2, Nav1.3 (Black et al., 1995a), Nav1.5 (Black et al., 1998), and Nav1.6 (Reese and Caldwell, 1999), and microglia have been shown to express Nav1.5 and Nav1.6 (Craner et al., 2005 and Black et al., 2009). Human red blood cells have been shown to express Nav1.4 and Nav1.7 (Hoffman et al., 2004). Although this article focuses on the Nav1.1–Nav1.9 pore-forming α-subunits of sodium channels, there is also evidence demonstrating the presence of AZD9291 cost sodium channel β-subunits in some nonexcitable cells (Oh and Waxman, 1994), where they are postulated to function as cell-adhesion molecules (Brackenbury et al.,

2010). As described below, voltage-gated sodium channels contribute to diverse effector functions of nonexcitable cells. This is all the more remarkable because, in general, estimated densities of sodium channels in nonexcitable cells are substantially lower than those in excitable cells (<1 versus 2–75 μm−2, respectively; see, e.g., Sontheimer et al., 1992). Spinal cord astrocytes in vitro are an exception and can express sodium

channels at densities estimated to be as high as 10 channels per μm2 (Sontheimer et al., 1992), which, although not supporting action potential electrogenesis close to resting potential, can support the production of all-or-none overshooting action-potential-like responses when the cells are hyperpolarized to levels that remove resting inactivation (Sontheimer and Waxman, 1992). The density of sodium channels in cells such as astrocytes in vitro depends DAPT cell line on the milieu to which the cells are exposed (Thio and Sontheimer, PTPRJ 1993 and Thio et al., 1993), raising the question of whether channel expression is an artifact of culture. Importantly, however, astrocytes within slices of hippocampus, cerebral cortex, spinal cord, and cerebellum also express sodium currents (Sontheimer and Waxman, 1993, Chvátal et al., 1995 and Bordey and Sontheimer, 2000). Thus, expression of these

channels within astrocytes can occur within a relatively normal milieu and is not an artifact of culture. Further confirmation of this comes from immunocytochemical studies that have demonstrated the expression of sodium channels in astrocytes in situ within both the rodent (Black et al., 1994 and Black et al., 1998) and the human (Black et al., 2010) brain. The expression of sodium channels in nonexcitable cells is not static and, on the contrary, may change markedly depending on the developmental and/or physiological state of the cells. For instance, differentiation of cells of the oligodendrocyte lineage, from oligodendrocyte precursor cells (OPCs) to mature myelinating oligodendrocytes, is accompanied by switches in patterns of phenotypic expression (see Levine et al., 2001), including the downregulation of sodium channels (Paez et al., 2009). OPCs express robust voltage-sensitive sodium currents.

, 2012 and many others). To address how

the observed NAcc activity relates to potentially distinct approach behaviors, McGinty et al. (2013) provide an unconventional but illuminating comparison. Nicola (2010) previously reported that NAcc dopamine transmission is required to perform the “flexible approach” task (which is the focus of McGinty et al., 2013), but not to perform a different, “inflexible approach” task. On this “inflexible” task, NAcc neurons only weakly predicted approach response speed, and no prediction learn more of response latency was possible. As noted by McGinty et al. (2013), the striking contrast between NAcc activity on the flexible and inflexible approach tasks may help explain why other studies that have separated cue- and movement-related components report no link between NAcc activity and the vigor of subsequent movement (e.g., Goldstein et al., 2012). An important issue for further work would be to isolate the precise task difference(s) responsible for this contrast, for instance, by separating the number of possible approach starting locations from the (un)predictability

of the cue and the associated re-engagement with Tyrosine Kinase Inhibitor Library mw the task upon cue onset. Along those same lines, the amount of experience with the task, and its dependence on motivational state and instrumental contingencies, may shape differentially the extent of NAcc involvement on the two tasks. Either way, the findings of McGinty et al. (2013) and Nicola (2010) provide a productive way forward in the untangling of the role of the NAcc in motivated behavior. A different key question about the cue-evoked, movement-predicting NAcc activity concerns precisely what is encoded. Does this activity signal a single number, indicating the level of vigor, or is there more to it? The NAcc mediates the Asenapine influence of a number of so-called “decision variables” on behavior: these include quantities such as expected (subjective) value, delay, effort, and others (Tremblay et al., 2009). McGinty et al. (2013) identify proximity to the lever at the time of the cue as

an important determiner of NAcc activity, an observation potentially compatible with contributions from a number of decision variables, including subjective value, delay, and effort. Untangling these possible contributions will probably yield new insights into the neural basis of normal as well as dysfunctional motivated behavior. For instance, studies of relapse (reinstatement) of drug use indicate that, both in humans and rodents, cues previously paired with drug reward are powerful drivers of relapse (Kalivas and McFarland, 2003). A related direction for future work stems from the observation that the NAcc can direct behavior in settings with more than a single approach target. For instance, Flagel et al.

, 2005). We found that 92% of all YFP positive cells located in layer V of the cortex colabeled

with CTIP2 while there was no colabeling with the transcription factor SATB2, which is expressed exclusively by callosal projection neurons in the cortex SCH727965 ( Alcamo et al., 2008 and Britanova et al., 2008) ( Figure 2C). Collectively these findings suggest that Shh is expressed by a significant portion of subcortical projection neuron subtypes. Previous studies have shown that cortical Shh expression peaks approximately at the second postnatal week of development and is downregulated and maintained at a lower expression level in the adult cortex (Charytoniuk et al., 2002). This pattern coincides with the period of peak dendritogenesis and synaptogenesis in the mouse cerebral cortex (Micheva PD173074 nmr and Beaulieu, 1996). To assess Shh function in the developing cortex, we utilized a conditional loss of function approach by specifically removing Shh from cortical pyramidal neurons without affecting patterning and specification in the early developing nervous system (Ericson et al., 1995, Roelink et al., 1995, Xu et al., 2005 and Xu et al., 2010), by crossing animals with an Emx1-ires-Cre knocked into the Emx1

locus ( Gorski et al., 2002) with animals carrying a conditional null allele of Shh ( Dassule et al., 2000) (ShhcKO). ShhcKO mice are viable with Phloretin no gross defects in the patterning or morphology of the brain. While the gross morphology of the brain is indicative of normal patterns of proliferation, we chose to investigate the possibility of a more subtle phenotype. While cortical neurogenesis is nearly complete before birth, gliogenesis continues on through postnatal development ( Ivanova et al., 2003). To assess whether cortical Shh had any role in the production or survival of glial cells during early postnatal development,

we administered a pulse of BrdU between postnatal day 1 to postnatal day 3 (P1–P3) and examined the number of labeled cells in both the cortex and spinal cord ( Figures S2C–S2E). We observed no change in cell death or proliferation in the postnatal brain and spinal cord of ShhcKO animals. We also analyzed whether loss of cortical Shh had a cell autonomous effect on the formation or maintenance of corticospinal axonal projections and found no differences between the conditional mutants and control animals ( Figure S2A), indicating that cortical Shh did not play a significant role in the maintenance or survival of neurons or glia in these regions during this window of neural development. To assess the involvement of Shh in the regulation of neuronal growth and synaptogenesis, we performed Golgi analysis on P21–P28 brains of ShhcKO mice and wild-type control littermates ( Figures 3A–3D).

e. 12–18, >18–49 and >49 years old. Two doses of vaccine at 6.6–7.5 log EID50 were administered 21 days apart. Immune responses after 1 and 2 doses in volunteers aged >18–49 year old vaccinated with PLAIV are shown in Table 3. Based on the results of this study, the GPO filed a registration dossier with the TFDA in early December 2010 as the first live influenza vaccine produced in Thailand. It will also file a registration dossier for all other age groups under study

after completion of the clinical trials. The GPO PLAIV contains 7 log EID50 for nasal administration of 0.25 ml/nostril. It is a liquid formulation kept frozen at −20 °C and thawed just before use. While real time stability studies are in progress, the stabilizers used and recommended storage conditions show the vaccine Pomalidomide research buy to be stable for at least 14 weeks at both −20 °C and 2–8 °C. Following the clinical study of H1N1 PLAIV and based on the experience acquired, the GPO decided to initiate the development of an H5N2 LAIV to be used against H5N1 avian influenza, which is still a major threat in the region. This is in line with its strategic goal of pandemic preparedness. Ca/ts virus pre-master seed A/17/turkey/Turkey/05/133

(H5N2) was provided by IEM, Russia and the first lot of H5N2 LAIV Modulators concentrated bulk vaccine Sotrastaurin mouse was produced with a high yield of 9 log EID50/0.5 ml. The vaccine is currently undergoing non-clinical testing as well as Megestrol Acetate testing for genotype and phenotype. Samples of the GPO H5N2 vaccine have been sent to the National Institute for public Health and the Environment (RIVM) for testing in ferrets, and Phase I clinical trials are planned to start in early 2011. Due to its experience with registration of the H1N1 LAIV, the GPO hopes to be able to register H5N2 as the second LAIV within a shorter time

frame. In case of future pandemics, it is likely that the GPO’s total industrial-scale pandemic IIV capacity of 30 million doses would be inadequate. Therefore, following completion of the development of its H5N2 LAIV, the GPO plans to develop and market a seasonal LAIV. In this way, if and when a pandemic hits, the GPO will be able to produce both PLAIV and PIIV, the former for the general population and the PIIV for use in the general population as well as high-risk groups, principally pregnant women, the elderly and persons with chronic diseases. This will allow adequate supplies of pandemic vaccine for the whole population, and even those of neighbouring countries. The experience gained in the laboratory-scale production of seasonal IIV and the development of pandemic H1N1 and H5N2 vaccines has prepared the GPO for the next stage of the influenza vaccine project, i.e. to produce seasonal IIV at the pilot and industrial scale.

Demographic data, medical history of chronic

conditions, date of vaccination and type of vaccine were collected using a structured questionnaire. For the assessment of influenza vaccine effectiveness, children were defined as vaccinated if they had received at least one dose more than 14 days before symptom onset. An influenza-confirmatory laboratory test was carried out in all children. The virus was detected through nasopharyngeal sample collection; stable viral transport medium was added to swabs. Specimens were collected and analysed by using a real-time reverse transcriptase-polymerase chain reaction (RT-PCR). In six centres the tests were analysed in internal Modulators laboratories, whereas Abiraterone in vivo the others sent the specimens to certified external laboratories. The first phase of the study was performed

in the 2011–2012 influenza season and was used as a pilot study to refine the 2012–2013 investigation. In order to concentrate enrolment and laboratory tests in the epidemic period the coordinator centre gave the start-up on the basis of data on influenza epidemics in Italy provided from the National surveillance of ILI incidence [9]. The inclusion of children took place between 1 February and 31 March 2012 Cilengitide datasheet (for the 2011–2012 season), and between 14 January and 15 March 2013 (for the 2012–2013 season). The inclusion periods were the same for all centres. Data were analysed according to a test-negative case-control study design: all children with a positive confirmatory laboratory test (to one of the viruses contained in the seasonal vaccine) were included as cases, whereas controls were children with a negative test. For effectiveness evaluation, odds of influenza vaccination were compared in cases and controls. The following paediatric hospitals and departments over were participating: Giannina Gaslini Paediatric Hospital (Genova); Regina Margherita Paediatric Hospital (Torino); Department of Paediatrics, University of Padova; Paediatric Department, Treviso Hospital (Treviso); Anna Meyer Children’s University Hospital (Firenze); Department of Paediatrics,

University of Perugia; Pharmacology and Paediatrics and Developmental Neuroscience, Università Cattolica S. Cuore (Roma); Bambino Gesù Paediatric Hospital (Roma); Santobono-Pausilipon Paediatric Hospital-Virologic Unit Cotugno (Napoli); Giovanni Di Cristina Paediatric Hospital (Palermo); University Hospital of Messina. A common study protocol was approved by the Ethics Committee of each clinical centre. The study was coordinated by the National Centre of Epidemiology of the National Institute of Health in Rome. Data were analysed with SPSS (v. 21.0). T-test was used to compare means, Wilcoxon–Mann–Whitney non-parametric test was used to compare medians and Chi-square test was used to compare percentages. Adjusted odds ratios (ORs) and 95% confidence intervals (CI) were estimated through a logistic regression model.

In our experience, the likelihood of a for profit manufacturer willing SB431542 mouse to fund and support production of a whole cell Tv vaccine is low because the technology is simple but also difficult to obtain patent protection. Thus the potential

for developing and testing a simple and inexpensive vaccine is limited by the expense of development and testing which is not offset by the potential profitability either due to the lack of patent protection or the fact that the key market is in low resource countries. A subunit vaccine could be more appealing to a manufacturer as patents could be set in place on the formulation of the vaccine or the process to purify select antigens. However, these vaccines would cost more to produce and not be as easily widely distributed in low economic settings. Therein lies a struggle to produce a vaccine that is affordable, but also profitable. A potential medical breakthrough for the control of Tv lies in novel vaccine development. This goal will only be achieved if resources to fund the vaccine development and clinical testing are obtained from a not for profit organization oriented to improving disease control and burden, such as WHO or the Gates Foundation. Ideally a collaborative effort of researchers,

manufacturers, and charitable organizations learn more will be required to achieve this attainable goal of vaccine design, testing and production, and Modulators reduction of T. vaginalis burden in humans. There are no conflicts of interest to be declared. The authors alone are responsible for the views expressed in this article and do not necessarily represent the views, decisions or policies of the institutions

with which they are affiliated. “
“Cervical cancer is an important public health issue. In 2008, worldwide around 530,000 new cases of cervical cancer until were reported, and 275,000 deaths [1]. In 2004, 16,000 women still died in the European Union from this disease even with a screening programme in most countries [2]. In other parts of the world the incidence and mortality are much higher with cervical cancer ranking in the top five of causes of death in women [1]. HPV was recognized as the cause of cervical cancer in 1992 [3] and it was later confirmed that virtually all cervical cancers contain oncogenic human papillomavirus (HPV) DNA [4]. This led to the conclusion that HPV is a necessary factor in the initiation of cervical cancer with the highest worldwide attributable fraction ever identified for a specific cause of a major human cancer [5]. The main histological types of cervical cancer are squamous cell carcinoma (SCC) and adenocarcinoma, of which the first accounts for 90–95% of invasive cancer cases. The development of SCC is a multistage disease beginning with pre-invasive lesions, which may regress, persist or progress towards invasive cancer. Genital warts (condyloma acuminata) are attributed to non-oncogenic HPV types [6], [7] and [8].

9% versus 67.8%), the effect for those adhering to the exercise protocol might have been higher than confirmed by the published results. The authors did not describe in detail how often the exercises should be performed during the first week (‘20 min, 3 times a day’). However, based on the study protocol previously published (Bleakley et al 2007) we assume that the exercises were prescribed daily during the first week. For general practitioners, as well as sports physicians and physiotherapists, seeing patients with acute ankle sprains in the clinic, these findings emphasise the importance of prescribing exercises in combination with the PRICE protocol in the first week after

injury to optimise rehabilitation. However, the optimal dosage of treatment, including Talazoparib PRICE, choice of exercises, intensity and frequency of the exercise protocol, requires Libraries further investigation. “
“The Impact of Event Scale-Revised (IES-R) is a self-report measure of current subjective distress in response to see more a specific traumatic event (Weiss and Marmar 1997). The 22-item scale is comprised

of 3 subscales representative of the major symptom clusters of post-traumatic stress: intrusion, avoidance, and hyperarousal (American Psychiatric Association 1994). The intrusion subscale includes 8 items related to intrusive thoughts, nightmares, intrusive feelings, and imagery associated with the traumatic event. The avoidance subscale includes 8 items related to avoidance of feelings, situations, and ideas. The hyperarousal subscale includes 6 items related to difficulty concentrating, anger and irritability, psychophysiological arousal upon exposure to reminders Sitaxentan and hypervigilance. The IES-R is a revised version of the Impact of Event Scale (Horowitz 1979) and was developed as the original version did not include a hyperarousal subscale. IES-R responses were also modified so the client was requested to report on the degree of distress rather than the frequency of the symptoms. Instructions to the client and scoring: The IES-R

takes approximately 10 minutes to complete and score with no special training required to administer the questionnaire. The client is asked to report the degree of distress experienced for each item in the past 7 days. The 5 points on the scale are: 0 (not at all), 1 (a little bit), 2 (moderately), 3 (quite a bit), 4 = (extremely). The sum of the means of each subscale instead of raw sums is recommended ( Weiss and Marmar 1997). Thus, the scores for each subscale range from 0 to 4 and the maximum overall score possible is 12. There are no specific cut-off scores for the IES-R although higher scores are representative of greater distress. Increased overall scores on all subscales may indicate the need for further evaluation. Reliability, validity and sensitivity to change: Test-retest reliability (r = −0.89 to 0.94) and internal consistency (Chronbach’s α) for each subscale (intrusion = 0.87 to 0.94, avoidance = 0.84 to 0.

, 2006). We identified Sema6D mRNA enriched in the chiasm in the rostral and middle sectors of the chiasm midline, similar to Nr-CAM mRNA ( Lustig et al., 2001 and Williams et al., 2006) ( Figure 1A). Sema6D colocalizes with Nr-CAM in RC2+ radial glia at the chiasm midline from E13.5 to E17.5 ( Figures 1B and 1C), although Sema6D expression extends dorsally along the ventricular zone of the third ventricle ( Figure 1A). In the retina, Sema6D is restricted to the optic disc, resembling the expression pattern of EphA4 in glial

cells at the optic nerve head ( Petros et al., 2006) (see Figure S1A available online). Sema6A and Sema6C are expressed in the region dorsal and lateral to the supraoptic area of the ventral diencephalon and, thus, are not candidates for regulating midline crossing ( Figure S1A). Sema3A, Sema3B, and Sema3D mRNAs are not expressed at the chiasm midline ( Figure S1A). The only known receptors for Sema6D are Plexin-A1 CHIR99021 and Plexin-A4, and these receptors can function in axon guidance independent of neuropilins (Takegahara et al., 2006, Toyofuku et al., 2004 and Yoshida et al., 2006). Plexin-A1 is expressed in the CD44+/SSEA-1+

early-born neurons caudal to the chiasm and in two oval groups of SSEA-1− cells caudal and slightly dorsal to the chiasm (Figure S1C). A raphe of Plexin-A1+/SSEA-1+ neurons extends between the palisade of Nr-CAM+/Sema6D+ radial glia that expresses Nr-CAM+/Sema6D+ (Figure 1D). In summary, Sema6D is expressed in Nr-CAM+ radial glia at the chiasm midline, and its receptor Plexin-A1 is expressed in the CD44+/SSEA-1+ neurons caudal to and intersecting the selleck chemical chiasm radial glia (Figure 1E). These expression patterns raise the possibility that Sema6D, Plexin-A1, and Nr-CAM might be involved in guiding RGCs across the chiasm midline. To identify the potential contribution Sodium butyrate of Sema6D in RGC divergence at the optic chiasm, we made use of our in vitro culture assay of uncrossed VT or crossed dorsotemporal (DT) retinal explants on dissociated

chiasm cells (Figure S2A). In dissociated chiasm cell cultures, 50.6% of cultured chiasm cells are RC2+ cells, almost all of which express both Sema6D and Nr-CAM, and 36.7% of cells are SSEA-1+ neurons, almost all of which express Plexin-A1 (data not shown). Axons from both DT and VT explants grow extensively on laminin substrates. When grown on chiasm cells, neurite outgrowth from VT explants was reduced by 68%, whereas DT explant neurite outgrowth was reduced only by 25% (DT plus chiasm was 0.75 ± 0.02 versus VT plus chiasm 0.30 ± 0.02; p < 0.01) (Figures S2B and S2C). Thus, on chiasm cells, crossed RGCs extend longer neurites than uncrossed RGCs, reflecting their differential behavior at the midline in vivo. Nonetheless, neurite outgrowth from crossed RGCs is moderately decreased on chiasm cells, suggesting the presence of inhibitory factors intrinsic to chiasm cells that dampen the growth of crossed RGCs and must be overcome during RGC traverse of the midline.

In other words, PCDH17 is expressed along the anatomically Tyrosine Kinase Inhibitor Library connected corticobasal ganglia pathways in a highly topographic manner. Because protocadherin 10 (PCDH10), another δ2-protocadherin family member, is highly expressed in the striatum (Aoki et al., 2003), we next compared expression patterns of both of these proteins in basal ganglia. Double immunostaining of PCDH17 and PCDH10 showed that while PCDH17 is distributed in the anterior striatum, PCDH10 is distributed in the posterior striatum (Figure 2A). Therefore, expression of the two protocadherins

was complementary along the anteroposterior axis. Their distributions are also complementary in the LGP and MGP; PCDH17 displays an inner distribution, but PCDH10 displays an outer distribution within these regions (Figure 2A). Furthermore, in contrast to the distribution of PCDH17 in the posterior SNr, PCDH10 is distributed in the anterior SNr (Figure 2A). Double-fluorescent in situ hybridization demonstrated that both PCDH17 and PCDH10 mRNAs also exhibit complementary

expression patterns in basal ganglia ( Figure S2). Thus, these findings indicate that PCDH17 and PCDH10 delineate topographic features of this pathway. We next compared the protein expression patterns BMS-354825 nmr of PCDH17 and PCDH10 in the cerebral cortex and thalamus, particularly in the prefrontal cortex and the mediodorsal

thalamus, as these regions are anatomically and functionally incorporated into the corticobasal ganglia-thalamocortical loops (McCracken and Grace, 2009; McFarland and Haber, 2002). In the prefrontal cortex, while PCDH17 is distributed in the medial prefrontal cortex, PCDH10 expression is higher in the orbitofrontal cortex, indicating partially complementary expression patterns (Figure 2B). In subregions of the mediodorsal thalamus, PCDH17 and PCDH10 expression are also expressed in a somewhat complementary Astemizole manner (Figure 2C). Thus, expression of PCDH17 and PCDH10 are largely complementary throughout the corticobasal ganglia-thalamocortical loop circuits in a highly topographic manner. We note that expression of PCDH17 and PCDH10 partially overlaps in some cortical and thalamic areas, which could explain the presence of integrative and converging trans-circuits in these areas (Draganski et al., 2008). We examined the subcellular localization of PCDH17 in basal ganglia using high-resolution structured illumination microscopy (SIM) to acquire 3D images with resolution approaching 100 nm (Schermelleh et al., 2008). We performed immunostaining of PCDH17 in addition to VGLUT1 and PSD-95, markers of the pre- and postsynaptic compartments of corticostriatal excitatory synapses, respectively.

We compared blood oxygen level-dependent (BOLD) activity during the delay period in the Willpower task, in which subjects must continually resist the temptation to select the available SS, with activity during the delay period in the Choice task, in which the SS option was not available. Because we were interested in effective implementations of self-control, we restricted this analysis to trials with LL outcomes only, thus controlling for EGFR inhibitor reward anticipation and delivery across conditions. We expected to find brain regions that have been previously associated with inhibition of prepotent responses,

executive function, and self-control (McClure et al., 2004, McClure et al., 2007, Hare et al., 2009, Figner et al., 2010, Kober et al., 2010, Cohen et al., 2012, Essex et al., 2012 and Luo et al., 2012). Confirming our hypothesis, this analysis revealed significant activations in bilateral DLPFC (peak −50, 10, 32; t(19) = Dolutegravir 14.39, p < 0.001, whole-brain family-wise error [FWE] corrected), bilateral IFG (peak −44, 42, 10; t(19) = 6.44, p < 0.001, whole-brain FWE corrected), and bilateral PPC (peak −32, −52, 44; t(19) = 8.80, p < 0.001, whole-brain FWE corrected) when subjects actively resisted temptations (Figure 3; Table S2). Additional willpower-related activations were observed in the cerebellum, ventral striatum, insula, posterior cingulate cortex, and parahippocampal gyrus (p < 0.05 whole-brain FWE corrected;

Table S2). To investigate the neural correlates of precommitment, we compared BOLD activity at decision onset during binding LL decisions in the Precommitment task with activity at decision onset during nonbinding (but otherwise identical) LL decisions in the Opt-Out task. Again, we restricted

this analysis to choices with LL outcomes only, to control for reward anticipation across conditions. In line with our predictions, this analysis revealed activity in left and right LFPC (peak −34, 58, −8; t(19) = 4.74, p = 0.014, small-volume FWE corrected; Figure 4A and Table S3). We performed additional analyses to test the selectivity of LFPC activation to trials with opportunities to Org 27569 precommit. As in our previous analyses, we focused on trials in which subjects chose LL to control for reward anticipation across conditions. First, we investigated whether the LFPC showed sustained activation when subjects actively resisted temptations by extracting the Willpower contrast estimate from our region of interest (ROI) in LFPC (−34, 56, −8; Boorman et al., 2009). LFPC activation was not significantly different from zero when subjects actively resisted temptations (beta = 0.2653, SE = 0.4249, t(19) = 0.64, p = 0.5294; Figure 4B). Directly contrasting BOLD responses from Precommitment trials in which subjects chose to precommit, against BOLD responses from Willpower trials in which subjects actively resisted temptations, revealed a significant cluster in right LFPC (40, 56, −12; t(19) = 4.78, p = 0.