This study compared the efficacy of the Wijma Delivery Expectancy/Experience Questionnaire (W-DEQ) and the Childbirth Attitudes Questionnaire (CAQ) in assessing fear of childbirth (FOC) among hospitalized pregnant women, aiming to identify a practical screening tool. A total of 184 pregnant women were recruited from the Northwest Women’s and Children’s Hospital using convenience sampling. Data were collected through the General Demographic Questionnaire, Fear of Birth Scale (FOBS), W-DEQ, and CAQ. Using the FOBS as a reference, the diagnostic performance of the W-DEQ and CAQ was evaluated via receiver operating characteristic curves and Bayesian discriminant analysis. The area under the curve (AUC) for the W-DEQ (0.888) was significantly higher than that of the CAQ (0.789; Z = −2.189, p < 0.05). Optimal cutoff values were 80.5 for the W-DEQ and 31.5 for the CAQ. Cross-validation revealed accuracy rates of 75.6% and 70.7%, respectively. The incidence of FOC, as assessed by the W-DEQ, CAQ, and FOBS, was 29.9%, 43.9%, and 37.2%. Both tools demonstrated good reliability and validity, but the W-DEQ showed superior performance. It is recommended as the preferred tool for assessing FOC among pregnant women in China due to its comprehensive evaluation capacity.

微RNA(miRNA)是一类重要的调节转录后基因表达水平的内源性非编码RNA,参与细胞生长和组织分化等多种生理病理过程.近年来,对miRNA在中枢神经系统疾病中的研究逐渐增多且多聚焦于某几个miR-NA.因此,本文综述了目前在中枢神经系统疾病中研究的热点miRNA,阐述了这些miRNA在阿尔茨海默病(AD)、帕金森病(PD)、抑郁症和药物成瘾中的表达变化及作用机制,以期为中枢神经系统疾病机制的研究和诊断治疗提供新方向.

目的 探究多巴胺D3受体在围绝经期抑郁症发病中的作用.方法 基于前期围绝经期抑郁动物模型,采用RT-PCR方法,研究围绝经期抑郁小鼠伏隔核D3受体mRNA的变化;进一步,采用D3受体敲除(D3 receptor knockout,D3RKO)小鼠与相同遗传背景的野生型(wild type,WT)小鼠,分别构建青年组与围绝经期小鼠,采用强迫游泳、悬尾实验检测小鼠抑郁样行为.结果 伏隔核D3受体mRNA在围绝经期明显下降(P<0.05);慢性束缚应激会诱导青年期小鼠D3受体mRNA下降(P<0.05);慢性束缚应激会诱导围绝经期小鼠D3受体进一步下降(P<0.05).围绝经期D3RKO小鼠相对于围绝经期WT小鼠,在强迫游泳实验中不动时间明显延长(P<0.05);围绝经期D3RKO小鼠相对于青年D3RKO小鼠,在强迫游泳、悬尾实验中不动时间明显延长(P<0.05);围绝经期不会明显改变WT小鼠不动时间(P>0.05).结论 伏隔核多巴胺D3受体在围绝经期明显下降;D3受体的大幅度下降或缺失可能参与围绝经期抑郁症的发病.

目的 初步探讨鼠李糖乳杆菌的产后抗抑郁作用及其潜在机制.方法 在雌性小鼠妊娠期间施用地塞米松磷酸钠建立产后抑郁症(PPD)模型.适应性喂养结束后,将受孕的50只雌性小鼠随机分为鼠李糖乳杆菌干预低剂量组(Ⅰ组)、鼠李糖乳杆菌干预高剂量组(Ⅱ组)、阳性对照组(Ⅲ组)、模型对照组(Ⅳ组)和空白对照组(Ⅴ组).通过灌胃给药进行干预,Ⅰ组和Ⅱ组小鼠分别给予鼠李糖乳杆菌1×107和1×108 CFU(kg·d),Ⅲ组小鼠给予1.8 mg/(kg·d)帕罗西汀,Ⅳ组和Ⅴ组小鼠给予等量的生理盐水,干预时间为4周.通过24 h食物消耗实验、旷场实验、糖水消耗实验检测各组小鼠的行为学表现,反相高效液相色谱法测定5-羟色胺(5-HT)、去甲肾上腺素(NE)及多巴胺(DA)的浓度,RT-qPCR法检测小鼠盲肠中粪肠球菌、双歧杆菌、乳酸杆菌和大肠杆菌的变化.结果 造模前各组小鼠摄食量、体质量变化率、旷场移动距离和速度、糖水消耗百分比差异均无统计学意义(P>0.05).造模后与Ⅴ组相比,Ⅰ组、Ⅱ组、Ⅲ组和Ⅳ组小鼠的摄食量和体质量变化率差异无统计学意义,而旷场移动距离、移动速度和糖水偏爱百分比明显降低,差异有统计学意义(P<0.05).鼠李糖乳杆菌干预后,与Ⅳ组相比,Ⅰ组、Ⅱ组小鼠的抑郁样行为得到改善,体质量变化率、旷场移动距离和速度、糖水偏爱百分比和单胺神经递质浓度较Ⅳ组显著增加(P<0.05),粪肠球菌、大肠杆菌和乳酸杆菌显著下降(P<0.05),双歧杆菌有上升趋势,但未见统计学差异;摄食量没有明显变化.结论 鼠李糖乳杆菌能够改善产后小鼠抑郁样行为,影响小鼠单胺类神经递质,调节肠道菌群,为产后抑郁相关研究提供了新的方向.

目的:探讨鼠李糖乳杆菌对小鼠产后抑郁样行为和运动能力的影响.方法:在小鼠妊娠期间施用地塞米松磷酸钠建立产后抑郁症(PPD)小鼠模型.将受孕的25只小鼠随机分为:鼠李糖乳杆菌干预低剂量组(Ⅰ组)、鼠李糖乳杆菌干预高剂量组(Ⅱ组)、阳性对照组(Ⅲ组)、模型对照组(Ⅳ组)和空白对照组(Ⅴ组).通过灌胃给药的方式进行干预,Ⅰ组和Ⅱ组小鼠分别给予鼠李糖乳杆菌1×107 CFU/(kg·d)和1×108 CFU/(kg·d),Ⅲ组小鼠给予1.8 mg·kg-1·d-1帕罗西汀,Ⅳ组和Ⅴ组小鼠给予等量的0.9％氯化钠溶液,干预时间为4周.通过24 h食物消耗实验、黑白箱实验、强迫游泳实验和悬尾实验检测各组小鼠的行为学表现.结果:造模前各组小鼠摄食量、体质量变化率、白箱停留时间和黑白箱穿梭次数、不动状态持续时间和悬尾不动时间方面,差异均无统计学意义(P>0.05).与造模前相比,造模后和干预后各组小鼠摄食量减少,体质量变化率增加(P<0.05);造模后和干预后Ⅰ组、Ⅱ组、Ⅲ组和Ⅳ组小鼠强迫游泳不动持续时间和悬尾不动时间增加.与造模后相比,干预后各组小鼠体质量变化率增加(P<0.05),干预后Ⅰ组、Ⅱ组和Ⅲ组小鼠强迫游泳不动持续时间和悬尾不动时间减少.造模后与Ⅴ组相比,其余组小鼠黑白箱穿梭次数有所减少,悬尾不动时间升高(P<0.05).干预后黑白箱穿梭次数各组间差异均无统计学意义(P>0.05);干预后与Ⅴ组比较,其余组小鼠的悬尾不动时间增加(P<0.01);与Ⅳ组比较,Ⅰ组、Ⅱ组和Ⅲ组的悬尾不动时间减少(P<0.01).结论:雌性小鼠妊娠期间施用地塞米松磷酸钠表现出产后抑郁样行为,鼠李糖乳杆菌干预后对产后小鼠的焦虑抑郁和运动能力有一定改善.

BACKGROUND:Middle-aged females, especially perimenopausal females, are vulnerable to depression, but the potential mechanism remains unclear. Dopaminergic and GABAergic system dysfunction is involved in the pathophysiology of depression. In the current study, we used 2-month-old and 11-month-old C57BL/6 mice as young and middle-aged mice, respectively. Chronic immobilization stress (CIS) was used to induce depressive-like behaviour, and the sucrose preference test (SPT), tail suspension test (TST) and forced swim test (FST) were used to assess these behaviours. We then measured the mRNA levels of dopamine receptor D1 (DRD1) and the GABAA receptors GABRA1, GABRB2 and GABRG2 in the nucleus accumbens (NAc) and prefrontal cortex (PFC).RESULTS:We found that immobility time in the FST was significantly increased in the middle-aged mice compared with the middle-aged control mice and the young mice. In addition, the preference for sucrose water was reduced in the middle-aged mice compared with the middle-aged control mice. However, CIS did not induce obvious changes in the performance of the young mice in our behavioural tests. Moreover, the middle-aged mice exhibited equal immobility times as the young mice in the absence of stress. Decreases in the mRNA levels of DRD1, GABRA1, and GABRB2 but not GABRG2 were found in the NAc and PFC in the middle-aged mice in the absence of stress. Further decreases in the mRNA levels of DRD1 in the NAc and GABRG2 in the NAc and PFC were found in the middle-aged mice subjected to CIS.CONCLUSIONS:Our results suggested that ageing could not directly induce depression in the absence of stress. However, ageing could induce susceptibility to depression in middle-aged mice in the presence of stress. CIS-induced decreases in DRD1 and GABRG2 levels might be involved in the increase in susceptibility to depression in this context.

C-藻蓝蛋白具有抗癌、抗氧化、抗炎活性等多种功能,然而其对乳腺癌细胞的抗癌作用及机制尚不明确.本研究应用不同浓度(0～500 μg/mL)的C-藻蓝蛋白处理人乳腺癌细胞系MDA-MB-468.研究显示,C-藻蓝蛋白以剂量依赖性方式抑制MDA-MB-468细胞的增殖并降低细胞的菌落形成能力.C-藻蓝蛋白通过上调了Fas和cleaved-caspase 3的表达并下调Bcl-2的表达来诱导细胞凋亡.C-藻蓝蛋白处理以剂量依赖性方式显著降低COX-2的表达并抑制细胞迁移能力.C-藻环蛋白以剂量依赖性方式促进p38 MAPK和JNK的磷酸化,p38 MAPK和JNK抑制剂处理可显著抑制C-藻红蛋白诱导的细胞死亡.本研究表明C-藻蓝蛋白能够抑制三阴性乳腺癌MDA-MB-468细胞的增殖,促进细胞凋亡,抑制细胞迁移能力.C-藻蓝蛋白的抗癌机制可能与激活p38 MAPK和JNK信号传导有关.

Objective: To examine the cellular distribution and the expression of CD200 and its receptor 1 (CD200R1) in human deciduas in first-trimester pregnant women with spontaneous early abortion (SEA) and normal pregnancy, and to explore their role in the etiology of SEA.Subjects and methods: Thirty-five women at 6-10-week gestation with SA and 30 women of similar gestational age with a healthy pregnancy were recruited. Expression of CD200 and CD200R1 in the deciduas was determined using immunohistochemistry, confocal laser scanning microscope, Western blot, and real-time PCR (RT-PCR).Results: The decidual stromal cells, glandular epithelial cells, and vessel endothelial cells during the first trimester of pregnancy express both CD200 and CD200R1 proteins. During this period, the expression of CD200 in glandular epithelial cells and vessel endothelial cells is significantly higher in normal pregnancy than that in women with SEA (0.3079 ± 0.0674 versus 0.2735 ± 0.0515; 0.4077 ± 0.1366 versus 0.3249 ± 0.0993); the expression of CD200R1 in stromal cells, decidual stromal cells, glandular epithelial cells is significantly higher during normal pregnancy than SEA (0.2574 ± 0.0588 versus 0.2292 ± 0.0415; 0.3617 ± 0.1046 versus 0.2804 ± 0.0640). Western blot analysis showed an approximately 44% decrease in CD200R1expression in decidua in the SEA versus the controls. Finally, in decidua, the expression of both CD200 protein and CD200R1 transcript are significantly higher in healthy first-trimester pregnancy than in SEA (CD200: 2.2089 ± 1.2754 versus 0.7241 ± 0.2143; CD200R1: 15.7843 ± 10.7085 versus 7.3381 ± 5.8529).Conclusions: Women with SEA have a lower level of CD200 and CD200R1 expression in deciduas compared with normal pregnant women suggesting that under physiological conditions, CD200 and CD200R1 expression by deciduas is important to prevent fetal loss ensure a successful pregnancy.

抑郁症已成为世界范围内的首要致残原因.抑郁症发病女性高于男性,围绝经期女性抑郁症发病明显增高,但是机制仍然不明确.抑郁症发病与多种递质紊乱有关,而在围绝经期,女性由于卵巢功能衰退,会出现多种激素水平波动,并伴随单胺类递质、神经活性甾体、GABA、脑源性神经营养因子等的改变,这些变化可能是导致女性围绝经期抑郁症发病的神经生物学机制.

目的 研究不同剂量甲基苯丙胺(methamphetamine,METH)对小鼠空间学习记忆的影响及可能机制.方法 以C57BL/6小鼠为研究对象,采用0.5、1.0、2.0mg/kg的METH或生理盐水,在每天的Morris水迷宫行为学习前腹腔注射给药,连续5d,每天4轮的定位航行实验训练,最后一次训练完24 h后进行空间探索实验,观察不同剂量METH对小鼠空间学习记忆的影响.测试后立即采用颈椎脱臼法处死小鼠,并剥离海马组织,采用Western blot方法检测海马中ERK1/2(extracellular signal-regulated kinase)、CREB(cAMP response element-binding protein)磷酸化水平的变化.结果 相比盐水组小鼠,1.0 mg/kg METH组小鼠爬台潜伏期明显缩短(P＜0.05),在目标象限的停留时间(P＜0.05)、穿台次数(P＜0.05)明显增加;0.5、2.0 mg/kg METH对小鼠空间学习记忆无明显影响,但是0.5 mg/kg METH组小鼠呈现记忆促进趋势,而2.0 mg/kg METH组小鼠呈现记忆破坏趋势;1.0 mg/kg METH组小鼠明显伴随海马中p-ERK1/2(P＜0.05)、p-CREB(P＜0.05)水平的增高.结论 1.0 mg/kg METH明显提高小鼠空间学习能力及记忆水平;在0.5、1.0、2.0 mg/kg的METH三个剂量之间,METH的效应呈倒U曲线型;海马中ERK1/2、CREB可能参与METH诱导的小鼠空间学习记忆的提高.

目的 :调查孕妇在妊娠期压力状况及其影响因素,为提出针对性的干预措施提供依据.方法 :收集陕西地区孕妇1044例,采用一般资料调查表 、妊娠压力量表对其进行问卷调查,分析其妊娠期间压力状况及影响因素.结果 :孕妇妊娠压力总分(26.28±14.25)分,按得分指标分类,轻度压力784例(75.1％),中度压力255例(24.4％),重度压力5例(0.5％);压力源各因子中,"为确保母子健康和安全而引发的压力感"得分指标最高,为43.57％.妊娠压力的主要影响因素为:居住地类别 、对住房的满意度 、与伴侣母亲的关系.结论 :经济状况及家庭成员情感支持是影响孕妇妊娠压力水平的重要因素,为经济困难者提供必要的社会援助 、为家庭情感支持不足者实施心理干预,是缓解妊娠压力,帮助其顺利度过妊娠期,提升母婴健康水平的重要措施.

目的 研究围绝经期小鼠抑郁样行为及相关脑区GABAA受体的改变.方法 采用2、8、12 m雌性C57BL/6小鼠,采用悬尾实验、强迫游泳实验检测小鼠不动时间的变化,研究小鼠抑郁样行为的改变.进一步,采用实时定量PCR方法检测海马,前额叶皮质中GABAA受体Gabra1、Gabrb2及Gabrg2的mRNA改变.结果 三组小鼠在悬尾实验、强迫游泳实验中不动时间无明显差异(P>0.05);海马、前额叶皮质中Gabra1、Gabrb2在12 m组小鼠明显降低(P<0.05);海马中Gabra1水平在3组之间呈逐渐下降,而前额叶皮质中Gabra1,海马、前额叶皮质中Gabrb2在8 m组呈一定程度上升,至12 m时明显下降(P<0.05);海马及前额叶皮质中Gabrg2在3组之间无明显差异(P>0.05).结论 无应激状态下,围绝经期小鼠抑郁样行为无明显变化;小鼠海马及前额叶皮质中Gabrg2可能参与该行为过程;海马、前额叶皮质中Gabra1,Gabrb2在围绝经期明显下降,可能参与应激诱导的围绝经期抑郁易感性.

目的:研究甲基苯丙胺(methamphetamine,METH)重复暴露诱导的小鼠空间学习记忆损伤中可能的分子机制.方法:前期研究发现,1.0mg·kg-1 METH连续给药20d,明显损伤小鼠空间学习记忆.基于此,我们进一步采用Western blot方法检测了海马、前额叶皮质、背侧纹状体中ERK1/2(extraeellular signal-regulated kinase)、CREB(cAMP response element-binding protein)磷酸化水平的变化.结果:METH组小鼠海马中ERK1/2磷酸化水平明显降低(P＜0.05),该变化与小鼠在目标象限停留时间百分比(P＜0.05)、穿台次数(P＜0.05)的改变呈明显相关;METH组小鼠前额叶皮质中ERK1/2磷酸化水平无明显变化;此外,METH组小鼠背侧纹状体中ERK1/2磷酸化水平明显降低(P＜0.05),但该变化与小鼠在目标象限停留时间百分比、穿台次数的改变均无明显相关性.进一步检测发现METH组小鼠海马中CREB磷酸化水平明显降低(P＜0.05),该变化与小鼠在目标象限停留时间百分比(P＜0.05)、穿台次数(P＜0.05)的改变呈明显相关.结论:1.0 mg·kg-1 METH重复暴露会降低小鼠海马中ERK1/2、CREB磷酸化水平,该降低可能参与着METH诱导的小鼠空间学习记忆损伤.

Methamphetamine (METH) administration results in addiction and memory impairment. Previous studies have suggested that levo-tetrahydropalmatine (l-THP), an alkaloid purified from the Chinese herb Corydalis, attenuates the behavioral changes induced by METH. Therefore, in this study, we explored whether l-THP could also protect against the METH-induced memory impairment examined using the Morris water maze (MWM). We found that low dose of METH (1.0 mg/kg) treated for 20 consecutive days prior to the MWM experiment impaired spatial memory retention but not acquisition in mice. In addition, high dose of METH (10.0 mg/kg) treated during the spatial learning phase for five consecutive days impaired both the acquisition and retention of spatial memory. Moreover, both of these impairments induced by METH were reversed by l-THP treatment, indicating a potential protective role of l-THP in METH use.

[目的]研究月经初潮年龄对经前期综合征症状及应对方式的影响.[方法]采用多阶段分层整群抽样的方法,随机抽取中国不同地区共10所医学高校2 379名女大学生为调查对象,采用自制问卷、月经症状量表和月经对策方式量表进行调查.[结果]不同初潮年龄段女大学生的经前期综合征症状得分比较差异有统计学意义(P＜0.01);不同初潮年龄段女大学生月经对策方式得分比较差异有统计学意义(P＜0.001).[结论]不同初潮年龄段女大学生经前期综合征症状及对策方式存在差异,应根据我国女大学生的健康状况提供针对性的健康指导.

This study aimed to investigate the effects of curcumin on macrophages polarization and possible mechanism involved, and to analyze the molecular basis of its antiatherosclerosis activity. RAW264.7 macrophages (M0) and M1 macrophages were treated with curcumin at 0, 6.25, 12.5, and 25 μmol/L with or without GW9662. Using real-time polymerase chain reaction and Western blot analysis, we examined the phenotype markers of M1 [iNOS, interleukin (IL)-1β, IL-6, and MCP-1] and M2 (KLF4, FIZZ1, and MGL1] macrophages. Curcumin reduced the expression of the M1 phenotype markers and upregulated the expression of proliferator-activated receptor γ in M0 and M1 macrophages and IKBα in M1 macrophages. When M1 macrophages were incubated with curcumin and GW9662, the expression of the M1 phenotype markers was decreased, while IKBα was upregulated. The expression of the M2 phenotype markers in M0 and M1 macrophages was upregulated after the curcumin treatment. When M0 and M1 macrophages were incubated with curcumin and GW9662, the expression of the M2 phenotype markers was reduced. Curcumin inhibited the M1 inflammation phenotype as a result of the direct activation of IKBα and polarized the macrophages to become M2 phenotype through the activation of proliferator-activated receptor γ. These findings provide new clues to develop new drug therapy for atherosclerosis.

A central problem in understanding the dopamine system in anxiety and depression is to specify functions of different members of the dopamine receptor family. Recent studies have reported that the dopamine D2/D3 receptor agonist pramipexole exerts an antidepressant-like effect in the chronic mild stress model and in the behavioral despair model, suggesting dopamine D3 receptor may be an important target for antidepressant actions. The aim of the present study was to examine the role of dopamine D3 receptor on the anxiety-like and depression-like behaviors induced by immobilization stress. We subjected D3 receptor knockout (D3KO) mice to a series of behavioral paradigms after acute (1 h) or chronic (1 h a day for 14 days) immobilization stress. The results showed that immobilization stress significantly altered the anxiety-like behaviors (open field test and elevated plus maze) and depression-like behaviors (tail suspension test) in both D3KO mice and their wild-type littermates. Moreover, further analysis of the data indicated that the D3KO mice, but not their littermates, failed to show a change in immobility time in the tail suspension test after the acute and chronic stress as compared to intact controls, suggesting an increased resistance to the immobilization stress given before behavioral tests. Although our study did not suggest a significant role of D3 receptor in regulating basal anxiety-like and depression-like behaviors, it demonstrated the mice lacking D3 receptor might be more resistant to stressful procedure than their WT littermates.

Persistent changes in behavior and psychological function that occur as a consequence of exposure to drugs of abuse are thought to be mediated by the structural plasticity of specific neural circuits such as the brain's dopamine (DA) system. Changes in dendritic morphology in the nucleus accumbens (NAc) accompany drug-induced enduring behavioral and molecular changes, yet ultrastructural changes in synapses following repeated exposure to drugs have not been well studied. The current study examines the role of DA D3 receptors in modulating locomotor activity induced by both acute and repeated methamphetamine (METH) administration and accompanying ultrastructural plasticity in the shell of NAc in mice. We found that D3 receptor mutant (D3−/−) mice exhibited attenuated acute locomotor responses as well as the development of behavioral sensitization to METH compared with wild-type mice. In the absence of obvious neurotoxic effects, METH induced similar increases in synaptic density in the shell of NAc in both wild-type and D3−/− mice. These results suggest that D3 receptors modulate locomotor responses to both acute and repeated METH treatment. In contrast, the D3 receptor is not obviously involved in modulating baseline or METH-induced ultrastructural changes in the NAc shell.

Drugs of abuse modulated learning and memory in humans yet the underlying mechanism remained unclear. The extracellular signal-regulated kinase (ERK) and the transcription factor cAMP response element-binding protein (CREB) were involved in neuroplastic changes associated with learning and memory. In the current study, we used a Morris water maze to examine the effect of methamphetamine (METH) on different processes of spatial memory in mice. We then investigated the status of ERK and CREB in the hippocampus and prefrontal cortex (PFC). We found that 1.0 mg/kg dose of METH facilitated spatial memory consolidation when it was injected immediately after the last learning trial. In contrast, the same dose of METH had no effect on spatial memory retrieval when it was injected 30 min before the test. Furthermore, 1.0 mg/kg dose of METH injected immediately after retrieval had no effect on spatial memory reconsolidation. Activation of both ERK and CREB in the hippocampus was found following memory consolidation but not after retrieval or reconsolidation in METH-treated mouse groups. In contrast, activation of both ERK and CREB in the PFC was found following memory retrieval but not other processes in METH-treated mouse groups. These results suggested that METH facilitated spatial memory consolidation but not retrieval or reconsolidation. Moreover, activation of the ERK and CREB signaling pathway in the hippocampus might be involved in METH-induced spatial memory changes.

An essential feature of drug addiction is that an individual continues to use drug despite the threat of severely adverse physical or psychosocial consequences. Persistent changes in behavior and psychological function that occur as a function of drugs of abuse are thought to be due to the reorganization of synaptic connections (structural plasticity) in relevant brain circuits (especially the brains reward circuits). In this paper we summarized evidence that, indeed, exposure to amphetamine, cocaine, nicotine or morphine produced persistent changes in the structure of dendrites and dendritic spines on cells in relevant brain regions. We also approached the potential molecular mechanisms of these changes. It is suggested that structural plasticity associated with exposure to drugs of abuse reflects a reorganization of patterns of synaptic connectivity in these neural systems, a reorganization that alters their operation, thus contributing to some of the persistent sequela associated with drug use-including addiction.