OBJECTIVE: The study investigated the mediation mechanisms between coronavirus disease 2019 (COVID-19) infection risk perception and depressive symptoms among pregnant women during the different periods of the COVID-19 pandemic.
METHODS: Study data were derived from a sample of 463 pregnant women in Hubei Province, the province with the most severe COVID-19 outbreak in China. Data were collected in two phases (during and after the acute phase of the COVID-19 pandemic) using the COVID-19 infection risk perception scales, the Edinburg Postnatal Depression Scale (EPDS), the Perceived Stress Scale (PSS), and the Peritrauma Distress Inventory (PDI). Mediation model analysis was used for data analysis, overall and by groups.
RESULTS: The level of depressive symptoms among pregnant women after the acute phase of the COVID-19 pandemic was moderate (median, 9.00 [25th percentile, 75th percentile = 5.00, 12.00]), higher than the acute group (median, 7.00 [25th percentile, 75th percentile = 4.50, 10.00]). Perceived stress and traumatic stress fully mediated the relationship between infection worry (total indirect effect, 0.39 [95% confidence interval, 0.24-0.54])/infection possibility (total indirect effect, 0.41 [95% confidence interval, 0.22-0.61]) and depressive symptoms among pregnant women during the acute phase of the COVID-19 pandemic, whereas the relationship was only fully mediated by perceived stress after the acute pandemic.
CONCLUSIONS: Effects of risk perception on depressive symptoms varied by periods of COVID-19. These findings have important implications for developing effective prevention and early psychoeducational intervention strategies for pregnant women with a high risk of depressive symptoms during different periods of emerging infectious diseases.

Background: Stress disorders, such as post-traumatic stress disorder (PTSD), are attracting much attention. However, the relationship between traumatic stress and inflammation is rarely discussed. Subjects and Methods: As studies have linked PTSD to altered susceptibility to various diseases, such a psychiatric condition may lead to long-term systematic changes in physiological functions. We searched PubMed with the keywords \"traumatic stress,\" \"stress disorders,\" \"post-traumatic stress disorder,\" and \"inflammation.\" Results: Based on 65 previously published studies, we reviewed the long-term effects of PTSD, as well as traumatic events, on inflammatory function from both epidemiological and biological perspectives. Post-traumatic stress disorder is related to the immune response, including an increase in inflammatory factors and a reduction in anti-inflammatory factors. Additionally, it has been demonstrated that traumatic stress disorder and immune disease share a common genetic basis at the gene expression level. Conclusions: Understanding this relationship is of great significance for optimizing treatment plans for patients with PTSD.

Anhedonia is common in individuals with traumatic experience. Anhedonia symptoms play an important role in posttraumatic psychopathology, and are related to various adverse outcomes. The current study is a preliminary neuroimaging study of the neural correlates of posttraumatic anhedonia symptoms. Resting-state fMRI data were acquired from 88 Chinese earthquake survivors. Whole brain analyses and exploratory ROI-to-ROI analyses were performed to examine the relationship between posttraumatic anhedonia symptoms and resting-state functional connectivity (rsFC) of reward-related subcortical nucleus including nucleus accumbens and ventral pallidum. The rsFC between left ventral pallidum and areas of bilateral posterior cingulate cortex (PCC) and precuneus cortex were found lower in the high posttraumatic anhedonia group, after controlling for sex, age and other posttraumatic stress symptoms. The rsFC between left ventral pallidum and PCC and the rsFC between left ventral pallidum and lateral parietal cortex were significantly lower in the high anhedonia group. Our findings suggest that decreased functional connectivity between the ventral pallidum and the brain default mode network (DMN) regions could be the neural correlates of posttraumatic anhedonia symptoms.

Sleep disturbances have been recognized as a core symptom of post-traumatic stress disorders (PTSD). However, the neural basis of PTSD-related sleep disturbances remains unclear. It has been challenging to establish the causality link between a specific brain region and traumatic stress-induced sleep abnormalities. Here, we found that single prolonged stress (SPS) could induce acute changes in sleep/wake duration as well as short- and long-term electroencephalogram (EEG) alterations in the isogenic mouse model. Moreover, the medial prefrontal cortex (mPFC) showed persistent high number of c-fos expressing neurons, of which more than 95% are excitatory neurons, during and immediately after SPS. Chemogenetic inhibition of the prelimbic region of mPFC during SPS could specifically reverse the SPS-induced acute suppression of delta power (1-4 Hz EEG) of non-rapid-eye-movement sleep (NREMS) as well as most of long-term EEG abnormalities. These findings suggest a causality link between hyper-activation of mPFC neurons and traumatic stress-induced specific sleep-wake EEG disturbances.

The molecular mechanism of fear memory is poorly understood. Therefore, the pathogenesis of post-traumatic stress disorder (PTSD), whose symptom presentation can enhance fear memory, remains largely unclear. Recent studies with knockout animals have reported that Rin1 and stathmin regulate fear memory. Rin1 inhibits acquisition and promotes memory extinction, whereas stathmin regulates innate and basal fear. The aim of our study was to examine changes in the expression of Rin1 and stathmin in different animal models of stress, particluarly traumatic stress. We used three animal traumatic stresses: single prolonged stress (SPS, which is a rodent model of PTSD), an immobilization-stress (IM) and a Loud sound stress (LSS), to examine the change and uniqueness in Rin1/stathmin expression. Behavioral tests of SPS rats demonstrated increased anxiety and contextual fear-conditioning. They showed decreased long-term potentiation (LTP), as well as decreased stathmin and increased Rin1 expression in the hippocampus and the amygdala. Expression of the stathmin effector, tubulin, and downstream molecules Rin1, Rab5, and Abl, appeared to increase. Rin1 and EphA4 were endogenously coexpressed in primary neurons after SPS stimulation. IM rats exhibited increased anxiety behavior and enhanced fear-conditioning to contextual and auditory stimuli. Similar changes in expression of Rin1/stathmin were observed in IM rats whereas no changes were observed in rats exposed to a loud sound. These data suggest that changes in expression of the Rin1 and stathmin genes may be involved in rodents with SPS and IM stresses, which provide valuable insight into fear memories under abnormal conditions, particularly in PTSD.

Brief and age-appropriate measures of trauma-related symptoms are useful for identifying children in need of clinical services. The current study examines the psychometric properties of the 23-item Child\'s Reaction to Traumatic Events Scale-Revised (CRTES-R). The CRTES-R includes subscales assessing hyperarousal, avoidance and intrusion. To date, no studies have examined the psychometric properties of this revised measure or cross-cultural differences in its factor structure. Two samples of (a) children (ages 6-21) who had experienced a hurricane in the USA or Grenada (N = 135), and (b) Ugandan children (ages 8-17) who had experienced a variety of traumatic events (N = 339) completed the CRTES-R in English or Lugandan. Confirmatory factor analysis supported an empirically adjusted model with three modified latent factors in both the English (χ2/df = 1.34, CFI = .90, RMSEA = .05) and Lugandan samples (χ2/df = 1.45, CFI = .93, RMSEA = .04). Although the analysis supported separate hyperarousal, avoidance and intrusion subscales, the items that loaded on each factor differed from the original CRTES-R subscales. The English version of the CRTES-R showed good concurrent validity with the Kauai Recovery Index measure of trauma symptoms. Those using the CRTES-R to assess children\'s experiences of the different symptom types should consider using the empirically-derived subscales described in this paper; however, those who wish to capture a broad spectrum of PTSD symptoms should consider using all the original CRTES-R items and calculating a total score.