The primary protein components of white matter include myelin basic protein (MBP) and 2’,3’-cyclic nucleotide 3’-phosphodiesterase (CNP). Alterations in their expression are significantly implicated in depression. This study investigated changes in MBP and CNP expression associated with depressive-like behaviors induced by chronic unpredictable stress (CUS) and evaluated therapeutic interventions using fluoxetine (FLU), an enriched environment (EE), or their combination. Male Sprague Dawley rats were randomly assigned to a control group and four CUS-exposed groups undergoing 6 weeks of stress. During the final 3 weeks of CUS, rats received daily fluoxetine (CUS + FLU group), were housed in EE (CUS + EE group), or received combined EE and fluoxetine (CUS + FLU + EE group). Depression-like behaviors were assessed through sucrose preference, forced swimming, and open field tests after CUS completion and at the end of weeks 4–6. Protein and mRNA expression levels of MBP and CNP in the prefrontal cortex were quantified via immunohistochemistry, western blot, and qRT-PCR. Three weeks following CUS exposure, rats demonstrated significant depression-like behavioral phenotypes. By the fifth week, these behavioral deficits were ameliorated in the CUS + FLU + EE, whereas the CUS + FLU and CUS + EE groups exhibited comparable behavioral recovery by week 6. Parallel molecular analyses revealed diminished protein and mRNA expression levels of MBP and CNP in the prefrontal cortex of CUS-exposed animals, accompanied by a pronounced elevation in IL-1β expression. Therapeutic interventions with FLU, EE, or their combination significantly attenuated these CUS-induced molecular alterations. The antidepressant effects correlated with restored MBP, CNP, and IL-1β expression levels, suggesting that MBP/CNP deficiencies in depression may involve IL-1β elevation. In particular, combined enriched environment and fluoxetine accelerated behavioral recovery.

BACKGROUND: Cognitive dysfunction is a core characteristic of schizophrenia, independent of positive and negative symptoms. It significantly impacts social reintegration, quality of life, and imposes a burden on families and society. This study investigates the prevalence and influencing factors of cognitive impairment in patients with stable schizophrenia on regular medication, with the hope of providing assistance to the cognitive improvement of patients. METHODS: A multistage stratified sampling approach was implemented to screen and enroll eligible patients with stable schizophrenia from five specialized psychiatric hospitals in Henan Province. Psychiatrists who had received standardized training conducted questionnaire responses and cognitive assessments for the patients, and quality control personnel reviewed the questionnaires. Binary Logistic analysis was used to detect the influencing factors of cognitive function. RESULTS: The valid questionnaires of 1,274 patients were collected from January 1, 2022, to December 31, 2023. The cognitive dysfunction rate of the patients with stable schizophrenia on regular medication was 66.2%. The risk factors for cognitive function, in descending order, are: first-generation antipsychotics (FGAs) (OR: 9.246, 95%CI: 1.021,1.093), family history (OR: 2.535, 95%CI: 1.349,4.762), negative symptoms (OR: 2.532, 95%CI: 1.735,3.695), mood stabilizers (OR: 1.882, 95%CI: 1.356,2.613), anticholinergic drugs (OR: 1.616, 95%CI: 1.161,2.249), combined medication (OR: 1.332, 95%CI: 1.009,1.760), high body mass index (BMI) (OR: 1.069, 95%CI: 1.030,1.111), longer duration of education (OR: 1.057, 95%CI: 1.021,1.093), and long duration of disease (OR: 1.045, 95%CI: 1.028,1.063). The protective factors, in descending order, are: taking 5-HT1A receptor partial agonist (OR: 0.657, 95%CI: 0.503,0.857) and having more children (OR: 0.817, 95%CI: 0.732,0.912). The sensitivity of the regression model for predicting cognitive function was 66.5%, and the specificity was 88.0%. CONCLUSIONS: Findings highlight the complex interplay of personal, familial, psychiatric, physical, and pharmacological factors in cognitive impairment. Medication use, especially FGAs, significantly influences cognitive function, underscoring the need for psychiatrists to closely monitor treatment regimens to mitigate cognitive decline and improve long-term outcomes in patients with stable schizophrenia.

INTRODUCTION:This study evaluated the efficacy and safety of lemborexant (LEM), a dual orexin-receptor antagonist, in participants with insomnia disorder in China. METHODS:E2006-J086-311 (Study 311; NCT04549168), a 1-month, multicenter, randomized, double-blind, placebo (PBO)-controlled, parallel-group study, enrolled adults (≥18 years) with insomnia disorder in China. Pairs of polysomnograms were conducted during a 7-day PBO run-in period (baseline), after the first 2 doses of LEM 10 mg (LEM10) or PBO, and after the last 2 doses at the end of 1 month of treatment. Objective sleep parameter assessments included latency to persistent sleep (LPS; primary endpoint) and secondary endpoints of sleep efficiency, wake after sleep onset (WASO), and total sleep time (TST; exploratory endpoint). Safety data were collected. RESULTS:Among 194 participants randomized (PBO, n = 100; LEM10, n = 94), the median age was approximately 42 years; most participants were female (PBO: 74.0 %; LEM10: 61.3 %). Following 1 month of treatment, mean (standard deviation [SD]) decreases from baseline in LPS were larger (improved) for the LEM10 treatment group (-39.47 min [46.147 min]) versus PBO (-21.71 min [42.809 min]; post hoc Box-Cox transformation, p = 0.0096). LEM10 demonstrated larger and statistically significant increases from baseline (improvements) in sleep efficiency (p < 0.0001) and TST (p < 0.0001) and significant decreases from baseline (improvement) in WASO (p = 0.0002) versus PBO and was well-tolerated. No new safety signals with LEM were observed in the current study compared with the known safety profile. CONCLUSIONS:LEM may be an important potential treatment option for patients with insomnia in China. TRIAL REGISTRATION:ClinicalTrials.gov identifier (first submitted on 09-09-2020): NCT04549168; Study protocol and statistical analysis plan may be accessed at: https://clinicaltrials.gov/study/NCT04549168.

The present investigation was designed to probe into the relationship between fluctuations in gamma - aminobutyric acid (GABA) levels and depression accompanied by suicidal behavior. It aimed to explore the potential mechanistic role of GABA in the suicide risk among patients with depression and appraise its potential as a biomarker. This study employed a single - center, prospective, cross - sectional design. A total of 106 subjects were enrolled and allocated into three groups: an experimental group (patients with depression and suicidal behavior, n = 36), a control group (patients with depression but without suicidal behavior, n = 40), and a healthy control group (n = 30). Serum GABA levels were quantified, and evaluations were conducted using the Hamilton Depression Scale (HAMD), the Beck Scale for Suicide Ideation (BSS), serum cortisol levels, and brain - derived neurotrophic factor (BDNF) levels. The serum GABA level was significantly lower in the experimental group (2.50 ± 0.40 µmol/L) compared to both the control group (3.00 ± 0.30 µmol/L, p < 0.01) and the healthy control group (3.50 ± 0.20 µmol/L, p < 0.01). Conversely, serum cortisol levels were markedly elevated in the experimental group (601.18 ± 79.86 nmol/L, p < 0.01), while BDNF levels were substantially reduced (15.0 ± 3.0 ng/mL, p < 0.01). Psychological assessment scores showed that the experimental group had the highest levels of depressive symptoms and suicidal ideation, with significantly elevated HAMD and BSS scores (p < 0.001). Correlation analyses revealed that serum GABA levels were negatively correlated with BSS scores (r = -0.8444, p < 0.001), HAMD scores (r = -0.7850, p < 0.001), and cortisol levels (r = -0.6427, p < 0.001), but positively correlated with BDNF levels (r = 0.6784, p < 0.001). A significant reduction in serum GABA levels is closely associated with increased depressive severity and suicide risk. These findings suggest that GABA plays a key role in the pathophysiology of depression and suicidal behavior, potentially through modulation of the HPA axis and neuroplasticity mechanisms. Serum GABA serves as a valuable biomarker for assessing suicide risk and represents a promising target for future therapeutic interventions in depression-related suicidality.

BACKGROUND:Research into the shared and distinct brain dysfunctions in patients with schizophrenia (SCZ) and major depressive disorder (MDD) has been increasing. However, few studies have explored the application of functional near-infrared spectroscopy (fNIRS) in investigating brain dysfunction and enhancing diagnostic methodologies in these two conditions. METHODS:A general linear model was used for analysis of brain activation following task-state fNIRS from 131 patients with SCZ, 132 patients with MDD and 130 healthy controls (HCs). Subsequently, seventy-seven time-frequency analysis methods were used to construct new features of fNIRS, followed by the implementation of five machine learning algorithms to develop a differential diagnosis model for the three groups. This model was evaluated by comparing it to both a diagnostic model relying on traditional fNIRS features and assessments made by two psychiatrists. RESULTS:Brain activation analysis revealed significantly lower activation in Broca's area, the dorsolateral prefrontal cortex, and the middle temporal gyrus for both the SCZ and MDD groups compared to HCs. Additionally, the SCZ group exhibited notably lower activation in the superior temporal gyrus and the subcentral gyrus compared to the MDD group. When distinguishing among the three groups using independent validation datasets, the models utilizing new fNIRS features achieved an accuracy of 85.90 % (AUC = 0.95). In contrast, models based on traditional fNIRS features reached an accuracy of 52.56 % (AUC = 0.66). The accuracies of the two psychiatrists were 42.00 % (AUC = 0.60) and 38.00 % (AUC = 0.50), respectively. CONCLUSION:This investigation brings to light the shared and distinct neurobiological abnormalities present in SCZ and MDD, offering potential enhancements for extant diagnostic systems.

BACKGROUNDS:Clinical studies to date have yet to establish distinct boundaries between depression in bipolar disorder (BD) and unipolar depression (UD), leading to misdiagnoses and even exacerbation of the conditions. This study aimed to explore the distinctions in the local gyrification index (LGI) between BD and UD, and to evaluate its potential diagnostic value as a biomarker. METHODS:LGI values across 68 cortical regions were measured from 42 patients with BD, 45 patients with UD, and 45 healthy controls (HCs) based on the Desikan-Killiany atlas. General linear model was performed to compare LGI values among the three groups. XGBoost classifier was implemented to develop a binary classification model for distinguishing BD from UD. Additionally, the correlation between clinical characteristics and LGI values was investigated separately within the BD and UD groups. RESULTS:Compared to HCs, individuals with BD and UD exhibited significantly reduced LGI values in various cortical regions. Nine LGI regions in the BD group displayed reduced values compared to the UD group, except for a singular increase in the left frontal pole (ηp2 = 0.173; P = 0.006). No significant association was found between LGI values and clinical characteristics within the patient groups. The XGBoost classifier achieved a distinction accuracy of 73.7 % between BD and UD, with the left frontal pole making the most significant contribution to the model. CONCLUSIONS:The findings suggest that LGI could be a relatively stable neuroimaging biomarker for distinguishing between BD and UD.

Chronic stress is the primary environmental risk factor for major depressive disorder (MDD), and there is compelling evidence that neuroinflammation is the major pathomechanism linking chronic stress to MDD. Mitogen-activated protein kinase (MAPK) phosphatase-1 (MKP-1) is a negative regulator of MAPK signaling pathways involved in cellular stress responses, survival, and neuroinflammation. We examined the possible contributions of MKP-1 to stress-induced MDD by comparing depression-like behaviors (anhedonia, motor retardation, behavioral despair), neuroinflammatory marker expression, and MAPK signaling pathways among rats exposed to chronic unpredictable mild stress (CUMS), overexpressing MKP-1 in the hippocampus, and CUMS-exposed rats underexpressing MKP-1 in the hippocampus. Rats exposed to CUMS exhibited MKP-1 overexpression, greater numbers of activated microglia, and enhanced expressions of neuroinflammatory markers (interleukin [IL]-6, [IL]-1β, tumor necrosis factor [TNF]-ɑ, and decreased phosphorylation levels of ERK and p38 in the hippocampus as well as anhedonia in the sucrose preference test, motor retardation in the open field, and greater immobility (despair) in the forced swimming tests. These signs of neuroinflammation and depression-like behaviors and phosphorylation levels of ERK and p38 were also observed in rats overexpressing MKP-1 without CUMS exposure, while CUMS-induced neuroinflammation, microglial activation, phosphorylation levels of ERK and p38, and depression-like behaviors were significantly reversed by MKP-1 knockdown. Moreover, MKP-1 knockdown promoted the activation of the MAPK isoform ERK, implying that the antidepressant-like effects of MKP-1 knockdown may be mediated by the ERK pathway disinhibition. These findings suggested that hippocampal MKP-1 is an essential regulator of stress-induced neuroinflammation and a promising target for antidepressant development.

BackgroundMitogen-activated protein kinase (MAPK) phosphatase-1 (MKP1) is upregulated in the hippocampus of patients with depression, while pharmacological inhibition of hippocampal MKP1 can mitigate depression-like behaviors in rodents. In addition, MAPK signaling regulates autophagy, and antidepressants were recently shown to target autophagic signaling pathways. We speculated that MKP1 contributes to depression by enhancing hippocampal autophagy through dephosphorylation of the MAPK isoform ERK1/2.MethodsWe established a rat depression model by exposure to chronic unpredictable mild stress (CUMS), and then examined depression-like behaviors in the sucrose preference test (SPT) and forced swimming test (FST) as well as expression changes in hippocampal MKP1, ERK1/2, phosphorylated ERK1/2, and autophagy-related proteins LC3II by Western blotting and immunostaining. These same measurements were repeated in rats exposed to CUMS following hippocampal infusion of a MKP1-targeted shRNA. Finally, the effects of MKP1 expression level on autophagy we examined in rat GMI-R1 microglia.ResultsCUMS-exposed rats demonstrated anhedonia in the SPT and helplessness in the FST, two core depression-like behaviors. Expression levels of MKP1 and LC3II were upregulated in the hippocampus of CUMS rats, suggesting enhanced autophagy, while pERK/ERK was downregulated. Knockdown of hippocampal MKP1 mitigated depression-like behaviors, downregulated hippocampal LC3II expression, and upregulated hippocampal pERK/ERK. Similarly, MKP1 knockdown in GMI-R1 cells upregulated pERK/ERK and reduced the number of LC3II autophagosomes, while MKP1 overexpression had the opposite effects.ConclusionEnhanced hippocampal autophagy via MKP1-mediated ERK dephosphorylation may contribute to the development of depression.

Autophagy can remove endogenous inflammasome and reduce pro-inflammatory cytokine releases. While, over-expression of proinflammatory cytokines may inhibit autophagy. The mTOR is a major regulator of the autophagic process, in which PI3K/Akt pathway underlies the upstream of mTOR and modulates its activity. Both inflammatory response and mTOR-PI3K/Akt expressions were up-regulated in schizophrenia. However, the inter-relationship between chronic inflammation and autophagy, whether inflammation suppresses autophagy via PI3K/Akt/mTOR signaling pathway, and how the imbalance between two immunities causes neuroinflammation and neuropathological changes remain unknown in schizophrenia. Thus, this study determined relationship between inflammation and PI3K/Akt/mTOR pathway in schizophrenia patients (SZ), and between autophagy and glia inflammatory/neuroprotective phenotypes in a mouse model of schizophrenia. 66 SZ and 44 healthy controls (CT) were enrolled. Clinical data as well as blood samples were collected. When compared to CT, peripheral autophagy factors MDC stain, and LC3 expression and autophagy activity were decreased, while the concentration of autophagy inhibitor P62, pro-inflammatory factors IL-1β, IL-6 and TNF-α concentrations were increased, and anti-inflammatory factors IL-10 and IL-4 were decreased in SZ. Blood microglia M1 marker IBA1 and astrocyte A1 S100B were up-regulated, while M2 CD206 and A2 P11 were downregulated. A negative correlation between inflammation and autophagy, and synaptic protein Beclin1 and MAP expression were found in SZ lymphocytes. In SZ lymphocytes, the PI3K/Akt/mTOR pathway was activated at both mRNA and protein levels. Then, IL-1 and IL-6 treatment significantly increased, while IL-10 decreased LC3 and Beclin 1 expression in SZ lymphocytes. Furthermore, 3-MA, an autophagy inhibitor, increased NLRP3, ASC, Caspase 1 and pro-inflammatory cytokines IL-1b and IL-6. Mouse model of schizophrenia induced by PolyI:C showed schizophrenia-like behaviors, such as increased spontaneous, impaired cognition and defected sensory-motor gating. In the brain, changes in proinflammatory cytokines, autophagy factors, glial phenotype patterns and synaptic protein were similar to peripheral changes in SZ. More important, clozapine or autophagy agonist RAPA reversed schizophrenia-like behavioral and neuropathological abnormalities, which were aborted by 3-MA. These data for the first time demonstrated imbalance between inflammation and autophagy may contribute to the neuropathology of schizophrenia.

Abstract Background Depression is an important public health burden, its risk of occurrence is associated with vitamin D deficiency and may also increase with age, while serum vitamin D levels are closely related to age. Objective The purpose of this study was to evaluate whether vitamin D and age are associated with depression after adjustment for each other. Materials and methods We extracted data from NHANES 2013–2018, including demographic characteristics, depression level, vitamin D level, physical activity, and body measures. A total of 15,156 adults aged 20 years or older (mean age 49.81 ± 17.67 years, 7301 males and 7855 females) were included. Depression was screened by PHQ-9. Vitamin D deficiency was defined by a serum vitamin D level < 30nmol/L. We performed binary logistic regression models to analyze the association between vitamin D, age and depression, respectively. Results Vitamin D levels were negatively associated with depression (P < 0.001). Vitamin D had a significant effect on depression (OR = 0.776, 95%CI: 0.682–0.884, P < 0.001), the effect remained significant after adjusted for confounding variables (OR = 0.761, 95%CI: 0.663–0.874, P < 0.001). Age was positively associated with depression (P < 0.001) and had a significant effect on depression (OR = 1.079, 98%CI: 1.032–1.128, P = 0.001), the effect remained significant after adjusted for confounding variables (OR = 1.092, 95%CI: 1.040–1.146, P < 0.001). Age and vitamin D levels were positively correlated (P < 0.001), and older age had a significant effect on vitamin D level (OR = 1.526, 95%CI: 1.416–1.645, P < 0.001), the effect remained significant after adjusted for confounding variables (OR = 1.371, 95%CI: 1.263–1.487, P < 0.001). In addition, the prevalence of depression was higher in females (2312/7855, 29.43%) than in males (1571/7301, 21.52%), and the difference was statistically significant (P < 0.001). Conclusions Vitamin D deficiency and older age are both associated with higher risk of depression, while older age is a protective factor for vitamin D deficiency.

Transforming growth factor (TGF)-β is a group of cytokines with anti-inflammatory effects in the TGF family, which participates in the development of stress and depression-related mechanisms, and plays roles in the regulation of inflammatory response in depression and the recovery of various cytokine imbalances. The core symptoms of depression is associated with TGF-β level, and the psychological symptoms of depression are related to TGF-β gene polymorphism. Various antidepressants may up-regulate TGF-β level through the complex interaction between neurotransmitters and inflammatory factors, inhibiting inflammatory response and regulating cytokine imbalance to improve depressive symptoms. Studies have shown that recombinant TGF-β1 protein has beneficial effects in mouse depression models, indicating TGF-β1 might be a potential therapeutic target for depression and nasal sprays having the advantage of being fast acting delivery method. This article reviews the research progress on dynamic changes of TGF-β level before and after depression treatment and the application of TGF-β level as an indicator for the improvement of depressive symptoms. We provide ideas for the development of new antidepressants and for the evaluation of the treatment efficacy in depression.

随着疫情防控策略的不断调整和变化,我们都深刻体会到新冠病毒的传播速度之快、感染范围之广,对人们的心身带来极大的冲击,尤其是老人"阳"了之后,因合并各种躯体疾病及多器官老化等因素,有些老年人没能挺过去而离世了. 俗话说:"家有一老,如有一宝",父母在,人生尚有来处,父母去,人生只剩归途,家中的老人就是我们这些常年在外奔波儿女们的精神依靠.当家中老人未能挺过病毒的攻击,会迅速失去代偿能力,我们可能无法参与临终关怀,甚至需要在几个小时内做出生死抉择,此刻,悲伤、无助便成了我们无法逃避的情绪.而对于很多人来说,这样的悲伤会绵延不断、无法摆脱,那么,我们应该如何应对老人离世的哀伤反应呢?

目的 探索邢台地区乳腺癌发病的影响因素,为降低乳腺癌的发病率提供依据.方法 选取2019年6月至2020年6月首次确诊的乳腺癌患者210例为观察组,同期体检中心体检的女性,按照1:1匹配选入对照组210例,调查2组人群的一般情况、月经和生育史、既往史、个人史、家族史及饮食情况,分析影响乳腺癌发病的因素.结果 影响乳腺癌发生的因素有超重(OR=1.960,95％CI:1.191～3.225)、肥胖(OR=3.242,95％CI:1.207～8.707)、月经初潮年龄(OR=0.471,95％CI:0.231～0.961)、有生育者首次足月产年龄(OR=1.995,95％CI:1.169～3.404)、母乳喂养(OR=0.429,95％CI:0.212～0.867)、乳腺癌家族史(OR=7.391,95％CI:2.215～24.667)、偶尔食用油炸食品(OR=0.136,95％CI:0.091～0.205)和从不食用油炸食品(OR=0.128,95％CI:0.087～0.189)、从不食用腌制食品(OR=0.141,95％CI:0.095～0.209).结论 超重和肥胖、有生育者首次足月产年龄越大、有乳腺癌家族史是乳腺癌的危险因素;月经初潮年龄大、有母乳喂养、偶尔和从不食用油炸食品、从不食用腌制食品是乳腺癌的保护因素.

Background: Exploratory eye movements (EEMs) and P300 are often used to facilitate the clinical diagnosis of depression. However, There were few studies using the combination of EEMs and P300 to build a model for detecting depression and predicting a curative effect. Methods: Sixty patients were recruited for 2 groups: high frequency repetitive transcranial magnetic stimulation (rTMS) combined with paroxetine group and simple paroxetine group. Clinical efficacy was evaluated by the Hamilton Depression scale-24(HAMD-24), EEMs and P300. The classification model of the auxiliary diagnosis of depression and the prediction model of the two treatments were developed based on a machine learning algorithm. Results: The classification model with the greatest accuracy for patients with depression and healthy controls was 95.24% (AUC = 0.75, recall = 1.00, precision = 0.95, F1-score = 0.97). The root mean square error (RMSE) of the model for predicting the efficacy of high frequency rTMS combined with paroxetine was 3.54 (MAE [mean absolute error] = 2.56, R-2 = -0.53). The RMSE of the model for predicting the efficacy of paroxetine was 4.97 (MAE = 4.00, R-2 = -0.91). Conclusion: Based on the machine learning algorithm, P300 and EEMs data was suitable for modeling to distinguish depression patients and healthy individuals. However, it was not suitable for predicting the efficacy of high frequency rTMS combined with paroxetine or to predict the efficacy of paroxetine.

抑郁症以长期持续的情感低落为最主要临床表现，据统计，全球约3.5亿人患有该疾病，每年造成的经济负担位于临床疾病前列，是最严重的公共卫生问题之一。近年来，抑郁症的患病率逐年增高，2008年，WHO将重度抑郁症列为世界范围内疾病负担的第三大原因，并预测到2030年时，抑郁症将升至第一位。虽然已经开展了大量针对抑郁症的基础研究，但是我们对抑郁症的发病机制仍然知之甚少。目前较为公认的观点认为生活中的应激事件是抑郁症发病的直接诱因，而遗传因素、心理因素以及社会环境因素等则是造成抑郁症易感人群的重要风险因素。

Objective:To investigate the role of mitogen-activated protein kinase phosphatase-1 (MKP-1) on depressive-like behaviors and hippocampal neuron apoptosis in chronic unpredictable mild stress (CUMS) rats.Methods:A total of 36 Sprague-Dawley male rats were randomly divided into 4 groups using a random number table, including the control group( n=8), CUMS group( n=8), virus control group( n=10), and MKP-1 down-regulated group( n=10), with 8 rats in each group. Except for the control group, rats in other groups were stressed by CUMS model of depression. Rats in the virus control group and MKP-1 down-regulated group received adeno-associated virus injections in the hippocampal CA1 and CA3 regions before CUMS modeling. Sucrose preference test, forced swimming test, and open field test were used to observe the behavioral changes of rats. Western blotting was used to detect the protein expression of MKP-1, B-cell lymphoma-2 gene (Bcl-2) and B-cell lymphoma-2 gene-related X protein (Bax), in the hippocampus. TUNEL staining was utilized to observe the morphology of apoptotic cells in the hippocampus CA1 area. Repeated measures variance was used to analyze body weight and behaviors, while an independent sample t-test was used to analyze protein levels. Results:Compared with the control group, the body weight of rats in the CUMS group decreased ( F=44.664); the sucrose preference rate decreased ( F=14.978); the forced swimming immobility time increased ( F=8.436); the number of defecation in the open field test increased ( F=9.572); the relative expression level of MKP-1 and Bax/Bcl-2 also significantly increased ( t=4.415,3.410), P<0.05 for all; Compared with the virus control group, rats in the MKP-1 down-regulation group showed a higher sucrose preference rate ( F=11.922) and a shorter forced swimming immobility time ( F=12.868), furthermore, the activity distance ratio in the central area increased ( F=6.291), the number of uprights in the open field test increased ( F=14.372), and the relative expression levels of MKP-1 and Bax/Bcl-2 ( t=3.775,6.193) decreased, P<0.05 for all. The number of DNA fragments in the nucleus of the hippocampal CA1 region of the CUMS group was significantly more than that of the control group. In comparison, the number of DNA fragments in the nucleus of the MKP-1 down-regulated group was substantially less than that of the virus control group. Conclusion:Down-regulation of MKP-1 gene alleviated depressive-like behavior and hippocampal neuron apoptosis in CUMS rats.

目的:探讨认知应对治疗(CCT)联合帕罗西汀对广泛性焦虑障碍(GAD)的短期临床疗效、社会功能以及认知功能的影响.方法:选取符合美国精神障碍诊断统计手册第5版(DSM-5)诊断标准的70例GAD患者,按随机数字表法分为CCT联合帕罗西汀组35例(31例完成)、帕罗西汀组35例(32例完成).两组患者分别在基线期以及治疗4周后完成焦虑自评量表(SAS)、汉密顿焦虑量表(HA-MA)、社会功能缺陷量表(SDSS)评估、事件相关电位P300检查、MATRICS共识认知成套测验(MC-CB)成套认知测验.结果:经过4周治疗后,CCT联合帕罗西汀组在SAS评分、HAMA评分、SDSS评分低于帕罗西汀组(P＜0.05),P300波幅、MCCB评分注意/警觉性、推理解决问题能力、社会认知领域显著高于帕罗西汀组(P＜0.05),CCT联合帕罗西汀组的总显效率(51.6％)显著高于帕罗西汀组(25％).结论:认知应对治疗联合帕罗西汀对GAD患者的治疗在短期内起到增效或协同作用,能够有效提高患者的社会功能,对患者的认知功能具有一定的改善作用.

目的 研究巴戟天寡糖胶囊联合阿戈美拉汀应用于老年抑郁症的治疗效果及对患者血清神经元特异性烯醇化酶(NSE)和髓鞘碱性蛋白(MBP)水平的影响.方法 将医院2019年3月—2020年2月诊治的老年抑郁症118例按照随机数字表法均分为两组,每组59例,对照组单独采用阿戈美他汀治疗,观察组采用巴戟天寡糖胶囊联合阿戈美拉汀治疗.观察比较两组的汉密尔顿焦虑量表(HAMA)、汉密尔顿抑郁量表(HAMD)、中医证型量化评分、血清NSE和MBP水平、用药不良反应发生情况、世界卫生组织生存质量评定量表(WHOQOL-100).结果 治疗前两组HAMA、HAMD评分比较,差异无统计学意义(P＞0.05),治疗后两组HAMA、HAMD评分均显著下降,并且观察组显著低于对照组(P＜0.05).治疗前两组中医证型量化评分总积分及精神症状、躯体症状、其他各项评分比较,差异均无统计学意义(P＞0.05),治疗后两组以上评分显著改善,观察组总积分及精神症状、躯体症状积分显著低于对照组(P＜0.05).治疗前两组血清NSE和MBP水平比较,差异均无统计学意义(P＞0.05),治疗后两组血清NSE和MBP水平显著下降,并且观察组显著低于对照组(P＜0.05).两组均无严重不良反应发生.治疗前两组WHOQOL-100总评分及各维度评分差异均无统计学意义(P＞0.05),治疗后两组WHOQOL-100总评分及各维度评分均显著改善,并且观察组的WHOQOL-100评分及生理健康、心理状态、独立能力及社会关系维度评分均显著高于对照组(P＜0.05).结论 巴戟天寡糖胶囊联合阿戈美拉汀应用于老年抑郁症的治疗效果满意,能够降低改善患者中医证型量化评分,缓解抑郁症状,改善血清NSE和MBP水平,巴戟天寡糖胶囊起到增效剂作用、并且具有良好的安全性,能够更显著地提升患者的生存质量.

目的 探讨价值取向综合干预措施对老年抑郁症患者生活质量及主观幸福感的影响.方法 选择2018年1月至2019年9月新乡医学院第二附属医院收治的86例老年抑郁症患者为研究对象,根据治疗方法将患者分为观察组(n=44)和对照组(n=42).对照组患者根据病情接受相应的常规药物治疗.观察组患者在对照组常规治疗基础上进行价值取向综合干预,包括一般性心理干预、认知干预、正念治疗、价值取向治疗,干预周期为3个月.分别于干预前、干预3个月时,采用简易应对方式问卷(SCSQ-19)评估患者在日常生活中遇到问题时所采取的态度和措施,包括积极应对和消极应对2个维度;采用世界卫生组织生存质量测定量表简表(WHOQOL-BREF)评估患者的生存质量,包含总体生存质量及生理功能、心理功能、环境领域和社会关系4个领域;采用纽芬兰纪念大学幸福度量表(MUNSH)评估患者的主观幸福感,包含正性情感和负性情感2个维度.结果 对照组患者干预3个月时的积极应对和消极应对维度评分与干预前比较差异无统计学意义(P>0.05);观察组患者干预3个月时的积极应对维度评分显著高于干预前,消极应对维度评分显著低于干预前(P<0.05);干预3个月时,观察组患者的积极应对维度评分显著高于对照组,消极应对维度评分显著低于对照组(P<0.05).对照组患者干预3个月后的总体生存质量及生理功能、心理功能、社会关系、环境领域评分与干预前比较差异无统计学意义(P>0.05);观察组患者干预3个月时的总体生存质量及生理功能、心理功能、社会关系、环境领域评分均显著高于干预前;干预3个月时,观察组患者的总体生存质量及生理功能、心理功能、社会关系、环境领域评分均显著高于对照组(P<0.05).对照组患者干预前与干预3个月的正性情感评分、负性情感评分、MUNSH总分比较差异无统计学意义(P>0.05);观察组患者干预3个月的正性情感评分、MUNSH总分均显著高于干预前,负性情感评分显著低于干预前(P<0.05);观察组患者干预3个月的正性情感评分、MUNSH总分显著高于对照组,负性情感评分显著低于对照组(P<0.05).结论 在常规药物治疗的基础上,价值取向综合干预能帮助老年抑郁症患者正确应对抑郁情绪,显著提高其生活质量和主观幸福感.