The role of perceived negative partner behavior in daily snacking behavior: A dynamical systems approach.

Past work suggested that psychological stress, especially in the context of relationship stress, is associated with increased consumption of energy-dense food and when maintained for long periods of time, leads to adverse health consequences. Furthermore, this association is moderated by a variety of factors, including emotional over-eating style. That being said, few work utilized a dynamical system approach to understand the intraindividual and interindividual fluctuations within this process. The current study utilized a 14-day daily diary study, collected between January-March 2020, where participants reported their partner's negative relationship behavior and their own snacking behavior. A differential equation model was applied to the daily dairy data collected. Results showed that snacking behavior followed an undamped oscillator model while negative relationship behavior followed a damped coupled oscillator model. In other words, snacking behavior fluctuated around an equilibrium but was not coupled within dyadic partners. Negative relationship behavior fluctuated around an equilibrium and was amplified over time, coupled within dyadic partners. Furthermore, we found a two-fold association between negative relationship behavior and snacking: while the association between the displacement of negative relationship behavior and snacking was negative, change in negative relationship behavior and snacking were aligned. Thus, at any given time, one's snacking depends both on the amount of negative relationship behaviors one perceives and the dynamical state a dyad is engaging in (i.e., whether the negative relationship behavior is "exacerbating" or "resolving"). This former association was moderated by emotional over-eating style and the latter association was not. The current findings highlight the importance of examining dynamics within dyadic system and offers empirical and methodological insights for research in adult relationships.

Social Regulation of the Neural Threat Response Predicts Subsequent Markers of Physical Health.

OBJECTIVE: Social support has been linked to a vast range of beneficial health outcomes. However, the physiological mechanisms of social support are not well characterized. Drawing on functional magnetic resonance imaging and health-related outcome data, this study aimed to understand how neural measures of "yielding"-the reduction of brain activity during social support-moderate the link between social support and health. METHODS: We used a data set where 78 participants around the age of 24 years were exposed to the threat of shock when holding the hand of a partner. At ages 28 to 30 years, participants returned for a health visit where inflammatory activity and heart rate variability were recorded. RESULTS: Findings showed a significant interaction between dorsal anterior cingulate cortex-related yielding and perceived social support on C-reactive protein levels ( ß = -0.95, SE = 0.42, z = -2.24, p = .025, 95% confidence interval = -1.77 to -0.12). We also found a significant interaction between hypothalamus-related yielding and perceived social support on baseline heart rate variability ( ß = 0.51, SE = 0.23, z = 2.19, p = .028, 95% confidence interval = 0.05 to 0.97). CONCLUSIONS: Greater perceived social support was associated with lower C-reactive protein levels and greater baseline heart rate variability among individuals who were more likely to yield to social support in the dorsal anterior cingulate cortex and hypothalamus years earlier. The current study highlights the construct of yielding in the link between social support and physical health.

Surgery induces neurocognitive disorder via neuroinflammation and glymphatic dysfunction in middle-aged mice with brain lymphatic drainage impairment.

Background: Brain lymphatic drainage impairment is a prevalent characteristic in both aging and neurodegeneration. Surgery is more likely to induce excessive neuroinflammation and postoperative neurocognitive disorder (PND) among patients with aging and neurodegeneration. We hypothesized that surgical trauma may aggravate PND through preexisting cerebral lymphatic drainage impairment. However, there remains limited understanding about the role of surgery in changes of neurocognitive function in the populations with preoperative brain lymphatic drainage impairment. This study aims to expand our insight into surgery-induced glymphatic dysfunction, neuroinflammation and PND in middle-aged mice with preoperative brain lymphatic drainage impairment. Materials and methods: Deep cervical lymph nodes ligation (LdcLNs) was performed on middle-aged mice to establish preoperative brain lymphatic drainage impairment. A month later, laparotomy was performed on these mice with or without LdcLNs followed by analysis of brain neuroinflammation, glymphatic function, neuronal damage, and behavioral test. Results: LdcLNs disrupted meningeal lymphatic drainage. In middle-aged mice with LdcLNs, surgery exacerbated more serious glymphatic dysfunction accompanied by aggravation of A1 astrocytes activation and AQP4 depolarization. Furthermore, surgery caused neuronal damage via reducing expression of neuronal nuclei (NeuN), post-synaptic density protein 95 (PSD95) and synaptophysin (SYP), as well as impairment in exploratory behavior and spatial working memory in middle-aged mice with LdcLNs. Additionally, surgery induced neuroinflammation with elevated microglia activation and increased the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1ß and IL-6, as well as activated more expression of HMGB1/TLR-4/NF-κB pathway in middle-aged mice with LdcLNs. Conclusion: Surgery exacerbates neuroinflammation and glymphatic dysfunction, ultimately resulting in neuronal damage and neurocognitive disorder in middle-aged mice with preoperative brain lymphatic drainage impairment. These results suggest that brain lymphatic drainage impairment may be a deteriorating factor in the progression of PND, and restoring its function may serve as a potential strategy against PND.

Characterization of circRNA-Associated-ceRNA Networks Involved in the Pathogenesis of Postoperative Cognitive Dysfunction in Aging Mice.

Postoperative cognitive dysfunction (POCD) is a clinical entity associated with declined cognitive function following surgery. It occurs more frequently in elderly patients. Recent studies have shown that circRNA-associated-ceRNA networks, constructed based on interactions between circRNA-miRNA and miRNA-mRNA, provide key insight into the molecular mechanisms underlying the pathogenesis of several neurological diseases. However, the mechanism of POCD remains undetermined. In this study, laparotomies were performed under isoflurane anesthesia on young (2-month-old) and aging (17-month-old) male C57BL/6 mice. The results showed that the aging mice were more likely than the young mice to develop POCD. Subsequently, differentially expressed circRNAs, miRNAs, and mRNAs were characterized by RNA sequencing the hippocampi of young and aging mice under control and surgery conditions. Six circRNAs, 6 miRNAs, and 203 mRNAs were identified to construct the circRNA-associated-ceRNA network for the control condition, while 13 circRNAs, 8 miRNAs, and 189 mRNAs were used for the circRNA-associated-ceRNA network for the surgery condition. Further Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of these two networks revealed that the circRNA-associated-ceRNA networks are involved in POCD pathogenesis though modulating the Wnt and VEGF signaling pathways, as well as neural processes associated with long-term synaptic depression and synaptic transmission. In particular, the mmu-miR-298-5P regulatory pathway identified in this study's mouse model suggests that mm9_circ_009789- and mm9_circ_004229-associated-ceRNA networks as closely related to the occurrence of POCD through regulating PKC signaling pathway, neural cell apoptosis and glycolipid metabolism pathway. These findings provide possible insight into the role of the circRNA-associated-ceRNA networks, helping to unravel the complexity of the molecular pathogenesis of POCD.

Seeing no pain: Assessing the generalizability of racial bias in pain perception.

Racial disparities in pain care may stem, in part, from perceptual roots. It remains unresolved, however, whether this perceptual gap is driven by general deficits in intergroup emotion recognition, endorsement of specific racial stereotypes, or an interaction between the two. We conducted four experiments (total N = 635) assessing relationships between biases in pain perception and treatment and biases in the perception of anger, happiness, fear, and sadness. Participants saw Black and White male targets making increasingly painful and angry (Experiment 1), happy (Experiment 2), fearful (Experiment 3), or sad expressions (Experiment 4). The effect of target race consistently varied based on the emotion displayed. Participants repeatedly saw pain more readily on White (vs. Black) male faces. However, while participants also saw sadness less readily on Black faces, perception of anger, fear, and happiness did not vary by target race. Moreover, the tendency to see pain less readily on Black faces predicted similar differences in recognizing (particularly negative) expressions, though only racial bias in pain perception facilitated similar biases in treatment. Finally, while endorsement of racialized threat stereotypes facilitated recognition of angry expressions and was marginally associated with impeded recognition of happy expressions on Black faces, gaps in pain perception were not reliably related to stereotype endorsement. These data suggest that while racial bias in pain perception is associated with a general bias in recognizing negative emotion on Black male faces, the effects of target race on pain perception are particularly robust and have distinct consequences for gaps in treatment. (PsycInfo Database Record (c) 2021 APA, all rights reserved).

The Delaware Pain Database: a set of painful expressions and corresponding norming data.

INTRODUCTION: Facial expressions of pain serve an essential social function by communicating suffering and soliciting aid. Accurate visual perception of painful expressions is critical because the misperception of pain signals can have serious clinical and social consequences. Therefore, it is essential that researchers have access to high-quality, diverse databases of painful expressions to better understand accuracy and bias in pain perception. OBJECTIVES: This article describes the development of a large-scale face stimulus database focusing on expressions of pain. METHODS: We collected and normed a database of images of models posing painful facial expressions. We also characterized these stimuli in terms of the presence of a series of pain-relevant facial action units. In addition to our primary database of posed expressions, we provide a separate database of computer-rendered expressions of pain that may be applied to any neutral face photograph. RESULTS: The resulting database comprises 229 unique (and now publicly available) painful expressions. To the best of our knowledge, there are no existing databases of this size, quality, or diversity in terms of race, gender, and expression intensity. We provide evidence for the reliability of expressions and evaluations of pain within these stimuli, as well as a full characterization of this set along dimensions relevant to pain such as perceived status, strength, and dominance. Moreover, our second database complements the primary set in terms of experimental control and precision. CONCLUSION: These stimuli will facilitate reproducible research in both experimental and clinical domains into the mechanisms supporting accuracy and bias in pain perception and care.