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MDL-WIS-PA-000005 REV 15 000005 REV 00 AD 01. • Activation energy from polarization resistance 100 25°C Span 200°C Span 0.75. The beta-hCG assay is a two-site immunoenzymatic 'sandwhich' immunoassay. A sample is added to a reaction vessel with anti-beta-hCG-alkaline phosphatase conjugate, and paramagnetic particles coated with goat- anti-mouse IgG mouse monoclonal anti-beta-hCG complexes. The serum hCG binds to the immobilized monoclonal anti-beta-hCG on the solid phase while, at the same time, the rabbit anti-beta-hCG-alkaline phosphatase conjugate reacts with different antigenic sites on the serum hCG. Separation in a magnetic field and washing removes material not bound to the solid phase. What type of reaction is this? Empathic responses underlie our ability to share emotions and sensations with others. We investigated whether observed pupil size modulates our perception of other's emotional expressions and examined the central mechanisms modulated by incidental perception of pupil size in emotional facial expressions. We show that diminishing pupil size enhances ratings of emotional intensity and valence for sad, but not happy, angry or neutral facial expressions. This effect was associated with modulation of neural activity within cortical and subcortical regions implicated in social cognition. In an identical context, we show that the observed pupil size was mirrored by the observers' own pupil size. This empathetic contagion engaged the brainstem pupillary control nuclei (Edinger-Westphal) in proportion to individual subject's sensitivity to this effect. These findings provide evidence that perception-action mechanisms extend to non-volitional operations of the autonomic nervous system. Empathic responses underlie our ability to share emotions and sensations with others. We investigated whether observed pupil size modulates our perception of other's emotional expressions and examined the central mechanisms modulated by incidental perception of pupil size in emotional facial expressions. We show that diminishing pupil size enhances ratings of emotional intensity and valence for sad, but not happy, angry or neutral facial expressions. This effect was associated with modulation of neural activity within cortical and subcortical regions implicated in social cognition. In an identical context, we show that the observed pupil size was mirrored by the observers’ own pupil size. This empathetic contagion engaged the brainstem pupillary control nuclei (Edinger–Westphal) in proportion to individual subject's sensitivity to this effect. These findings provide evidence that perception–action mechanisms extend to non-volitional operations of the autonomic nervous system. Human society operates through cohesive social relationships between individuals. A characteristic feature of our social interactions is the ability to understand other people's mental and emotional states. In parallel, humans have a tendency to mimic the body postures, gesticulations (Kendon, ), emotional facial expressions (Dimberg et al., ) and elements of speech, such as accents (Matarazzo and Wiens, ), of others. It is suggested that this tendency, typically occurring without conscious intent, facilitates emotional understanding across individuals, an ability encapsulated within the broader concept of empathy (Hatfield et al., ). Until recently the study of empathy lacked a convincing neurobiological substrate. ![]() However, the discovery of mirror neurons within the premotor cortex, which respond during performance and observation of the same action by a conspecific has provided a potential neural mechanism mediating how we understand other people's actions and intentions (di Pellegrino et al.,; Rizzolatti et al., ). Concurrent development and extension of action–perception models of motor behaviour and imitation (Prinz, ) to the domain of feelings and emotions (Preston and de Waal, ) suggest a common neural representation for the perception of actions and feelings in others and their experience in self, and provides the basis for a neuroscientific account of intersubjectivity (Gallese, ). Recent neuroimaging studies provide supporting evidence for action–perception models of empathy by showing shared neural activation when experiencing touch (Keysers et al.,; Blakemore et al., ), disgust (Wicker, ) and pain (Singer et al.,; Morrison et al.,; Jackson et al., ) in oneself and when perceiving these sensations and feelings in others. Common neuronal networks are also activated when subjects imitate or observe different emotional facial expressions (Carr et al., ). We investigated the role of pupil size in emotional perception and then interrogated our data to determine whether perception–action models and mimicry extend to a function that is exclusively mediated by the autonomic nervous system. Pupil size is sensitive to change in ambient light flux, but in addition, pupillary constriction occurs to other stimulus attributes such as onset of colour change, spatial structure or coherent movement (Barbur, ). These stimulus-specific pupil responses have a longer latency than a subcortical pupillary light reflex (240 vs 180 ms) and are likely to be mediated via cortical influences on the mid-brain, parasympathetic efferent, Edinger–Westphal nuclei (Wilhelm et al.,; Barbur, ). Conversely, pupil enlargement (reflex pupillary dilatation) occurs in tasks requiring either physical (lifting weights) or mental effort, including tasks with a high working memory load (Kahneman and Beatty, ). Emotional arousal, regardless of valence, is also believed to be reflected in the magnitude of pupillary dilatation (Hess and Polt,; Partala et al.,; Steinhauer and Hakerem, ), an effect exploited by Venetian women in the 17th century through the use of belladonna (meaning beautiful lady) eye drops. We used face stimuli with different emotional expressions and pupil sizes to address the following questions: First, does incidental observation of varying pupil size modulate our perception and judgment of another's emotional state? Second, if so, what are the neural structures associated with this modulation? Third, does the observer's own pupil size, change as a function of perceived pupil size, and in particular is there evidence for pupillary contagion? Finally, if such a mechanism is proposed, how is it instantiated neurally? We addressed the first question in a behavioural study in which subjects were asked to rate a series of emotional facial expressions on three dimensions, how positive or negative the emotional expression appeared, the perceived intensity of the emotion and the attractiveness of the face. Responses were made using a visual analogue scale. Picture stimuli representing 20 different facial identities depicting expressions of happiness, sadness, anger and neutrality were used. These were manipulated in terms of pupil size, to produce a series of 320 images with pupil areas 64, 80, 100 and 180% of the original. The latter three questions were addressed in a combined fMRI and pupillometry study. A second group of subjects were shown the same emotional facial stimuli as used in the behavioural study. Importantly, there was no difference between average luminosities of the stimuli across pupil size for any emotional expression. Each emotional facial expression was displayed centrally for 500 ms, and subjects were asked to judge the subject's age (older or younger than 25 years). We tested whether linearly varying pupil size in the context of different facial expressions was associated with correlated changes in regional neural activity. Using each individual subject's pupillometry data, we then assessed whether an observer's own pupil size was modulated by observed pupil size in the facial expressions and, in particular, whether there was mirroring of response, indicating ‘pupillary contagion’. An index of each individual's sensitivity to pupillary contagion was then determined and used as a regressor to determine brain regions where activity correlated with this effect. Subjects The participants in the behavioural study were 31 healthy subjects [23 female, mean age (±s.d.) 26.1 (±6.9) years]. Three subjects were left handed, all had normal or corrected to normal vision and none had a history of trauma or surgery to the eye. One subject had a history of depression and was treated with venlafaxine 150 mg at the time of the study. All other subjects were, excluding the oral contraceptive, medication free with no history of neurological or psychiatric illness. Participants for the imaging study were 15 healthy subjects [8 females, mean age (±s.d.) 22.0 (±3.5) years]. All were right handed, had normal or corrected vision, no structural brain abnormality and no past neurological or psychiatric history. All subjects bar one denied drug use within the last 6 months. The outstanding subject smoked cannabis intermittently and had last smoked it 2 weeks prior to scanning. Informed consent was obtained in accordance with the declaration of Helsinki (), and the procedures were approved by the Joint Ethics Committee of the National Hospital and Institute of Neurology, London. Subjects were recruited from a database and given a small financial reimbursement for their involvement in the study. Stimuli and behavioural data analysis Stimuli for both studies were colour photographs of happy, sad, angry and neutral faces of 10 male and 10 female identities taken from the Karolinska Directed Emotional Faces Set (KDEF, Lundqvist D., Flykt A. And Ohman A.; Department of Neurosciences, Karolinska Hospital, Stockholm, Sweden, 1998). Pupil areas were measured, and replica images of pupils 64, 80, 100 and 180% of the area of the original produced using Adobe® Photoshop® were made. Brightness and contrast were manipulated using Photoshop® to ensure that pupils were clearly visible in all images while ensuring that the images remained naturalistic. Brightness and contrast manipulations were identical across pupil sizes for each facial identity and emotional expression. Luminosity of the images was measured with a Ganzfeld device fitted to a Minolta CS-100A chromameter. Average luminosity did not differ across pupil size [mean (s.d.) 2.02 (0.24) cd/m 2] and there was no interaction between emotion and pupil size [ANOVA F(3, 316) = 0.001, P = 1.000]. In the behavioural study, the images were presented in a 400 × 400 pixel array on a 21′′ Sony GDM-F520 CRT, performed in a dark, sound-proofed experimental room. Ratings of emotional intensity, negativity or positivity and attractiveness were obtained sequentially for each face, emotion, and pupil size combination using a mouse-controlled cursor on a visual analogue scale displayed on the screen. Images were shown in random order with each facial identity, emotion and pupil size combination shown once. Images remained on the screen until each of the dimensions had been rated. Subjects took between 30 and 65 min to complete the task, which was broken by three short breaks. All subjects described feeling fatigued in the final session and a minority in the last two sessions. To ensure that ratings were not influenced by fatigue only ratings for the first two-thirds of faces presented were subsequently analysed. Mean ratings for each emotion–pupil combination were determined for each subject and used in second-level repeated-measures ANOVAs. In the imaging study, all faces were displayed in a 400 × 400 pixel array and back-projected onto a mirror mounted on the magnetic resonance imaging (MRI) head coil. Each face was shown centrally for 500 ms, followed by a central fixation cross at the level of the nasion on a grey background. The interstimulus interval was 3.0 s. Images were shown in random order with each facial identity, emotion and pupil size combination shown once (a total of 320 images with an additional 30 null events displayed as a grey 400 × 400 pixel array). Participants were asked to make an age judgment using a right-index-finger button-press for older than 25 years and a right-middle-finger button-press for younger than 25 years by using a button box held in the right hand. Tasks for both studies were written and presented, and behavioural responses logged via a desktop computer running Cogent software on a Matlab platform (Mathwork, Nantick MA). Two further short (. Physiological data recording and analysis Pupil diameter was monitored online throughout fMRI scanning by an infrared eye tracker (Applied Sciences Laboratories, Waltham MA, Model 504) recording at 60 Hz. Pupil recordings were analysed for each trial type separately (i.e. For each pupil size and emotion combination) using purpose written routines in Matlab. Subjects with greater than 50% signal loss during more than half of the trials in either the 500 ms prior to the initiation of the pupillary light response or the 500 ms following maximal pupillary constriction were rejected. Data for each of the remaining participants were then interpolated to 100 Hz and mean pupil size at all points during the interstimulus interval determined. Individuals’ mean pupil recordings during each trail type were normalized with respect to their overall mean pupil size during the 500 ms prior to stimulus onset. The effects of stimuli on participants’ pupil size were recorded during the 500 ms period following maximal pupillary constriction. Non-physiological recordings relating to blink responses, periods of non-fixation or poor signal during this period were identified and replaced with the individual's time-specific mean pupil size for that trial type. Individual's mean pupil size in the 500 ms time window following maximal pupillary constriction was determined for each trial. These values were mean normalized by subtracting individuals’ grand mean pupil size for this period across all trails and the resulting values combined across subjects and used in a repeated measure ANOVA. Behavioural ratings of emotional facial expressions Subjects rated facial expressions of sadness with small pupils as significantly more negative [repeated measures ANOVA, main effect of pupil size, F(3, 90) = 4.340, P = 0.007], with decreasing pupil size linearly modulating ratings of how negative the sad faces were perceived to be [ANOVA F(1, 30) = 11.05, P = 0.002]. Rating of emotional intensity also showed a trend in the same direction [repeated measures ANOVA F(3, 90) = 2.053, P = 0.11]. Contrast of the two extreme values, 64 and 180%, indeed showed that expressions of sadness with smaller pupils were also rated as significantly more intense [ F(1, 30) = 4.575, P = 0.041]. These effects were apparently implicit: at debriefing, subjects were unaware of the pupil manipulations even when directly prompted. Pupil size had no significant effect on ratings for any of the other emotions (). Interestingly, while women did not rate men with larger pupils as more attractive, there was a trend in this direction for the eight men's attractiveness ratings of women with happy expressions (repeated measures ANOVA contrast 64 vs 180% F(1, 39) = 2.85, P = 0.10). Imaging data Functional imaging datasets were analysed by SPM2 using the general linear model applied at each voxel across the whole brain. We examined how activity within different brain regions was modulated as a function of perceived pupil size in the context of each emotional expression. Specifically, we included parametric regressors reflecting observed pupil size for each emotional expression. We then tested for brain areas in which activity increased linearly with linearly decreasing pupil size for each expression. Pursuing our behavioural findings showing significant effects only for sad faces, we focused on observations relating to brain responses evoked during presentation of sad faces (details for observed changes for the other three emotions are given in ). Despite the very subtle change in the visual stimulus (the largest vs smallest pupil conditions represented a change in less than 0.1% of the total viewable area), presentation of smaller pupils in the context of sad facial expressions was associated with significantly greater neural activity in left amygdala, right and left superior temporal sulci, left frontal operculum, left insula and right dorsal anterior cingulate as well as right cerebellum and left primary visual cortex (, ). Interestingly, many of these brain regions are independently implicated in processing socially relevant stimuli (Brothers and Ring, ). This is consistent with the suggestion that the perception of pupil size in the context of sad facial expressions represents a highly salient social signal and engages brain regions underlying social cognition. Pupillometry data Pupillometry data were available for 9 of the 15 subjects recruited for the combined fMRI and pupillometry study. We computed correlations between the subjects’ own pupil response (evoked by each stimulus presentation) and the pupil size of the observed emotional face stimuli to determine if incidental processing of pupil size in another modulated the pupil size of the observer. Strikingly, we found that the observer's own pupil size was significantly smaller when viewing sad faces with small pupils than when viewing those with larger pupils [repeated measures ANOVA, main effect of observed pupil size, F(3, 24) = 5.04, P = 0.008]. The size of observers’ own pupil response also showed a significant linear relationship with the pupil size displayed on the sad face stimuli [ F(1, 8) = 27.22, P = 0.001]. These effects were most marked in the 500 ms period following maximal pupillary constriction induced by the light reflex. The timing of this peak is of interest in so far that this latency is consistent with evidence for higher order influences on the pupil mediated via inhibition of the Edinger–Westphal nuclei that are expressed at a latency of 600–800 ms and which persist while the stimulus is maintained (Steinhauer and Hakerem, ). Influences mediated via the direct sympathetic innervation of the dilator pupillae muscle occur with a much later peak latency of approximately 1200 ms. Furthermore, in high-ambient-light conditions, such as our study, tonic pupil size is decreased by high parasympathetic tone. In these conditions inhibitory influences on the Edinger–Westphal nuclei are believed to be the dominant mechanism through which higher order processes influence pupil size (Steinhauer and Hakerem, ). It is noteworthy that there was no effect of observed pupil size on the observers’ own pupil response when the subjects viewed neutral, happy or angry expressions (). Mechanism of observed pupillary contagion Finally, to explore the mechanism underlying the observed autonomic contagion for sad faces we examined the fMRI data in two further analyses. Previous studies highlight the action of cortical influences on the pupils through modulation of inhibitory input to the mid-brain Edinger–Westphal nuclei (Wilhelm et al.,; Barbur, ). We therefore tested for brain areas where activity correlated with a linear increase in pupil size for sad facial expressions to identify greater, presumed inhibitory, inputs to this mid-brain region. Notably, we observed enhanced neural activity in two symmetric regions within the mid-brain (, ) and also in the right angular gyrus. The mid-brain activity encompassed the Edinger–Westphal nuclei, which regulate parasympathetic efferents to the pupil. Again, no significant change was seen in either the mid-brain or parietal region in response to changes in observed pupil size depicted on happy, angry or neutral facial expressions. ( A) Mid-brain regions showing a significant correlation with linearly increasing pupil size in the context of expressions of sadness. Both regions shown are significant at P ≤ 0.001 uncorrected. All activations are shown overlaid. In addition, we wished to determine whether individual differences in sensitivity to pupillary contagion were associated with corresponding differences in brain activity across individuals. We therefore performed a between-subject analysis using indices of subjects’ individual sensitivity to pupillary contagion as a regressor of interest. This analysis also showed significant correlations with activity in many of the regions sensitive to observed pupil size, including left frontal operculum, amygdala and superior temporal sulcus (STS) () as well as a midline mid-brain region that lay within and between the mid-brain regions active in response to observed pupil size (, ). Furthermore correlational analysis of the peak voxel within this mid-brain region suggested that pupillary contagion may account for up to 80% of the between-subject variance in this region, thus supporting our contention that the mechanism for the mirrored change in pupil size involves the brainstem Edinger–Westphal nuclei. Interestingly this regression analysis across the whole brain also identified regions including an area close to the left intraparietal sulcus not observed in our earlier analysis. DISCUSSION In the present study, we demonstrate for the first time that perception–action mechanisms extend to non-volitional responses that engage the autonomic nervous system. Under conditions of normal room illumination, pupil size is predominately under the control of the parasympathetic Edinger–Westphal nuclei in order to optimize ambient lighting and stimulus luminance. The Edinger–Westphal nuclei are also implicated in mechanisms through which non-luminance attributes of visual stimuli, including spatial structure and colour transiently change pupillary responses (Wilhelm et al.,; Barbur, ). Higher cortical regions also modulate pupil size via the Edinger–Westphal nuclei, reflecting attributes including the informational value of a stimulus and task difficulty. Two mechanisms are implicated; a direct pathway via descending direct cortical inputs and an indirect pathway via ascending reticular inputs to the Edinger–Westphal nuclei (Steinhauer and Hakerem, ). Our findings extend these observations empirically by demonstrating a behaviourally selective adaptation of Edinger–Westphal responses in a social context and highlight a functional imitative mechanism contributing to social communication. We show that perceived pupil size is a selective and salient agent in social interaction influencing the vicarious understanding of expressed sadness and inducing a coherent modulation of the observer's own pupil size. Our findings highlight an involuntary, incidental processing and mimicry of pupil size in the context of sadness. It is noteworthy that the neural systems supporting this mechanism encompass cortical regions implicated in cognitive appraisal and detailed visual representation of social signals, the amygdala, a motivational or affective centre and brainstem autonomic nuclei. The cortex surrounding the STS is implicated in processing of socially meaningful postures and movements such as head position, eye gaze direction, lip reading, hand gestures and biological motion (Allison et al., ). Studies on theory of mind extend these findings to suggest that posterior STS is generally sensitive to stimuli that signal dispositions, agency or intentional activity (Frith and Frith, ). Additionally neuroimaging evidence suggests a role for the dorsal anterior cingulate in sympathetic arousal and generation of galvanic skin conductance responses (Critchley et al., ). It is interesting that we observed this region to be automatically engaged with decreases in pupil size (a parasympathetic effect) suggesting the possibility of an organ-specific patterned autonomic response. In a broader context, a discrete set of brain regions are implicated in social cognition including medial prefrontal cortex, STS and, critically, the amygdala (Brothers and Ring,, Kawashima et al., ). Damage to the amygdala in humans impairs social and empathic behaviour and also the explicit recognition of facial expressions of fear (Adolphs et al., ) and sadness (Adolphs and Tranel, ). Interestingly, recognition of fear may be enhanced by directing patients with amygdala damage to focus on the eyes (Adolphs et al., ). Our data suggest that a similar strategy may ameliorate acquired deficits in sadness perception. Interestingly, activity within left frontal operculum, an area not typically implicated in social cognition, also reflected pupillary size in the context of perceived sadness. This region, however, is activated during both performance and observation of actions in others (Grezes and Decety, ). Accordingly our observation suggests that the frontal operculum may contribute to empathic understanding of sadness through this mirror system. This contribution may be through either a direct influence of the motor mirror system on pupillary control centres or through an indirect route with activation of the mirror system because of an associated enhanced motor mimicry of the perceived facial expression. Thus, Carr and colleagues () found frontal operculum activity when subjects were instructed to either mimic emotional facial expressions or simply passively view them. Our regression analysis showing greater activity in the frontal operculum in individuals with higher pupillary contagion scores would support either of these proposed mechanisms. It is noteworthy that other regions including the cerebellum and right parietal lobe were also recruited in processing of pupillary effects related to sadness. While these regions are not typically included within the social brain network, the activation in our study may reflect the attentional tracking of the salient role of pupils in sadness processing. Further studies are needed to integrate fully these findings with lesion data reporting affective consequences following cerebellar or parietal damage (Adolphs et al.,; Schmahmann and Sherman, ). Over the variety of analyses performed consistent effects of pupil size were found only for expressions of sadness. Significant neural activity differences were observed for happy and angry (and, to a lesser extent, neutral) expressions, which are likely to arise from neural processing of different observed pupil sizes in these contexts. However, these effects did not extend to associated activity in pupil control centres and, as demonstrated in the separate behavioural experiment, are unlikely to have any meaningful impact on direct judgments of emotion intensity or valence. Further interpretation of the impact of this neural processing on other cognitive, behavioural and physiological functions was outside the scope of the experiment. Previous studies examining the contributions of specific facial features to the recognition of emotional expressions may inform this relative specificity. Visual scan path studies, for example, show that recognition of sad faces is associated with a greater number and duration of fixations to the eyes region when compared with recognition of happy facial expression, associated with a greater number of fixations around the mouth (Williams et al., ). Differentiation of Duchenne, or emotional smiles, from posed or non-emotional smiles, does involve fixations in the eye region. However, the focus is on the crow's feet area, lateral to that used in the recognition of sadness (Williams et al., ). Studies identifying salient facial feature information at multiple spatial scales using the ‘bubbles’ technique also support a central contribution of the eye to sadness recognition (Smith et al., ). The observation that β-adrenoreceptor blockade specifically impairs the recognition of sad facial expressions, but not the other basic emotions, links sadness perception to central and peripheral correlates of autonomic arousal responses (Harmer et al., ). Although not addressed within the present study, we anticipate an opposite effect of pupil size when processing fear. The saliency of the eye region to fear recognition is established (Adolphs et al., ), yet it remains uncertain if pupillary signals play a role in this. Nevertheless, lid retraction and facial pallor during the experience of fear indicate a marked enhancement of sympathetic facial responses, leading us to predict a likely association between perceived intensity of fear response and sympathetic pupillary dilatation. Together, this study provides the first evidence to support a role for the autonomic nervous system in perception–action models of empathy exemplified in the emotion of sadness. Our data suggest that incidental processing of pupil size when viewing faces with sad emotional expressions modulates the perceived intensity of the observed emotion and results in an empathic modulation of the observers’ own pupil size. Owing to the automaticity of pupillary reflexes, we predict that this is likely to be independent of conscious awareness of observed pupil size. Furthermore, observed pupil size modulates activity in brain regions that are central to social cognition and in regions implicated in the mirroring of others actions. We show that the mechanism for the mirrored change in pupil involves the brainstem parasympathetic Edinger–Westphal nuclei. Together these data identify the neural substrates through which automatic mirroring of another's autonomic pupil size may enhance empathic appraisal and understanding of their feelings of sadness. • Adolphs R, Tranel D. Impaired judgments of sadness but not happiness following bilateral amygdala damage. Journal of Cognitive Neuroscience. 2004; 16(3):453–62. [] • Adolphs R, Damasio H, Tranel D, Damasio AR. Cortical systems for the recognition of emotion in facial expressions. Journal of Neuroscience. 1996; 16(23):7678–87. [] • Adolphs R, Tranel D, Hamann S, Young AW, Calder AJ, Phelps EA, Anderson A, Lee GP, Damasio AR. Recognition of facial emotion in nine individuals with bilateral amygdala damage. 1999; 37:1111–7. [] • Adolphs R, Gosselin F, Buchanan TW, Tranel D, Schyns P, Damasio AR. A mechanism for impaired fear recognition after amygdala damage. 2005; 433:68–72. [] • Allison T, Puce A, McCarthy G. Social perception from visual cues: role of the STS region. Trends in Cognitive Neuroscience. 2000; 4(7):267–78. [] • Barbur JL. Learning from the pupil – studies of basic mechanisms and clinical applications. In: Chalupa LM, Werner JS, editors. The Visual Neurosciences. Cambridge, MA: MIT Press; 2004. • Blakemore SJ, Bristow D, Bird G, Frith C, Ward J. Somatosensory activations during the observation of touch and a case of vision-touch synaesthesia. 2005; 128:1571–83. [] • Brothers L, Ring B. Mesial temporal neurons in the macaque monkey with responses selective for aspects of social stimuli. Behavioural Brain Research. 1993; 57(1):53–61. [] • Carr L, Iacoboni M, Dubeau M-C, Mazziotta JC, Lenzi GL. Neural mechanisms of empathy in humans: a relay from neural systems for imitation to limbic areas. Proceedings at New York Academy Sciences. 2003; 100(9):5497–502. [] [] • Critchley HD, Elliott R, Mathias CJ, Dolan RJ. Neural activity relating to generation and representation of galvanic skin conductance responses: a functional magnetic resonance imaging study. Journal of Neuroscience. 2000; 20(8):3033–40. [] • Deichmann R, Gottfried JA, Hutton C, Turner R. Optimized EPI for fMRI studies of the orbitofrontal cortex. 2003; 19:430. [] • Dimberg U, Thunberg D, Elmehed K. Unconscious facial reactions to emotional facial expressions. Psychological Science. 2000; 11(1):86–9. [] • di Pellegrino G, Fadiga L, Fogassi L, Gallese V, Rizzolatti G. Understanding motor events: a neurophysiological study. Experimental Brain Research. 1992; 91(1):176–80. [] • Frith U, Frith CD. Development and neurophysiology of mentalizing. Philosophical Transactions of the Royal Society of London. Series B, Biological sciences. 2003; 358(1431):459–73. [] [] • Gallese V. The manifold nature of interpersonal relations: the quest for a common mechanism. Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences. 2003; 358(1431):517–28. [] [] • Grezes J, Decety J. Functional anatomy of execution, mental simulation, observation, and verb generation of actions: a meta-analysis. Human Brain Mapping. 2001; 12:1–19. [] • Harmer CJ, Perrett DI, Cowan PJ, Goodwin GM. Administration of the beta-adrenoceptor blocker propranolol impairs the processing of facial expressions of sadness. 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When you click the 'Go to Site' button you will have an opportunity to review and confirm the debit card features, terms and conditions. © 2017 Copyright Credit World Pty Ltd. All rights reserved. The DebitCards.com.au brand and logo are trademarks of Pixel Capital Pty Ltd. Operated by Credit World Ltd ABN 11 128 435 861, Australian Credit Licence Number 397589, Credit Ombudsman Service Number M0008295. ![]() Debit Card FAQ’s Can I use my Debit Card at ATMs that display the NYCE logo? Feel free to use your Debit Card at any location that displays the NYCE symbol. As of Nov 7th, 2012, our cards are part of the NYCE network (prior to this date, your card was part of the STAR network). ![]() If you have a STAR logo on your current card, you may continue to use it as normal. It will be accepted anywhere the NYCE logo appears. When the card expires, it will be replaced with a new card displaying the NYCE logo. Do I pay a fee for using a First Commonwealth ATM? No fee is charged to our Debit Card cardholders who use a First Commonwealth ATM. For a list of our ATM locations, simply Where am I permitted to use my Debit Card to make purchases? You can use your Debit Card at any of over 20 million merchants worldwide who display the MasterCard® logo. Do I pay a fee when I use my Debit Card to make purchases? No fee is charged to you for using the Debit Card to make purchases. However, when using your card internationally you may be assessed a cross border and/or a currency conversion fee from the MasterCard Network. These fees are passed through directly to the cardholder and are the cardholder's responsibility. Can I return items that I purchase with my Debit Card? Think of your Debit Card as another form of cash or check. If you need to return merchandise that was purchased with your Debit Card, go ahead! If given a choice by the merchant, should I select debit or credit when using my Debit Card? With the Debit Card, you can select either debit or credit. ![]() No matter which choice you make, the money will be deducted directly from your checking account balance. First Commonwealth suggests you select credit so that your transaction will be processed quickly through the MasterCard network. Simply sign your receipt and you’re on your way! What do I do if I lose my Debit Card? Immediately notify our Engagement Center at 1-800-711-BANK (2265). For after hours, please call our automated banking line at 1-888-711-BANK (2265) and select the option to report a lost or stolen card. How do I keep track of Debit Card purchases and transactions? You should always keep your receipts in a safe place until you are able to enter them into your checking account register. Also, your monthly checking account statement will list all your Debit Card transactions. Can I view my Debit Card purchases online? Simply enroll for Online Banking and view all your Debit Card activity online. Online Banking is free and enrollment only takes a few minutes. Can I use my Debit Card when I’m renting a car? Your Debit Card can be used when paying for your car rental expenses. However, most car rental companies will not accept a Debit Card when making a reservation or at reservation check-in counters. You should always contact your car rental company in advance for details. ![]() ![]() Ok so I have this new Astone UMPC. There are numerous touchscreen laptops in that price grade. In my Windows 10 tablet to activate USB TETHERING. Kills four birds with one stone. Of course what would be even better is a Galaxy Note 7 - especially with the above peripherals. It would be more bulky than just the tablet, but would eliminate a need for anything else. Not far off for that UMPC I've always wanted. Paul StJohn Mackintosh • 5 years ago. I have just upgraded the iPad to air navigation pro version 4.0 and I would just like to say it is absolutely brilliant. Easy to do a flight plan, easy to edit it, north up or track up, genuine UK flight map (£15.00 or so extra) Touch to edit the flight plan by dragging the line, awesome and for 23 quid, amazing. Astone UMPC Touchscreen LCD Laptop 60GB Wifi Webcam 0 results. You may also like. ![]() The first thing to do is to get the latest BIOS from Samsung, Version 20MA from. While on the site, also download the and Video drivers (same page) for Windows Vista, the only drivers I updated after installing Windows 7 as well as the ““, again for Windows Vista. The Easy Button Manager will allow you to use the four programmable keys in the dial on the right side of the device. The other application that I tested, the “Menu UI” loaded but didn’t work properly as it seems to be unable to talk to Windows 7. So don’t bother installing that one. I wasn’t interested in any of the other apps, so I left them out to begin with. Ratings based on results of the 2017 ConsumerLab.com Survey of Supplement Users. More information at *These statements have not been evaluated by the Food and Drug Administration. These products are not intended to diagnose, treat, cure or prevent any disease. For our website and catalog, the MSRP is the 'Manufacturer's Suggested Retail Price.' The MSRP is understood to mean the price at which a manufacturer will recommend a retailer sell a product for in stores, on the internet, or in catalogs. The MSRP of National brand items are dictated to Swanson by each manufacturer. For Swanson brand items, the MSRP is calculated based on a varying percentage above the product's base price. © 2017 Swanson Health Products – –. ![]() Testosterone supplement natural for women and older men, ways to increase low levels, herbal, vitamin Low T treatment, risks and side effects. Nutrition Tips to Boost Testosterone Naturally. Superfoods that support healthy levels of testosterone. To “Nutrition Tips to Boost Testosterone. ![]() ![]() I have a problem that I hope you can help. One of my patients recently purchased Transitions Flat top 28 plastic lenses, and she came back complaining that the lenses do not turn dark. I tested the lenses myself and the lenses will only turn to about 30% darkness even after few hours of exposure to the sun. I informed the lab of the problem and re-ordered the lenses; however the new lenses have the same problem. The patient is angry and I am not sure what to do. She had Transitions before and she knows and expects that the lenses should get much darker. Could anyone tell me why Transitions lenses would not turn dark? Would it be advisable to change the lenses to Sunsensors? Hello drpark111, At temps in the high 80's on non overcast days, the Transitions 1.50 Gray will darken to at least 20 to 25% Transmission. (75 to 80% tint depending on time of day, brightness of the sun). Between 11 and 2 are the brightest time of day, and UV is at its peak. Sometimes perception is the lens is not that dark. A quick way to demonstrate the change is to cover half of each lens with a post it note. Take them outside, activate them for a few minutes and peel off the post it. It is very dramatic to see how much the lens has changed. BTW, you do not have to leave a lens outside for extended periods to make it dark. After two or 3 minutes (on a normal day) the lens will darken to whatever the conditions at that time allow. Now, in mid winter when UV is low, extended time outside may darken the lens darker than in the intial few minutes but that is because the cold temps slow the chemical reaction. It may take 5 minutes or so to hit maximum darkness on cold, overcast winter days. Also, AR will not affect performance. If AR did affect the performance, you normally see a problem with the AR, it will have purple or red reflect in the normal green reflect. ![]() This is from a layer not having the proper thickness or somehow was put in out of order. It has been a while since I saw one of these. I hope this helps. “My patients are very interested in the new Transitions Vantage lenses but. Transitions line of performance sunwear. To activate the photochromic. ![]() Feel free to call if you have any questions. Best regards, Jim. EyeFitWell, Cold temps slow down the chemical reaction of uv darkening a lens. By that I mean the molecule is held longer in the open (or colored) position. The millions of molecules in a photochromic lens open and close rapidly, heat and cold affect the speed of the reactions. Whenever more molecules are in the open position, the darker the lens, heat up the lens and more molecules will be in the closed (or clear) position, the lens will not be as dark. This is part of what we call balance of properties. All putting a lens in a fridge will do is cause one activation cycle to be darker than normal. It will not make the lens darker than normal in future activations and that is the urban myth that went along with placing eyewear in the fridge (or freezer) Jim. EyeFitWell, Transitions and all other non glass/mineral photochromic lenses activate on their first exposure to UV light. There is no magic bullet. The performance on the first activation is as good as the UV index of the hour and day or the strength of the UV wavelength of a UV bulb if it is done in doors. If the lens is cold or colder than a lens at ambient temps, it will get darker, for that one performance cycle, that's it. It wont be jmped to a new dimension of performance. I visit many labs every year, I have yet to have a lab tell me they put Transitions in a freezer/refrigerator. Best regards, Jim. Hi Carrie, Transitions Optical does not or ever produced glass photochromic lenses.Corning was the originator of glass photochromics! I see you heat treated the glass product, this is for improving impact capabilities. I do not recall that this treatment kicked in the silver halide technology of glass (mineral) photochromic lenses. Whenever I ordered glass samples from Corning, I conditioned them by exposing them to full sunlight, then reversed the reaction placing them in a dark area until they were clear. If you have any questions about Transition lenses or what's right for you, please give us a call or leave a comment in the comments section below. Transition lenses are some of the most impressive lenses on the market, and millions of happy Transitions wearers come back for a new pair with every. Oct 11, 2008 About a year later my hubby got new glasses with the transition lenses and they did not tell him. To activate it just put them in the freezer over. Green-gray color when activated. Percent Transmission. With No-Glare Treatment. With No-Glare Treatment. Transitions XTRActive Lenses and Transitions VI Lenses—Clarity and Speed to Darkness. ![]() I did this several times. This conditioning did several things, mainly eliminated the yellow tinge of a spanking new blank and the lens performed closer to what a patient would experience in everyday tasks. I hope this helps. PicLens instantly transforms your browser into a full-screen, 3D experience for viewing images on the web. Photos will come to life via a cinematic presentation that goes well beyond the confines of the traditional browser window. With PicLens, browsing and viewing images on the web will never be the same again. Piclens works with a growing number of websites: Photo Sites • Flickr• Photobucket• Picasa Web Albums• deviantART• Smugmug Social Networking • Facebook• MySpace• Bebo• Hi5• Friendster Image Search • Google Images• Yahoo Images• Ask Images• Live Images• AOL Images. With version 1.00 you can have a second slideshow option: The great PicLens/Cooliris addon. You only need to activate the in your options. Click on 'View. Jun 26, 2007. Firefox plugin PicLens from Cooliris provides full screen immersive picture browsing of Flickr and other web sites that support Media RSS. To use PicLens, a. ![]() ![]() Oct 20, 2006 PicLens is a new photo viewing plug in from CoolIris. The tool lets user watch a full screen slide show of any photo series from Flickr, Photobucket. ![]() Backup and Restore Office 2016 Activation or Product Key After you install Microsoft Office 2016 and activate it, you may want to back up its activation or product key in case you need to reinstall Office 2016 in future. Now this post will show how to. • • Part 1: How to backup Office 2016 product key It’s very necessary to make a backup for the product key in case of loss. If you have a backup, then you won’t need to spend time or money to find or re-buy the product key when you need to use the key to reinstall or activate Office 2016 again. The product key typically contains 25 digits, which makes it hard to manually remember and write it down. Hence, to backup Office 2016 product key easily, you can use one specialized tool. Step 1: Get installed on your computer. Then launch it. Tips: The Product Key Finder is a specialized tool that can find and backup keys for various software products installed on computer. Step 2: Click on Start Recovery. Step 3: It will discover and list the product keys of all software currently installed on your computer, click on Save to File and save the keys in a notepad file for easier viewing. Step 4: Save the notepad which stores the keys in a safe place, such as on a flash drive, or on any cloud storage service. Part 2: How to backup and restore Office 2013/2016 activation Once you successfully, the activation info is stored on your local disk. However, system restallation or some other actions will wipe the activation info. Hence, you can backup the activation in advance so that you can simply restore it after you reinstall Office 2016, which can save you the bother of reactivation. To backup Office 2016 activation on Windows 10/8, just go to C: Windows System32 spp, and then copy and paste the store folder into a safe place. To restore the activation, do as follows Step 1: Make sure Office 2016 is installed. Close all open Office 2016 document. Step 2: Open Command Prompt as administrator. Type net stop sppsvc and hit Enter to stop the Software Protection Platform service. Step 3: Replace the original store folder with the backup store folder. ![]() Step 4: Open Command Prompt as administrator.Type net start sppsvc and hit Enter to start the Software Protection Platform service. Step 5: Open Office 2016 app, and it can be automatically activated. Considerations: 1. To order a backup disk for Office 2016 on a Windows PC. Provided you have a valid Office 2007 product key. Jun 23, 2013. I just installed and activated Office 2003. I got it second hand and it supposedly has never have been installed before, (with the product key on the CD case) but no way to tell. So I would like to be sure I can reinstall it if necessary and not be told it's been installed too many times, if I reinstall or buy a new. Jan 30, 2014. How to backup and restore activation for Office 2013, 2010, 2007, 2003 and XP. Ever since Microsoft introduced product. As long as have installed the same edition of Office, with the same product key, on the same edition of Windows, it can restore the activation. Backing up the activation from an edition of. The activation files only can be restored on the same computer. Windows system installed on the computer should has been activated. ![]() ![]() Got a strange one today. One of my customers had their PC die and because of the age it was not worth repairing so they bought a new box from us. I sold it with Windows 7 Pro but used the downgrade rights so that they could keep their existing XP Pro installation, which I transfered over from the old computer and updated Windows for the new hardware. Windows XP reactivated with no problems over the internet. Office 2003 however won't activate over the internet. It says that they have reached the limit of the number of times the product can be activated. This is normally not an issue as you activate by phone and tell the operater what's happened and they give you the activation code. ![]() ![]() This time however they seemed stumped and the system wasn't giving them an activation code. They said to uninstall and reinstall Office and try activate again. So I did this and got the same error when trying over the internet so called Microsoft again and had the same problem. This time they said DON'T try to activate over the internet, just call us back and we'll activate it for you. So again I did this but they were again stumped so got me to call Microsoft Support (0800 800 004). I did this and when I told them what I was trying to do they said they no longer support Office 2003 and activation won't work any more! Thanks Microsoft! Can anyone confirm if this is true and Office 2003 will no longer activate? The information below covers the Office 2003 Hack and more. Office 2003 Activation Hack. If you’re searching for the Office 2003 Hack, you have come to the right place! The information below covers the Office 2003 Hack and more. Office 2003 Activation Hack If you’re searching for the Office 2003 Hack, you have come to the right place! If you’re here looking for a way to crack Microsoft Office 2003 Product Registration, then you’re in the wrong place (unless you’re here to see if you’re safe from hackers! Look to your left and test yourself). We are simply providing instructions for the 2003 quick brown fox activation hack / Easter egg (type) which is in no way illegal. Office Hack for 2003 actually came from one of the coders said to be directly involved in creating office 2003. Microsoft is aware of the Office 2003 hack and according to Serial-Crack (specializes in Activation Hacks such as these) states that ‘This is by design and considered a product feature’. Rumor has it that this hack will also work on future versions of Microsoft Office. Serial-Crack reported ‘I thought I would get creative with the Activation Hack and changed a few numbers, I bumped the code to 2005,2006 and my system just stopped. It took me awhile, but I found that keeping the code at 200,99 worked great’ Fair warning here that running the Office 2003 Hack may slow down your system or your PC may become sluggish, but only during the activation process. Reports state that the 2003 Hack takes anywhere from a few seconds to two minutes depending on your processing speed. To execute the Office 2003 Hack, and this works with earlier versions as well, simply enter the code ‘= rand (200,99)’. See detailed hack code below. Office 2003 Activation Hack Instructions • Open a blank Word document • Type =rand(200,99) • Press Enter • Wait for 30 seconds. This Activation Hack will generate code / text and should complete within a few seconds. Serial-Crack refers to the code as the quick brown fox text. Speaking of Hacks – Have you been hacked but don’t know it? Copy this text into your clipboard: =rand(200,99) This is a private clipboard data test. Now follow the link to see if you’re giving away your personal information! If you see your clipboard data displayed on the next screen, then any website can view your clipboard data! Not good depending on what you copy and paste! Reader Interactions. 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