Correlations among childhood trauma, autistic traits and dysexecutive functions in college students / 中国心理卫生杂志

Objective:To explore the relations among childhood trauma,autistic traits and dysexecutive functions in college students.Methods:Totally 2757 college students were assessed with the Childhood Trauma Questionnaire (CTQ).Sixty-three college students were randomly selected as the abused group according to the subscale cutoff point of CTQ Scale defined by Bernstein,and 93 students were randomly selected from students without history of childhood trauma as the control group.They were assessed with the Self-Rating Depression Scale (SDS),Autism Spectrum Quotient (AQ) and Dysexecutive Questionnaire (DEX) to measure depression,autistic traits and abnormality of executive functions,respectively.The individuals from the top and below 27％ of CTQ and AQ scores were defined as higher or lower-level different types of abused group and higher or lower-level autistic traits group,respectively.Results:The differences of DEX scores between higher or lower-level four types of CTQ (emotional abuse,physical abuse,sexual abuse,emotional neglect and physical neglect) and between higher or lower-level autistic traits group were significant (Ps ＜0.05).DEX scores in all higher-level groups were higher than all lower-level groups.Regression analysis showed that DEX score could be positively predicted by scores of emotional abuse,AQ and SDS (β =0.17-0.32,P ＜0.05).SDS score was a mediator between scores of emotional abuse and DEX,and between scores of autistic traits and DEX (95％ confidence interval were 0.05-0.32 and 0.07-0.55,respectively).Conclusion:Childhood trauma and autistic traits may positively predict dysexecutive function,and depression may play a mediating role between emotional abuse and dysexecutive function,and between autistic traits and dysexecutive function.

Effect of doxazosin and metoprolol on vascuIar remodeling in rats with hypertension induced by abdominal aorta coarctation / 中国药理学与毒理学杂志

OBJECTIVE To investigate the effect of doxazosin(DOX) and metoprolol( MET) on vascular remodeling in rats with abdominal aorta coarctation (AAC). METHODS An animal model was established by AAC. Two weeks later, the rats were treated with DOX (10 mg.kg-1 per day) or MET (20 mg.kg-1 per day) for six weeks. Blood pressure was measured using carotid artery intubation with a MP150 polygraph. The media thickness, wall cross-sectional area and thickness / internal diameter ratio were calculated by morphometry. Vascular fibrosis was evaluated by Masson′s trichrome staining. The collagen and fibronectin expression in vascules was measured by Western blotting. RESULTS Compared with the sham group 〔(17.6±0.5)kPa〕, the mean arterial blood pressure in the model group〔(23.3±0.7)kPa〕 was significantly increased(P<0.05), but was lowered by DOX 〔(20.5±0.7)kPa〕 and MET 〔(19.0±0.4) kPa〕 (P<0.05). Moreover, HE staining showed that tunica media thickness, artery vessel area and thickness / inner diameter in the model group were increased by 39.5%, 46.4% and 27.0%(P<0.05), respectively. The tunica media thickness was decreased by 16.0% and 26.1%( P<0.05), respectively, the artery vessel area by 22.8% and 26.1%(P<0.05), respectively, and the thick-ness / inner diameter by 17.0% and 26.0%( P<0.05) when the rats were treated with DOX and MET. Masson staining showed that the collagen accumulation in vascules increased, suggesting that AAC induced fibrosis. Meanwhile, vascular fibrosis induced by AAC was also reduced by MET or DOX. Western blotting also proved that the increase of collagen and fibronectin induced by AAC could be attenuated by DOX and MET(P<0.05). CONCLUSION DOX and MET are effective in suppressing the role of norepi-nephrine in vassels, which can attenuate AAC-induced vassels remodeling by preventing the binding between norepinephrine and adrenoceptors.

Effects of HIP in protection of HSP70 for stress-induced cardiomyocytes injury and its glucorticoid receptor pathway.

Moderate levels of stress can be beneficial to health, while stress overload can cause injury or contribute to diseases. Despite a number of studies of adaptation or stress damage, the mechanisms of adaptation and stress damage remain far from clear. The effect and mechanisms of adaptation on cardiomyocytes damage caused by stress overload are discussed in this study. Data showed that mild repeated stress mitigated stress overload-induced cardiomyocyte injury both in an animal model of restraint stress and in H9C2 cells with GC (glucocorticoid) treatment. HSP70, HIP expression and interaction between HSP70 and HIP increased during adaptation induced by mild stress both in animals and H9C2 cells. Overexpression or inhibition of HSP70 in H9C2 cells with pCDNA-3.1-Hsp70 or KNK437 (HSP70 inhibitor) showed that HSP70 can protect H9C2 cells from GC-induced cell damage. A luciferase assay showed that Hsp70 plays its protective role through inhibition of GR transcription activity dependent on the interaction with HIP. These results indicated that HSP70 may promote adaptation with its interacting protein HIP, and increased levels of HSP70 and its interacting protein HIP during adaptation may play a protective role on stress-overload-induced cardiomyocyte injury.

Potentral of plasma level of HSP70 as a biological marker of military stress / 军事医学

Objective To study the possibility of the plasma level of heat shock protein 70(HSP70) being used as a bi-ological marker of military stress .Methods Soldiers who returned from a 6-month-navigation were chosen as subjects , the HSP70 level of plasma was measured with the ELISA assay and stress questionnaires and Self -rated Health Measurement Scale (SRHMS) were used to measure the stress level .Results The soldiers′plasma level of HSP70 was 31.40%higher than that of the control .The stress questionnaire indicatesd that the level of thinking and anxiety , negative mood and somat-ic symptoms were higher than normal .The SRHMS indicated that the level of physiological health ,mental health and social health was lower than normal .The plasma level of HSP70 was associated with the level of military stress .Conclusion The plasma level of HSP70 may be used as an important predictor of military stress .It can predict the level of military stress injury.

Effect of different military stress loads and modes on level of stress hormones in rats / 军事医学

Objective To systematially observe the different patterns and leves of military stress on modified multitle-platform method the level of stress-related hormones in rats .Methods A sleep deprivation model was established by water environment modified multiple-platform method(MMPM).A restraint stress model was established by self-made bondage cage.Chronic unpredictable mild stress ( CUMS) model was established by action control , cage damp, cage tilt, night lightening, water and food fasting , empty bottles stimulation and group feeding methods .Cortisol, catecholamines and 5-HT levels were detected to observe the different military stress loads and modes on the level of stress hormones .Results The level of serum cortisol increased significantly ( P <0.05 ) after 5 days of sleep deprivation .The level of serum catecholamines increased significantly (P<0.05) after 1 day of sleep deprivation.The cortisol concentration increased and the level of 5-HT decreased in serum after 4 weeks CUMS.The level of catecholamines increased significantly (P<0.05) after 2-8 weeks of CUMS, increased significantly (P<0.05) after 1 week of restraint stress , and returned to normal after 3-4 weeks of restraint stress .The level of serum cortisol increased significantly after 3 -4 weeks of restraint stress . Conclusion Cortisol levels gradually increased with the level of stress in different military stress modes , which can serve as an index to evaluate the level of different stress modes .

Phosphorylated nerve growth factor-induced clone B (NGFI-B) translocates from the nucleus to mitochondria of stressed rat cardiomyocytes and induces apoptosis.

Stress induces cardiac dysfunction and cardiomyocyte injury, and while current data indicate that mitochondria play a key role in this process, the mechanisms remain unknown. In this study, we found that in rats, restraint stress induced nerve growth factor-induced clone B (NGFI-B) translocation from the nucleus to mitochondria in cardiomyocytes. This translocation promoted cytochrome c release from mitochondria to the cytoplasm, which ultimately resulted in cardiomyocyte apoptosis. We also found that stress induced oversecretion of glucocorticoids and activated the protein kinase A (PKA) pathway in cardiomyocytes. Enhanced PKA activity increased NGFI-B serine phosphorylation, which caused NGFI-B to translocate from the nucleus to mitochondria. Moreover, a PKA peptide inhibitor blocked NGFI-B serine phosphorylation and translocation. Our data demonstrate that stress affects cardiomyocytes by inducing NGFI-B mitochondrial translocation via serine phosphorylation, which in turn initiates mitochondrial-mediated apoptosis.

Comparative Proteomics Analysis of Hippocampal Proteins From Chronic Stressed Rats / 生物化学与生物物理进展

Chronic stress can induce hippocampus injury such as neuron loss, dendrite atrophy, but its mechanism and molecular basis remain unclear up to now. To understand the molecular mechanism on protein level and find the crucial proteins which correlated with chronic stress-induced injury, two-dimensional electrophoresis was applied to separate the hippocampal total proteins of control group and restraint stressed rats, then the differential expressed proteins were detected by image analysis and identified by matrix assisted laser desorption /ionization time of flight mass spectrometry (MALDI-TOF-MS) as well as database searching. Moreover, the 2-DE results were verified on the mRNA level by semi-quantitative RT-PCR. The hippocampal 2-DE map with high resolution and good reproducibility of control and stress group rats were obtained. Fourteen differentially expressed protein spots were detected and eleven proteins were successfully identified, most of these proteins were involved in the process of energy metabolism and signal transduction. These results provide a clue for elucidating the mechanism of chronic stress-induced hippocampal injury and are useful for elevating the adaptability to stress.

Protective effect of heat-stress preconditioning on anoxic endothelial cells and its mechanism / 中国病理生理杂志

AIM: To observe the protective effect of heat stress preconditioning on endothelial cells under anoxia and explore its mechanism. METHODS: The endothelial cells were divided into 4 groups: (1) anoxia; (2) heat stress; (3) heat stress preconditioning + hypoxia; (4) control. LDH activity was measrued by using Automatic Biochemistry Analysis-Meter. Cell death rate was determined by trypan blue, NO production was tested by measuring NO - 2/NO - 3 content in cellular culture medium by using Griess assay. RESULTS: LDH release and cell death rate of the anoxia endothelial cells significantly increased compared with control; 39℃ heat stress preconditioning reduced those increment by 29、47%, 33.67% respectively. 41℃ heat stress preconditioning has no protection against the anoxia-induced injury in endothelial cells. The NO production in anoxic endothelial cells decreased markedly. 39℃ heat stress preconditioning induced the increase in NO production in endothelial cells, but 41℃ heat stress preconditioning made the NOS activity decrease. The NO production was correlated negatively with LDH release and cell death rate in anoxic endothelial cells. CONCLUSION: The heat stress preconditioning within the limits can protect the endothelial cells from anoxia injury. The increase in NO in endothelial cells may play an important role in the mechanism of the protective effect.

Mitochondrial membrane mechanism of rat heart injury induced by stress / 中国病理生理杂志

AIM: To investigate the effects of stress on the opening of mitochondrial membrane permeability pore (PTP) in rat heart and explore the possible molecular mechanism underlying PTP opening. METHODS: Stress animal model was established. After strained for differnet time, all rats were killed and PTP opening degree were examined by spectrophotometer. Bcl-2, Bax expression levels were determined by Western blot. RESULTS: Stress induced PTP opning, Bcl-2 expression inhibition and Bax level elevation in myocardial mitochondria. CONCLUSION: PTP opening was the important mitochondrial mechanism of stress-induced heart injury. Decrease in Bcl-2 expression and increase of Bax level may be an important molecular basis for PTP opening.