BACKGROUND:Asthma is a common chronic inflammatory airway disease, characterized clinically by recurrent wheezing, shortness of breath, chest tightness, and cough. The roles of inflammatory cells such as T cells, eosinophils, and basophils in asthma are now well established. Recent studies have further revealed that the nervous system is not merely a "bystander" to the inflammatory response. Consequently, the peripheral nerves and the neural nuclei involved in asthma have attracted increasing research interest. SUMMARY:This review summarizes the currently identified peripheral and central nerves implicated in transmitting airway inflammatory signals in asthma. It describes the principal mechanisms through which various brain nuclei - including nucleus tractus solitarius, paraventricular nucleus, and amygdala - participate in asthma regulation. We also discuss whether these nuclei interact to form specific neural circuits that modulate the disease. First-line anti-inflammatory medications remain ineffective for a subset of patients, and current pharmacological interventions targeting neural pathways show limited clinical efficacy. KEY MESSAGES:A clear elucidation of the neural circuits regulating asthma would advance our understanding of its pathogenesis, offer new directions and targets for drug development, and raise the possibility of treating asthma through direct central nervous system interventions.

BackgroundThe incidence of cognitive impairment in patients with depressive disorder is high， and the causes and mechanisms of which deserve more attention. It is usual that the thyroid hormone levels in patients with depressive disorder alter. Further research is needed to explore whether the cognitive function changes in patients with depressive disorder are related to thyroid hormone levels.ObjectiveTo explore the improvement of cognitive function in patients with first-episode depressive disorder after escitalopram and paroxetine treatment， and to analyse its correlation with thyroid hormone levels， so as to look for potential biomarkers of cognitive function change in patients with depressive disorder.MethodsFrom March 2021 to March 2022， 120 patients who met the diagnostic criteria of the International Classification of Diseases， tenth edition （ICD-10） for depression and were hospitalized at Shandong Mental Health Center were selected as the research objects. They were randomly divided into two groups by random number table method with 60 patients in each group. The two groups were treated with escitalopram （starting dose 5 mg/d） and paroxetine （starting dose 20 mg/d） for 6 weeks. Before and 6 weeks after the treatment， levels of thyroid stimulating hormone （TSH）， free thyroxine （FT4） and free triiodothyronine （FT3） were tested respectively. Depression degree and cognitive function level were assessed using the Hamilton Depression Scale-17 item （HAMD-17） and Montreal Cognitive Assessment （MoCA）， respectively. Pearson or Spearman correlation analysis was used to examine the correlation between the MoCA score difference before and after the treatment and the post-treatment level of thyroid hormone.ResultsBefore and 6 weeks after the treatment， the time effect of HAMD-17 total score in both groups was statistically significant （F=1 236.568， P<0.01）. Also， the time effect， group effect as well as interaction effect of time and group of MoCA total score in both groups were statistically significant （F=79.186， 6.026， 20.417， P<0.05 or 0.01）. The time effect， group effect as well as the interaction effect of time and group for FT3 level and FT4 level were statistically significant in both groups （F=75.973， 20.287， 0.961， 84.194， 0.142， 8.299， P<0.05 or 0.01）. According to the simple effect analysis. After the treatment， the MoCA total score in both groups was higher than that before treatment， while FT3 and FT4 levels were lower than those before treatment （F=15.864， 5.421， 8.524， 6.443， 7.628， 3.639， P<0.01）. After the 6-week treatment， the MoCA total score as well as FT3 and FT4 level differences in escitalopram and paroxetine groups were of statistical significance （t=5.841， -0.705， -2.349， P<0.05 or 0.01）. The MoCA score difference before and after treatment in paroxetine group was positively correlated with FT3 and FT4 levels after treatment （r=0.276， 0.382， P<0.05 or 0.01）.ConclusionBoth escitalopram and paroxetine can improve cognitive function in patients with first-episode depressive disorder. The improvement may be related to the changes in serum FT3 and FT4 levels.

目的:探讨丙戊酸镁联合舍曲林治疗伴有非自杀性自伤(NSSI)行为青少年抑郁症患者的效果.方法:选择2021年1月1日—2021年12月30日山东省精神卫生中心儿童病房的住院患者,抽取伴有NSSI行为的青少年抑郁障碍患者,通过随机数字表法分为实验组61例和对照组69例.对照组口服舍曲林单一治疗,实验组在对照组基础上联合丙戊酸镁缓释片口服治疗.比较两组治疗前后甲状腺功能、认知水平和抑郁状态.结果:两组治疗6周后TT3、TT4、FT3、FT4水平低于治疗前,实验组TSH水平高于治疗前(P<0.05),而对照组治疗前后TSH水平比较,差异无统计学意义(P>0.05),且实验组及对照组治疗前后TT3、FT3、TT4、FT4比较,差异无统计学意义(P>0.05);两组治疗后PDQ-D评分及MADRS评分低于治疗前,且实验组低于对照组(P<0.05);Spearman相关性分析显示,实验组治疗后PDQ-D评分减分率与TT4水平呈正相关(P<0.05);多因素分析显示,丙戊酸镁是治疗前后TT4、TSH水平变化的影响因素(P<0.05).结论:丙戊酸镁能够辅助舍曲林改善伴有NSSI行为的青少年抑郁障碍患者认知功能及抑郁状态,其对认知功能的改善与甲状腺激素水平变化相关.

Self-injury has become a significant public health problem, especially happens in adolescents. Previous studies have suggested that self-injury is related to numerous factors. At present, the occurrence mechanism of self-injury is still unclear, and there is a lack of reliable biological markers in its diagnosis and therapeutic target so far. Previous studies have suggested that self-injury may be related to hypothalamic pituitary adrenal(HPA) axis, β-endorphins, opioids and other hormones. Hypothalamic pituitary thyroid(HPT) axis and hypothalamic pituitary gonadal(HPG) axis are endocrine systems connecting nerves and hormones. Many studies suggested that various hormones in HPT axis and HPG axis of self-injury patients with other mental disorders (such as major depression and bipolar disorder) were abnormal. At present, there are few studies on the relationship between self-injury and HPT axis and HPG axis. There are differences in results even among studies on the same hormones, and some studies involve suicide attempts and even behaviors. Some studies have confirmed that self-injury is related to suicide, expanding the possibility of exploring the correlation between self-injury and hormones. This study will review the relationship between self-injury and hormonal changes.

Abstract Background: Patients with depression frequently experience cognitive impairment. Our purpose is to determine whether thyroid hormones mediate the effect of depression on cognitive impairment. Methods: A total of 119 depressed patients were enrolled (mean age 32 years, 56.30% female). The Montreal Cognitive Assessment Scale, the 17-item Hamilton Depression Scale, and thyroid hormone levels, including free triiodothyronine (FT3), free thyroxine (FT4), and thyroid-stimulating hormone (TSH), were evaluated at intervals of 8 weeks. In order to describe the temporal relationship between depression and cognitive impairment, we initially used cross-lagged panel analysis. After that, linear regression analysis was utilized to show how depression and thyroid hormones are related to one another. To further investigate the causal role of thyroid hormones in depression and cognitive impairment, a causal mediation model was created. Results: The cross-lagged panel analysis showed that there was a significant cross-lagged path coefficient from baseline depression to follow-up cognition(β=－0.284, P=0.002) . Baseline depression had an impact on FT3 (F = 1.880, P＜0.05) and FT4 (F = 2.466, P＜0.05), according to a linear regression analysis. Baseline depression were affected by baseline FT4 ( = 0.316, t = 2.687, P＜0.05). The link between baseline depression and follow-up cognitive performance was revealed to be partially mediated by serum FT4 levels, according to the causal mediation analysis (a=0.008, se=0.004, p=0.022, CI=0.001/0.016). Conclusion: Serum FT4 levels may be biological markers of cognitive impairment in patients with depression and may mediate the effect of depression on cognitive impairment.

ObjectiveNon-suicidal self-injury (NSSI) is the intentional and repeated direct injury to one’s bodily tissues or organs without the intent to die, which is not socially sanctioned and does not result in death. This study will be the first to explore the relationship between NSSI behavior and thyroid hormone and sex hormone levels in male adolescents with depression.MethodsAmong the inpatients in the children’s ward of Shandong Mental Health Center, eighty male patients with first-episode depressive disorder were randomly selected. Forty male adolescent depressed patients with NSSI behaviors were set as the NSSI group, and forty male adolescent depressed patients without NSSI behaviors were set as the No-NSSI group. Their thyroid hormones (free triiodothyronine, free thyroxine, and thyroid stimulating hormone) and sex hormones (estradiol, progesterone, and testosterone) were measured, and the severity of self-injury in the NSSI group was assessed using the Adolescent Self-Injury Questionnaire. The NSSI group was tested again after 6 weeks of sertraline treatment for biological indicators and assessed by the Self-Injury Questionnaire to compare the hormonal differences between the NSSI group and the No-NSSI group and compare the differences of each index before and after treatment in the NSSI group.ResultsT3/T4 (p = 0.001) and FT3 (p = 0.023), TSH levels (p < 0.001) were lower in the NSSI group than in the No-NSSI group before treatment, and FT4 (p = 0.036) and T (p < 0.001) levels were higher than in the No-NSSI group. T3/T4 levels were higher in the NSSI group after treatment (p < 0.001). FT4 (p < 0.001) and T (p = 0.001) levels and self-injury questionnaire scores (p < 0.001) decreased after treatment in the NSSI group. In the NSSI group at baseline, FT4 levels were negatively correlated with self-injury questionnaire scores (r = −0.459, p = 0.003) and testosterone levels were positively correlated with self-injury questionnaire scores (r = 0.383, p = 0.015), and in the NSSI group after treatment, FT4 difference was negatively correlated with self-injury questionnaire score reduction rate (r = −0.037, p = 0.019), and testosterone difference was positively correlated with self-injury questionnaire score reduction rate (r = 0.424, p = 0.006). Logistic regression analysis showed that low TSH and high testosterone levels were independent risk factors for the development of non-suicidal self-harming behaviors in male adolescent depressed patients.ConclusionChanges in thyroid hormone and sex hormone levels may be associated with non-suicidal self-injurious behavior in male adolescent depressed patients.

目的 调查分析社区护士对精神卫生知识的知晓率及相关影响因素,为下一步加强精神卫生防治提供参考.方法 选取2019-08来自山东省16个地市23个县(区、市)86个乡镇卫生院(社区服务中心)的255名社区护士为研究对象,通过纸质问卷调查社区护士精神卫生知识知晓率,分析其影响因素.结果 山东省社区护士精神卫生知识回答总体正确率为87.64％.其中第2条(63.5％)、4条(64.7％)、6条(67.1％)和20条(58.8％)回答正确率均＜80％.Lo-gistic 回归分析结果显示,学历和精神卫生防治工作经验是影响知晓率的相关因素,差异有统计学意义.其中第2条正确率与护士学历呈正相关(OR=1.771,95％CI为1.223～2.564,P=0.02),第6条与参与社区精神卫生防治工作年限呈正相关(OR=1.249,95％CI为1.127～1.383,P＜0.01).结论 山东省社区护士的精神卫生知识知晓率较低,对精神疾病认识不足;社区护士学历水平和精神卫生防治工作经验是精神卫生知晓率影响因素.建议采取相关措施提高山东省社区护士精神卫生知识技能.

Purpose Agitation is prevalent among inpatients with schizophrenia. The aim of this study was to investigate whether biochemical parameters are associated with agitation in schizophrenia. Patients and Methods Agitation was evaluated by the Positive and Negative Syndrome Scale-Excited Component questionnaire (PANSS-EC). Fasting serum levels of C-reactive protein (CRP), free triiodothyronine (FT3), free thyroxine (FT4), thyroid-stimulating hormone (TSH), uric acid (UA), creatinine, glucose and lipids were measured. Results The analysis included 154 inpatients with schizophrenia (71 with agitation, 83 without agitation) and 75 healthy control subjects. Patients with schizophrenia and agitation had higher serum levels of CRP, FT3, FT4 and UA as well as lower levels of serum TSH and creatinine than patients without agitation (all P < 0.05). Multivariate logistic regression analysis indicated that serum CRP (odds ratio [OR] = 1.470, P = 0.001), FT3 (OR = 13.026, P < 0.001), TSH (OR = 0.758, P = 0.033) and creatinine (OR = 0.965, P = 0.004) were significantly associated with agitation in schizophrenia. CRP, FT3, TSH and creatinine achieved an area under the ROC curve of 0.626, 0.728, 0.620 and 0.663 respectively in discriminating schizophrenia with or without agitation. Conclusion Increased serum CRP and FT3 levels and decreased serum TSH and creatinine levels are independent risk factors for agitation in hospitalized patients with schizophrenia. Inflammation, thyroid hormones and renal function may be involved in the pathogenesis of agitation in schizophrenia.

Accumulating evidence has already indicated that traditional Chinese medicine (TCM) possesses tremendous potential for treating neurodegenerative diseases. Astragalus, also named Huangqi, is a famous traditional medical herb that can be applied to treat cerebral ischemia and prevent neuronal degeneration. Nevertheless, the underlying mechanisms remain largely unexplored. In the present study, Astragalus-containing serum (ASMES) was prepared and added into the culture medium of PC12 cells to explore its neuroprotective effect on 6-hydroxydopamine (6-OHDA)-caused neuronal toxicity. Our data showed that ASMES significantly ameliorated the cellular viability of cultured PC12 cells against the neurotoxicity induced by 6-OHDA (P < 0.05). Moreover, ASMES significantly decreased the cell apoptosis triggered by 6-OHDA (P < 0.01). Furthermore, 2′,7′-dichlorofluorescin diacetate assay was performed to detect the changes in oxidative stress, and we showed that 6-OHDA elevated the production of reactive oxygen species (ROS), whereas ASMES significantly reversed these changes (P < 0.01). Besides, mitochondrial membrane potential (MMP) assay showed that ASMES could restore 6-OHDA-damaged MMP in cultured PC12 cells (P < 0.05). In conclusion, Astragalus could protect PC12 cells from 6-OHDA-caused neuronal toxicity, and possibly, the ROS-mediated apoptotic pathway participated in this process. Collectively, our findings provided valuable insights into the potential in treatment of neurodegenerative diseases.

事件相关电位P300在抑郁症不同研究角度都有大量的研究,近几年一些新视角的研究补充了以往研究的空缺.本文从事件相关电位P300与抑郁症、P300在单双相抑郁及抑郁不同分型中的应用、P300与脑源定位技术相结合在抑郁症中的应用及P300对抑郁症严重程度和疗效评估4个角度进行综述.

目的 系统评价唑吡坦与阿普唑仑治疗失眠患者的有效性及安全性.方法 计算机检索数据库,纳入唑吡坦、阿普唑仑治疗失眠症的随机对照试验,进行Meta分析.结果 纳入9项研究,共计760例患者,两组研究的匹兹堡睡眠质量指数量表(PSQI)减分值比较差异具有统计学意义[P=0.007,OR(95％CI)=-2.32(-4.00～-0.64)];两组不良反应发生率比较差异具有统计学意义[P=0.002,OR(95％CI)=0.40(0.23～0.71)].两组PSQI评分总有效率和睡眠障碍量表(SDRS)有效率比较,差异均无统计学意义(P>0.05).结论 与阿普唑仑相比,唑吡坦治疗失眠症的有效性和安全性更优.

目的 观察艾司西酞普兰对植入永久性心脏起搏器患者伴发焦虑抑郁症状的改善与C-反应蛋白(CRP)水平的变化.方法 将81例植入永久性心脏起搏器并伴发焦虑抑郁症状的患者随机分为研究组(40例)和对照组(41例),研究组给以艾司西酞普兰系统治疗,对照组给以氟西汀系统治疗,共4周.在基线、治疗后第1、2、4周末对两组进行汉密尔顿抑郁量表(HAMD)、汉密尔顿焦虑量表(HAMA)、治疗中需处理的不良反应症状量表(TESS)评定.在基线、治疗后第4周末对两组CRP水平进行测定.结果 治疗4周后,研究组治疗有效率高于对照组(P<0.05).治疗后第1周末,研究组HAMA、HAMD评分均较基线时降低(P<0.05).治疗后第2、4周末,两组HAMA、HAMD评分均较各自基线时降低(P<0.05).治疗后第1、2、4周末,研究组HAMA、HAMD评分均低于对照组(P<0.05).研究组不良反应发生率低于对照组(P<0.05).治疗后第4周末,两组CRP水平均较各自基线时下降(P<0.05),且研究组CRP水平低于对照组(P<0.05).两组HAMA减分值、HAMD减分值与CRP降低值均呈正相关(P<0.05).结论 艾司西酞普兰可有效、快速改善植入永久性心脏起搏器患者伴发的抑郁焦虑症状,且与患者CRP水平变化相关,安全性较高.

目的 探讨奥氮平对青少年精神分裂症患者甲状腺激素、血清泌乳素和血清尿酸水平的影响.方法 选取53例青少年精神分裂症患者,使用奥氮平单药治疗4周,分别在入院时和治疗后第4周末抽取空腹静脉血检测甲状腺功能五项、血清泌乳素和血清尿酸.甲状腺功能五项指标包括总三碘甲状腺原氨酸(TT3)、总甲状腺素(TT4)、促甲状腺素(TSH)、游离三碘甲状腺原氨酸(FT3)、游离甲状腺素(FT4).结果 青少年精神分裂症患者在奥氮平单药治疗4周后,TT4、FT3、FT4水平较治疗前下降(P<0.05),TSH和血清泌乳素水平较治疗前升高(P<0.05).治疗前后TT3、TT4、FT3、FT4、泌乳素、尿酸的差值均分别与基线TT3、TT4、FT3、FT4、泌乳素、尿酸水平呈负相关(P<0.05).基线TT3、TT4、FT3、FT4、尿酸水平分别是治疗前后TT3、TT4、FT3、FT4、尿酸差值的影响因素(P<0.05).性别、年龄、基线泌乳素水平是治疗前后泌乳素差值的影响因素(P<0.05).结论 奥氮平治疗青少年精神分裂症患者时,会出现甲状腺功能、泌乳素水平的变化.治疗前后甲状腺功能、泌乳素、尿酸的差值与其各自基线值有关,泌乳素水平变化同时受性别、年龄等因素影响.

目的 探讨CYP2D6基因多态性与利培酮治疗精神分裂症的相关性.方法 共计收集296例精神分裂症患者,并进行CYP2D6基因多态性检测.根据检测结果,将98例检测结果08CYP2D6基因检测为TT、10CYP2D6基因检测为GG、06CYP2D6基因检测为CC,基因型分析结果为*10/*10,代谢型为IM的患者视为研究组,将198例其他基因型的患者视为对照组,均应用利培酮系统治疗,共6周.在基线和治疗后第2、4、6周末使用阳性和阴性综合征量表(PANSS)、临床总体印象量表-病情严重程度(CGI-SI)、治疗中需处理的不良反应症状量表(TESS)评定疗效和安全性.结果 在治疗后第6周末,研究组的利培酮用量低于对照组(P<0.05).治疗后第4、6周末,两组CGI评分、PANSS总分及各因子分均较各自基线时降低(P<0.05).在治疗后第2、4、6周末,研究组的TESS评分及不良反应例次数均低于对照组(P<0.05).在治疗后第6周末,研究组的总不良反应发生率低于对照组(P<0.05).结论 CYP2D6基因多态性检测结果:08CYP2D6基因检测为TT、10CYP2D6基因检测为GG、06CYP2D6基因检测为CC、基因型分析结果为*10/*10,代谢型为IM的精神分裂症患者选用利培酮系统治疗,可取得较好的临床疗效,更低的药物治疗剂量,更高的治疗安全性.

Objective To investigate the effect of attributional retraining group therapy ( ARGT) combined with closabine on the negative symptoms and quality of life in refractory schizophrenia patients. Methods The refractory schizophrenia patients were divided into ARGT combined with clozapine therapy group(study group,n=56) and clozapine alone group(control group,n=54). The positive and negative syn-drome scale( PANSS) was used to assess the symptoms of all patients at baseline and 8 weeks later. The quality of life(QOL) of the patients was assessed by GQOLI-74 at baseline and 8 weeks after treatment. The side effects were evaluated by treatment emergent symptom scale(TESS) before and after treatment. SPSS18. 0 was used for statistical analysis. Results At baseline,there was no significant difference in PANSS score between the two groups. After 8 weeks,the total score of PANSS (79. 41±11. 64) and the score of negative symptoms (28. 68 ±2. 74) in the study group were lower that those of control group(83. 06±11. 58,30. 61± 2. 12),and the differences were statistically significant(t=7. 68,7. 10,both P<0. 05). The scores of positive symptoms,cognitive symptoms,emotional symptoms and aggression symptoms in the study group had no sta- tistical differences compared with the control group (all P>0. 05). There were no significant differences in the scores of material life,mental health,physical health and social function between the two groups at base-line (P>0. 05). After 8 weeks,the total score of GQOLI- 74 (206. 37±14. 37),material life score (48. 69± 6. 35),body health score ( 52. 83± 7. 32),mental health score ( 51. 66 ± 4. 63) and social function score (53. 62± 6. 17) of the study group were higher than those of control group((182. 00± 12. 56),( 44. 62± 6. 11),(48. 52±5. 52),(45. 26±4. 66),(46. 18±5. 32))(t=4. 67,5. 26,3. 26,4. 92,3. 25,all P<0. 05). There was no significant difference in TESS score between the two groups(P<0. 05). Conclusion ARGT combined with clozapine can improve the negative symptoms and the quality of life of patients with refractory schizophrenia.

重度抑郁障碍是一种普遍的、致残的且累及多方面的慢性精神疾病.认知障碍是临床症状和诊断标准的核心,是重度抑郁障碍患者功能恢复的主要决定因素.认知功能障碍表现在多个领域,包括执行能力、学习及记忆能力、信息处理速度和注意力及专注度,并与社会心理和职业成就相关.本文的主要目的是描述抑郁障碍及认知障碍的总体特征及两者之间从器质性内部结构至社会心理外部因素的关联性.

Recent studies have revealed that the gut microbiota participates in the psychiatric behavior changes in disorders associated with alcohol. But it still remains unknown whether alcoholism is involved in changes in gut microbiota and its underlying mechanism is also not clear. Here, we tested the gut microbiota of patients with alcoholism and conducted fecal microbiota transplantation (FMT) from patients with alcoholism to C57BL/6J mice whose gut microbiota had been sharply suppressed with antibiotics (ABX). Then we evaluated their alcohol preference degree, anxiety, and depression-like behaviors and social interaction behaviors, together with molecular changes in the medial prefrontal cortex (mPFC) and nucleus accumbens (NAc). Our data indicated that the gut microbiota of patients with alcoholism was drastically different from those of the healthy adults. The abundance of p_Firmicutes was significantly increased whereas p_Bacteroidetes was decreased. Compared to mice transplanted with fecal microbiota from healthy male adults, the mice accepting fecal microbiota from patients with alcoholism showed (a) anxiety-like and depression-like behaviors, (b) decreased social interaction behaviors, (c) spontaneous alcohol preference, and (d) decreased brain-derived neurotrophic factor (BDNF), alpha 1 subunit of GABA type A receptor (α1GABAA R) in mPFC and decreased metabotropic glutamate receptors 1 (mGluR1), protein kinase C (PKC) ε in NAc. Overall, our results suggest that fecal microbiota from patients with alcoholism did induce a status like alcohol dependence in C57BL/6J mice. The decreased expression of BDNF, α1GABAA R, and mGluR1/ PKC ε may be the underlying mechanism.

目的 探讨齐拉西酮联合舍曲林治疗精神分裂症的疗效.方法 将60例精神分裂症患者随机分为研究组和对照组,各30例,研究组服用齐拉西酮联合舍曲林系统治疗,对照组单用齐拉西酮系统治疗,共治疗8周,在基线及治疗后第2、4、8周末采用阳性和阴性综合征量表(PANSS)和阴性症状量表(SANS)评价疗效,治疗中需处理的不良反应症状量表(TESS)评定不良反应.结果 治疗后第4、8周末,两组PANSS总分及各因子分、SANS评分均较基线时降低(P<0.05).治疗后第4、8周末,研究组PANSS总分及各因子分、SANS评分均低于对照组(P<0.05).两组不良反应发生率比较差异无统计学意义(P>0.05).结论 齐拉西酮联合舍曲林可安全有效治疗精神分裂症,短期效果优于单一用药.

Serum interleukin (IL)-6 levels in schizophrenia correlate with the severity of negative symptoms. This study aimed to explore the potential immune mechanism of SSRI augmentation in the management of patients with treatment-resistant schizophrenia, assessing changes in IL-6 and CRP amounts. This was a randomized double-blind, placebo-controlled, 8-week study of escitalopram augmentation in 62 schizophrenic patients treated in 2016-2017 at the Shandong Mental Health Center. Twenty-nine healthy controls were also included. Patients received add-on escitalopram or placebo for 8 weeks. Serum IL-6 and CRP were measured at baseline and 8 weeks. The primary outcome was the Positive and Negative Syndrome Scale (PANSS). After 8 weeks of treatment, reductions in total PANSS, negative subscore, and affective subscore were more important in escitalopram treated patients than in the placebo group (all P < 0.05). Escitalopram significantly decreased CRP and IL-6 levels (both P < 0.05). At baseline, IL-6's effects on negative and cognitive symptoms represented 16.2% and 20.1%, respectively; at week 8, these effects were 22.7% and 20.8% on negative and cognitive symptoms, respectively. CRP had no impact on any PANSS score. Overall, escitalopram augmentation may be a useful addition for schizophrenic patients with persistent negative symptoms. Changes in IL-6 may be associated with negative and cognitive symptoms.

Alcohol addiction can cause brain dysfunction and threatens both individuals and society. Recently, emerging studies have suggested the dysbiosis of gut microbiota induced by alcohol exposure contributed to the reward-seeking behaviors as well as anxiety, depression. In the current study, animal model of chronic alcohol exposure was established by providing mice with gradient concentrations of alcohol from 2%, 4%, and 6% to 8% for 21 days. Moreover, three fecal microbiota transplantation (FMT) plans were innovatively designed to explore the potential effects of FMT from 3 healthy donors on alcohol-induced neuropsychic behaviors. To our knowledge, for the first time, e found that anxiety and depression after alcohol intake were gradually relieved with the extension of transplantation. Although the two-week FMT starting at the end of alcohol treatment had few effects, the transplantation started at 8% ethanol exposure alleviated alcohol-induced depression in tail suspension test. More importantly, accompanied by three-week exposure, the tive-n eek FMT significantly decreased anxiety-like behaviors in open field test and depression in tail suspension test. These data validated the role of gut microbiota in alcohol addiction and indicated the modulation of healthy donor FMT on alcohol-related anxiety and depression, providing a new target for treating alcohol addiction by targeting microbiota.