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The ongoing Israel-Hamas war is posing additional challenges for mental health workers in an already stressful workplace. This study centres on the psychological effects of the shared traumatic reality on mental health workers, arising from the Israel-Hamas war. One month after exposure to the terrorist attack of 7 October 2023 and the outbreak of war following this event, 147 mental health workers completed questionnaires regarding a variety of variables such as demographics, anxiety symptoms, acute stress symptoms, media-induced secondary trauma, personal resilience, National resilience (NR), and post-traumatic growth (PTG). The study found that mental health workers with previous trauma displayed higher anxiety symptoms, acute stress symptoms, and media-induced secondary trauma. Additionally, acute stress and anxiety were positively correlated with media-induced secondary trauma. Religiosity, personal resilience, and NR were found associated with lower anxiety and acute stress symptoms. Religiosity was also positively correlated with personal resilience, NR, and PTG. The PTG of mental health workers working with trauma survivors and evacuees was higher compared to that of other mental health workers. Both adverse and adaptive reactions were evident among mental health workers. While traumatic stress is expected, individual, professional, and NR factors may mitigate its effects. Providing training, social support, regulated media exposure, stress management, and meaning-focused coping strategies can help safeguard workers' well-being.
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BACKGROUND: It is unclear how exposure to and perception of community trauma creates a mental health burden. This study aimed to examine the psychological distress trends among community residents in acute stress reaction, acute stress disorder, and post-traumatic stress disorder phases following the Seoul Halloween crowd crush. METHODS: A three-wave repeated cross-sectional survey was conducted with participants after the incident. Analysis of covariance (ANCOVA) with post hoc Bonferroni test was adopted to examine temporal changes in psychological distress and psychological outcomes resulting from media impacts. A two-way ANCOVA was adopted to examine the interaction effects of time and relevance to victims on psychological distress. RESULTS: A total of 807, 1,703, and 2,220 individuals participated in the three waves. Anxiety (estimated mean [standard error of the mean]: 2.28 [0.03] vs. 2.12 [0.02] vs. 2.03 [0.02]; P < 0.001), depression (2.22 [0.03] vs. 2.01 [0.02] vs. 1.90 [0.02]; P < 0.001), and anger (2.70 [0.03] vs. 2.66 [0.02] vs. 2.49 [0.02]; P < 0.001) gradually improved. However, sense of safety initially worsened and did not recover well (2.96 [0.03] vs. 2.75 [0.02] vs. 2.77 [0.02]; P < 0.001). The interaction effect of time and relevance to the victim were significant in depression (P for interaction = 0.049), anger (P for interaction = 0.016), and sense of safety (P for interaction = 0.004). Among participants unrelated to the victim, those exposed to graphics exhibited higher levels of anxiety (2.09 [0.02] vs. 1.87 [0.07]; P = 0.002), depression (1.99 [0.02] vs. 1.83 [0.07]; P = 0.020), and anger (2.71 [0.03] vs. 2.47 [0.08]; P = 0.003) at W2 and higher anger (2.49 [0.02] vs. 2.31 [0.06]; P = 0.005) at W3. CONCLUSION: Community residents indirectly exposed to trauma also experienced psychological distress in the early stages after the incident. A significant impact of media which might have served as a conduit for unfiltered graphics and rumors was also indicated.
Subject(s)
Anxiety , Depression , Stress Disorders, Post-Traumatic , Humans , Male , Female , Cross-Sectional Studies , Stress Disorders, Post-Traumatic/psychology , Stress Disorders, Post-Traumatic/epidemiology , Adult , Depression/epidemiology , Depression/psychology , Anxiety/epidemiology , Anxiety/psychology , Middle Aged , Psychological Distress , Surveys and Questionnaires , Seoul/epidemiology , Mass Media , Anger , Stress Disorders, Traumatic, Acute/psychology , Young Adult , Aged , Media ExposureABSTRACT
Acute Stress Disorder (ASD) is a psychiatric condition that can develop shortly after trauma exposure. Although molecular studies of ASD are only beginning, groups of metabolites have been found to be significantly altered with acute stress phenotypes in various pre-clinical and clinical studies. ASD implicated metabolites include amino acids (ß-hydroxybutyrate, glutamate, 5-aminovalerate, kynurenine and aspartate), ketone bodies (ß-hydroxybutyrate), lipids (cortisol, palmitoylethanomide, and N-palmitoyl taurine) and carbohydrates (glucose and mannose). Network and pathway analysis with the most prominent metabolites shows that Extracellular signal-regulated kinases and c-AMP response element binding (CREB) protein can be crucial players. After highlighting main recent findings on the role of metabolites in ASD, we will discuss potential future directions and challenges that need to be tackled. Overall, we aim to showcase that metabolomics present a promising opportunity to advance our understanding of ASD pathophysiology as well as the development of novel biomarkers and therapeutic targets.
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A single exposure to stress can induce functional changes in neurons, potentially leading to acute stress disorder or post-traumatic stress disorder. In this study, we used in vivo wide-field optical mapping to simultaneously measure neural calcium signals and hemodynamic responses over the whole cortical area. We found that cortical mapping to whisker stimuli was altered under acute stress conditions. In particular, callosal projections in the anterior cortex (primary/secondary motor, somatosensory forelimb cortex) relative to barrel field (S1BF) of somatosensory cortex were weakened. On the contrary, the projections in posterior cortex relative to S1BF were mostly unchanged or were only occasionally strengthened. In addition, changes in intra-cortical connection were opposite to those in inter-cortical connection. Thus, the S1BF connections to the anterior cortex were strengthened while those to the posterior cortex were weakened. This suggests that the well-known barrel cortex projection route was enhanced. In summary, our in vivo wide-field optical mapping study indicates that a single acute stress can impact whole-brain networks, affecting both neural and hemodynamic responses.
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Individuals might be exposed to intense acute stress while having to make decisions with far-reaching consequences. Acute stress impairs processes required for decision-making by activating different biological stress cascades that in turn affect the brain. By knowing which stress system, brain areas, and receptors are responsible for compromised decision-making processes, we can effectively find potential pharmaceutics that can prevent the deteriorating effects of acute stress. We used a systematic review procedure and found 44 articles providing information on this topic. Decision-making processes could be subdivided into 4 domains (cognitive, motivational, affective, and predictability) and could be referenced to specific brain areas, while mostly being impaired by molecules associated with the sympathetic-adrenal-medullar and hypothalamic-pituitary-adrenal axes. Potential drugs to alleviate these effects included α1 and ß adrenoceptor antagonists, α2 adrenoceptor agonists, and corticotropin releasing factor receptor1/2 antagonists, while consistent stress-like effects were found with yohimbine, an α2 adrenoceptor antagonist. We suggest possible avenues for future research.
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Polysulfides are endogenously produced in mammals and generally associated with protective functions. Our aim was to investigate the effect of dimethyl trisulfide (DMTS) in a mouse model of acute stress. DMTS activates transient receptor potential ankyrin 1 (TRPA1) channels and leads to neuropeptide release, potentially that of substance P (SP). We hypothesize that DMTS might inhibit the degrading enzymes of endocannabinoids, so this system was also investigated as another possible pathway for mediating the effects of DMTS. Trpa1 gene wild-type (WT) and knockout (KO) mice were used to confirm the role of the TRPA1 ion channel in mediating the effects of DMTS. C57BL/6J, NK1 gene KO, and Tac1 gene KO mice were used to evaluate the effect of DMTS on the release and expression of SP. Some C57BL/6J animals were treated with AM251, an inhibitor of the cannabinoid CB1 receptor, to elucidate the role of the endocannabinoid system in these processes. Open field test (OFT) and forced swim test (FST) were performed in each mouse strain. A tail suspension test (TST) was performed in Trpa1 WT and KO animals. C-FOS immunohistochemistry was carried out on Trpa1 WT and KO animals. The DMTS treatment increased the number of highly active periods and decreased immobility time in the FST in WT animals, but had no effect on the Trpa1 KO mice. The DMTS administration induced neuronal activation in the Trpa1 WT mice in the stress-related brain areas, such as the locus coeruleus, dorsal raphe nucleus, lateral septum, paraventricular nucleus of the thalamus, and paraventricular nucleus of the hypothalamus. DMTS may have a potential role in the regulation of stress-related processes, and the TRPA1 ion channel may also be involved in mediating the effects of DMTS. DMTS can be an ideal candidate for further study as a potential remedy for stress-related disorders.
Subject(s)
Disease Models, Animal , Mice, Inbred C57BL , Mice, Knockout , Sulfides , TRPA1 Cation Channel , Animals , TRPA1 Cation Channel/metabolism , TRPA1 Cation Channel/genetics , Mice , Sulfides/pharmacology , Male , Substance P/metabolism , Stress, Psychological/metabolism , Stress, Physiological/drug effects , Proto-Oncogene Proteins c-fos/metabolismABSTRACT
Cardiovascular diseases are the leading cause of death worldwide. Pathophysiologically, metabolic and inflammatory processes contribute substantially to the development and progression of cardiovascular diseases. Over the past decade, the role of disease-propagating inflammatory processes has been strengthened and reframed, leading to trials testing anti-inflammatory drugs for the treatment of atherosclerosis and its complications. Despite these achievements, further research in both pre-clinical and clinical studies is warranted to explore new targets, to better identify responders, and to refine therapy strategies to combat inflammation in human disease. Environmental disturbances, so-called lifestyle-associated cardiovascular risk factors, greatly alter the immune system in general and leukocytes in particular, thus affecting the progression of atherosclerosis. Epidemiological studies have shown that exposure to mental stress can be closely linked to the occurrence of cardiovascular disease. Here, we describe how acute and chronic mental stress alter the immune system via neuroimmune interactions, thereby modifying vascular inflammation. In addition, we identify gaps that still need to be addressed in the future.
Subject(s)
Neuroimmunomodulation , Stress, Psychological , Humans , Stress, Psychological/immunology , Stress, Psychological/complications , Neuroimmunomodulation/immunology , Neuroimmunomodulation/physiology , Inflammation/immunology , Models, Immunological , Cardiovascular Diseases/immunology , Atherosclerosis/immunologyABSTRACT
OBJECTIVE: This review aims to present an updated overview of cardiac disease-induced trauma and stress-related disorders such as acute stress disorder (ASD), adjustment disorder (AjD), and posttraumatic stress disorder (PTSD). First, the prevalence of these disorders, their diagnostic criteria, and their differences from other trauma-related disorders are described. Special challenges in diagnosis and treatment are identified, with various screening tools being evaluated for symptom assessment. Additionally, the risk factors studied so far for the development of symptoms of cardiac-induced posttraumatic stress disorder and the bidirectional relationship between posttraumatic stress disorder and cardiovascular diseases are summarized. Various therapeutic interventions, including pharmacological approaches, are also discussed. Finally, various areas for future research are outlined. BACKGROUND: Experiencing a cardiovascular disease, particularly a life-threatening cardiac event, can potentially lead to stress-related disorders such as ASD, AjD, and cardiac disease-induced PTSD (CDI-PTSD). If left untreated, these disorders are associated with a worsening cardiac prognosis and higher mortality rates. Approaching treatment through a trauma-focused lens may be beneficial for managing CDI-PTSD and stress-related disorders. CONCLUSION: Future research should explore treatment options for both the patients and the caregivers as well as investigate the long-term effects of trauma-focused interventions on physical and mental health outcomes.
Subject(s)
Stress Disorders, Post-Traumatic , Humans , Stress Disorders, Post-Traumatic/therapy , Stress Disorders, Post-Traumatic/etiology , Stress Disorders, Post-Traumatic/diagnosis , Heart Diseases/etiology , Heart Diseases/therapy , Risk Factors , Adjustment Disorders/diagnosis , Adjustment Disorders/therapy , Adjustment Disorders/etiology , Adjustment Disorders/psychology , Prevalence , Comorbidity , Stress Disorders, Traumatic, Acute/therapy , Stress Disorders, Traumatic, Acute/diagnosis , Stress Disorders, Traumatic, Acute/etiology , Stress Disorders, Traumatic, Acute/psychologyABSTRACT
Stressors can initiate a cascade of central and peripheral changes that modulate mesocorticolimbic dopaminergic circuits and, ultimately, behavioral response to rewards. Driven by the absence of conclusive evidence on this topic and the Research Domain Criteria framework, random-effects meta-analyses were adopted to quantify the effects of acute stressors on reward responsiveness, valuation, and learning in rodent and human subjects. In rodents, acute stress reduced reward responsiveness (g = -1.43) and valuation (g = -0.32), while amplifying reward learning (g = 1.17). In humans, acute stress had marginal effects on valuation (g = 0.25), without affecting responsiveness and learning. Moderation analyses suggest that acute stress neither has unitary effects on reward processing in rodents nor in humans and that the duration of the stressor and specificity of reward experience (i.e., food vs drugs) may produce qualitatively and quantitatively different behavioral endpoints. Subgroup analyses failed to reduce heterogeneity, which, together with the presence of publication bias, pose caution on the conclusions that can be drawn and point to the need of guidelines for the conduction of future studies in the field.
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BACKGROUND: Anxiety disorders are one of the most common mental disorders. Ghrelin is a critical orexigenic brain-gut peptide that regulates food intake and metabolism. Recently, the ghrelin system has attracted more attention for its crucial roles in psychiatric disorders, including depression and anxiety. However, the underlying neural mechanisms involved have not been fully investigated. METHODS: In the present study, the effect and underlying mechanism of ghrelin signaling in the nucleus accumbens (NAc) core on anxiety-like behaviors were examined in normal and acute stress rats, by using immunofluorescence, qRT-PCR, neuropharmacology, molecular manipulation and behavioral tests. RESULTS: We reported that injection of ghrelin into the NAc core caused significant anxiolytic effects. Ghrelin receptor growth hormone secretagogue receptor (GHSR) is highly localized and expressed in the NAc core neurons. Antagonism of GHSR blocked the ghrelin-induced anxiolytic effects. Moreover, molecular knockdown of GHSR induced anxiogenic effects. Furthermore, injection of ghrelin or overexpression of GHSR in the NAc core reduced acute restraint stress-induced anxiogenic effects. CONCLUSIONS: This study demonstrates that ghrelin and its receptor GHSR in the NAc core are actively involved in modulating anxiety induced by acute stress, and raises an opportunity to treat anxiety disorders by targeting ghrelin signaling system.
Subject(s)
Anxiety , Ghrelin , Nucleus Accumbens , Rats, Sprague-Dawley , Receptors, Ghrelin , Signal Transduction , Stress, Psychological , Animals , Ghrelin/metabolism , Nucleus Accumbens/metabolism , Nucleus Accumbens/drug effects , Male , Anxiety/metabolism , Anxiety/psychology , Receptors, Ghrelin/metabolism , Receptors, Ghrelin/genetics , Rats , Stress, Psychological/metabolism , Stress, Psychological/psychology , Signal Transduction/drug effects , Signal Transduction/physiology , Behavior, Animal/drug effectsABSTRACT
BACKGROUND: Maxillofacial trauma often results in visible facial disfigurements and can lead to psychological complications such as post-traumatic stress disorder (PTSD). However, PTSD often remains unrecognized and un/undertreated. The goal of the current systematic review was to determine the incidence of PTSD after maxillofacial trauma, associated risk factors, assessment tools employed, and management. METHODS: A literature search was conducted in PubMed, Google Scholar, Semantic Scholar, and Cochrane Library databases following PRISMA guidelines up to March 2024. Collected variables included the number of patients included, PSTD assessment tool, PTSD incidence, and risk factors and management. The meta-analysis was conducted using random effect models in STATA 16. RESULTS: The review included 14 studies (1633 patients, male=1025, female=230, not mentioned=378). Assessment tools varied widely among studies. Meta-analysis revealed a pooled incidence of PTSD of 27 % (n = 14, 95 % CI, 24 %-30 %) at 1-3 months post-trauma and 10 % (n = 3, 95 % CI, 3 %-17 %) at the 6-12 months follow-up, with a statistically significant 60 % reduction between these periods. CONCLUSION: The overall incidence of PTSD following maxillofacial trauma was 27 % at 1-3 months and decreased to 10 % after 6 months. The emphasis should be given to the importance of early intervention strategies and awareness among the treating surgeon to prevent PTSD.
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Many everyday decisions, including those concerning our health, finances and the environment, involve choosing between a smaller but imminent reward (e.g., 20 now) and a later but larger reward (e.g., 40 in a month). The extent to which an individual prefers smaller imminent rewards over larger delayed rewards can be measured using delay discounting tasks. Acute stress induces a cascade of biological and psychological responses with potential consequences for how individuals think about the future, process rewards, and make decisions, all of which can impact delay discounting. Several studies have shown that individuals focus more on imminent rewards under stress. These findings have been used to explain why individuals make detrimental choices under acute stress. Yet, the evidence linking acute stress to delay discounting is equivocal. To address this uncertainty, we conducted a meta-analysis of 11 studies (14 effects) to systematically quantify the effects of acute stress on monetary delay discounting. Overall, we find no effect of acute stress on delay discounting, compared to control conditions (SMD = -0.18, 95% CI [-0.57, 0.20], p = 0.32). We also find that neither the gender/sex of the participants, the type of stressor (e.g., physical vs. psychosocial) nor whether monetary decisions were hypothetical or incentivized (i.e. monetary decisions were actually paid out) moderated the impact of acute stress on monetary delay discounting. We argue that establishing the effects of acute stress on the separate processes involved in delay discounting, such as reward valuation and prospection, will help to resolve the inconsistencies in the field.
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BACKGROUND: On 7 October 2023, hundreds of armed Hamas fighters breached the security border fence and entered Israel from the Gaza Strip. More than 1400 Israeli citizens were murdered, and 239 individuals were kidnapped. Many Israeli citizens experienced these occurrences as psychologically traumatic events that caused stress and uncertainty. OBJECTIVES: The present study aimed to examine the relationship between exposure to war (in more distant circles), intolerance of uncertainty (IU) and disengaged coping on acute stress symptoms (ASS). First, we examined whether exposure to war and IU were directly associated with ASS. Second, we tested the mediating role of disengaged coping in the relationship among war exposure, IU and ASS. METHODS: This cross-sectional study involved 393 Israeli citizens. Participants answered questionnaires on exposure to war, IU, coping strategies and ASS. RESULTS: The study results indicate that higher exposure and higher levels of IU were directly associated with more intensive ASS, and this association was partially mediated by higher use of disengaged coping strategies. CONCLUSIONS: Individuals during wartime are at risk of experiencing high levels of ASS and developing ASD. However, degree of exposure to war alone was not associated with ASS, but it was related to personal resources and coping strategies.
Subject(s)
Adaptation, Psychological , Humans , Male , Female , Israel , Cross-Sectional Studies , Adult , Uncertainty , Surveys and Questionnaires , Middle Aged , Stress Disorders, Traumatic, Acute/psychology , Young Adult , Coping SkillsABSTRACT
This study aimed to investigate the potential protective effects of Dexmedetomidine (DEX) against acute kidney injury (AKI) induced by acute stress (AS). Wistar rats were divided into five groups: Control, DEX, AS, AS + DEX, and AS + A438079. The results showed that AS led to AKI by increasing inflammatory biomarkers and oxidative stress-related indicators. The acute stress model in rats was successfully established. Renal function, histopathology, oxidative stress, and inflammation were assessed. Localization of P2X7 receptor (P2X7R) was determined by immunofluorescence. Additionally, the key inflammatory proteins of the P2X7R/NF-κB/NLRP3 signaling pathway were measured by Western blotting. DEX significantly improved kidney function, alleviated kidney injury, and reduced oxidative stress and inflammation. DEX inhibited the activation of the P2X7R, decreased the expression of NF-κB, NLRP3 inflammasome, and Caspase-1, and inhibited the expression of interleukin-1ß (IL-1ß) and tumor necrosis factor α (TNFα). Furthermore, DEX also alleviated AS-induced AKI by inhibiting the excessive production of reactive oxygen species (ROS) and reducing oxidative stress. In conclusion, DEX attenuates AS-induced AKI by mitigating inflammation and oxidative stress through the inhibition of the P2X7R/NF-κB/NLRP3 pathway in rats.
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When animals perceive an acute stressor like a predator, they typically undergo a suite of physiological changes that function to improve survival during the encounter, such as elevation in cardiac output, to supply more energy to muscles. If bodily energy is limited, such as by parasites or infections, these functions could become less efficient and lessen host survival. In the aquatic world of microorganisms, individuals can become colonized by other organisms on their surface (epibionts), which could sap energy from their host from their weight, or even compete with the host for food. Here, we tested if one epibiont (a ciliated protozoan, Vorticella spp.) affects its hosts' ability to mount a physiological stress reaction. We collected wild daphnia (Daphnia ambigua) that had varying burdens of these on their bodies and exposed them to a simulated stressor (crushed daphnia, to simulate nearby predation) under a microscope while monitoring for changes in their heart rates in real time. Out of 121 daphnia, those with no Vorticella epibionts showed no meaningful changes in their heart rate after exposure, but those with light or heavy burdens showed immediate elevations (within 5 min). Moreover, the heart rates of heavily burdened daphnia continued to rise for 1.5 h thereafter, to as much as 17% higher than at baseline. These patterns were unexpected, as they suggest that the ciliated epibionts act to elevate their hosts' physiological reaction, rather than dampen it, perhaps by churning the water column around the host, thereby enhancing the chemical alarm cue. The procedures used in this study may be useful for future investigations into the acute stress reactions of daphnia or other microorganisms.
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Impaired activity of the hypothalamic-pituitary axis and reduced blood levels of glucocorticoids (GCs) are signature features of stress-related maladies. Recent evidence suggests a possible role of the tryptophan metabolite kynurenic acid (KYNA) in this context. Here we investigated possible causal relationships in adult male rats, using stress-induced fear discrimination as a translationally relevant behavioral outcome measure. One week following adrenalectomy (ADX) or sham surgery, animals were for 2 h either physically restrained or exposed to a predator odor, which caused a much milder stress response. Extracellular KYNA levels were determined before, during and after stress by in vivo microdialysis in the prefrontal cortex. Separate cohorts underwent a fear discrimination procedure starting immediately after stress termination. Different auditory conditioned stimuli (CS) were either paired with a foot shock (CS+) or non-reinforced (CS-). One week later, fear was assessed by re-exposing the animals to each CS. Separate groups of rats were treated with the KYNA synthesis inhibitor BFF-816 prior to stress initiation to test a causal role of KYNA in fear discrimination. Restraint stress raised extracellular KYNA levels by â¼85 % in ADX rats for several hours, and these animals were unable to discriminate between CS+ and CS-. Both effects were prevented by BFF-816 and were not observed after exposure to predator odor or in sham-operated rats. These findings suggest that a causal connection exists between adrenal function, stress-induced KYNA increases, and behavioral deficits. Pharmacological inhibition of KYNA synthesis may therefore be an attractive, novel option for the treatment of stress-related disorders.
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Monitoring stress levels of farmed Atlantic salmon (Salmo salar) is important to ensure fish welfare and optimize farm operations. Feces could be a promising matrix for assessing stress responses in fish, based on their properties of low-invasive sampling and allowing repeated sampling over time. Meanwhile, elevated levels of cortisol metabolites (CMs) in feces indicate the increases in plasma cortisol levels (PLA) after exposure to acute stress. However, the dynamics of fecal CMs following acute stress in Atlantic salmon remain unclear. In this study, a confinement stress involving chasing and crowding was conducted to investigate the responses of gastrointestinal CMs to an acute stressor in Atlantic salmon. The post-smolts, with an average weight of 155.21 g, were sampled before and at 30 min, 1.5, 6, 12, 18, 24, 36, and 48 h after the onset of stress. Blood and gastrointestinal contents from the stomach, proximal intestine, and distal intestine of each fish were collected and subsequently analyzed, using competitive enzyme-linked immunosorbent assay (ELISA). The results demonstrated that the pre-stress level of PLA was low (4.28 ± 6.13 ng/ml) and reached a peak within 30 min following stress. The levels of CMs in gastrointestinal contents from stomach (SCMs), proximal intestine (PCMs), and distal intestine (DCMs) in pre-stress group were 0.82 ± 0.50, 18.31 ± 6.14 and 16.04 ± 6.69 ng/g, respectively. Gastrointestinal CMs increased significantly within 30 min and the peak levels of SCMs (3.51 ± 3.75 ng/g), PCMs (68.19 ± 23.71 ng/g) and DCMs (65.67 ± 23.37 ng/g) were found at 1.5 h post-stress. The significant increases in PCMs and DCMs post-stress validate the biological relevance of measuring intestinal CMs for assessing acute stress responses in Atlantic salmon. No significant difference was noted between PCMs and DCMs across all samples, suggesting that intestinal contents can serve as a suitable matrix compared with feces when measuring the responses of CMs to acute stress. The time lag between the peak of PLA levels and their reflection in the intestinal contents exceeded 1 h, indicating that using intestinal contents as a matrix to assess stress levels in fish can extend and delay the sampling window. This study highlights valuable guidance for determining the optimal times to utilize intestinal contents for measuring stress responses, providing further insights into the dynamics of fecal CM following acute stress.
Subject(s)
Feces , Hydrocortisone , Salmo salar , Stress, Physiological , Animals , Hydrocortisone/blood , Stress, Physiological/physiology , Feces/chemistry , Crowding , Gastrointestinal Tract/metabolism , Gastrointestinal Contents/chemistryABSTRACT
BACKGROUND: In the context of persistent wars and conflicts worldwide, the impact of acute, excessive and constant exposure to media coverage of such events on mental health outcomes becomes a serious problem for public health, and requires therefore urgent investigation to inform an effective prevention and management response. The objective of the present study was to test the hypothesis that war-related media exposure is directly and indirectly associated with insomnia through depression and perceived stress among adults from the general population of different Arab countries. METHODS: A cross-sectional study was carried-out two weeks after the beginning of Israel-Gaza war on the 7th of October 2023. An anonymous online survey and a snowball sampling method were adopted to collect data. A sample of 2635 general population adults (mean age of 23.98 ± 7.55 years, 73.1% females) took part of this study. RESULTS: The results of the mediation analysis showed that, after adjusting over potential confounders, depression and perceived stress fully mediated the association between war media exposure and insomnia; higher war media exposure was significantly associated with higher depression (Beta = 0.13; p < .001) and perceived stress (Beta = 0.07; p < .001), whereas higher depression (Beta = 0.43; p < .001) and perceived stress (Beta = 0.31; p < .001) were significantly associated with higher insomnia. It is of note that war media exposure was not significantly and directly associated with insomnia (Beta = - 0.01; p = .178 and Beta = 0.02; p = .098 respectively). CONCLUSION: The present study is the first to provide evidence that more time spent viewing the horrors of war is significantly associated with insomnia. In addition, symptoms of stress and depression were present as early as two weeks following the beginning of the war, and played a significant role in mediating the association between war media coverage and insomnia. These findings suggest that timely screening for, and management of depression and stress symptoms in clinical and preventive programs might be beneficial for community adults who have been heavily and indirectly exposed to war through media, and present with insomnia.
Subject(s)
Depression , Sleep Initiation and Maintenance Disorders , Stress, Psychological , Humans , Female , Male , Sleep Initiation and Maintenance Disorders/epidemiology , Sleep Initiation and Maintenance Disorders/psychology , Cross-Sectional Studies , Adult , Israel/epidemiology , Depression/epidemiology , Stress, Psychological/epidemiology , Young Adult , Middle East/epidemiology , Mass Media/statistics & numerical data , Adolescent , Surveys and Questionnaires , Middle Aged , WarfareABSTRACT
BACKGROUND: Adjustment and stress-related disorders are prevalent among psychiatric service users. Despite their prevalence, little is known about their prognosis. To reduce that gap, the present article documents the service use and diagnostic outcomes of people with adjustment or stress-related disorders presenting at Singapore's largest psychiatric emergency department. METHODS: Administrative data from 2014 to 2021 was retrieved to follow a group of 683 service users whose first-ever psychiatric presentation in 2014 warranted a diagnosis of adjustment or stress-related disorder. People were grouped a priori depending on whether different diagnoses were recorded within 7 days, 9 months, after 9 months or not at all. Survival curves characterized conversion to other diagnoses and engagement with healthcare services. Service use outcomes include the number of hospitalizations, outpatient appointments, emergency department visits, and prescriptions. RESULTS: Sixty-one percent (n = 417) never received another diagnosis over the 8-year period. This group used emergency services most and received the most pharmacotherapy shortly after their first visit. Of those who received another diagnosis, depression, personality disorders, and psychotic disorders were the most common. Those who received another diagnosis within 7 days (n = 70, 10%) received it on their first day of hospitalization (IQR 1-1), making the most use of inpatient services. The group who received another diagnosis within 9 months (n = 105, 15%) did so after 42 days (IQR 26-84) and had the highest relative number of deaths. Those who received another diagnosis after 9 months (n = 91, 13%) did so after 1,134 days (IQR 613-1,823) and had the longest period of engagement but made the least use of any psychiatric service, potentially suggesting a group whose early index diagnosis heralded vulnerability to future disorders. CONCLUSIONS: A large group of service users with acute stress or adjustment disorders will likely never be given another psychiatric diagnosis and appear to disengage following an initial period of high-intensity service use. The group that received a different diagnosis after the 9-month mark had prolonged contact with services but low intensity of service use and may represent a target for preventative intervention to help them improve their stress-managing skills and avoid developing other disorders.
Subject(s)
Adjustment Disorders , Humans , Male , Female , Adult , Middle Aged , Adjustment Disorders/epidemiology , Adjustment Disorders/diagnosis , Adjustment Disorders/psychology , Singapore/epidemiology , Longitudinal Studies , Hospitalization/statistics & numerical data , Emergency Service, Hospital/statistics & numerical data , Patient Acceptance of Health Care/statistics & numerical data , Young Adult , Emergency Services, Psychiatric/statistics & numerical data , Mental Health Services/statistics & numerical dataABSTRACT
Macrobrachium rosenbergii is an essential species for freshwater economic aquaculture in China, but in the larval process, their salinity requirement is high, which leads to salinity stress in the water. In order to elucidate the mechanisms regulating the response of M. rosenbergii to acute low-salinity exposure, we conducted a comprehensive study of the response of M. rosenbergii exposed to different salinities' (0‱, 6‱, and 12‱) data for 120 h. The activities of catalase, superoxide dismutase, and glutathione peroxidase were found to be significantly inhibited in the hepatopancreas and muscle following low-salinity exposure, resulting in oxidative damage and immune deficits in M. rosenbergii. Differential gene enrichment in transcriptomics indicated that low-salinity stress induced metabolic differences and immune and inflammatory dysfunction in M. rosenbergii. The differential expressions of MIH, JHEH, and EcR genes indicated the inhibition of growth, development, and molting ability of M. rosenbergii. At the proteomic level, low salinity induced metabolic differences and affected biological and cellular regulation, as well as the immune response. Tyramine, trans-1,2-Cyclohexanediol, sorbitol, acetylcholine chloride, and chloroquine were screened by metabolomics as differential metabolic markers. In addition, combined multi-omics analysis revealed that metabolite chloroquine was highly correlated with low-salt stress.