Publications by authors named "Shu Chang He"

Article Synopsis
  • The study examines how childhood trauma interacts with genetic variations in the serotonin (5-HT) and endocannabinoid (eCB) systems to predict burnout in individuals.
  • Results show that certain genetic polymorphisms, especially FAAH rs324420, influence the relationship between childhood trauma, job stress, and burnout symptoms like reduced personal accomplishment and emotional exhaustion.
  • It concludes that these genetic factors together may impact how childhood experiences affect burnout, highlighting the complexity of these interactions in mental health.
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Both the BDNF gene rs6265 and the FKBP5 gene rs1360780 polymorphisms are independently associated with adult psychotic-like experiences, when exposed to high childhood abuse; however, it remains unclear whether the relationship between childhood abuse and burnout is moderated by these two single nucleotide polymorphisms (SNPs). Furthermore, there is an interaction between glucocorticoid receptor transcriptional activity and BDNF signaling. Therefore, we investigated the interaction of these two SNPs with childhood trauma in predicting burnout.

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The oxytocin receptors located in the corticotropin-releasing factor neurons of the paraventricular nucleus are stimulated by oxytocin. Oxytocin functions as the regulator of the corticotropin-releasing factor system and in turn promotes sleep quality. The objective of this study was to examine the main and genotype-genotype interactive effects of the oxytocin receptor gene (OXTR) polymorphisms on sleep quality.

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Background: Job burnout is related to both environmental and genetic factors. However, previous studies on job burnout in teachers have mainly focused on potential stressors in the environment, while ignoring genetic factors. Brain-derived neurotrophic factor (BNDF) may be a pathogenic factor involved in burnout symptoms.

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Background: Empathy refers to an individual's ability to experience the emotional and cognitive processes of another person during social interactions. Although many studies have examined the effects of genetic variation on emotional empathy, little is currently known about whether genetic factors may influence cognitive empathy. This study investigated the relationship between BDNF rs11030101 genotype, job stress, and empathy, especially cognitive empathy, in a Chinese Han population.

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Rationale: Job stress can lead to job burnout, and BDNF polymorphism has been found to be involved in its psychopathological mechanism. Research needs a better understanding of the important role of gene × environment (i.e.

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Background: Job burnout is a stress-related syndrome influenced by both genetic and environmental factors. Poor sleep quality acting as a stressor may lead to job burnout. The oxytocin receptor gene (OXTR) related to stress reactivity may also exert an effect on job burnout.

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Background: Some studies have shown that long-term exposure to job stress could result in burnout, and BDNF polymorphism may play an important role in its psychopathological mechanism. However, the inter-relationships between the job-related stress, serum BDNF level, BDNF genotype and job burnout have not been examined. This study was to explore the job stress × BDNF rs2049046 interaction and the role of serum BDNF level in job burnout in a Chinese Han population.

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Background: Burnout is a worked-related stress syndrome caused by long-term exposure to a stressful environment. Dysregulation of the hypothalamic- pituitary- adrenal (HPA) axis may be involved in both stress and burnout; an evaluation of genetic polymorphisms which alter activity in the HPA may be predictive of how likely an environment is to produce burnout.

Methods: Using a cross-sectional design, this study examined whether corticotrophin-releasing hormone receptor 1 (CRHR1) gene polymorphism rs110402 is a risk factor for burnout; further, it explores whether the interaction of stress × CRHR1 gene predicts burnout in the healthcare workers in a Chinese Han population.

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Objective: Many studies have reported that long-term exposure to job-related stress can lead to burnout, which may be influenced by genetic and environmental factors. Burnout correlates with depression. This study investigated whether one tag polymorphism rs6354 in 5-HTT gene modulated the influence of job-related stress on burnout in the medical professionals in a Chinese Han population, which to our best knowledge has not been explored.

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Background: Chronic exposure to job-related stress can lead to depression and BDNF polymorphism may play an important role in this process. The role of the stress × BDNF Val66Met interaction in depression has been studied widely using childhood stress, but few studies have utilized chronic stress in adulthood as a moderator. This study was to examine the chronic stress × BDNF Val66Met interaction in job-related depression in the healthcare workers in a Chinese Han population, which has not been reported yet.

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Cognitive deficits have been regarded as one of the most significant clinical symptoms of depressive disorder. Accumulating evidence has shown that apolipoprotein B (ApoB) levels, which are responsible for inducing neurodegeneration, may be involved in cognitive deficits. This study examines cognitive deficits, and the correlation of serum ApoB levels with cognitive deficits of depressive disorder.

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Excessive free radical production leading to oxidative stress may be involved in the pathophysiology of schizophrenia. Oxidative stress increases serum thioredoxin (TRX), a redox-regulating protein with antioxidant activity recognized as an oxidative-stress marker. The aim of this study was to assess the clinical significance of serum TRX levels in various stages of schizophrenia.

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Objective: To study the possible mechanism of Al neurotoxicity, we evaluated the oxidative function injury of mitochondria in the primary cultured neurons that were exposed to various concentrations of AlCl3.

Methods: Neurons from newborn SD rats were primarily cultured. Then they were exposed to AlCl3 of 0 micromol/L, 50 micromol/L, 100 micromol/L, and 500 micromol/L.

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