The interaction of occupational stress and job burnout on depressive symptoms in railway workers in Fuzhou city.

BACKGROUND: To explore the relationship between occupational stress, burnout and depressive symptoms among railroad workers in Fuzhou, and to analyze the interaction of burnout and occupational stress on depressive symptoms. METHODS: In this study, 861 railway employees of Fuzhou railway bureau were randomly selected from January to April, 2022. Occupational stress inventory revised edition (OSI-R), China job burnout inventory (CMBI) and Symptom Checklist-90 (SCL-90) were used to investigate the occupational stress, job burnout and depressive symptoms of railway workers. Interactions associated with depressive symptoms were assessed by linear hierarchical regression analysis and SPSS macros (PROCESS). RESULTS: Occupational stress, job burnout and depressive symptoms accounted for 50.58%, 93.47%, and 11.19% of the study population, respectively. There were intergroup differences between age, marriage status, and length of service (P < 0.05). Occupational stress and job burnout are the main risk factors for depressive symptoms (OR: 2.01, 95% CI: 1.17-3.45; 1.94, 1.69-2.23, respectively). More importantly, further analysis of the interaction between occupational stress and job burnout showed that those with high levels of job burnout had a high-risk effect on depressive symptoms at high levels of occupational stress. CONCLUSION: Occupational stress and job burnout are risk factors for depressive symptoms among railroad workers in Fuzhou City. The interaction of job burnout and occupational stress increases the risk of depressive symptoms.

The mechanism by which piR-000699 targets SLC39A14 regulates ferroptosis in aging myocardial ischemia/reperfusion injury.

Myocardial ischemia/reperfusion (I/R) injury is a classic type of cardiovascular disease characterized by injury to cardiomyocytes leading to different types of cell death. The degree of irreversible myocardial damage is closely related to age, and ferroptosis is involved in cardiomyocyte damage. However, the mechanisms underlying ferroptosis regulation in aging myocardial I/R injury are still unclear. The present study aims to explore the underlying mechanism of piRNA regulation in ferroptosis. Using left anterior descending coronary artery ligation in an aging rat model and a D-galactose-induced rat cardiomyocyte line (H9C2) to construct an aging cardiomyocyte model, we investigate whether ferroptosis occurs after reperfusion injury in vitro and in vivo. This study focuses on the upregulation of piR-000699 after hypoxia/reoxygenation treatment in aging cardiomyocytes by observing hypoxia/reoxygenation (H/R) injury indicators and ferroptosis-related indicators and clarifying the role of piR-000699 in H/R injury caused by ferroptosis in aging cardiomyocytes. Bioinformatics analysis reveals that SLC39A14 is a gene that binds to piR-000699. Our data show that ferroptosis plays an important role in I/R injury both in vivo and in vitro. Furthermore, the results show the potential role of piR-000699 in regulating SLC39A14 in ferroptosis in aging cardiomyocytes under hypoxia/reoxygenation conditions. Together, our results reveal that the mechanism by which piR-000699 binds to SLC39A14 regulates ferroptosis in aging myocardial I/R injury.

Maternal immune activation mediated prenatal chronic stress induces Th17/Treg cell imbalance may relate to the PI3K/Akt/NF-κB signaling pathway in offspring rats.

Maternal immune activation (MIA), defined as elevated levels of inflammatory markers beyond the normal range, can occur due to psychological stress, infection, and other disruptions during pregnancy. MIA affects the immune system development in offspring and increases the risk of immune-related disorders. Limited studies have investigated the effects of prenatal stress on offspring's immune system. In this study, pregnant rats were exposed to chronic unpredictable mild stress (CUMS) during pregnancy, involving seven different stressors. We examined the impact of prenatal stress stimuli on the offspring's immune system and observed activation of the PI3K/Akt/NF-κB signaling pathway, resulting in an imbalance of Th17/Treg cells in the offspring's spleen. Our findings revealed increased plasma levels of corticosterone, IL-1ß, and IL-6 in female rats exposed to prenatal stress, as well as elevated serum levels of IL-6 and TNF-α in the offspring. Furthermore, we identified a correlation between cytokine levels in female rats and their offspring. Transcriptome sequencing and qPCR experiments indicated differentially expressed mRNAs in offspring exposed to prenatal stress, which may contribute to the imbalance of Th17/Treg cells through the activation of the Gng3-related PI3K/Akt/NF-κB pathway.

Prenatal chronic stress impairs the learning and memory ability via inhibition of the NO/cGMP/PKG pathway in the Hippocampus of offspring.

Numerous clinical and animal studies have found that antenatal chronic stress can lead to pathological changes the hippocampal development from embryos to adult, but the mechanisms are not well understood. Proteomic analyses provide a new insight to explore the potential mechanisms of this impairment. In this study, gestating rats were subjected to chronic unpredictable mild stress (CUMS) during pregnant days using nine different stimulations, and the changes of the learning and memory performance and the expression of proteins in the hippocampus of offspring were measured. It was found that prenatal chronic stress led to growth retardation, impaired spatial learning and memory ability in the offspring. Furthermore, prenatal stress caused various degrees of damage to neurons, Nissl body, mitochondria and synaptic structures in hippocampal CA3 region of offspring. In addition, 26 significantly different expressed proteins (DEPs) were found between the two groups by using isoquantitative tag-based relative and absolute quantification (iTRAQ) proteomics analysis. Further analyses of these DEPs showed that involved with different molecular functions and several biological processes, such as biological regulation and metabolic processes. Among these, the KEGG pathway enrichment showed that learning and memory impairment was mainly associated with the cyclic guanosine monophosphate protein kinase G (cGMP-PKG) pathway. At the same time, compared with OPC group, the NO, nNOS and cGMP level were significantly decreased, and the expression of PKG protein was also dropped. All of these results suggested that pregnant rats exposed to chronic psychological stress might impair spatial learning and memory ability of offspring, by disturbing the NO/cGMP/PKG signaling pathway.

Contribution of hippocampal BDNF/CREB signaling pathway and gut microbiota to emotional behavior impairment induced by chronic unpredictable mild stress during pregnancy in rats offspring.

Background: Numerous studies have shown that exposure to prenatal maternal stress (PMS) is associated with various psychopathological outcomes of offspring. The accumulating evidence linking bacteria in the gut and neurons in the brain (the microbiota-gut-brain axis) has been aconsensus; however, there is a lack of research on the involvement mechanism of gut microbiota in the regulation of the BDNF/CREB signaling pathway in the hippocampus of prenatally stressed offspring. Methods: Pregnant rats were subjected to chronic unpredictable mild stress (CUMS) to establish the prenatal maternal stress model. The body weight was measured and the behavioral changes were recorded. Offspring were tested to determine emotional state using sucrose preference test (SPT), open-field test (OFT) and suspended tail test (STT). Gut microbiota was evaluated by sequencing the microbial 16S rRNA V3-V4 region, and the interactive analysis of bacterial community structure and diversity was carried out. The expression of hippocampal BDNF, TrkB and CREB mRNA and proteins were respectively measured using RT-PCR and Western blotting. Results: Prenatal maternal stress increased maternal plasma corticosterone levels, slowed maternal weight gain and caused depression-like behaviors (all P < 0.05). In offspring, prenatal maternal stress increased plasma corticosterone levels (P < 0.05) and emotional behavior changes (depression-like state) were observed (P < 0.05). The species abundance, diversity and composition of the offspring's gut microbiota changed after the maternal stress during pregnancy (P < 0.05). Compared with the control group's offspring, the species abundance of Lactobacillaceae was dropped, while the abundance of the Muribaculaceae species abundance was risen. Concurrent, changes in the hippocampal structure of the offspring and decreases in expression of BDNF/CREB signaling were noted (P < 0.05). Conclusions: Prenatal maternal stress leads to high corticosterone status and abnormal emotion behavior of offspring, which may be associated with the abnormal BDNF/CREB signaling in hippocampus of offspring caused by the change of gut microbiota composition.

The association between undiagnosed diabetes and cognitive function: findings from the China health and retirement longitudinal study.

BACKGROUND: The cognitive function of people with diabetes has gained an increasing interest in recent years, and this study focuses on exploring the relationship between undiagnosed diabetes and cognitive function among the middle-aged and elderly people in China. METHODS: The data came from the China Health and Retirement Longitudinal Study (CHARLS) which was conducted between July and October 2015. 9855 subjects were enrolled in the study. Executive function and episodic memory were used to assess cognitive function. The subjects were divided into three groups: no diabetes, diagnosed diabetes, and undiagnosed diabetes, and weighted multiple linear regression models were established to evaluate the association of undiagnosed diabetes with cognitive function. RESULTS: After controlling for covariates, undiagnosed diabetes was statistically associated with executive function (ß = -0.215, P < 0.01). In the age group of ≥65 years, undiagnosed diabetes was statistically associated with executive function (ß = -0.358, P < 0.01) and episodic memory (ß = -0.356, P < 0.01). When adjusting for confounders, no statistically significant associations were found between diagnosed diabetes and cognitive function except in 45-54 age group (ß = 0.374, P < 0.05). CONCLUSIONS: The cross-sectional study suggested that undiagnosed diabetes was linked to poor cognitive function, especially in the elderly population. Timely diagnosis and active treatment of diabetes are important to reduce the occurrence of cognitive impairment. Further prospective cohort studies are required to articulate the association between undiagnosed diabetes and cognitive function.

Lycium barbarum polysaccharide attenuates emotional injury of offspring elicited by prenatal chronic stress in rats via regulation of gut microbiota.

Stress during pregnancy is not only detrimental to a woman's own physical and mental health, but can also cause changes in the intrauterine environment and even have an impact on later growth and development, this study was designed to understand the changes of gut microbiota in the maternal and offspring caused by prenatal chronic stress, and to explore the regulatory effect of LBP on gut microbiota, and then to improve the emotional damage caused by prenatal chronic stress in the offspring. A rat model of prenatal chronic stress was made and used LBP to intervene by gavage. Fresh feces of offspring were collected, the concentration of microbial metabolites were tested by ELISA. Illumina MiSeqPE300 sequencing technology was used to determine the sequence of 16S rRNA V3-V4 of microorganisms. On the PND 42, the emotional function of offspring were tested by open-field test (OFT), sucrose preference test (SPT) and tail of suspend test (TST). Results indicated that stress factors increased the plasma corticosterone level of rats during pregnancy and they appeared depressive behaviors. The body weight of offspring during prenatal chronic stress was lower than the control group, and the plasma corticosterone level was increased. Prenatal chronic stress had a significant impact on emotional performance of the offspring on OFT, SPT and TST. Alpha diversity of gut microbiota and microbiota composition in offspring of prenatal chronic stress was attenuated and some relationships existed between these parameters. LBP treatment reduced offspring's plasma corticosterone level and improved their body weight, changed the emotional function, increased the diversity of gut microbiota. Collectively, these findings disclose that prenatal chronic stress not only causes emotional injury on the offspring, but also changes the gut microbiota of the mother and offspring; LBP may regulate the intestinal flora of the mother, then reducing the influence of stress factors on the emotional injury of offspring.

Association between dietary fatty acid patterns based on principal component analysis and fatty acid compositions of serum and breast milk in lactating mothers in Nanjing, China.

This study aimed to comprehensively analyze dietary fatty acids (FAs) to evaluate their association with FA compositions of maternal serum and breast milk and assess their effects on mothers and infants. Overall, 121 healthy lactating Chinese mothers at 30-50 days of postpartum were enrolled and instructed to complete a Food Frequency Questionnaire, together with venous blood and breast milk sample collections. Dietary FA patterns were derived by principal component analysis with varimax rotation. Serum and breast milk FA compositions were detected using capillary gas chromatography and presented as relative concentrations (weight percentage of total FAs, %). Daily energy intake, absolute intake of most nutrients, and percentage of energy intake provided by these nutrients significantly varied among the different dietary FA patterns. There were significant differences in serum polyunsaturated fatty acid (PUFA) levels (P = 0.011); in monounsaturated fatty acid and PUFA proportions in breast milk with respect to four patterns (P = 0.002 and P = 0.026, respectively); and in n-6 PUFA, n-3 PUFA, linoleic acid, γ-linolenic acid, α-linolenic acid, and docosahexaenoic acid levels in breast milk (P = 0.027, P = 0.007, P = 0.048, P = 0.034, P = 0.020, and P = 0.002, respectively). Furthermore, maternal weight retention and length-for-age z scores, weight-for-age z scores and head circumference-for-age z scores of infants with respect to the four patterns exhibited significant differences (P = 0.038, P = 0.030, P = 0.034, and P<0.001, respectively). The results demonstrated the effect of dietary FA patterns on FA compositions of serum and breast milk, and patterns mainly characterized by LC-PUFA may have potentially beneficial effects on maternal postpartum recovery and infant growth.

Reproducibility and relative validity of a semi-quantitative food frequency questionnaire for the Chinese lactating mothers.

BACKGROUND: The dietary nutritional status of the lactating mothers is related to maternal health and has a significant impact on the growth and development of infants through the secretion of breast milk. The food frequency questionnaire (FFQ) is the most cost-effective dietary assessment method that can help obtain information on the usual dietary pattern of participants. Until now, the FFQs have been used for different populations in China, but there are few FFQs available for the lactating mothers. We aimed to develop a semi-quantitative, 156-item FFQ for the Chinese lactating mothers, and evaluate its reproducibility and relative validity. METHODS: A total of 112 lactating mothers completed two FFQs and one 3-d dietary record (3DR). The first FFQ (FFQ1) was conducted during postpartum at 60-65 days and the second FFQ (FFQ2) during subsequent follow-up at 5 weeks. The 3DR was completed with portion sizes assessed using photographs taken by the respondent before and after eating (instant photography) 1 week after FFQ1. RESULTS: For reproducibility, the Spearman's correlation coefficients for food ranged from 0.34 to 0.68, and for nutrients from 0.25 to 0.61. Meanwhile, the intra-class correlation coefficients for food ranged from 0.48 to 0.87, and for nutrients from 0.27 to 0.70. For relative validity, the Spearman's correlation coefficients for food ranged from 0.32 to 0.56, and for nutrients from 0.23 to 0.72. The energy-adjusted coefficients for food ranged from 0.26 to 0.55, and for nutrients from 0.22 to 0.47. Moreover, the de-attenuation coefficients for food ranged from 0.34 to 0.67, and for nutrients from 0.28 to 0.77. The Bland-Altman plots also showed reasonably acceptable agreement between the two methods. CONCLUSIONS: This FFQ is a reasonably reproducible and a relative valid tool for assessing dietary intake of the Chinese lactating mothers.

The mechanism of enriched environment repairing the learning and memory impairment in offspring of prenatal stress by regulating the expression of activity-regulated cytoskeletal-associated and insulin-like growth factor-2 in hippocampus.

BACKGROUND: Prenatal stress can cause neurobiological and behavioral defects in offspring; environmental factors play a crucial role in regulating the development of brain and behavioral; this study was designed to test and verify whether an enriched environment can repair learning and memory impairment in offspring rats induced by prenatal stress and to explore its mechanism involving the expression of insulin-like growth factor-2 (IGF-2) and activity-regulated cytoskeletal-associated protein (Arc) in the hippocampus of the offspring. METHODS: Rats were selected to establish a chronic unpredictable mild stress (CUMS) model during pregnancy. Offspring were weaned on 21st day and housed under either standard or an enriched environment. The learning and memory ability were tested using Morris water maze and Y-maze. The expression of IGF-2 and Arc mRNA and protein were respectively measured by using RT-PCR and Western blotting. RESULTS: There was an elevation in the plasma corticosterone level of rat model of maternal chronic stress during pregnancy. Maternal stress's offspring exposed to an enriched environment could decrease their plasma corticosterone level and improve their weight. The offspring of maternal stress during pregnancy exhibited abnormalities in Morris water maze and Y-maze, which were improved in an enriched environment. The expression of IGF-2, Arc mRNA, and protein in offspring of maternal stress during pregnancy was boosted and some relationships existed between these parameters after being exposed enriched environment. CONCLUSIONS: The learning and memory impairment in offspring of prenatal stress can be rectified by the enriched environment, the mechanism of which is related to the decreasing plasma corticosterone and increasing hippocampal IGF-2 and Arc of offspring rats following maternal chronic stress during pregnancy.

Biomarkers of endothelial dysfunction in patients with primary focal segmental glomerulosclerosis.

AIM: Endothelial dysfunction occurs in nephrotic syndrome (NS) and may constitute a link between NS and vascular complications. Focal segmental glomerulosclerosis (FSGS) is a common cause of NS. This study aimed to assess endothelial markers at different stages of FSGS and define whether they were associated with thromboembolic complications and disease activity. METHODS: Forty-four patients with nephrotic-range proteinuria and biopsy-proven primary FSGS were included in this study. Nine of them had concurrent thromboembolisms. Thirty-two sex- and age- matched healthy volunteers served as controls. Endothelial markers including circulating endothelial cells (CECs), soluble thrombomodulin (sTM), von Willebrand factor (vWf), soluble vascular cell adhesion molecule-1 (sVCAM-1) and sE-selectin were assessed at the commencement of the study in all participants and were repeated at 2, 6 and 12 months of follow-up in patients without thromboembolisms. RESULTS: Patients with FSGS during active stage showed significantly higher levels of CECs, sTM, vWf, sVCAM-1 and sE-selectin when compared with controls. Moreover, patients with thromboembolisms had higher CECs and vWf than those without thromboembolisms. In patients without thromboembolisms, endothelial markers except sE-selectin had inverse correlations with serum albumin and were positively related to cholesterol. Multiple analyses showed that cholesterol and serum albumin were independent predictors of CECs and sTM, and vWf and sVCAM-1, respectively. At follow-up, these markers systematically decreased as the disease went into remission, but the increase in vWf and sVCAM-1 persisted even in patients obtaining complete remission for nearly a year. In patients with no response, levels of endothelial markers exhibited no obvious change. CONCLUSION: Patients with FSGS had elevated markers of endothelial dysfunction, which were largely related to the activity of the disease. Meanwhile, levels of CECs and vWf were higher in patients concurrent with thromboembolisms.