Emotion recognition and eye tracking of static and dynamic facial affect: A comparison of individuals with and without traumatic brain injury.

Diminished social functioning is often seen after traumatic brain injury (TBI). Mechanisms contributing to these deficits are poorly understood but thought to relate to impaired ability to recognize facial expressions. Static stimuli are often used to investigate ability post-TBI, and there is less evidence using more real-life dynamic stimuli. In addition, most studies rely on behavioral responses alone. The present study investigated the performance of a TBI group and matched non-TBI group on static and dynamic tasks using eye-tracking technology alongside behavioral measures. This is the first study to use eye tracking methodology alongside behavioral measures in emotion recognition tasks in people with brain injury. Eighteen individuals with heterogeneous TBI and 18 matched non-TBI participants were recruited. Stimuli representing six core emotions (Anger, Disgust, Fear, Happy, Sad, and Surprise faces) were selected from the Amsterdam Dynamic Facial Expression Set (ADFES). Participants were instructed to identify the emotion displayed correctly whilst eye movement metrics were recorded. RESULTS: Results of analyses showed that TBI patients had First Fixation to nose for all emotion stimuli, shorter Fixation Duration and lower Fixation Count to eyes, were generally slower to classify stimuli, and less accurate than non-TBI group for the static task. Those with TBI were also less accurate at identifying Angry, Disgust, and Fear stimulus faces compared to the non-TBI group during the dynamic unfolding of an emotion. CONCLUSION: In the present study, those with TBI had atypical eye scan patterns during emotion identification in the static emotion recognition task compared to the non-TBI group and were associated with lower identification accuracy on behavioral measures in both static and dynamic tasks. Findings suggest potential disruption to oculomotor systems vital for first stage perceptual processing. Arguably, these impairments may contribute to diminished social functioning.

The cooking task: making a meal of executive functions.

Current standardized neuropsychological tests may fail to accurately capture real-world executive deficits. We developed a computer-based Cooking Task (CT) assessment of executive functions and trialed the measure with a normative group before use with a head-injured population. Forty-six participants completed the computerized CT and subtests from standardized neuropsychological tasks, including the Tower and Sorting Tests of executive function from the Delis-Kaplan Executive Function System (D-KEFS) and the Cambridge prospective memory test (CAMPROMPT), in order to examine whether standardized executive function tasks, predicted performance on measurement indices from the CT. Findings showed that verbal comprehension, rule detection and prospective memory contributed to measures of prospective planning accuracy and strategy implementation of the CT. Results also showed that functions necessary for cooking efficacy differ as an effect of task demands (difficulty levels). Performance on rule detection, strategy implementation and flexible thinking executive function measures contributed to accuracy on the CT. These findings raise questions about the functions captured by present standardized tasks particularly at varying levels of difficulty and during dual-task performance. Our preliminary findings also indicate that CT measures can effectively distinguish between executive function and Full Scale IQ abilities. Results of the present study indicate that the CT shows promise as an ecologically valid measure of executive function for future use with a head-injured population and indexes selective executive function's captured by standardized tests.

Preoperative immunonutrition and its effect on postoperative outcomes in well-nourished and malnourished gastrointestinal surgery patients: a randomised controlled trial.

BACKGROUND/OBJECTIVES: Invasive procedures such as surgery cause immunosuppression, leading to increased risk of complications, infections and extended hospital stay. Emerging research around immune-enhancing nutrition supplements and their ability to reduce postoperative complications and reduce treatment costs is promising. This randomised controlled trial aims to examine the effect of preoperative immunonutrition supplementation on length of hospital stay (LOS), complications and treatment costs in both well-nourished and malnourished gastrointestinal surgery patients. SUBJECTS/METHODS: Ninety-five patients undergoing elective upper and lower gastrointestinal surgery were recruited. The treatment group (n=46) received a commercial immuno-enhancing supplement 5 days preoperatively. The control group (n=49) received no supplements. The primary outcome measure was LOS, and secondary outcome measures included complications and cost. RESULTS: A nonsignificant trend towards a shorter LOS within the treatment group was observed (7.1 ± 4.1 compared with 8.8 ± 6.5 days; P=0.11). For malnourished patients, this trend was greater with hospital stay reduced by 4 days (8.3 ± 3.5 vs 12.3 ± 9.5 days; P=0.21). Complications and unplanned intensive care admission rates were very low in both the groups. The average admission cost was reduced by AUD1576 in the treatment group compared with the control group (P=0.37). CONCLUSIONS: Preoperative immunonutrition therapy in gastrointestinal surgery has the potential to reduce the LOS and cost, with greater treatment benefit seen in malnourished patients; however, there is a need for additional research with greater patient numbers.

Investigating the 'latent' deficit hypothesis: age at time of head injury, implicit and executive functions and behavioral insight.

This study investigated the 'latent deficit' hypothesis in two groups of head-injured patients with predominantly frontal lesions, those injured prior to steep morphological and corresponding functional maturational periods for frontal networks (28 years. The latent deficit hypothesis proposes that early injuries produce enduring cognitive deficits manifest later in the lifespan with graver consequences for behavior than adult injuries, particularly after frontal pathology (Eslinger, Grattan, Damasio & Damasio, 1992). Implicit and executive deficits both contribute to behavioral insight after frontal head injury (Barker, Andrade, Romanowski, Morton, & Wasti, 2006). On the basis of morphological and behavioral data, we hypothesized that early injury would confer greater vulnerability to impairment on tasks associated with frontal regions than later injury. Patients completed experimental tasks of implicit cognition, executive function measures and the DEX measure of behavioral insight (Behavioral Assessment of the Dysexecutive Syndrome: Wilson, Alderman, Burgess, Emslie, & Evans, 1996). The Early Injury group were more impaired on implicit cognition tasks compared to controls that Late Injury patients. There were no marked group differences on most executive function measures. Executive ability only contributed to behavioral awareness in the Early Injury Group. Findings showed that age at injury moderates the relationship between executive and implicit cognition and behavioral insight and that early injuries result in long-standing deficits to functions associated with frontal regions partially supporting the latent deficit hypothesis.

Implicit cognition is impaired and dissociable in a head-injured group with executive deficits.

Implicit or non-conscious cognition is traditionally assumed to be robust to pathology but Gomez-Beldarrain et al. recently showed deficits on a single implicit task after head injury. Laboratory research suggests that implicit processes dissociate. This study therefore examined implicit cognition in 20 head-injured patients and age- and IQ-matched controls using a battery of four implicit cognition tasks: a serial reaction time task (SRT), mere exposure effect task, automatic stereotype activation and hidden co-variation detection. Patients were assessed on an extensive neuropsychological battery, and MRI scanned. Inclusion criteria included impairment on at least one measure of executive function. The patient group was impaired relative to the control group on all the implicit cognition tasks except automatic stereotype activation. Effect size analyses using the control mean and standard deviation for reference showed further dissociations across patients and across implicit tasks. Patients impaired on implicit tasks had more cognitive deficits overall than those unimpaired, and a larger dysexecutive self/other discrepancy (DEX) score suggesting greater behavioural problems. Performance on the SRT task correlated with a composite measure of executive function. Head injury thus produced heterogeneous impairments in the implicit acquisition of new information. Implicit activation of existing knowledge structures appeared intact. Impairments in implicit cognition and executive function may interact to produce dysfunctional behaviour after head injury. Future comparisons of implicit and explicit cognition should use several measures of each function, to ensure that they measure the latent variable of interest.

Impaired implicit cognition with intact executive function after extensive bilateral prefrontal pathology: a case study.

LR has extensive bilateral pathology to prefrontal cortices after head injury and marked changes to interpersonal and social behavior relative to his premorbid state. WAIS scores revealed intact IQ at superior levels, equivalent to premorbid ability as measured by the NART. LR performed at normal levels on a battery of executive function tasks, as did eight age- and IQ-matched controls. However, he showed impaired implicit learning on a serial reaction time task, and performed differently from controls on a mere exposure effect task. This case supports claims that implicit cognition may underpin some aspects of normal social functioning.

Quality of relationships and structural properties of social support networks of female survivors of abuse.

The purposes of this study were to examine the structural properties of the social support networks of female survivors of violence and abuse and to investigate the quality of the relationship, and specific level of satisfaction, survivors have with their social support networks. Participants averaged 5.8 persons in their social support networks. Their levels of satisfaction with the emotional, practical, financial, guidance, and socializing support they received from members of their social support networks were higher with respect to close friends and coworkers than with respect to family members and professionals (e.g., attorneys and social workers). The most common type of support provided by close friends who were themselves victims of abuse was emotional, guidance, and socializing support, and the most satisfying support was the financial and practical help that came from parents or family. An interesting finding was the significant presence of men in the survivors' social support networks. Overall satisfaction with the quality of support from the social support networks was high, and satisfaction with support from men was comparable, if not higher, than support from women. Multiple regression models revealed that satisfaction with support networks was a potent predictor of self-esteem, emotional health, and loneliness. Intimacy, especially in terms of exclusiveness and trust or loyalty, with at least a few members of the support network contributed significantly to the variance in self-esteem, emotional health, and loneliness among the abused women. The size of the support network also emerged as a limited contributor to well-being. Implications and applications are discussed for professionals working with female survivors of abuse.

Sex hormone modulation of serotonin-induced coronary vasodilation in isolated heart.

The present study was designed to evaluate the differences in the coronary vasodilator actions of serotonin (5-HT) in isolated heart obtained from naive or castrated male and female rats that were treated with either estrogen or testosterone. Hearts from 12 groups of rats were used: male and female naive animals, castrated, castrated and treated with 17beta-estradiol (0.5 microg kg(-1) day(-1)) for 7 or 30 days, and castrated and treated with testosterone (0.5 mg kg(-1) day(-1)) for 7 or 30 days. After treatment, the vascular reactivity of the coronary bed was evaluated. Baseline coronary perfusion pressure (CPP) was determined and dose-response curves to 5-HT were generated. Baseline CPP differed between male (70 +/- 6 mmHg, N = 10) and female (115 +/- 6 mmHg, N = 12) naive rats. Maximal 5-HT-induced coronary vasodilation was higher (P<0.05) in naive female than in naive male rats. In both sexes, 5-HT produced endothelium-dependent coronary vasodilation. After castration, there was no significant difference in baseline CPP between hearts obtained from male and female rats (75 +/- 7 mmHg, N = 8, and 83 +/- 5 mmHg, N = 8, respectively). Castration reduced the 5-HT-induced maximal vasodilation in female and male rats (P<0.05). Estrogen treatment of castrated female rats restored (P<0.05) the vascular reactivity. In castrated male rats, 30 days of estrogen treatment increased (P<0.05) the responsiveness to 5-HT. The endothelium-dependent coronary vasodilator actions of 5-HT are greater in female rats and are modulated by estrogen. A knowledge of the mechanism of action of estrogen on coronary arteries could aid in the development of new therapeutic strategies and potentially decrease the incidence of cardiovascular disease in both sexes.

Sex hormone modulation of serotonin-induced coronary vasodilation in isolated heart

The present study was designed to evaluate the differences in the coronary vasodilator actions of serotonin (5-HT) in isolated heart obtained from naive or castrated male and female rats that were treated with either estrogen or testosterone. Hearts from 12 groups of rats were used: male and female naive animals, castrated, castrated and treated with 17ß-estradiol (0.5 æg kg-1 day-1) for 7 or 30 days, and castrated and treated with testosterone (0.5 mg kg-1 day-1) for 7 or 30 days. After treatment, the vascular reactivity of the coronary bed was evaluated. Baseline coronary perfusion pressure (CPP) was determined and dose-response curves to 5-HT were generated. Baseline CPP differed between male (70 Ý 6 mmHg, N = 10) and female (115 Ý 6 mmHg, N = 12) naive rats. Maximal 5-HT-induced coronary vasodilation was higher (P<0.05) in naive female than in naive male rats. In both sexes, 5-HT produced endothelium-dependent coronary vasodilation. After castration, there was no significant difference in baseline CPP between hearts obtained from male and female rats (75 Ý 7 mmHg, N = 8, and 83 Ý 5 mmHg, N = 8, respectively). Castration reduced the 5-HT-induced maximal vasodilation in female and male rats (P<0.05). Estrogen treatment of castrated female rats restored (P<0.05) the vascular reactivity. In castrated male rats, 30 days of estrogen treatment increased (P<0.05) the responsiveness to 5-HT. The endothelium-dependent coronary vasodilator actions of 5-HT are greater in female rats and are modulated by estrogen. A knowledge of the mechanism of action of estrogen on coronary arteries could aid in the development of new therapeutic strategies and potentially decrease the incidence of cardiovascular disease in both sexes

Acute pressor actions of ouabain do not enhance the actions of phenylephrine or norepinephrine in anesthetized rats.

The inhibition of high-affinity isoforms of the Na+,K+-ATPase by nanomolar levels of ouabain has been proposed to enhance the actions of vasoconstrictor agents that act via a Ca+2-dependent mechanism. The present study tested this hypothesis by evaluating the effects of ouabain (6 and 18 microg/kg, i.v.) on the vasopressor actions of phenylephrine and norepinephrine in anesthetized, reflex-blocked rats. In separate groups of animals, dose-response curves for increases in diastolic pressure produced by phenylephrine were generated after the administration of saline (control), ouabain (18 microg/kg), L-omega-N-nitro arginine methyl ester (L-NAME, 3 micromol/kg) and angiotensin II (15 ng/kg per min). Treatment with ouabain (18 microg/kg) produced an increase in diastolic pressure of 19+/-3 mm Hg but did not significantly alter the potency or maximal response produced by phenylephrine. In contrast, treatment with angiotensin II and L-NAME, agents known to enhance the actions of alpha-adrenoceptor agonists, increased the potency of phenylephrine. In animals in which the pressor actions of norepinephrine were evaluated before and after the administration of ouabain (6 microg/kg), ouabain did not alter the pressor response to norepinephrine. Blockade of alpha-adrenoceptors with phentolamine was found to attenuate as well as partially reverse the increase in diastolic pressure produced by ouabain. These observations suggest that ouabain produces a pressor response by actions on sympathetic nerve endings as well as on vascular smooth muscle and that these actions do not alter the sensitivity to phenylephrine or norepinephrine.

The effect of acute ethanol exposure on the chronotropic and inotropic function of the rat right atrium.

Consumption of ethanol (CH2CH3OH), both acutely and chronically, is known to affect cardiac function and may alter the autonomic control of the heart. This study investigated the effects of two modes of acute exposure to ethanol on the chronotropy and inotropy of the rat right atrium with emphasis on alterations in the adrenergic responses. Atria from rats infused with an anesthetizing level of ethanol for 21 h showed a tendency for a greater increase of the unstimulated beating rate with isoproterenol (ISO), while both unstimulated inotropy and the inotropic response to ISO were significantly decreased compared with the control. Right atria in the presence of ethanol in-vitro demonstrated decreased basal active tension development and decreased inotropic responses to ISO. No alteration of the chronotropic response to ISO was evident with any concentration of ethanol. These results demonstrate both an immediate as well as a persistent effect of ethanol on right atrial chronotropy and inotropy. Alterations in the G-stimulatory subunit of the adenylate cyclase system and alterations in myofilament binding of Ca2+ are consistent with these observed ethanol effects.

Cocaine metabolism in hyperthermic patients with excited delirium.

The half-life of cocaine in clinical experiments has been reported to range from 60 to 90 min. It has been previously suggested that elevated temperature may accelerate the metabolism of cocaine. However, there is no clinical data to indicate the presence of hyperthermia like that seen in excited delirium alters the half-life of cocaine. We report the results of half-life determinations from serial cocaine concentrations in two patients with excited delirium. Both patients presented to the emergency department with classic findings of excited delirium that included hyperthermia, agitation, and cardiovascular aberrations. One patient died despite aggressive therapeutic intervention. Cocaine and metabolite concentrations were determined by an extractive alkylation mass spectrometry procedure. Presenting cocaine concentrations in patient 1 and patient 2 were 0.387 and 0.266 mg/L respectively. Results from pharmacokinetic modeling of the serial concentrations show that the half-life of cocaine was not significantly accelerated, despite the presence of hyperthermia. Data from these two cases provide further evidence that catastrophic reactions to cocaine are independent of amount or route of administration, and that the metabolism of cocaine, at least in these patients, was not altered by hyperthermia.

Long-term nitric oxide inhibition and chronotropic responses in rat isolated right atria.

The long-term administration of nitric oxide synthesis inhibitors induces arterial hypertension accompanied by left ventricular hypertrophy and myocardial ischemic lesions. Because the enhancement of sympathetic drive has been implicated in these phenomena, the current study was performed to determine the potency of beta-adrenoceptor agonists and muscarinic agonists on the spontaneous rate of isolated right atria from rats given long-term treatment with the nitric oxide inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME). Atrial lesions induced by long-term treatment with L-NAME were also evaluated. Long-term L-NAME treatment caused a time-dependent, significant (P<0.05) increase in tail-cuff pressure compared with control animals. Our results showed that the potency of isoproterenol, norepinephrine, carbachol, and pilocarpine in isolated right atria from rats given long-term treatment with L-NAME for 7, 15, 30, and 60 days was not affected as compared with control animals. Addition of L-NAME in vitro (100 microl/L) affected neither basal rate nor chronotropic response for isoproterenol and norepinephrine in rat heart. Stereological analysis of the right atria at 15 and 30 days revealed a significant increase on amount of fibrous tissues in L-NAME-treated groups (27+/-2.3% and 28+/-1.3% for 15 and 30 days, respectively; P<0.05) as compared with the control group (22+/-1.1%). Our results indicate that nitric oxide does not to interfere with beta-adrenoceptor-mediated and muscarinic receptor-mediated chronotropic responses.

Inhibition of nitric oxide synthase causes profound enhancement of the Bezold-Jarisch reflex.

The Bezold-Jarisch reflex function was evaluated in rats made hypertensive by the chronic oral intake of a nitric oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME, averaging 35 mg/kg/day), for 3, 6, and 12 days (n = 9/group) and in untreated control rats (CR, n = 9/group). L-NAME-treated rats showed a marked hypertension (MAP: 148 +/- 3, 182 +/- 4, and 179 +/- 4 mm Hg, respectively) compared with CR (110 +/- 2 mm Hg). The 6- and 12-day groups showed tachycardia (447 +/- 20 and 466 +/- 13 beats/min, respectively) when compared with CR (355 +/- 10 beats/min). When compared with CR, left ventricular hypertrophy was observed in rats treated with L-NAME for 6 and 12 days. The Bezold-Jarisch reflex, a decrease in heart rate (HR) accompanied by a decrease in diastolic arterial pressure (DAP), was evoked in a dose dependent manner by the intravenous injection of 5-hydroxytryptamine (5-HT, 5 to 10 microg/kg). Relative to responses observed in CR, 5-HT at 10 microg/kg caused a four- to fivefold greater decrease in HR and a two- to threefold greater decrease in DAP in all the L-NAME treatment groups. Using a Langendorff technique, we observed a significant increase in the responsiveness of the pacemaker to acetylcholine (1.25 to 80 microg/mL). These data suggest that the pharmacological inhibition of the nitric oxide synthase causes profound changes in the mechanisms of cardiovascular regulation as shown by a marked enhancement of the Bezold-Jarisch reflex in L-NAME-treated rats. The enhancement of this reflex seems to be in great part due to the hyperresponsiveness of the cardiac pacemaker to cholinergic stimulation.

Sino-aortic denervation causes right atrial beta adrenoceptor down-regulation.

Rat isolated right atria obtained 1 wk after sinoaortic denervation were less sensitive to the chronotropic actions of beta-agonists than were tissues obtained from animals that underwent sham surgery or no surgery at all. The potencies, but not the maximal responses for two high efficacy agonists, norepinephrine and isoproterenol, were reduced about 3- to 4-fold. Sino-aortic denervation (SAD) caused about a 3-fold decrease in potency and about a 60% decrease in maximal response for a low efficacy agonist, prenalterol. The changes in the actions of these agonists occurred in the absence of any changes in the subtype of beta receptor mediating the chronotropic response. The results of analyses of the data for prenalterol showed that SAD caused a decrease in the operational efficacy of this agonist without any changes in its KD value for beta-1 adrenoceptors. SAD had no effect on the responses of the tissue to blockade of uptake 1 and uptake 2, suggesting no compensatory changes in the removal processes caused the decreased potency. The results of radioligand binding assays showed that SAD caused a decrease in the maximal binding of 125I-cyanopindolol without altering its KD. Also, the results of competition binding assays confirmed the lack of effect of SAD on the KD for prenalterol. The SAD-induced changes in the actions of agonists acting at right atrial beta-1 receptors were caused by a down-regulation of beta-1 adrenoceptors, which probably occurred in response to SAD-induced increases in sympathetic tone.

Characterization of the antinociceptive properties of cimetidine and a structural analog.

The antinociceptive and pharmacological properties of the H2 receptor antagonist cimetidine and a novel cimetidine analog, SKF92374, were characterized. On both the hot-plate and tail-flick nociceptive tests, cimetidine and SKF92374 induced complete, dose-related analgesic responses when injected into the lateral ventricle of rats. SKF92374 showed strong similarities to cimetidine in analgesic efficacy, slope of dose-response curves and chemical structure, suggesting that these compounds share a common analgesic mechanism. In contrast, histamine induced submaximal antinociceptive effects, and the H3 antagonist thioperamide, a known HA-releasing drug, had little or no analgesic effects. Compared with cimetidine, SKF92374 showed very weak activity (400-fold lower affinity) on H2 receptors in vitro (isolated guinea pig atrium) and in vivo (rat gastric secretion). In addition, SKF92374 (100 microM) had neither agonist nor antagonist action on guinea pig ileum H1 receptors. SKF92374 was also a weak competitive antagonist of N alpha-methylhistamine-induced inhibition of electrically induced contractions of the guinea pig ileum (Kd = 5.2 microM), an H3 receptor-mediated response. Autoradiographic binding assays in guinea pig brain confirmed a weak antagonism of H3 receptors by SKF92374. The compound (up to 10 microM) also had no effect on unpurified rat brain histamine N-methyltransferase activity. These results support the hypothesis that cimetidine induces analgesia by a novel brain mechanism unrelated to H1, H2 or H3 receptors.

Effect of short-term treatment with gastrin and related peptides on gastrointestinal histamine H2-receptors.

The effects of short-term, 7-day, treatment with synthetic 15-leucine human gastrin I, pentagastrin or sulfated cholecystokinin-8 on the activity of histamine (HA)-stimulated adenylate cyclase in membranes isolated from guinea pig gastric mucosa and H2-receptor-mediated contractions of isolated ilea were evaluated. Treatment with each of the peptides produced a decrease in the maximal rate of HA-stimulated adenylate cyclase. The decreases in the maximal rate occurred without any effect on the potency of HA or any effect on basal rates of activity. In animals treated with pentagastrin, but not with cholecystokinin octapeptide sulfate, the contractile activity of dimaprit, a selective H2-agonist, was decreased. In animals treated with pentagastrin, the contractile actions of pentagastrin on isolated ileal preparations were increased. A 7-day treatment with the H2-antagonist, tiotidine, did not alter the potency of or the maximal response for HA-stimulated adenylate cyclase activity. Co-treatment with tiotidine prevented the effects of pentagastrin on gastric mucosal HA-stimulated adenylate cyclase. Treatment with pentagastrin did not alter the sensitivity of the gastric mucosal H2-receptor to inhibition by tiotidine. The effects of treatment with gastrin on NaF-stimulated adenylate cyclase activity also were determined. Treatment with gastrin did not alter the actions of NaF, suggesting that the coupling between the Gs subunit and the catalytic subunit of adenylate cyclase was not altered.(ABSTRACT TRUNCATED AT 250 WORDS)

Supersensitivity and changes in the active population of beta adrenoceptors in rat right atria in early sepsis.

We have investigated the effect of sepsis induced by cecal ligation and puncture on the chronotropic actions of beta adrenoceptor agonists on isolated right atria. The present findings show that right atria obtained from rats in an early stage of sepsis were supersensitive to the chronotropic actions of the beta-agonists, isoproterenol (ISO), fenoterol (FEN) and prenalterol (PREN). The supersensitivity to the chronotropic actions of ISO and FEN was much greater than that which developed to PREN. The positive chronotropic actions of isobutylmethylxanthine and forskolin were not affected by sepsis. The receptor subtypes mediating the responses to ISO, FEN and PREN by control and septic right atria were characterized by functional assays using selective beta-1 and beta-2 antagonists. The results showed that the chronotropic response produced by all three agonists on right atria obtained from control rats were mediated by beta-1 receptors. In contrast, the chronotropic actions of ISO and FEN on atria from septic rats were mediated by what appears to be beta-2 receptors and those of PREN by beta-1 receptors.