, 2002; Alix et al., 2007). Arabidopsis has been used to visualize infection biology of P. brassicae (Mithen & Magrath, 1992). The availability of synteny maps between Arabidopsis and Brassica spp. has allowed the identification of resistance loci in Brassica spp. first identified in Arabidopsis (Suwabe et al., 2006). Global analysis of host gene expression at different time points postinfection has been possible

using Arabidopsis genome arrays, and this has allowed the identification of host genes that may be important for infection by Plasmodiophora (Siemens et al., 2006). Genes of interest can then be studied further by transforming into Arabidopsis or by utilizing the bank of insertion lines available in Arabidopsis (Puzio et al., 2000; Siemens et al., 2006). Many of the host plants that Polymyxa spp. infect are not well characterized genetically, have fewer genetic tools available

and they have long generation check details times. Also, the roots of cereals can be difficult to visualize by microscopy as they are thicker in diameter than those of Arabidopsis. This can sometimes make the visual detection of Polymyxa in roots difficult. Therefore, if infection of Arabidopsis by Polymyxa spp. can be demonstrated, this could be a valuable tool in increasing our understanding of http://www.selleckchem.com/products/pexidartinib-plx3397.html plant–Polymyxa interactions. This study aimed to look at the potential for infection of Arabidopsis by Polymyxa spp. under controlled environment conditions using Polymyxa-infested soils. Arabidopsis thaliana ecotypes Landsberg erecta (Ler-0) and Columbia (Col-0) were used for this study (supplied by A. Cuzick, Rothamsted Research, UK). These ecotypes were chosen because they are genetically distinct and mapping populations are available. Seeds were sown into sterile Levingtons No. 2 compost containing Adenosine triphosphate sand and stratified for 4 days in the dark at 4 °C. Pots were then removed and placed in a greenhouse under short-day length conditions (8 h day at 20 °C, 16 °C night, light levels 200–300 μmol m−2 s−1). Once the seedlings had produced their first true leaves, they

were transferred to 10 cm pots containing infectious soils diluted 1 : 2, soil to sterile sand and grown as before. Two UK soils were used: one from Wiltshire, which was infested with SBCMV (Lyons et al., 2008), and one from Woburn, where Polymyxa was present, but no associated virus had ever been identified (Ward et al., 2005; R. Lyons, pers. commun.). For each soil, five seedlings of each ecotype were planted. Plants were then allowed to grow for 2 months. Flowering bolts were removed upon development to prolong vegetative growth. Roots were removed from pots and vigorously washed in sterile, distilled water. Portions of root were then mounted in sterile water under a coverslip and examined using an Axiophot (Zeiss) light microscope with bright field illumination.

To understand the neural bases of this inhibition and its possible odour specificity, we carried out a detailed analysis of the response characteristics of the different neuron types from the periphery to the central level. We examined the response patterns of pheromone-sensitive and plant volatile-sensitive neurons in virgin and mated male find more moths. By using intracellular recordings, we showed that mating changes the

response characteristics of pheromone-sensitive antennal lobe (AL) neurons, and thus decreases their sensitivity to sex pheromone. Individual olfactory receptor neuron (ORN) recordings and calcium imaging experiments indicated that pheromone sensory input remains constant. On the other hand, calcium responses to non-pheromonal odours (plant volatiles) increased after mating, as reflected

by increased firing frequencies of plant-sensitive AL neurons, although ORN responses to heptanal remained unchanged. We suggest that differential processing of pheromone and plant odours allows mated males to transiently block their central pheromone detection system, and increase non-pheromonal odour detection in order to efficiently locate Dabrafenib mouse food sources. “
“Detecting a change in a visual stimulus is particularly difficult when it is accompanied by a visual disruption such as a saccade or flicker. In order to say whether a stimulus has changed across such a disruption, some many neural trace must persist. Here we investigated whether two different regions of the human extrastriate visual cortex contain neuronal populations encoding such a trace. Participants viewed a stimulus that included various objects and a short blank period (flicker)

made it difficult to distinguish whether an object in the stimulus had changed or not. By applying transcranial magnetic stimulation (TMS) during the visual disruption we show that the lateral occipital (LO) cortex, but not the occipital face area, contains a sustained representation of a visual stimulus. TMS over LO improved the sensitivity and response bias for detecting changes by selectively reducing false alarms. We suggest that TMS enhanced the initial object representation and thus boosted neural events associated with object repetition. Our findings show that neuronal signals in the human LO cortex carry a sustained neural trace that is necessary for detecting the repetition of a stimulus. “
“Aged humans exhibit severe deficits in visual motion perception and contrast sensitivity under various levels of spatial and temporal modulation. Previous studies indicated that many of these deficits are probably mediated by the neural degradation of the central visual system.

In what follows, we consider what our results say about the functionality of the SEF, and about the application of ICMS in cognitive neuroscience. We consider first the effects of ICMS-SEF on error rates and RTs. One of the most prominent effects of ICMS-SEF is to greatly increase the propensity of anti-saccade errors made toward a contralateral cue (relative to the stimulating electrode; Fig. 2A). While ICMS-SEF also decreased

the propensity of pro-saccade errors made away from a contralateral cue (Fig. 2B), it is doing more that simply promoting the generation of a contralateral saccade: ICMS-SEF also increased substantially the propensity of anti-saccade errors selleck products made toward an ipsilateral cue (Fig. 2B, although this was less than the increase in propensity for contalateral anti-saccade errors), and decreased the propensity of pro-saccade errors made away from an ipsilateral cue (Fig. 2A). These

changes in error propensity cannot be attributed to decreased RTs, as might have been Ixazomib ic50 expected from a speed–accuracy tradeoff. Instead, the marked increase in anti-saccade errors accompanied substantial increases in RTs, regardless of direction (Fig. 3). We observed a more subtle and much smaller lateralized effect of SEF stimulation on pro-saccade RTs, with RTs increasing or decreasing for ipsilateral or contralateral pro-saccades, respectively. This latter result resembles that reported previously (Yang et al., 2008). One plausible explanation of our results is that ICMS-SEF selectively disrupts the animal’s ability to generate an anti-saccade, regardless of whether the animal was initially instructed to

make a pro- or anti-saccade. This disruption is somewhat lateralized, given the greater increase in propensity for contralateral vs. ipsilateral anti-saccade errors, but clearly effects anti-saccades in both directions. Exactly how such disruption occurs remains to be determined, but it could be that short-duration ICMS-SEF suppresses subsequent activity in the SEF that is required for anti-saccade generation, or perhaps resets the SEF back to the state adopted at the start of the trial. While this type of mechanism would also have to produce the pattern of neck EMG responses we Casein kinase 1 observed (see below), it would explain the bilateral increase in anti-saccade errors, the bilateral decrease in pro-saccade errors and the bilateral increase in the RTs of correct anti-saccades. We favor this interpretation over an alternative explanation that SEF stimulation favors the production of pro-saccades, given the greater level of SEF activity on anti- vs. pro-saccades (Amador et al., 2004), and because a simple bias toward pro-saccades fails to explain the longer RTs for ipsilateral anti-saccade errors compared with ipsilateral pro-saccades.

[14] The original Bohan and Peter criteria require at least two of elevated muscle enzymes, myopathic EMG, or muscle biopsy – the latter two being relatively invasive within a juvenile population. Both cohorts [1, 2] comment on their marked reduction in undertaking muscle biopsy in the last decade. The Australian cohort has also ceased EMG testing in favour of MRI. The CARRA registry reports MRI as the most commonly performed study in nearly all enrollees, and was more likely (91%) than EMG (50%)

or muscle biopsy (76%) to reveal abnormalities consistent with JDM.[13] Gowdie et al.[2] performed MRI in 50% of children with JDM and in 97% showed evidence of myositis. MRI has rapidly becoming the preferred non-invasive test indicating muscle inflammation, displacing muscle biopsy and EMG in the diagnosis of JDM and it is heartening to see the CARRA registry including MRI evidence

of myositis as a fifth selleck kinase inhibitor diagnostic/classification criterion for definite diagnosis of JDM.[13] Management of JDM with corticosteroids in conjunction with weekly methotrexate as the mainstay of therapy is based on consensus opinions rather than randomized trials due to the rarity of this serious illness.[15, 16] Use of methotrexate was 100% in the 2002–2011 series of Prasad et al., as compared to only 63% in Gowdie’s series which increased to 86% amongst their post year 2000 patients. A CARRA treatment survey indicated that more than 80% of North American paediatric rheumatologists would use methotrexate GDC-0980 mw as part of initial therapy for moderate JDM.[17] Comparably over 90% of the UK JDM group patients received treatment with methotrexate

and corticosteroids,[6] similar to the CARRA group in whom 95% had been treated with corticosteroids and 92% with methotrexate.[13] Furthermore, all three CARRA JDM consensus treatment protocols include methotrexate.[15, 16] Both the JDM cohorts published in this issue portray changing pattern of diagnostic (use of MRI) and therapeutic approach (use of methotrexate) over the years, apart from highlighting similarities and differences across ethnicities. However, such cohorts are neither designed, nor powered to assess treatment outcome of JDM. The rarity and low incidence of JDM precludes RCTs in the acute management of JDM even with collective cohorts such as CARRA and the UK JDM group. Alternatives to the RCT model of almost evidence such as comparative effectiveness research are eagerly awaited in this movement sapping disease. “
“Aim:  To determine the prevalence of rheumatic musculoskeletal disorders (RMSD) in type 2 diabetes mellitus (T2DM) and study their risk factors. Methods:  Diagnosed patients of T2DM attending the diabetic clinic in a premier teaching institution in south India were interviewed and requested to mark their RMS pain sites on a mannequin and intensity of pain on a visual analogue scale (VAS). A complete RMS examination was done and diagnoses were noted.

[14] The original Bohan and Peter criteria require at least two of elevated muscle enzymes, myopathic EMG, or muscle biopsy – the latter two being relatively invasive within a juvenile population. Both cohorts [1, 2] comment on their marked reduction in undertaking muscle biopsy in the last decade. The Australian cohort has also ceased EMG testing in favour of MRI. The CARRA registry reports MRI as the most commonly performed study in nearly all enrollees, and was more likely (91%) than EMG (50%)

or muscle biopsy (76%) to reveal abnormalities consistent with JDM.[13] Gowdie et al.[2] performed MRI in 50% of children with JDM and in 97% showed evidence of myositis. MRI has rapidly becoming the preferred non-invasive test indicating muscle inflammation, displacing muscle biopsy and EMG in the diagnosis of JDM and it is heartening to see the CARRA registry including MRI evidence

of myositis as a fifth Selleck PLX4032 diagnostic/classification criterion for definite diagnosis of JDM.[13] Management of JDM with corticosteroids in conjunction with weekly methotrexate as the mainstay of therapy is based on consensus opinions rather than randomized trials due to the rarity of this serious illness.[15, 16] Use of methotrexate was 100% in the 2002–2011 series of Prasad et al., as compared to only 63% in Gowdie’s series which increased to 86% amongst their post year 2000 patients. A CARRA treatment survey indicated that more than 80% of North American paediatric rheumatologists would use methotrexate Olaparib manufacturer as part of initial therapy for moderate JDM.[17] Comparably over 90% of the UK JDM group patients received treatment with methotrexate

and corticosteroids,[6] similar to the CARRA group in whom 95% had been treated with corticosteroids and 92% with methotrexate.[13] Furthermore, all three CARRA JDM consensus treatment protocols include methotrexate.[15, 16] Both the JDM cohorts published in this issue portray changing pattern of diagnostic (use of MRI) and therapeutic approach (use of methotrexate) over the years, apart from highlighting similarities and differences across ethnicities. However, such cohorts are neither designed, nor powered to assess treatment outcome of JDM. The rarity and low incidence of JDM precludes RCTs in the acute management of JDM even with collective cohorts such as CARRA and the UK JDM group. Alternatives to the RCT model of Lck evidence such as comparative effectiveness research are eagerly awaited in this movement sapping disease. “
“Aim:  To determine the prevalence of rheumatic musculoskeletal disorders (RMSD) in type 2 diabetes mellitus (T2DM) and study their risk factors. Methods:  Diagnosed patients of T2DM attending the diabetic clinic in a premier teaching institution in south India were interviewed and requested to mark their RMS pain sites on a mannequin and intensity of pain on a visual analogue scale (VAS). A complete RMS examination was done and diagnoses were noted.

In this study, a soil-borne, glyphosate-resistant bacterium was selected and identified as Enterobacter. The EPSPS in this strain was found to have buy Mitomycin C been altered to a resistant one. A total of 42 differentially expressed genes (DEGs) in the glyphosate were screened using microarray techniques. Under treatment, argF, sdhA, ivbL, rrfA-H were downregulated, whereas the transcripts of speA, osmY, pflB, ahpC, fusA, deoA, uxaC, rpoD and a few ribosomal protein genes were upregulated. Data were verified by quantitative real-time PCR on selected

genes. All transcriptional changes appeared to protect the bacteria from glyphosate and associated osmotic, acidic and oxidative stresses. Many DEGs may have the potential to confer resistance to glyphosate alone, and some may be closely related to the shikimate pathway, reflecting the complex gene interaction network for glyphosate resistance. “
“Yersinia polynucleotide phosphorylase (PNPase), a 3’-5’ exoribonuclease, has been shown to affect growth during several stress responses. In E. coli, PNPase is one of the subunits of a multi-protein complex known as the degradosome, but also has degradosome-independent

functions. The carboxy–terminus of E. coli ribonuclease E (RNase E) serves as the scaffold upon which PNPase, enolase (a glycolytic enzyme), and RhlB helicase all have been shown to bind. In the yersiniae, only PNPase has thus far been shown to physically interact with RNase PR-171 manufacturer E. We show by bacterial two-hybrid and co-immunoprecipitation assays that RhlB and enolase also interact with RNase E. Interestingly, although PNPase is required for normal growth at cold temperatures, assembly of the yersiniae degradosome was not required. However, degradosome assembly was required for growth in the presence of reactive oxygen species. These data suggest that while the Y. pseudotuberculosis PNPase plays a role in the oxidative stress response through a degradosome-dependent mechanism, PNPase’s Vasopressin Receptor role during cold stress is degradosome-independent.

2012 Federation of European Microbiological Societies. Published by Blackwell Publishing Ltd. All rights reserved “
“To examine why we failed in direct sequencing of rRNA gene internal transcribed spacer (ITS) in Pleurotus nebrodensis, we obtained monokaryons of P. nebrodensis (00489 and 00491) using a protoplast monokaryonization technique. PCR products of ITS amplifications were sequenced. There was a base pair insertion/deletion difference between the two nuclei of P. nebrodensis that led to failure in direct sequencing. Internal transcribed spacer regions (ITS1, ITS2, and 5.8S rRNA gene) of the nuclear ribosomal repeat are widely used in fungal systematics and phylogeny (Gardes & Bruns, 1993; Kårén et al., 1997; Cooke et al., 2000; Manter & Vivanco, 2007; Nilsson et al., 2009).

Trials containing voluntary electromyographic activity were excluded from further analysis. The effect of the attention locus (baseline, attention to hand, visual attention) on MEP amplitudes (series 1) was examined using repeated-measures anova with factors of Condition and ISI. For SICI and ICF, separate anova s with Condition and ISI as a repeat factor were analysed. More detailed information is given

in the Results. If appropriate, correction for multiple comparisons was used. For all experiments significance was set at P < 0.05. The behavioural results showed similar values for the visual and the attention-to-hand tasks (correct answers: visual attention 87.77 ± 6.5%; Epacadostat supplier attention to hand, cutaneous stimulation above

the FDI muscle area 92.48 ± 1.7%; attention to hand, cutaneous stimulation above ADM area 93.32 ± 2.0%), indicating similar difficulty PI3K targets for the two tasks and suggestive of similar levels of attentional demand. Figure 3(A) shows the MEP amplitude in the three blocks of trials (no attention, attention to hand, visual attention) as the difference between the two attention blocks and the no-attention block. An anova on the MEP amplitudes (no attention, 1.2 ± 0.1 mV; attention to hand, 0.87 ± 0.3 mV; visual attention, 1.87 ± 0.2 mV) revealed a significant effect of Condition (F2,22 = 23.67, P < 0.001). Post-hoc analysis confirmed that visual attention significantly increased the MEP size compared with baseline

(P < 0.001) and compared with attention to the hand (P < 0.005). Attention to the hand (at this location of the stimulus, i.e. the dorsum manum) did not significantly change the MEP size compared with baseline, although there was a trend (P = 0.06) towards suppression (Fig. 3). There was no difference in any condition between SICI measured at an ISI of 2 or 3 ms. Figure 3(B) shows the mean SICI in the three conditions as the difference between the two attention tasks and the baseline task, Figure 4 shows corresponding Diflunisal absolute values. Two-way anova on the amount of SICI (in % unconditioned test MEP) (no attention: 2 ms, 54.1 ± 8.6; 3 ms, 62.9 ± 13.8; attention to hand: 2 ms, 62.1 ± 15.2; 3 ms, 59.5 ± 12.4; visual attention: 2 ms, 76.5 ± 14.3; 3 ms, 78.1 ± 12.4) revealed a significant main effect of Condition (F2,22 = 4.24, P < 0.05), no significant effect of ISI (F1,11 = 0.06, P > 0.5) and no significant interaction of both (F2,22 = 0.43, P > 0.5). Post-hoc analysis showed that SICI was less effective during visual attention both when compared with the baseline task (P < 0.05) and the attention-to-hand task (P < 0.05). There was no difference in the amounts of ICF (in % unconditioned test MEP) at the two ISIs (no attention: 12 ms, 167.5 ± 23.5; 15 ms, 163.2 ± 20.8; attention to hand: 12 ms, 149.0 ± 14.1; 15 ms, 146.2 ± 18.4; visual attention: 12 ms, 159.1 ± 24.1; 15 ms, 137.5 ± 22.1).

211684) of the European Commission within its Seventh Framework Programme. The authors thank Dr Anna Rusznyak for critically reading the manuscript. Please note: Wiley-Blackwell is not responsible for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding

author for the learn more article. “
“Vibrio parahaemolyticus is an enteric pathogen, which can cause acute gastroenteritis in humans after consumption of raw or partially cooked seafood, and specific molecular markers are necessary for its accurate identification by PCR methods. In the present study, 23 protein-coding sequences were identified by the comparative genomics method Epigenetic inhibitor as V. parahaemolyticus-specific candidate markers. We targeted the irgB gene (vp2603), coding for iron-regulated virulence regulatory protein IrgB, in order to develop a PCR method for the detection of V. parahaemolyticus. PCR specificity was identified by amplification of 293 V. parahaemolyticus templates and by the loss of a PCR product with 11 strains from other Vibrio species and 35 non-Vibrio bacterial strains. The PCR assay had the 369-bp fragment and the sensitivity of 0.17 pg purified genomic DNA from V. parahaemolyticus. Furthermore, a multiplex PCR assay for the detection of total and virulent strains of V. parahaemolyticus

was developed by targeting irgB, tdh and trh genes. These data indicated that

the irgB gene is a new and effective marker for the detection of V. parahaemolyticus. In addition, this study demonstrates that genome sequence comparison has a powerful application in identifying specific markers for the detection and identification of bacterial pathogens. Vibrio parahaemolyticus is a Gram-negative bacterium commonly found in marine and estuarine environments around the world (Daniels et al., 2000). This organism may lead to acute gastroenteritis Teicoplanin characterized by diarrhea, headache, vomiting, nausea and low fever, after consumption of raw or partially cooked fish or shellfish (Tuyet et al., 2002; DePaola et al., 2003). Outbreaks of V. parahaemolyticus have been reported from many countries and regions such as China (Liu et al., 2004b), Japan (Alam et al., 2002), the United States (McLaughlin et al., 2005) and some European countries (Martinez-Urtaza et al., 2005). Therefore, early detection and identification of V. parahaemolyticus strains in clinical and food samples is essential for diagnosis and implementing timely risk management decisions. However, the detection of V. parahaemolyticus using conventional culture- and biochemical-based assays is time consuming and laborious, requiring more than 3 days. Those strains that produce thermostable direct hemolysin (TDH) and/or TDH-related hemolysin (TRH) are considered virulent for humans (Dileep et al., 2003; Zhang & Austin, 2005).

As with the DR task, aged monkeys are slower to learn the task and perform more poorly Staurosporine purchase as delay intervals are increased (Shamy et al., 2011). Behavioral flexibility is another frontal-dependent cognitive process that is compromised with aging. This has been studied using a variety of tasks, notably extradimensional set-shifting and reversal tasks in humans (Ridderinkhof et al., 2002; Marschner et al., 2005; Weiler et al., 2008), monkeys (Bartus et al., 1979; Lai et al., 1995; Voytko, 1999; Moore et al., 2003) and rats (Stephens et al., 1985; Barense et al., 2002; Schoenbaum et al., 2002; Nicolle & Baxter, 2003; Mizoguchi et al., 2010). Interestingly,

lesions of area 9 in marmoset monkeys affected extradimensional set-shifting performance, whereas lesions of the orbital PFC affected histone deacetylase activity reversal performance (Dias et al., 1996). These data suggest that these tasks rely on different brain structures within the PFC. Extradimensional set-shifting refers to the problem of switching attention between cues that are in different perceptual dimensions in order to perform the task correctly. An example

of this is to train a rat to use light cues to determine which arm to select in a maze, and then shift the relevant cue to an auditory stimulus. When the extradimensional set-shifting occurs, the rat must shift its strategy and follow the sound cue in order to select the correct baited arm (e.g., Insel et al., 2012). In contrast, reversal learning refers to adapting a behavior to the changing contingencies required to reach a goal. For example, a rat can initially learn to press a lever in a ‘light-on’ condition to receive reward. After a reversal, the rat must adapt its behavior to press during the ‘light-off’ condition (e.g., Nomura et al., 2004). In parallel to the age-related cognitive deficits discussed above, aging is also associated with changes in attentional processes (Gazzaley & D’Esposito, 2007; Prakash et al., 2009; Hedden et al., 2012). This is accompanied by a greater susceptibility to distraction or interference during the delay period of a working memory task in humans (Bowles & Salthouse, 2003; Campbell et al., 2012) and monkeys (Bartus & Dean,

1979; PTK6 Prendergast et al., 1998). Additionally, fMRI studies in older adults have reported that there is increased activity in brain regions mediating distraction (Milham et al., 2002; Stevens et al., 2008), and in cases where task-irrelevant stimuli are presented (Gazzaley et al., 2005). One of the most consistent finding in the literature on aging brain is a decline in the volume of the PFC of humans, monkeys and rodents. This decline is one of the earliest changes detected, and for almost fifty years it was thought that the decrease in frontal lobe volume was the result of cell loss (Haug, 1986; Peters, 2002). The early reports of cell loss, however, turned out to be an error resulting from differential shrinkage of young and aged tissue during processing (Haug et al.

In the control condition, the ADM was activated independently and matched a target force line (5% of MVC) displayed on the computer monitor for the entire duration of 5 s trials. TMS was delivered Bortezomib purchase randomly between the 1.5 and 3.75 s time points of these control trials in the experimental block trial blocks. In the other three experimental conditions, an index finger flexion movement was performed in response to an acoustic tone delivered randomly between the 1.5 and 3.75 s time points of the 5 s trials while the ADM was performing the same isometric force production task throughout the trial as in the control condition. For index finger flexion,

subjects were instructed to react as fast as possible to the acoustic tone, rapidly increase the force to the

line displayed on the monitor, hold this force throughout the trial, and quickly terminate the force at the end of the trial. The three experimental conditions involving index finger flexion were distinguished by the time in which TMS was delivered relative to the onset of the FDI EMG and will be referred to as the pre-motor, phasic, and tonic conditions. These conditions correspond to the following movement phases and TMS delivery times – pre-motor (20 ms before FDI EMG onset), phasic (the first peak of FDI EMG), and tonic (during INCB024360 in vivo contraction at the target force level). In summary, subjects had to accurately maintain a constant target force with the ADM throughout each trial in all conditions, despite sometimes having to concurrently produce a rapid index finger flexion force at random times. This, combined with the low target forces Progesterone and the requirement to use visual feedback to monitor the target forces of both muscles (sometimes simultaneously), made it a difficult motor task. Accordingly, pilot work found that 30–60 practice trials were required for a subject to become proficient. The goal of the initial practice

trial blocks was to provide the subjects with sufficient practice to correctly execute the motor task before progressing to the final practice trial block and experimental trial block. Accordingly, subjects performed two initial practice blocks of 30 trials. TMS was not applied during these practice blocks. At the end of the initial practice blocks, the investigators and each subject were confident that they could correctly execute the motor task. After the initial practice blocks, subjects could perform the motor task correctly and displayed consistent reaction times to the acoustic tone. Therefore, the aim of the final practice block was to determine the individual reaction time of each subject in order that TMS could be delivered at the appropriate times relative to the FDI onset in the pre-motor, phasic, and tonic movement phases in the forthcoming experimental trial blocks (Beck et al., 2008; Beck & Hallett, 2010). Upon completion of the final practice block (20 trials), a custom-written analysis script in Signal 4.