The impacts of normal operations cannot be eliminated, but they c

The impacts of normal operations cannot be eliminated, but they can be managed in space and time to minimize effects on culture and environment. Accidents, however, have the potential to cause the most widespread impacts of any of the threats posed by shipping. The record from the nearby Aleutian Islands [77] suggests that over time one or more spills may be close to inevitable. Increasing tug, salvage and spill response capabilities

in the Bering Strait and PLX3397 chemical structure Northwest Arctic should be considered, especially during peak vessel traffic periods. Such capacity could also aid in search and rescue if needed. Local training in emergency response could also Selleckchem Carfilzomib enhance the region׳s ability to respond promptly while other assets are en route. Identifying risks and associated regulatory measures is a first step, but taking action will depend also on effective governance of vessel traffic at local, national, and international levels. Bering Strait region communities

will need to develop the technical and human capacity to work effectively with mariners and regulators, to identify community needs and priorities and to implement measures such as local use of AIS and communication systems. National governments will need to continue to develop appropriate regulatory frameworks, including local outreach and involvement as well as standards that are consistent with other such efforts in Arctic waters. Internationally, cooperation between the U.S. and Russia would be a big step forward and would pave the way for recognition of Farnesyltransferase appropriate measures by the IMO. In this light, Table 2 outlines the progression from voluntary recommendations to domestic and international regulations. While voluntary recommendations may not be enforceable, they can also be made more quickly than formal regulations, compliance may be high, and they are a significant step towards formal regulations. Formal regulations are likely to take longer to develop and implement, but carry extra

weight. Both approaches have a role in a system of effective governance for vessel traffic. In summary, vessel traffic in the Bering Strait region is an economic opportunity, and also an opportunity for sound management of environmental and cultural risks. This paper presents a framework for various actions that can be taken locally, nationally, and internationally to reduce risks from vessel traffic, consistent with the principle of freedom of the seas as well as with responsible standards of care for vessel operations in areas. Acknowledging the risks and taking appropriate action proactively can help vessel traffic proceed without hindrance, while also protecting an important ecosystem and the cultures that depend on it, while both remain vibrant and healthy.

The poor diversity of the zooplankton community and of copepods a

The poor diversity of the zooplankton community and of copepods appears to be a characteristic feature of several small basins on the Egyptian Mediterranean coast, particularly those receiving land-based effluents (e.g. Abdel-Aziz & Dorgham 2002, Abdel-Aziz 2004). The number of

zooplankton species recorded during the present study (42 taxa including larval stages) is slightly higher than that recorded (37 taxa) by Abou-Zeid (1990) and El-Serehy et al. (2001). This may be because their studies did not take into account the western lagoon connected with the lake, or the continuous dredging activities in the main lake and shipping lane, which renew the lake’s water masses. In general, the low number of species recorded in the lake can be attributed to the continuous discharge of wastewater, which leads to increasing nutrient concentrations and hence the dominance of just a few

species. This was confirmed by Ludsin et al. (2001) and Prepas & Charette (2003), who concluded that the biodiversity of most aquatic systems decreases with increasing nutrient load as a result of increasing eutrophication. During the study period, the zooplankton standing crop in Lake Timsah showed an annual average zooplankton of 22 026 individuals m−3. This average is comparable with the study of Abou-Zeid (1990) in the lake (23 419 individuals m−3), even though his vertical samples did not cover the whole lake. Also, this value indicated that the lake is less productive than Lake Buroullus (183 000 individuals m−3) during 1987 (Aboul-Ezz Isotretinoin 1995), Afatinib cell line Lake Maryout with approximately 117 000 individuals m−3 during 1996–1997 (Abdel-Aziz & Aboul-Ezz 2004), Lake Idku with 326 000 individuals m−3 during 2000 (Aboul-Ezz & Soliman 2000) and Lake Manzalah with 5 × 106 individuals m−3 (El-Sherif et al. 1994).

The seasonal pattern of the zooplankton standing crop was characterized by conspicuously high numbers in summer and a lower peak in autumn, with minimum densities being recorded in winter. Copepods were by far the most important group of zooplankton in the study area, comprising 77.7% of the total population, and the seasonal variation in the total zooplankton population was governed mostly by variations in this group. This dominance of copepods was documented previously in the same area (Abou-Zeid 1990, Ghobasy et al. 1992), in the Suez Canal area (El-Serehy et al. 2001), in the eastern Mediterranean (e.g. Nour El-Din 1987, Dowidar 1988) and at other coastal sites of the Arabian Gulf (Yamazi 1974, Michel et al. 1986, Dorgham & Hussein 1997). The Pearson correlation revealed that temperature and pH were the common factors controlling copepod abundance in the Lake Timsah (r = 0.617 and 0.541 respectively). This is in agreement with Goldman & Horne (1983) and Rodriguez et al. (1995), who found that temperature was the main factor affecting zooplankton production.

, 2006), when we found the protein levels of GluR1

to hav

, 2006), when we found the protein levels of GluR1

to have returned to control levels. There is evidence, however, of increased GluR1 mRNA expression after 3 and 7 days of voluntary exercise (Molteni et al., LDK378 price 2002). Nonetheless, Chen et al. (2007) have demonstrated that voluntary and forced exercise may activate distinct signaling pathways, which could explain the different findings between voluntary exercise (Molteni et al., 2002) and the present protocol. During development, GluR1 and GluR2 are related to increases of length and complexity of dendritic arborizations (Chen et al., 2009). This doesn’t appear to be a mechanism involved in the changes that occur in the adult brain and the ones observed here, as we noticed increases of MAP2 and NF68 after exercise despite the decreased levels of GluR1 and unaltered levels of

GluR2/3. MAP2 is an early and sensitive marker of neuronal damage following traumatic brain injury (Huh et al., 2003), and has not yet been associated with exercise-dependent plasticity. Increased levels of MAP2 mRNA in the granule cell dendrites have been associated with the induction of LTP in hippocampal perforant path/granule cell synapses in rats (Roberts et al., 1998) and with some forms of hippocampus-mediated memory processes (Fanara et al., 2010). On the other hand, decreased levels of MAP2 and NFs have been associated with hypercortisolism (Cereseto et al., 2006). Our findings revealed increases of MAP2 protein and mRNA, together with increased MK0683 cell line immunoreactivity and levels of NF68. To the best of our knowledge, this is the first evidence of changes of protein levels of NFs and MAP2 in response to exercise, despite reports of increased dendritic

length (Stranahan et al., 2007) and complexity (Eadie et al., 2005). Together with previous literature, the present data can be interpreted as a beneficial plastic effect. In fact, increased perikaryal levels of NF proteins are thought to be neuroprotective in diseases such as amyotrophic lateral sclerosis, due to NF association to calcium-binding proteins (for a review, Cyclic nucleotide phosphodiesterase see Julien, 1999). It is noteworthy, however, that the increase of MAP2 preceded the increase of MAP2 mRNA, whereas no NF mRNA has changed after exercise. Changes of protein levels in the absence of mRNA changes may be explained by protein accumulation due to increased protein stability and/or decreased protein degradation, which also applies to SYN and GFAP data. Exercise-induced astrocytic changes have also been previously reported. It was observed that astrocytic density and GFAP levels increase in the cortex and striatum after 3 and 6 weeks of treadmill exercise (Li et al., 2005). In the SGZ, GFAP-expressing cells increase after 7 days of wheel running (Komitova et al., 2005).

It is important to note that 80% of the HCV genotype 1-infected p

It is important to note that 80% of the HCV genotype 1-infected patients in this study had subgenotype 1a, which has reportedly been more difficult HKI-272 price to treat than subgenotype 1b when using protease inhibitor-based direct-acting antiviral regimens.32, 33 and 34 Combination regimens that include ombitasvir and ABT-450/r with or without RBV have been studied in genotype 1-infected patients in other phase 2 and phase 3 studies. In a phase 2b trial evaluating various

combinations of ombitasvir, ABT-450/r, the nonnucleoside polymerase inhibitor dasabuvir, and RBV administered for 8, 12, or 24 weeks in genotype 1-infected patients, SVR24 rates up to 96.2% in treatment-naïve patients and 95.3% in prior pegIFN/RBV-null responder patients were observed.29 A phase 2 study assessing a 12-week regimen of ABT-450/r and ombitasvir without RBV in genotype 1b-infected patients reported SVR12 rates of 95.2% in treatment-naïve patients and 90.0% in GSK2126458 manufacturer prior pegIFN/RBV-null responder patients.30 In phase 3 trials, a regimen of ombitasvir/ABT-450/r and dasabuvir with RBV was evaluated in treatment-naïve and pegIFN/RBV treatment-experienced HCV genotype 1-infected patients with and without cirrhosis. Regimens of ombitasvir/ABT-450/r and dasabuvir with RBV achieved SVR12 rates up to 96% in each of the large patient populations evaluated in these trials.17, 21 and 31

Other phase 3 trials evaluated this regimen with and without RBV.18 SVR12 rates of 97.0% and 90.2% were observed in HCV subgenotype 1a-infected patients receiving ombitasvir/ABT-450/r and dasabuvir with and without RBV, respectively.18 SVR12 rates in HCV subgenotype 1b-infected patients receiving ombitasvir/ABT-450/r and dasabuvir with and without RBV were 99.0% and 99.5%, respectively.18 Response rates in this study in HCV genotype 2-infected patients were high Florfenicol despite 80% of the patients having subgenotype 2b infection, which has been identified as more difficult

to treat with pegIFN-containing regimens than subgenotype 2a.22, 35 and 36 The exploratory regimens in this study resulted in SVR in some HCV genotype 3-infected patients, but the overall SVR rates in this group of patients were low. The results of this study also indicate that the safety and tolerability of both the RBV-containing and RBV-free regimen compare favorably to pegIFN-based therapy. Patients receiving these all-oral regimens avoid the subcutaneous injections required for pegIFN therapy. Also, the rates of adverse events commonly associated with pegIFN treatment, such as fatigue, headache, nausea, and depression, were lower in patients in this study than previously reported in patients receiving pegIFN.37 One patient in this study had a grade 3 bilirubin elevation; this elevation was predominantly indirect bilirubin, consistent with the known effect of protease inhibitors on the organic anion-transporting polypeptide 1B1.

70 In the European Society for Clinical Nutrition and Metabolism

70 In the European Society for Clinical Nutrition and Metabolism (ESPEN) guidelines, Weijs et al72 propose using “ideal body weight” to more accurately estimate protein requirements for underweight (body mass index [BMI] <20 kg/m2) and obese (BMI >30 kg/m2) patients. Some recommendations are specific to protein, whereas others recommend protein as part of an oral nutrition this website supplement (ONS) or enteral nutrition formula. With increased protein

intake, older people may experience improved bone health, cardiovascular function, wound healing, and recovery from illness.73 These benefits also have the potential to help older people meet the health challenges of illness. The latest Cochrane update from 2009 indicates that protein-energy supplementation reduces mortality, especially in older, undernourished subjects and in patients with geriatric conditions.74 Table 3 summarizes studies and recommendations for protein intake in older people who are hospitalized in ward

or critical care settings. Results of a retrospective study of undernourished older people in a Dutch hospital (n = 610) showed that only 28% met protein targets (n = 172).78 For the study, subjects were identified Selumetinib ic50 by nutrition screening on admittance. Of those screened, 15% were malnourished and included in the study; 40% of patients older than 65 had multiple diseases. Energy targets were determined with the Harris-Benedict equation, then adjusted by +30% for activity or disease; protein targets were 1.2 to 1.7 g protein/kg BW/d. In a French study, the sickest patients in a group of older adults in short- or long-stay care settings were found to be the most undernourished, and fell

particularly about short of protein targets (intake of 0.9 g protein/kg BW/d, compared with 1.5 g/kg BW/d goal). Patients categorized to be at a nutritional “steady state” were able to meet their energy and protein goals (25–30 kcal/kg BW/d and 1.0 g protein/kg BW/d).79 The frailty syndrome has a place on the continuum between the normal physiological changes of aging and the final state of disability and death.4 and 80 Frailty worsens age-related changes in protein metabolism, further increasing muscle protein catabolism and decreasing muscle mass.81 Higher protein consumption has been associated with a dose-responsive lower risk of incident frailty in older women.82 Incorporating more protein into the diet is thus a rational strategy for frailty prevention. Older adults (average age 84) with hip or leg fracture who entered the hospital undernourished did not meet estimated energy or protein targets. Individual energy requirements were estimated by age, gender, activity level, and disease-related metabolic stress; protein requirements were estimated at 1.0 g protein/kg BW/d. With diet alone, patients were able to meet only 50% of energy and 80% of target protein intake.

, 2004) The Akt family of kinases, i e , Akt1, Akt2, and Akt3, p

, 2004). The Akt family of kinases, i.e., Akt1, Akt2, and Akt3, plays arolein processes that are well known as hallmarks of cancer, such as sustained angiogenesis, unlimited replicative potential, and tissue invasion and metastasis (Hanahan and Weinberg, 2011). Moreover, Akt activation mediates

the expression of N-cadherin and metalloproteinases and plays aroleintum or invasion and metastasis by inducing EMT (Park et al., 2001, Higuchi et al., 2001, Grille et al., 2003 and Wallerand et al., 2010). Recently, Steelman et al. (2011) demonstrated that the activation of AKT-1 increased the resistance of MCF-7 cells to radiation. Additionally, Toker and Yoeli-Lerner (2006) showed that Akt1 might have a dual role in tumorigenesis, not only promoting it by suppressing apoptosis but also inhibiting it by suppressing invasion and metastasis. The specific role of AKT in terms of cell motility and invasion seems PI3K Inhibitor Library chemical structure to depend on the cell type and the pathways that are activated. Many of the enzymes that either mediate the

Akt signal, such as MDM2 (Zhou et al., 2001), or regulate Akt activity, such as the tumor suppressor PTEN (Li et al., 1997), are frequently mutated in human tumors. As such, Akt activity is up-regulated, thus increasing tumor cell growth and survival. In several mammalian systems, activated Akt1 correlates with cell migration and invasion. While constitutively active Akt1 can enhance the ability of some cells to invade (Steelman et al., 2011, Kim et al., 2001 and Arboleda et al., 2003), Akt1 can also have the JNK inhibitors opposite effect

in normal or less invasive cells (Arboleda et al., 2003). Moreover, the increased activation of Akt1 correlates with increased proliferation and anchorage-independent growth. However, the effects of activated Akt1 on cell migration and invasiveness depend on the type of cells and tissues in which its action is being studied (Steelman et al., 2011, Kim et al., 2001, Arboleda et al., 2003, Enomoto et al., 2005, Irie et al., 2005 and Yoeli-Lerner et al., 2005). Yoeli-Lerner et al. (2005) and Toker and Yoeli-Lerner (2006) revealed that the expression of activated Dolichyl-phosphate-mannose-protein mannosyltransferase Akt1 potently blocks the migration and invasion of three distinct breast cancer cell lines through Matrigel in vitro. In fibroblasts, Akt signaling enhances the activation of various small GTPases, leading to remodeling of the actin cytoskeleton and enhancing cell motility ( Enomoto et al., 2005). Similarly, the expression of activated Akt in fibrosarcoma or pancreatic cancer cells increases their ability to invade through Matrigel ( Park et al., 2001 and Kim et al., 2001). Liu et al. (2006) demonstrated that cells expressing activated Akt1 show increased proliferation and resistance to apoptosis. Additionally, the invasiveness and motility of the cells were substantially decreased by the down-regulation of Rho activity.

The viability of the cells (>90%)

was determined before h

The viability of the cells (>90%)

was determined before harvesting and freezing for ascities production. Mice were first inoculated intraperitoneally with monoclonal antibody-producing hybridoma cells; thereafter, the ascites fluid was collected and purified (1st Base, Singapore, ProSci Incorporated, USA). Further purification with Protein A agarose (Thermo Scientific, USA) and elution with 0.1 M citrate buffer containing 0.05% sodium azide were carried out. The eluate was concentrated in a centrifugal filter unit (Millipore, USA), washed with HDAC inhibitor sterile phosphate buffered saline (PBS) and stored as a 1 mg/ml stock containing 0.05% sodium azide and 0.1% glycerol. Sections were immunostained with a primary antibody solution which contained goat anti-CRF RI/II antibody (SC1757, 1:1000, Santa Cruz, USA), mouse anti-relaxin-3 antibody (1:1000), rabbit anti-tryptophan hydroxylase 2 (TPH2) antibody (AB5572, 1:1000, Chemicon, USA) or rabbit anti-glial fibrillary acidic protein (GFAP) antibody (Z0334, 1:1000, Dako, Denmark). Stained sections were subsequently visualised with donkey anti-goat Alexa Fluor 555 (1:400), donkey anti-mouse Alexa Fluor 488 (1:400) or goat anti-rabbit Alexa Fluor 488 (1:400) secondary

antibodies, after which slides were washed and CDK and cancer mounted using Prolong Antifade with DAPI (Invitrogen, Singapore)

and viewed with a fluorescence microscope. The CRF RI/II polyclonal antibody used here was raised against the C-terminus of human CRF1, which is conserved across rat and mouse CRF1. Its specificity has been demonstrated previously by Chen et al. (2000) in experiments in which pre-incubation with the antigenic peptide abolished CRF1 signals in western blots and staining in mouse brain sections. In mouse heart sections known to express only CRF2, no staining was observed (Chen et al., 2000). To evaluate the specificity of this antibody in the NI neurons, a 10× relative concentration of the CRF blocking peptide (C-20P, Santa Cruz, USA) was pre-incubated with a 1:1000 dilution of click here the antibody overnight at 4 °C. NI sections were then incubated in this solution overnight and then further processed for CRF RI/II staining. Total RNA was extracted from the tissue and purified according to the manufacturer’s instructions for PureLink RNA mini kit (Invitrogen, Singapore). The amount of RNA was quantified with a NanoDrop UV–vis spectrophotometer (Thermo Scientific, USA). Approximately 1 µg of total RNA was reverse transcribed with oligo(dT) primers using ImProm-IITM Reverse Transcription system (Promega, USA).

Thus, if the (only) observed positivity is a P3, the question the

Thus, if the (only) observed positivity is a P3, the question then becomes: where is the P600? If the present late positivity is a P3, the lack of a distinct P600 entails that there is no P600 as a general, necessary consequence

of syntactic processing, or at the very least that it depends on specific (as of yet unspecified) aspects of the task. In either case, a model of the P600 as natural correlate of automatic syntactic processing must be amended. In addition, the assumption that the present Selleck NVP-BKM120 paradigm only elicited a P3 but no P600 is at odds with results demonstrating that the P600, in fact, has a stronger propensity to appear in task-relevant contexts than when task relevance and syntactic manipulation status do not coincide. As noted in the introduction section, the P600

– following both syntactic and semantic anomalies – is enhanced Alpelisib by more explicit tasks (Hahne and Friederici, 2002, Haupt et al., 2008, Osterhout et al., 1996 and Osterhout et al., 2002). It is greatly attenuated and often absent (Batterink and Neville, 2013 and Hasting and Kotz, 2008; Royle, Drury, & Steinhauer, 2013) when subjects do not consciously attend to grammatical violations – in contrast to syntax-sensitive negativities, which often remain rather unaffected by task (e.g. Haupt et al., 2008). It also appears highly unlikely that the use of an immediate-response paradigm led to a higher likelihood for a P3 in this Levetiracetam study as opposed to previous sentence processing experiments employing similar violation paradigms and delayed reaction. It has been established that the P3 follows the event affording decision making and response selection, not response execution. A direct comparison of immediate and delayed response tasks (e.g. Grent-‘t-Jong et al., 2011 and Praamstra et al., 1994) reveals that a P3 is always seen on the critical

stimulus itself, whether it is immediately followed by a response or not. In other words: the P3 does not “wait for the ‘go’ signal”. In accordance with these findings from non-linguistic paradigms, a P3 is expected following task-relevant violations in typical (delayed-response) EEG sentence processing experiments just as for the present immediate-response paradigm. Finally, it may be questioned if passive perception and comprehension is indeed the more “natural” mode of language processing, as opposed to “preparation for situated action” (Barsalou, 1999). In summary, when the present study is considered in light of the full range of existing data, there is no principled reason to assume that the paradigm employed here should have been more susceptible to eliciting a P3 effect than previous violation studies on sentence processing. The fact that the only positivity following the processing of structural information in our study is RT-aligned thus has implications for our understanding of the P600.

, 2008) we also observed high CK serum levels in both strains wit

, 2008) we also observed high CK serum levels in both strains within 3 h of injury. Furthermore, these histomorphometric and sacolermal permeability analysis after 24 h of injury confirms that the delay in muscular regeneration between mouse strains was not due to acute tissue damage induced by B. jararacussu venom. Endogenous danger signals activate Toll-like receptors (TLR 2, 4, and 9) and induce homeostatic or harmful responses, depending on the physiological context, thus explaining contradictory reports showing that TLR4-deficient mice develop harmful noninfectious lung inflammation (Zhao et al., 2010), but not in the model of cardiac ischemia (Zhao et al., 2009) or brain injury (Caso et al., 2007).

In the Selleck Alpelisib skeletal muscle injury model with cardiotoxin it was suggested that

TLR3 may exert a protective role in muscle regeneration (Mathes and Lafyatis, 2011). MyD88 is utilized by most TLRs with exception of TLR3 that learn more utilizes TRIF to activate the NF-κB pathway and IRF3 pathway. TLR4 utilizes MyD88 adapter molecule to activate the NF-κB pathway and TRIF adapter molecule to activate the IRF3 pathway inducing production of proinflammatory cytokines (McGettrick and O’Neill, 2010). In the noninfectious lung inflammation, the TLR4 anti-inflammatory signaling is dependent upon a MyD88-independent pathway (Zhao et al., 2010). C3H/HeJ mice used in the present study have a mutation in the cytoplasmic domain caused by substitution of a proline residue for histidine at position 712 in the TLR4 polypeptide chain that halts the activation of both signaling pathways (Poltorak et al., 1998). TLR4-deficient mice showed 10-fold more F4/80-positive macrophages in the injury site in comparison with wild-type mice in 10 DPI, suggesting that such persistence is associated with delayed transition to the early differentiation stage of myogenesis. Delayed muscle repair observed in our study suggests

that TLR4 plays a protective role in muscle regeneration although further studies with knockout mice (MyD88−/− and TRIF−/−) are necessary to determine main signaling pathway involved in the skeletal injury induced by intramuscular injection of B. jararacussu venom. Edema formation and influx of inflammatory cells with subsequent loss of muscle Fossariinae mass during later stages of tissue regeneration is regarded as a critical event of venom poisoning caused by snakes of the Bothrops genus (Barbosa et al., 2008; Doin-Silva et al., 2009). The edematogenic effect is related to widespread damage in the local microvasculature due to release of venom proteases (Escalante et al., 2011; Neto and Marques, 2005). Edema formation as evidenced by increased muscle mass was consistently observed in both TLR-deficient and wild-type mice up to 3 days after venom extract injection. Nonetheless, TLR4-deficient mice showed a significant increase in edema formation comparing to TLR4 wild-type mice, which was an indication that TLR4 probably control mechanisms related to edematogenic effect.

, 2003) and the automated anatomical labelling (AAL) atlas ( Tzou

, 2003) and the automated anatomical labelling (AAL) atlas ( Tzourio-Mazoyer et al., 2002) of SMA, angular gyrus, insula, superior frontal medial cortex and precuneus. The resulting statistical maps were overlaid onto a normalized T1-weighted MNI template (colin27) and the coordinates reported correspond to the MNI coordinate system. The repeated-measures ANOVA revealed a significant main effect for agency [F(1,17) = 5.96, p < .05] with participants giving significantly shorter interval estimates in the active compared to the passive condition on the judgement error. There was

an unsurprising significant main effect of delay [F(2,34) = 16.49, p < .001] with more pronounced underestimation of the action–effect interval at longer delays. There was also a significant interaction of both factors [F(2,34) = 6.48, Alectinib purchase p < .01] ( Fig. 1). This interaction arose because selleck chemical the difference in judgement error between active and passive conditions increased with action-tone delay. The interval estimation task was analysed by parametrically modulating the action onset

with the judgement error of the action-tone interval. We then contrasted the active with the passive condition based on the fact that the active condition should involve a shortening of the awareness of the interval, whereas the passive condition should not. This analysis identifies brain regions that correlate with the compression of the action-tone interval more strongly in the active than in the passive condition. The previous literature gave strong predictions about involvement of specific regions in the experience of agency: the angular gyrus and the SMA (see Etofibrate Introduction) but also insula, frontomedian cortex and precuneus. Therefore we used a small volume correction within anatomically defined mask of these structures of interest. We identified a significant cluster within the SMA ROI family-wise error corrected p < .05 after small volume correction at −11, −8, 74 (cluster

size = 7 voxels) ( Fig. 2). Closer inspection confirmed that the cluster was located in left BA6, effectively on the margin between the lateral portion of BA6 comprising the dorsal premotor cortex, and the medial portion comprising the SMA proper. We applied a similar small volume correction to the bilateral angular gyrus, insula, frontomedian cortex and precuneus ROI, but found no significant difference between the parametric regressors for the active and passive conditions (nor in the reverse contrast) surviving correction within these areas. A whole brain analysis of the contrast between the parametric regressors for the active and passive condition with a statistical criterion of p < .001 uncorrected for multiple comparisons again revealed the same SMA cluster at −11, −8, 74, but no other significant clusters. Further, no significant clusters of activation were found in the reverse contrast.