(1) Background: Currently, numerous qualitative research studies on food and its influence on health are being conducted. In qualitative research, data are obtained by analyzing participants\' responses. However, silence during conversation has been little studied. The aim of this study was to interpret the silences in the narratives of elderly people living alone about the potential risks of not keeping a healthy diet. (2) Methods: This is a descriptive and interpretative observational study under the qualitative research paradigm following a phenomenological and ethnographic perspective. The study was developed in two phases with people over 65 years old. In the first phase, from June 2021 to January 2022, 90 interviews, 12 life history analyses, 58 food diaries and 51 free listings (cultural domain technique) were conducted. In the second phase, from March to June 2022, 3 participatory workshops and 24 pile sorts (cultural domain technique) were conducted, as well as 3 focus groups. Only data from participants over 65 years old living alone are analyzed in this paper. The ATLAS-ti (Version 22) qualitative analysis software was used for coding and data analysis. (3) Results: The results show that elderly people living alone would sometimes remain silent during the various conversations conducted within the research. This silence reflects their desire to downplay the risks to their health from not eating well due to their unwanted loneliness. The people participating in our research had chronic health problems, financial insecurity and emotional problems. (4) Conclusions: We concluded that elderly people living alone are unable to maintain a healthy diet because they downplay their risk of malnutrition. This mindset is caused by their loneliness and bolstered by a situation of learned helplessness and social injustice.

In the last decade, activity-dependent strategies for labelling multiple immediate early gene (IEG) ensembles in mice have generated unprecedented insight into the mechanisms of memory encoding, storage, and retrieval. However, few strategies exist for brain-wide mapping of multiple ensembles, including their overlapping population, and none incorporate capabilities for downstream network analysis. Here, we introduce a scalable workflow to analyze traditionally coronally-sectioned datasets produced by activity-dependent tagging systems. Intrinsic to this pipeline is simple multi-ensemble atlas registration and statistical testing in R (SMARTR), an R package which wraps mapping capabilities with functions for statistical analysis and network visualization. We demonstrate the versatility of SMARTR by mapping the ensembles underlying the acquisition and expression of learned helplessness (LH), a robust stress model. Applying network analysis, we find that exposure to inescapable shock (IS), compared to context training (CT), results in decreased centrality of regions engaged in spatial and contextual processing and higher influence of regions involved in somatosensory and affective processing. During LH expression, the substantia nigra emerges as a highly influential region which shows a functional reversal following IS, indicating a possible regulatory function of motor activity during helplessness. We also report that IS results in a robust decrease in reactivation activity across a number of cortical, hippocampal, and amygdalar regions, indicating suppression of ensemble reactivation may be a neurobiological signature of LH. These results highlight the emergent insights uniquely garnered by applying our analysis approach to multiple ensemble datasets and demonstrate the strength of our workflow as a hypothesis-generating toolkit.

Fetal hypoxia and maternal stress frequently culminate in neuropsychiatric afflictions in life. To replicate this condition, we employed a model of prenatal severe hypoxia (PSH) during days 14-16 of rat gestation. Subsequently, both control and PSH rats at 3 months old were subjected to episodes of inescapable stress to induce learned helplessness (LH). The results of the open field test revealed an inclination towards depressive-like behavior in PSH rats. Following LH episodes, control (but not PSH) rats displayed significant anxiety. LH induced an increase in glucocorticoid receptor (GR) levels in extrahypothalamic brain structures, with enhanced nuclear translocation in the hippocampus (HPC) observed both in control and PSH rats. However, only control rats showed an increase in GR nuclear translocation in the amygdala (AMG). The decreased GR levels in the HPC of PSH rats correlated with elevated levels of hypothalamic corticotropin-releasing hormone (CRH) compared with the controls. However, LH resulted in a reduction of the CRH levels in PSH rats, aligning them with those of control rats, without affecting the latter. This study presents evidence that PSH leads to depressive-like behavior in rats, associated with alterations in the glucocorticoid system. Notably, these impairments also contribute to increased resistance to severe stressors.

TMP269, a class IIA histone deacetylase inhibitor with selectivity, that has a protective effect on the central nervous system, yet its specific mechanism of action remains ambiguous. Although major depressive disorder (MDD) is highly prevalent, its pathophysiology is poorly understood. Recent evidence suggests that histone deacetylase 5 plays a key role in the pathological process of depression and the fact that preclinical studies have shown HDAC5 to be a potential antidepressant target, the search for natural drugs or small molecule compounds that can target HDAC5 may be a potential therapeutic strategy for the treatment of depression. In addition, we examined the role of the Brain-derived neurotrophic factor (BDNF), an important neurotrophic factor for neuronal survival and growth, as a potential downstream target of HDAC5. We found downward revision of HDAC5 levels in the hippocampus ameliorated depressive-like behavior in LH (Learned helplessness) mice. Furthermore, injection of HDAC5 overexpressing adenoviral vectors in the hippocampal dentate gyrus of wild-type mice produced a somewhat depressive-like phenotype. Pharmacological, immunofluorescence and biochemical experiments showed that TMP269 could produce antidepressant effects by inhibiting mouse hippocampal HDAC5 and thus modulating its downstream BDNF. Over all, TMP269 mitigated LH-induced depressive-like behaviors and abnormalities in synapse formation and neurogenesis within the hippocampus. These findings suggest potential beneficial effects of TMP269 on depression.

The interactions between infants and caregivers are critical to infant development and caregiver well-being. Traditional developmental research has primarily emphasized the infant\'s development when studying infant-caregiver interactions, but a less commonly assessed feature of those interactions is the effect of the infant\'s crying on the caregiver\'s behavior. Using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) method (Moher et al., Public Library of Science Medicine, 6(7), e1000097, 2009), we conducted a systematic review of the literature evaluating the effects of crying on caregiver behavior. We searched for peer-reviewed articles in the Scopus and Web of Science Core Collection databases that included research studies in which researchers observed and manipulated infant crying and simultaneously measured features of caregiver behavior (actual or analogue). We used this body of literature to evaluate the existing evidence of the effects of crying on caregiver behavior, address the limitations and current gaps in our understanding of those interactions, and identify areas for future behavioral research.

UNASSIGNED: : Environmental deprivation, a type of childhood maltreatment, has been reported to constrain the cognitive developmental processes such as associative learning and implicit learning, which may lead to functional and morphological changes in the ventral pallidum (VP) and pessimism, a well-known cognitive feature of major depression. We examined whether neonatal isolation (NI) could influence the incidence of learned helplessness (LH) in a rat model mimicking the pessimism, and the number of vesicular glutamate transporter 2 (VGLUT2)-expressing VP cells and Penk-expressing VP cells.
UNASSIGNED: : The number of escape failures from foot-shocks in the LH test was measured to examine stress-induced depression-like behavior in rats. The number of VGLUT2-expressing VP cells and Penk-expressing VP cells was measured by immunohistochemistry.
UNASSIGNED: : In NI rats compared with Sham rats, the incidence of LH in adulthood was increased and VGLUT2-expressing VP cells but not Penk-expressing VP cells in adulthood were decreased. VGLUT2-expressing VP cells were decreased only in the LH group of NI rats and significantly correlated with the escape latency in the LH test.
UNASSIGNED: : These findings suggest that the aberrant VP neuronal activity due to environmental deprivation early in life leads to pessimistic associative and implicit learning. Modulating VP neuronal activity could be a novel therapeutic and preventive strategy for the patients with this specific pathophysiology.

UNASSIGNED: Learned helplessness (LH) is the psychological state in which an individual experiences multiple failures and setbacks and experiences a sense of loss when facing the current situation. It is a significant burden for lung cancer patients that can impair quality of life and lead to physical, social, and psychological difficulties. Thus, this study aimed to determine the level of LH among patients with lung cancer and identify factors associated with LH.
UNASSIGNED: From August 2022 to March 2023, 237 patients with lung cancer from Chongqing University Cancer Hospital were selected for this study. A general information questionnaire, the LH scale, the Brief Illness Perception questionnaire, the Strategies Used by People to Promote Health questionnaire, the Medical Coping Modes questionnaire, and the Self-esteem scale were used for the investigation. Multiple linear regression was employed to identify influencing factors for LH in patients with lung cancer.
UNASSIGNED: The total LH score of patients with lung cancer was 52.19±11.20. Multiple linear regression analysis showed that illness perception (β=0.249, P=0.001), self-efficacy (β=-0.194, P=0.017), and resignation coping mode (β=0.267, P<0.001) were the main influencing factors of LH (P<0.05), which explained 42.0% of the total variance.
UNASSIGNED: The score of LH in patients with lung cancer was at a moderate level in this study. Illness perception, self-efficacy, and resignation coping mode have been found to impact LH among patients with lung cancer. Healthcare professionals should implement effective interventions, such as promoting self-efficacy, encouraging positive coping, and reducing illness perception, to alleviate LH.

UNASSIGNED: To explore the predictive effect of effort-reward imbalance on students\' learning engagement and to elucidate the underlying mechanism, 796 students were selected for a survey.
UNASSIGNED: The participants were required to complete four scales: the Effort-reward Imbalance Scale, the Learning Engagement Scale, the Learned Helplessness Questionnaire, and the Perceived Social Support Scale.
UNASSIGNED: (1) Students\' effort-reward imbalance significantly and negatively predicts their learning engagement; (2) Learned helplessness serves as a mediator in the relationship between students\' effort-reward imbalance and learning engagement; (3) Social support plays a moderating role in the association between effort-reward imbalance and learned helplessness. High levels of social support can buffer the impact of an effort-reward imbalance on learned helplessness, and the protective effect of social support is more obvious when the effort-reward imbalance is low.
UNASSIGNED: The present study revealed how an effort-reward imbalance affects learning engagement among students through the dimensions of learned helplessness and perceived social support. The constructed model not only further clarifies the mechanism underlying the relationship between effort-reward imbalance and learning engagement but also holds significant implications for guiding students\' education.

BACKGROUND: Although findings from both animal and clinical research indicate that the blood-brain barrier (BBB) contributes to the pathogenesis of various psychiatric disorders (including depression), the underlying mechanisms are unknown. We investigated the levels of the tight-junction proteins claudin-5 and aquaporin-4 (AQP-4) in astrocytes of learned helplessness (LH) rats (an animal model of depression) and non-LH rats (a model of resilience).
METHODS: We administered inescapable mild electric shock to rats and then identified the LH and non-LH rats by a post-shock test. The expressions of claudin-5 and AQP-4 in several brain regions of the LH and non-LH rats were then evaluated by a western blot analysis.
RESULTS: The levels of both claudin-5 and AQP-4 in the CA-1 and CA-3 hippocampal areas of the LH group were significantly lower than those of the control group, whereas those of the non-LH rats were not significantly different from those of the control and LH rats.
CONCLUSIONS: These results suggest that LH rats but not non-LH rats experienced down-regulations of claudin-5 and AQP-4 in the CA-1 and CA-3. It is possible that a region-specific modulation of claudin-5 and AQP-4 is involved in the mechanisms of vulnerability but not resilience in depression.

BTRX-246040, a nociceptin/orphanin FQ peptide receptor antagonist, is being developed for the treatment of depressive patients. However, the underlying mechanism of this potential antidepressant is still largely unclear. Here, we studied the antidepressant-related actions of BTRX-246040 in the ventrolateral periaqueductal gray (vlPAG).
The tail suspension test, forced swim test, female urine sniffing test, sucrose preference test, and learned helplessness (LH) combined with pharmacological approaches were employed to examine the antidepressant-like effects and drug effects on LH-induced depressive-like behavior in C57BL/6J mice. Electrophysiological recordings in vlPAG neurons were used to study synaptic activity.
Intraperitoneal administration of BTRX-246040 produced antidepressant-like behavioral effects in a dose-dependent manner. Systemic BTRX-246040 (10 mg/kg) resulted in an increased frequency and amplitude of miniature excitatory postsynaptic currents (EPSCs) in the vlPAG. Moreover, slice perfusion of BTRX-246040 directly elevated the frequency and amplitude of miniature EPSCs and enhanced the evoked EPSCs in the vlPAG, which were blocked by pretreatment with the nociceptin/orphanin FQ peptide receptor agonist Ro 64-6198. In addition, intra-vlPAG application of BTRX-246040 produced antidepressant-like behavioral effects in a dose-dependent manner. Moreover, intra-vlPAG pretreatment with 6-cyano-7-nitroquinoxaline-2,3-dione reversed both systemic and local BTRX-246040-mediated antidepressant-like behavioral effects. Furthermore, both systemic and local BTRX-246040 decreased the LH phenotype and reduced LH-induced depressive-like behavior.
The results suggested that BTRX-246040 may act through the vlPAG to exert antidepressant-relevant actions. The present study provides new insight into a vlPAG-dependent mechanism underlying the antidepressant-like actions of BTRX-246040.