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Background: Previous studies of emotion recognition abilities of people with eating disorders used accuracy to identify performance deficits for these individuals. The current study examined eating disorder symptom severity as a function of emotion categorization abilities, using a visual cognition paradigm that offers insights into how emotional faces may be categorized, as opposed to just how well these faces are categorized., Methods: Undergraduate students (N = 87, 50 women, 34 men, 3 non-binary) completed the Bubbles task and a standard emotion categorization task, as well as a set of questionnaires assessing their eating disorder symptomology and comorbid disorders. We examined the relationship between visual information use (assessed via Bubbles) and eating disorder symptomology (EDDS) while controlling for anxiety (STAI), depression (BDI-II), alexithymia (TAS), and emotion regulation difficulties (DERS-sf)., Results: Overall visual information use (i.e. how well participants used facial features important for accurate emotion categorization) was not significantly related to eating disorder symptoms, despite producing interpretable patterns for each emotion category. Emotion categorization accuracy was also not related to eating disorder symptoms., Conclusions: Results from this study must be interpreted with caution, given the non-clinical sample. Future research may benefit from comparing visual information use in patients with an eating disorder and healthy controls, as well as employing designs focused on specific emotion categories, such as anger., (© 2024. The Author(s).)

Although it is well established that moderate-to-vigorous physical activity (MVPA) buffers against declines in cognitive health, less is known about the benefits of light physical activity (LPA). Research on the role of LPA is crucial to advancing behavioral interventions to improve late life health outcomes, including cognitive functioning, because this form of physical activity remains more feasible and amenable to change in old age. Our study examined the extent to which increases in LPA frequency protected against longitudinal declines in cognitive functioning and whether such a relationship becomes pronounced in old age when opportunities for MVPA are typically reduced. We analyzed 9-year data from the national Midlife in the United States Study (n = 2,229; M age = 56 years, range = 33-83; 56% female) using autoregressive models that assessed whether change in LPA frequency predicted corresponding changes in episodic memory and executive functioning in middle and later adulthood. Increases in LPA frequency predicted less decline in episodic memory (β = 0.06, p = .004) and executive functioning (β = 0.14, p < .001) over the 9-year follow-up period, even when controlling for moderate and vigorous physical activity. Effect sizes for moderate and vigorous physical activity were less than half that observed for LPA. Moderation models showed that, for episodic memory, the benefits of increases in LPA frequency were more pronounced at older ages. Findings suggest that increases in LPA over extended periods of time may help slow age-related cognitive declines, particularly in later life when opportunities for MVPA are often diminished., (© 2024. The Author(s).)

Napping benefits long-term memory formation and is a tool many individuals use to improve daytime functioning. Despite its potential advantages, approximately 47% of people in the United States eschew napping. The goal of this study was to determine whether people who endorse napping at least once a week (nap+) show differences in nap outcomes, including nap-dependent memory consolidation, compared with people who rarely or never nap (nap-). Additionally, we tested whether four weeks of nap practice or restriction would change sleep and performance profiles. Using a perceptual learning task, we found that napping enhanced performance to a greater degree in nap+ compared with nap- individuals (at baseline). Additionally, performance change was associated with different electrophysiological sleep features in each group. In the nap+ group, spindle density was positively correlated with performance improvement, an effect specific to spindles in the hemisphere contralateral to the trained visual field. In the nap- group, slow oscillatory power (0.5-1 Hz) was correlated with performance. Surprisingly, no changes to performance or brain activity during sleep emerged after four weeks of nap practice or restriction. These results suggest that individual differences may impact the potential benefits of napping on performance and the ability to become a better napper.

A beneficial effect of gesture on learning has been demonstrated in multiple domains, including mathematics, science, and foreign language vocabulary. However, because gesture is known to co-vary with other non-verbal behaviors, including eye gaze and prosody along with face, lip, and body movements, it is possible the beneficial effect of gesture is instead attributable to these other behaviors. We used a computer-generated animated pedagogical agent to control both verbal and non-verbal behavior. Children viewed lessons on mathematical equivalence in which an avatar either gestured or did not gesture, while eye gaze, head position, and lip movements remained identical across gesture conditions. Children who observed the gesturing avatar learned more, and they solved problems more quickly. Moreover, those children who learned were more likely to transfer and generalize their knowledge. These findings provide converging evidence that gesture facilitates math learning, and they reveal the potential for using technology to study non-verbal behavior in controlled experiments., (Copyright © 2016 Cognitive Science Society, Inc.)

Throughout history, psychologists and philosophers have proposed that good sleep benefits memory, yet current studies focusing on the relationship between traditionally reported sleep features (e.g., minutes in sleep stages) and changes in memory performance show contradictory findings. This discrepancy suggests that there are events occurring during sleep that have not yet been considered. The autonomic nervous system (ANS) shows strong variation across sleep stages. Also, increases in ANS activity during waking, as measured by heart rate variability (HRV), have been correlated with memory improvement. However, the role of ANS in sleep-dependent memory consolidation has never been examined. Here, we examined whether changes in cardiac ANS activity (HRV) during a daytime nap were related to performance on two memory conditions (Primed and Repeated) and a nonmemory control condition on the Remote Associates Test. In line with prior studies, we found sleep-dependent improvement in the Primed condition compared with the Quiet Wake control condition. Using regression analyses, we compared the proportion of variance in performance associated with traditionally reported sleep features (model 1) vs. sleep features and HRV during sleep (model 2). For both the Primed and Repeated conditions, model 2 (sleep + HRV) predicted performance significantly better (73% and 58% of variance explained, respectively) compared with model 1 (sleep only, 46% and 26% of variance explained, respectively). These findings present the first evidence, to our knowledge, that ANS activity may be one potential mechanism driving sleep-dependent plasticity.

Although previous research has shown personality and sleep are each substantial predictors of health throughout the lifespan, little is known about links between personality and healthy sleep patterns. This study examined Big Five personality traits and a range of factors related to sleep health in 436 university students (M(age) = 19.88, SD = 1.50, 50% Male). Valid self-report measures of personality, chronotype, sleep hygiene, sleep quality, and sleepiness were analyzed. To remove multicollinearity between personality factors, each sleep domain was regressed on relevant demographic and principal component-derived personality factors in multiple linear regressions. Results showed that low conscientiousness and high neuroticism were the best predictors of poor sleep (poor sleep hygiene, low sleep quality, and increased sleepiness), consistent with other research on predictors of poor health and mortality risk. In this first comprehensive study of the topic, the findings suggest that personality has a significant association with sleep health, and researchers could profitably examine both personality and sleep in models of health and well-being.

Background: Twenty-four hour ambulatory blood pressure thresholds have been defined for the diagnosis of mild hypertension but not for its treatment or for other blood pressure thresholds used in the diagnosis of moderate to severe hypertension. We aimed to derive age and sex related ambulatory blood pressure equivalents to clinic blood pressure thresholds for diagnosis and treatment of hypertension., Methods: We collated 24 hour ambulatory blood pressure data, recorded with validated devices, from 11 centres across six Australian states (n=8575). We used least product regression to assess the relation between these measurements and clinic blood pressure measured by trained staff and in a smaller cohort by doctors (n=1693)., Results: Mean age of participants was 56 years (SD 15) with mean body mass index 28.9 (5.5) and mean clinic systolic/diastolic blood pressure 142/82 mm Hg (19/12); 4626 (54%) were women. Average clinic measurements by trained staff were 6/3 mm Hg higher than daytime ambulatory blood pressure and 10/5 mm Hg higher than 24 hour blood pressure, but 9/7 mm Hg lower than clinic values measured by doctors. Daytime ambulatory equivalents derived from trained staff clinic measurements were 4/3 mm Hg less than the 140/90 mm Hg clinic threshold (lower limit of grade 1 hypertension), 2/2 mm Hg less than the 130/80 mm Hg threshold (target upper limit for patients with associated conditions), and 1/1 mm Hg less than the 125/75 mm Hg threshold. Equivalents were 1/2 mm Hg lower for women and 3/1 mm Hg lower in older people compared with the combined group., Conclusions: Our study provides daytime ambulatory blood pressure thresholds that are slightly lower than equivalent clinic values. Clinic blood pressure measurements taken by doctors were considerably higher than those taken by trained staff and therefore gave inappropriate estimates of ambulatory thresholds. These results provide a framework for the diagnosis and management of hypertension using ambulatory blood pressure values.

In this study we sought to determine whether early myocardial fibrosis is associated with depletion of vasoactive intestinal peptide (VIP) in the heart, thereby suggesting a possible pathogenetic role for depletion of myocardial VIP levels in the development of fibrosis in the heart. Spontaneously hypertensive rats (SHRs) and normotensive control Wistar-Kyoto rats (WKYs) were assigned randomly to low, intermediate or high sodium diets and their blood pressure was recorded twice weekly for 4 weeks. At the end of this period the rats were anaesthetised, blood was sampled for plasma VIP concentration and the hearts were harvested for histology and determination of the concentration of VIP in the heart. The degree of myocardial fibrosis increased with increasing dietary sodium intake in both the WKYs (P < 0.001) and the SHRs (P < 0.01). Myocardial VIP concentration decreased with increasing dietary sodium intake in the WKYs (P < 0.01) and in the SHRs (P < 0.01). There was a negative correlation between myocardial VIP concentration and the degree of myocardial fibrosis in both the WKYs (P < 0.0005) and the SHRs (P < 0.005). Dietary sodium intake induces myocardial fibrosis in a dose-dependent manner. Further, in early myocardial fibrosis resulting from increasing dietary sodium intake in both normotensive and hypertensive rats the concentration of VIP in the heart was negatively correlated with the degree of fibrosis. This suggests a possible role for depletion of VIP in the myocardium in the pathogenesis of myocardial fibrosis.

In the Dahl salt-sensitive hypertensive rat, a diet containing L-arginine, the natural substrate for nitric oxide synthase, abrogates the hypertension. We postulated that nitric oxide synthase inhibition might induce a salt-sensitive form of hypertension and that this salt sensitivity might be linked to a loss of the regulatory effect of sodium ingestion on angiotensin II (Ang II) and angiotensinogen. Male Wistar-Kyoto rats were randomised to a diet containing 0.008 %, 2.2 % or 4.4 % sodium chloride and to treatment with the NO synthase inhibitor L-NAME (10 mg kg(-1) day(-1)) in the drinking water, or drinking water alone (Controls) for 4 weeks. Blood pressure was measured by tail cuff plethysmography twice weekly. After 4 weeks, the rats were anaesthetised and truncal blood collected for determination of angiotensinogen, renin, angiotensin I (Ang I), Ang II and aldosterone concentrations as well as angiotensin-converting enzyme (ACE) activity. Systolic blood pressure increased with increasing dietary sodium intake in the L-NAME-treated rats (P < 0.05). Plasma renin and aldosterone concentrations decreased with increasing dietary sodium intake in both Control and L-NAME-treated rats. Ang I and ACE activity were unchanged by increasing dietary sodium intake. In contrast, the plasma concentration of Ang II and angiotensinogen increased with increasing dietary sodium (P < 0.05 and P < 0.005, respectively). Treatment with the Ang II receptor blocker, losartan, reversed the blood pressure increase. We conclude that treatment with L-NAME induces an increase in blood pressure that is at least in part salt sensitive. Further, the salt-sensitive component appears to be Ang II-dependent, as it was associated with increasing plasma Ang II levels and could be reversed by treatment with an Ang II receptor antagonist.

1. In view of previous observations that the metabolism of vasoactive intestinal peptide (VIP) is significantly increased in sodium-depleted rabbits, we wished to determine whether a high sodium intake also leads to alterations in VIP metabolism. We performed metabolic clearance studies in rabbits maintained on a high sodium diet and normal control diets. These studies were performed both before and after the administration of 1.5 mmol kg-1 of sodium intravenously to observe the effects of an acute increase in body sodium. 2. The rabbits maintained on the high sodium diet had a significantly lower basal plasma VIP level (P less than 0.025), a lower metabolic clearance rate (MCR) of the peptide (P less than 0.025) and a lower secretion rate (P less than 0.005), compared with the normal control animals. These differences were maintained following the intravenous sodium infusion. 3. The administration of the intravenous sodium infusion resulted in a further decrease in MCR in the rabbits on the high sodium diet (P less than 0.05). 4. These results confirm that VIP metabolism is affected by high dietary intake of sodium, as well as a low sodium intake, adding further support to the hypothesis that VIP may be involved in sodium homeostasis.

To determine whether vasoactive intestinal peptide (VIP) might act as a humoral mediator for a proposed portal or hepatic sodium monitor, we measured plasma VIP levels and urinary sodium excretion after portal and intravenous sodium loading in rabbits equilibrated on normal and low sodium diets. Sodium excretion was significantly less after intravenous (2 h: p less than 0.005; 4 h; p less than 0.005; 8 h; p less than 0.025) than after portal sodium administration in rabbit on a low-sodium diet. Plasma VIP levels fell after intravenous (p less than 0.005) but not after intraportal sodium in this group. To determine whether this fall in VIP levels reflected increased metabolism or decreased secretion, metabolic clearance studies were performed in rabbits on a low sodium diet. The metabolic clearance rate of VIP and its theoretical secretion rate increased after intravenous sodium loading in rabbits on a low salt diet (MCR, p less than 0.025; SR, p less than 0.05). We conclude, therefore, that in rabbits on a low-salt diet, intravenous sodium increases VIP metabolism, causing a decrease in plasma levels that may explain the difference in sodium excretion.

1. Reports that a greater natriuresis occurs after gastric rather than intravenous sodium loads suggest that a gastric sodium monitor exists which releases a humoral natriuretic factor. As vasoactive intestinal peptide (VIP) is natriuretic, it might act as this mediator. To determine whether it released from the gut in response to sodium we measured VIP levels in portal and systemic plasma of anaesthetized rabbits after a gastric sodium load. Levels of VIP in systemic plasma were also measured in conscious rabbits after gastric and portal sodium loads to determine the contributions of anaesthesia or increased sodium concentration in the portal tract to any observed rise in systemic VIP levels. 2. In the anaesthetized rabbit study portal and systemic VIP levels had both increased significantly from control values by 5 min after the sodium load in the low salt diet group (P less than 0.025, portal: P less than 0.05, systemic). By 10 min the levels in systemic and portal plasma were equal. 3. In the conscious rabbits an increase in systemic VIP levels was observed in the group on a low salt diet after a gastric but not a portal sodium load. 4. We conclude that VIP is released in response to gastric sodium loads in rabbits on low salt diets and that hepatic metabolism of VIP is reduced in this group.

1. Reports that gastric sodium loads cause a greater natriuresis than those administered intravenously, suggest that a gastric or portal sodium monitor exists which releases a humoral natriuretic factor. To determine whether cholecystokinin octapeptide (CCK-8) had direct renal natriuretic effects (and was therefore a candidate for this gut-derived natriuretic factor) we compared the natriuretic response to CCK-8 infused intravenously with that infused directly into the renal artery of six conscious male rabbits. 2. CCK-8 produced a significant log dose-dependent decrease in the fractional excretions of calcium (P less than 0.05) and magnesium (P less than 0.005) and a log dose-dependent increase in fractional sodium excretion (P less than 0.025). The significant decreases in the fractional excretions of calcium and magnesium were accompanied by log dose-dependent falls in their plasma levels (calcium, P less than 0.05, and magnesium, P less than 0.005), indicating movement of calcium and magnesium to extravascular sites. Studies of tissue calcium and magnesium levels in response to CCK-8 infusion showed that calcium accumulated in kidney and skeletal muscle. 3. We conclude that CCK-8 has direct renal natriuretic effects at the tubular level and could be the gut-derived natriuretic factor. In addition to its effects on sodium excretion, CCK-8 causes renal retention and increased gut absorption of calcium and magnesium with movement of these ions to extravascular sites.