocities has been proven to be a predictor of ischemic stroke, the site of brain ischemia does not correlate with the vessel in which blood flow velocity was found to be increased. This finding suggests that factors other than major cerebral artery stenosis concur to determine Chloroambucil brain ischemia [6]. In fact, rheological or hemodynamic impairment might undermine parenchymal lesions. A recent study pointed out that SCD patients have an impaired cerebral blood flow autoregulation compared with age-matched healthy subjects, independently from their hemolysis

rate [7]. Furthermore, small vessels disease might play a role in the stroke pathogenesis of these children. Side-to-side asymmetry of blood flow velocity is a common finding during TCD examination of the major arteries, both in adult than in children, but it is considered pathological whenever velocity values lie outside a standard range [8]. Nevertheless, a recent study indicated that SCD patients have a slightly wider physiological range of blood flow velocity values than normal children [9]. Furthermore, since SCD patients harbor a widespread tortuosity of intracranial vessels [3] and [4], a significant TAMM asymmetry might just represent this anatomical variation and not necessarily a pathological finding. Finally, we have also to consider some of the limits related to the TCD equipment: different location of the sample volume and/or angle of insonation when recording from each side; in fact, in children the temporal acoustic window is larger than in adults, allowing the operator to insonate the artery from different angles with potential measurement errors [9].

, Inc. (West Grove, PA, USA). 5′thiol-modified oligonucleotide primer (Pri)1 [5′-(5ThioMC6-D//iSp18)CCTTGAACCTGTGCCATTTGAATATATTAAGACTATACGCGGGAACA-3′] where iSp18 is an 18-atom hexa-ethyleneglycol spacer connecting the thiol reactive group and the DNA sequence, Pri2 (5′-CCTTGAACCTGTGCCATTTG-3′) and Pri3 (5′-GTCCCTCCATCTTCCTACTGTTCCACATGTTCCCGCGTATAGTCTT-3′)

Pexidartinib were obtained from IDT, (Coralville, IA, USA). Biotinylated forward primer 5B-HRM1-F (5′-CTCATCACCACGCTCCATTA-3′) and its non-biotinylated form (HRM1-F) and reverse primer HRM1-R (5′-TCTTCCACCTCCATGGTGTC-3′) were obtained from Generi Biotech (Hradec Králove, Czech Republic). SYTO-9 and geneticin (G418) were obtained from Invitrogen (Eugene, OR, USA). Glutaraldehyde was bought from Fluka, Chemie GmbH (Buchs, Switzerland). All other chemicals were from Sigma-Aldrich (St. Louis, MO, USA). BMMCs were isolated from C57BL/6 mice according to the previously reported protocol (Volná et al., 2004). All mice were maintained and used in accordance with the Institute of Molecular Genetics guidelines.

The cells were seeded in complete culture medium RPMI-1640 containing 10% heat inactivated (56 °C, 30 min) fetal bovine serum (FBS), 50 μM 2-mercaptoethanol, antibiotics (100 U/ml penicillin and 100 μg/ml streptomycin) and further supplemented with fresh rSCF (15 ng/ml) and 10% culture supernatant of confluent D11 cells as a source of IL-3 (Cao et al., 2007). BMMCs were cultured mTOR signaling pathway at 37 °C in an atmosphere of 5% CO2 in air. D11 cells were grown adherent in tissue culture flasks in Dulbecco’s modified Eagle medium (DMEM) supplemented with 10% heat inactivated FBS, antibiotics and 0.3 mg/ml of geneticin. The cells were detached from the flasks by incubation for 5–10 min at room temperature with 0.05% trypsin in phosphate buffered saline Bumetanide (PBS; 10 mM phosphate, pH 7.4, 150 mM NaCl) supplemented with 0.02% EDTA. After centrifugation at 280 ×g for 5 min, cells were resuspended in DMEM-10% FCS with geneticin. After 3 days of culturing, the medium was

aspirated and fresh DMEM medium without geneticin was added. Cells were cultured for additional week. Supernatant containing IL-3 was then collected, centrifuged at 5500 ×g for 15 min, filtered through a 0.22 μm membrane and stored in aliquotes at − 20 °C. For determination of SCF, supernatant from cultured BMMCs was collected daily for 5 days. Functionalized Au-NPs were prepared as previously described (Hill and Mirkin, 2006) with some modifications. One milliliter of 30 nm Au-NPs solution was incubated for 30 min at room temperature with 4 μg of polyclonal antibody (anti-IL-3 or anti-SCF) under gentle shaking. Ten microliters of 10% Tween 20 was then added, followed after 5 min by 50 μl of 2 M NaCl in 10 mM PBS (Hurst et al., 2008). The particles were then modified with 5′-thiolated oligonucleotide (final concentration 4 nmol/ml) under gentle shaking at 4 °C.

Stimuli that enhance cAMP levels (e.g., prostaglandin E2 or PDE4 inhibitors) suppress SIK2 activity and robustly potentiate IL-10 production by macrophages and dendritic cells (DCs), a phenotype that can be mimicked by small molecules that directly inhibit SIK2 [ 24••, 25 and 26]. Whereas recombinant IL-10 supplementation is ineffective in Crohn’s disease (CD) patients [ 27], perhaps due to insufficient delivery to the gut mucosa [ 28], these data suggest that SIK2 inhibition may be effective at increasing IL-10 levels directly in this tissue. The additional ability of SIK2 inhibitors to suppress production of IL-12 and other inflammatory cytokines

makes this kinase a promising target for further investigation see more in IBD [ 24,26]. Studies from genetics, physiology and chemical biology continue to implicate kinases as potential targets for restoring normal cytokine function in disease (Table XAV-939 purchase 1). Novel polymorphisms in leucine-rich repeat kinase 2 (LRRK2, a gene previously linked to Parkinson’s disease)

confer increased risk of IBD [ 29]. Functional studies suggest that LRRK2 regulates production of reactive oxygen species and inflammatory cytokines by macrophages [ 30 and 31]. In addition, SNPs near IRAK1, which encodes a kinase required for production of interferons (IFNs) following viral infection, confer increased risk of systemic lupus erythematosus [ 32]. The serum/glucocorticoid-regulated kinase 1 (SGK1) regulates differentiation of TH17 cells, a CD4+ T cell subset that produces IL-17A and other inflammatory cytokines, in response to environmental factors including NaCl; small-molecule inhibition of SGK1 suppresses high salt-induced TH17 development [ 33 and 34]. Mechanism-of-action studies have implicated the phoshatidylinositol kinase PIKfyve as the target of the clinical candidate apilimod, an inhibitor of IL-12/23 production discovered through phenotypic screening [ 35• and 36]. Targeting kinases implicated

in cytokine regulation, Guanylate cyclase 2C with novel inhibitors or those repurposed from other indications, is a critical step for testing novel therapeutic hypotheses and may yield valuable starting points for drug development. Signaling cascades downstream of immune receptors converge on transcription factors to regulate cytokine expression. The clinical success of calcineurin inhibitors, which suppress IL-2 production following T cell receptor stimulation by preventing dephosphorylation of NFAT [17], demonstrates the utility of small molecules that target transcriptional regulation in immune cells. In addition to acute transcriptional responses, activation of immune cells leads to chromatin modifications that can promote acquisition of distinct effector states [6, 7, 8 and 9].

and (d) latitudes and longitudes which coincide with the proposed boundaries for ‘divisions’. The latest changes of FAO fishing areas’ boundaries were in 1999 between areas 51 and 57 (as a consequence Sri Lanka moved from the Western to the Eastern Indian Ocean area) and in 2001 between areas 57 and 71 in the Australian–Indonesian region to match the border between the IOTC and WCPFC areas of competence. At its 22nd Session [22], the CWP reconfirmed the conditions to be met before changing boundaries between trans-isomer mouse major fishing areas: (a) no country should object the proposed change; (b) no Regional Fishery Body

(RFB) should object the change and effort should be made to reconcile boundaries between RFBs jurisdictions and those of the FAO Major Fishing Areas; and (c) countries involved in the proposed change should be able to provide to FAO revision of historical capture statistics according to new boundary. Other proposals to modify the boundary between areas 47 and 51 to match the ICCAT-IOTC border, the northern boundary between areas 57 and 71, and the southern boundary between 57 and 81 are pending until these requirements are met. The FAO Major Fishing Areas are often considered too large and coarse to correspond to stocks and allow detailed analysis of catch trends [23].

However, many major fishing areas are further subdivided into statistical subareas and divisions [24]. For several areas in which FAO and non-FAO regional fishery commissions are in place, catch data14 are also available by ‘statistical divisions’, providing a finer geographical resolution. FAO is receiving increasing requests Nivolumab purchase to incorporate more detailed catch location in the database, in particular to distinguish EEZ catches from catches in the high seas. A first step was undertaken for the Southeast Atlantic fishing area. Statistical divisions for this area have been revised in agreement between FAO and SEAFO, which Convention covers the high seas in the Southeast

Atlantic, with the PAK5 aim of obtaining separate data between catches taken inside and outside EEZs of coastal states [25]. A similar proposal [26] to modify statistical divisions in the Eastern Central Atlantic was also submitted to the CECAF.15 Definition of inland waters varies among countries and in some cases there is uncertainty in classifying a water bodies as marine or inland waters and hence assigning the catch to the relevant fishing area. Salinity cannot be always used to define boundaries because in some areas it fluctuates with tides and season and there are also inland water bodies which are highly saline (e.g. Caspian Sea). On the other hand, aquatic animals which are considered as freshwater species can tolerate changes in salinity and can be caught in maritime regions which have low salinities (e.g. Baltic Sea) due to river outflows.

At day 91, over-represented functions could not be identified due to the limited number of differentially expressed genes at ≤ 14 mg/L SDD. At higher concentrations, functions associated with immune response, lipid metabolism, small molecule biochemistry, metabolism and cell death were similarly over-represented in duodenum (Table 3) and jejunum (Supplementary Table S4). Table 4 lists selected genes with respective fold inductions and corresponding EC50 values, grouped according to the most over-represented

functional categories presented in Table 2 and Table 3. For example, genes associated with immune CAL-101 cell line response (e.g., Anxa2, Blnk, Ccl24, Il1rl1, Il33 and Clec7a) were differentially expressed at days 8 and 91. Genes associated with expression at both time points preceded

and coincided with minimal histiocytic infiltration after 90 days of SDD exposure. Several antigen processing and presentation genes, including Ciita, Tap2, B2m, and Cd74 were significantly suppressed (− 1.6- to − 7.9-fold) following Cr(VI) exposure. At day 91, Il1b was significantly decreased 1.5-fold at ≥ 60 mg/L SDD, and Tnf was moderately repressed (1.4-fold) at ≥ 60 mg/L SDD. These findings are consistent with decreases in pro-inflammatory cytokines TNFα and IL-1β in the duodenum at ≥ 60 mg/L SDD ( Thompson et al., 2011b). SDD induced (~ 1.5- to 6.7-fold) several redox-sensitive Nrf2 transcription factor targets, including Atf4, Gpx1, Gpx2, Gsr, Mt1, Prdx1, and Stip1 ( Table 4). These genes are involved in antioxidant,

detoxification, and cytoprotective functions. Induction ABT-263 order of genes associated with the Nrf2 pathway (IPA canonical pathway is shown in Supplementary Fig. S5) suggests activation of defense mechanisms in response to oxidative stress, consistent with the reduced GSH/GSSG ratio and elevated protein carbonyls (oxidation) in duodenum ( Thompson et al., 2011b). Carbonyl reductase (Cbr3), also regulated by Nrf2 ( Ebert et al., 2010), was elevated at the four lowest concentrations at day Phosphoglycerate kinase 91 ( Supplementary Table S2). Out of 57 unique mouse Nrf2 target genes (from IPA Nrf2-mediated oxidative stress response canonical pathway), SDD elicited the dose-dependent differential expression (induced and repressed) of 42–68% of all Nrf2 targets in the duodenum or jejunum at 8 and 91 days (ǀfold changeǀ > 1.5, P1(t) > 0.999). When the filtering criteria were relaxed (ǀfold changeǀ > 1.2, P1(t) > 0.90), the number of differentially expressed Nrf2 pathway associated increased to 73–87% ( Supplementary Table S5). In addition to genes in the Nrf2 pathway, SDD also induced (up to 6-fold) members of the glutathione transferase and peroxidase families, including Gsto2, Gstt2, Gstm2, Gstm5, Gsta3, Gsta4, Gstp1, and Gpx2 ( Supplementary Table S5), further suggesting an oxidative stress response. Nrf2 activation can also be linked to increases in duodenal GSH levels (Thompson et al., 2011b).

A different management strategy has been taken for each rock either alternating total bans with no ban (Cabo Cebes), partial bans (Maste) or no bans (Picones). All three zones exhibit positive trends however this is more pronounced in the alternating total ban strategy. Still, it is important to take into account that due to the total bans few data points are available for the Cabo Cebes zone. To ensure the flexibility of the plan, the fishers hold emergency meetings throughout the fishing season to determine the status of the plan

and the measures necessary to sustain the resource ( Table 2). Thus, the incorporation of the community in the management process empowered the resource users, by providing them with a key role in the decision-making Palbociclib mouse process as was expressed during the focus groups, and endorsed the integration of fishers׳ knowledge in the guidelines. Furthermore, the adaptability of a co-management plan permitted the careful incorporation of gooseneck barnacle life history traits into the guidelines and the development of innovations ABT-199 manufacturer within the plans (Table 2). Before the establishment of the co-management system research on the distribution and life history traits of the resource was carried out to determine its exploitation potential [32], it is complemented each year by follow-up research performed by the DGPM. Careful attention is placed to protect juveniles

in the co-management system by setting a minimum harvest size of 4 cm. Nonetheless, according to fishers׳ knowledge and scientific information P. pollicipes larvae usually settle on the adults [33], thus by-catch is unavoidable. The system adapted by allowing a few individuals below

size as long as they do not surpass a 10% of the landings. Another important trait is P. pollicipes reproduction occurring asynchronously during the summer, from April to September [34] and [35]. Once the government officials obtained this information, a fishing season from October to April (both inclusive) was proposed to allow Sorafenib mw juveniles to settle during the summer. After negotiation all the cofradías agreed to the fishing season. However, according to the Cabo Peñas stakeholders in the focus group and interviews, the seven-month fishing campaign was no longer suitable to the needs of the plan. Consequently, since the 2004–2005 season Cabo Peñas exploits one third of their area during the summer. Another example of the co-management system׳s capacity to adapt to changes is the change in daily TAC implemented in the 2004–2005 campaign (Table 2). Due to decreased landings observed by the DGPM and the cofradías, daily TAC was reduced from 8 to 6 kg for most of the campaign with the exception of the high season (December), where it would remain at 8 kg. However, the Cabo Peñas cofradía petitioned to maintain the 8 kg TAC, it was agreed that they would harvest 8 kg during pre-established dates determined at the beginning of the season.

In the present study, we have investigated and compared the restorative efficiency of OLP and RLP transplants, in three different therapeutic windows (acutely, 2-week and 4-week delayed), after a complete thoracic spinal cord transection in adult rats. By the twelfth week after transplantation, animals selleck products with OLP or RLP showed a discrete and similar hindlimb motor improvement. All transplants produced comparable results for spinal cord tissue sparing and sprouting, evaluated

using GFAP and GAP-43 immunohistochemistry. Acute transplantation of OLP and RLP seems to foster some limited supraspinal axonal regeneration, as indicated by the presence of cells stained by retrograde tracing in brainstem nuclei. However, retrogradely labeled cells in cortical areas were only observed following acute RLP transplantation. A larger number of 5-HT positive fibers were

found in the cranial stump of the OLP and RLP groups compared to the lesion and caudal regions analyzed. CGRP fibers were present in considerable number at the SCI site in both transplantation types. Although the mechanisms Onalespib clinical trial underlying the regenerative properties of OECs in the SCI site are not completely elucidated, reduction of glial scarring (Lu et al., 2006), facilitation of axon re-entry into the host–graft interface (Li et al., 2005), reduction of proteoglycan expression (García-Alías et al., 2004), angiogenesis (Richter et al., 2005),

remyelination (Sasaki et al., 2006) and growth-factors release (Lipson et al., 2003) are considered the main benefits of this cell transplantation (Tetzlaff et al., 2011). We were selleck screening library able to detect the presence of OECs in the lamina propria before and after grafting in the transection site, but the limitations of our study were the lack of the OECs quantification and the inability to investigate the possible migratory properties of these cells after transplantation. Nevertheless, some aspects of OECs behavior after transplantation have been previously documented. In an olfactory nerve injury, OECs were seen to remain at the lesion site forming a conduit that can guide regenerating nerve axons, analogously to Schwann cells after a peripheral nerve injury (Li et al., 2005 and Williams et al., 2004). After a cervical spinal cord injury model, Lu et al. (2006) failed to demonstrate any unique migratory properties of OECs, concluding that these cells probably spread due to pressure at the injection site, without active migration. On the other hand, Richter et al. (2005) showed a superior migratory ability of OECs derived from lamina propria when compared to OECs derived from OB after crush of spinal cord dorsolateral funiculus at the C3–C4 level. Thus, the migratory capacity of these cells after transplantation into different injury sites is still controversial.

fil.ion.ucl.ac.uk/spm/) working on Matlab 2010b (MathWorks, Inc., http://www.mathworks.com, MA, USA). All functional volumes were subjected to standard preprocessing procedures (Friston, Ashburner, Kiebel, & Penny, 2007), including spatial realignment, co-registration with the anatomical scan, normalization [on the Montreal Neurological Institute (MNI)

space with 2 × 2 × 2 mm3 voxels] using the unified segmentation of the anatomical scan and smoothed with an isotropic 6 mm full width half-maximum (FWHM) Gaussian kernel. Time series from each voxel were high-pass filtered (1/128 Hz cutoff) and the preprocessed Navitoclax price functional volumes were then submitted to fixed-effects analysis (i.e., first level analysis, FFX) using a block design, applying the general linear model to each voxel (Friston et al., 1995 and Worsley and Friston, 1995) and using an auto-regressive [AR(1)] function to account for temporal correlations between voxels across the whole brain. Afterwards, the data were submitted to second-level analysis (random effect analysis, RFX) in order to generalize the results for

the population. All conditions were modeled in a full factorial model (ANOVAs) 3 × 2 (F1: condition; F2: task). The coordinates derived from these analyses (cluster maxima) were converted from MNI coordinates to Talairach and Tournoux stereotaxic coordinates using the icbm2tal script ( Lancaster et al., 2007) in order to associate Hydroxychloroquine order Idoxuridine the results with an anatomical location ( Talairach & Tournoux, 1988). The WFU pickAtlas software ( Maldjian et al., 2004 and Maldjian et al.,

2003) was used to define anatomical locations based on the Talairach Daemon atlas database ( Lancaster et al., 2000) and the automatic anatomical labeling (AAL) tool ( Tzourio-Mazoyer et al., 2002). Anatomical labels were assigned according to the nearest gray matter position. All illustrations are based on this neurological convention. Statistical parametric maps (SPMs) were assessed to determine the brain activation associated with each experimental context (simple effects). Effects were recognized at p < .05 corrected for multiple comparisons at the voxel level (FWE). SPMs were also computed to compare brain activity across tasks in the active condition (dynamic vs static) as well as between AO + MI and AO in the dynamic task. Significant differences were recognized at p < .001, uncorrected at the voxel level but with an extended cluster threshold of 240 contiguous voxels (pcluster < .05; false discovery rate (FDR) corrected) for topological analysis ( Chumbley & Friston, 2009). In this manuscript, all locations are presented in MNI coordinates (x, y, z) and the Tables provide details of the local maxima for each cluster. In the first part of this study, the pattern of brain activation in each experimental task was studied with simple effect comparisons (contrast between task and resting state).