目的获取新兵的情绪智力情况,为有针对性地对新兵的心理卫生工作提供依据。方法应用情绪智力技能问卷,测量士兵的10种情绪智力技能,并考查情绪智力技能问卷与传统智商分数以及人格测验中的心理健康分数之间的关系。结果士兵智商分数与决策、自尊及时间管理间呈正相关,相关系数(r)分别为0.301、0.321和0.287(P<0.05);心理健康分数与各个情绪技能间呈中度相关(P<0.01)。结构效度,同一领域内分测验间相关比较高,而从属于不同领域的分测验之间相关比较低。结论士兵情绪智力技能与智商及心理健康状况有一定的关联性。情绪智力技能问卷的信度、效度结果比较理想,但仍存在一些问题,需要作进一步的研究。

In our previous study, we proposed that there may be an unknown pathway in the upper stream of the known signal transduction pathway of Ciliary neurotrophic factor (CNTF) that mediates the neuro-protective function of CNTF In the present experiment, we observed that the neuro-protective function of the non-classic signal transduction pathway in a L-NMDA (a glutamic acid ion type receptor atagonist) induced hippocampal neuron injury model, using primary culture rat hippocampal neurons, continuous photography and gp130 immunohistochemical assay. The results showed that L-NMDA induced injurious reaction of hippocampal neurons, and CNTF was able to inhibit the toxic action of L-NMDA on hippocampal neurons. Additionally, when JAK/STATs in the known classic signal transduction pathway of CNTF were blocked by PTPi-2, the protective effect of CNTF against L-NMDA injury still existed. L-NMDA caused a rapid increase in the concentration of hippocampal intracellular free [Ca2+](i). CNTF was able to attenuate L-NMDA-induced elevation of [Ca2+](i), and blocking JAK/STATs in the known classic signal transduction pathway of CNTF did not affect L-NMDA-induced elevation of [Ca2+](i), indicating that, apart from the known classic signal transduction pathway, there may be some other transduction pathways for CNTF to exert the protective effect on hippocampal neurons, and this pathway is related to[Ca2+].

先前我们曾提出,在已知的CNTF信号传导通路上游可能存在新途径介导其神经保护作用.运用原代培养大鼠海马神经元、活细胞连续照相、活细胞计数、活细胞内游离[Ca2+]测定及gp130免疫组化等方法,以Glu离子型受体激动剂L-NMDA诱发海马神经元损伤为细胞损伤模型,用JAK/STATs阻断剂PTPi-2阻断CNTF已知的经典信号传导途径,观察CNTF非经典信号传导途径的神经保护功能,并探讨其可能机制.结果表明,L-NMDA可引起海马神经元的损伤反应,CNTF可有效抑制L-NMDA对神经元的毒性作用; 使用PTPi-2阻断已知的CNTF经典信号传导途径中JAK/STATs后,CNTF保护海马神经元抵抗L-NMDA的损伤作用仍然存在.L-NMDA可引起海马神经细胞内游离Ca2+浓度([Ca2+]i)迅速升高,CNTF可显著减弱L-NMDA引起的[Ca2+]i升高,阻断CNTF的经典信号传导途径中JAK/STATs并不影响L-NMDA引起的[Ca2+]i升高,表明除了已知的经典信号传导通路,CNTF发挥保护海马神经元作用还有其他信号传导途径,这一途径与胞内[Ca2+]有关.

军队是一个特殊的职业群体,人格特质对军事活动和行为可产生较大影响,人格因素在应激所致心理问题中的作用也存在差别.研究和探讨不同军事人员的性格特征,是甄选和淘汰不合格人员、提高军人的心理素质、制定科学规范有效的干预措施的基础,这对有效实施个性化应激管理,保证安全作业,提高作业绩效,增强部队的战斗力,减少非战斗减员有着重要意义.本文就不同人格特质在战时、平时,噪声环境,高原环境,潜艇人员以及渡海登陆演习等军事应激中的作用、特点进行综述.

Objective:To observe the effect of ciliary neurotrophic factor (CNTF) on the increase of hippocampal neurons -[Ca~(2+)-]_i induced by thapsigargin (Tg), a sarco/endoplasmic reticulum Ca~(2+)-ATPase (SERCA2a) inhibitor. Methods: The primarily cultured hippocampal neurons of newborn SD rats(within 24 h of delivery) were prepared after 10-14 d culture. The intracellular -[Ca~(2+)-]_i was measured with Fura-2/AM in real time. The neurons were divided into 3 groups. Group A (n=20), EGTA (3 mmol/L);Group B (n=40), EGTA (3 mmol/L) + Tg (10 μmol/L);and Group C (n=12), EGTA (3 mmol/L) +Tg (10 μmol/L) +CNTF (500 U/μl). Results: When the extracellular Ca~(2+) was chelated by enough EGTA, -[Ca~(2+)-]_i was ≤(30.73±7.25) nmol/L; after EGTA+Tg was added, -[Ca~(2+)-]_i significantly increased(-[Ca~(2+)-]_i≥-[91.55±12.24-] nmol/L); and after EGTA+Tg+CNTF was added, -[Ca~(2+)-]_i was markedly reduced compared with that in group B (-[Ca~(2+)-]_i≤-[26.09±7.16-] nmol/L, P0.01). Conclusion: CNTF can significantly decrease the inhibitive effect of Tg on SERCA2a and thus reduce the cytoplasm -[Ca~(2+)-]_i, suggesting that CNTF may improve the uptaking of -[Ca~(2+)-]_i from cytoplasm and reduce the Ca~(2+) load in hippocampal neurons.

The hippocampus is one of the most important brain areas involved in stress response and plays a critical role in memory processes. In recent years, many studies have been achieved on the individual differences in the vulnerability to stress and memory, and the effects of cell adhesion molecules (CAMs) in memory. This paper reviews the main research results.

Objective:The neuro-protective effects of CNTF on hippocampal neurons via unknown transduction pathway were observed and its mechanism was investigated. Damaged hippocampal neurons, which induced by ionotrophic glutamate receptor agonist L-NMDA, were used as damaged model. JAKSTATs inhibitor PTPi-2 was used to block the classical transduction pathway of CNTF. Method:Primary culture hippocampal neurons,confinuous photography of the living cells and number of living cells count were carried out. Result:L-NMDA could damage neurons. This damaged effect was dose-dependent when the process went on 1—2h and was time-dependent when the concentration of L-NMDA arranged from 0μmolL to 500μmolL. CNTF could decrease damaged effects on hippocampal neurons induced by L-NMDA. The protective effects of CNTF on hippocampal neurons still existed after JAKSTATs was blocked by PTPi-2. Conclusion:CNTF can exhibit protective effects on injured hippocampal neurons.The effects might be performed via unknown rapid pathway besides already known transduction pathway.

有机体暴露于不同的应激源,神经内分泌反应不同.因此,应激可以被视为反映特异性中枢解剖和功能回路存在与否的反应.近年来,研究者对特异性应激回路已做过部分讨论[1-3],这些应激回路分别参与交感神经元和肾上腺髓质以及HPA轴活性的调节.本文通过分析五种不同的应激源在中枢神经系统可能的作用途径和靶细胞,发现不同的应激源在唤起应答和在神经回路中的作用均有所不同.

有机体暴露于不同的应激源,神经内分泌反应不同.因此,应激可以被视为反映特异性中枢解剖和功能回路存在与否的反应.近年来,研究者对特异性应激回路已做过部分讨论[1-3],这些应激回路分别参与交感神经元和肾上腺髓质以及HPA轴活性的调节.本文通过分析五种不同的应激源在中枢神经系统可能的作用途径和靶细胞,发现不同的应激源在唤起应答和在神经回路中的作用均有所不同。

介绍心理应激学的产生、发展以及现代应激观念,系统地分析护理人员的应激源、应激机制及应对措施,旨在现代应激观的指导下,增强护理人员成功应对应激源的能力,促进护理管理者有效采取应激干预措施.