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Background: Nonsuicidal self-injury (NSSI) among adolescents is a growing global concern. However, effective interventions for treating NSSI are limited. Method: A 36-week quasi-experimental study design of parent--child group resilience training (intervention group) for adolescents aged 12-17 years was used and compared with treatment-as-usual (control group). The primary endpoint was the frequency of NSSI assessed with the Ottawa Self-Injury Inventory (OSI), and the secondary endpoints were the levels of depression, hope, resilience, and family adaptability and cohesion as assessed by the 24-item Hamilton depression rating scale (HAMD-24), Herth Hope Scale (HHS), Connor- Davidson Resilience Scale (CD-RISC), and Family Adaptability and Cohesion Evaluation Scale, second edition (FACES-II-CV), respectively. Result: A total of 118 participants completed the trial. Both groups showed a significant reduction in NSSI frequency after 12, 24, and 36 weeks of intervention (p< 0.05), although the intervention group did not differ significantly from the control group. After 12, 24, and 36 weeks of intervention, the CD-RISC, HHS, HAMD-24, and FACES-II-CV scores in the intervention and control groups improved over baseline (p< 0.05). Furthermore, the intervention group had higher scores on the CD-RISC, HHS, and FACES-II-CV and lower scores on the HAMD-24 than the control group after 12, 24, and 36 weeks of intervention (p < 0.05). Conclusion: Parent--child group emotional regulation and resilience training showed promise as treatment options for NSSI among adolescents, leading to increased hope, resilience, and improved family dynamics among NSSI teens. Moreover, NSSI frequency significantly decreased in the intervention group compared to baseline. [ABSTRACT FROM AUTHOR]

Background Non-suicidal self-injury (NSSI) is a frequent and prominent phenomenon in major depressive disorder (MDD). Even though its prevalence and risk factors are relatively well understood, the potential mechanisms of NSSI in MDD remain elusive. Aims To review present evidence related to the potential mechanisms of NSSI in MDD. Methods According to Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 guidelines, articles for this systematic review were searched on Medline (through PubMed), Embase (through Elsevier), PsycINFO (through OVID) and Web of Science databases for English articles, as well as China National Knowledge Infrastructure (CNKI), SinoMed, Wanfang Data, and the Chongqing VIP Chinese Science and Technology Periodical (VIP) Databases for Chinese articles published from the date of inception to 2 August 2022. Two researchers (BW, HZ) independently screened studies based on inclusion and exclusion criteria and assessed their quality. Results A total of 25 157 studies were searched. Only 25 of them were ultimately included, containing 3336 subjects (1535 patients with MDD and NSSI, 1403 patients with MDD without NSSI and 398 HCs). Included studies were divided into 6 categories: psychosocial factors (11 studies), neuroimaging (8 studies), stress and hypothalamic-pituitary-adrenal (HPA) axis (2 studies), pain perception (1 study), electroencephalogram (EEG) (2 studies) and epigenetics (1 study). Conclusions This systematic review indicates that patients with MDD and NSSI might have specific psychosocial factors, aberrant brain functions and neurochemical metabolisms, HPA axis dysfunctions, abnormal pain perceptions and epigenetic alterations. [ABSTRACT FROM AUTHOR]

Background: Non-suicidal self-injury (NSSI) is common in adolescent MDD, which is also a risk factor for suicide. However, there is few research on biomarkers and predictors about treatment response of NSSI. The purpose of this study was to find the difference of P300 between adolescent MDD with NSSI and healthy controls, and to explore whether the baseline electrophysiological level can predict the change of NSSI after treatment. Methods: We collected 62 first-episode drug-naïve MDD adolescents with NSSI (MDD with NSSI group) and 44 healthy controls (HC group). The demographic data, HAMD score, self-injury frequency and electrophysiological level of NSSI group and HC group were collected. The HAMD score, frequency of NSSI in was also collected after 8 weeks of antidepressant treatment. Results: Compared to HC, the latency of the N2, P3a, and P3b components were significantly prolonged, whereas the amplitude of P3a and P3b were decreased in the MDD with NSSI group (P < 0.001). The frequency of selfinjury decreased significantly after treatment (P < 0.001). Regression analysis showed that the amplitudes of P3b had a significant positive predictive effect on the rate of change of NSSI frequency after 8 weeks. Conclusion: P3b at baseline can be used as potential predictor for the reduction of NSSI in adolescent MDD. [ABSTRACT FROM AUTHOR]

Background: Due to substantial comorbidities of major depressive disorder (MDD) and anxiety disorder (AN), these two disorders must be distinguished. Accurate identification and diagnosis facilitate-effective and prompt treatment. EEG biomarkers are a potential research hotspot for neuropsychiatric diseases. The purpose of this study was to investigate the differences in EEG power spectrum at theta oscillations between patients with MDD and patients with AN. Methods: Spectral analysis was used to study 66 patients with MDD and 43 patients with AN. Participants wore 16-lead EEG caps to measure resting EEG signals. The EEG power spectrum was measured using the fast Fourier transform. Independent samples t-test was used to analyze the EEG power values of the two groups, and p < 0.05 was statistically significant. Results: EEG power spectrum of the MDD group significantly differed from the AN group in the theta oscillation on 4-7Hz at eight electrode points at F3, O2, T3, P3, P4, FP1, FP2, and F8. Conclusion: Participants with anxiety demonstrated reduced power in the prefrontal cortex, left temporal lobe, and right occipital regions. Confirmed by further studies, theta oscillations could be another biomarker that distinguishes MDD from AN. [ABSTRACT FROM AUTHOR]

Immune dysfunction has been implicated in the pathogenesis of schizophrenia (SZ). Despite previous studies showing a broad link between immune dysregulation and the central nervous system of SZ, the exact relationship has not been completely elucidated. With immune infiltration analysis as an entry point, this study aimed to explore the relationship between schizophrenia and the immune system in more detail from brain regions, immune cells, genes, and pathways. Here, we comprehensively analyzed the hippocampus (HPC), prefrontal cortex (PFC), and striatum (STR) between SZ and control groups. Differentially expressed genes (DEGs) and functional enrichment analysis showed that three brain regions were closely related to the immune system. Compared with PFC and STR, there were 20 immune-related genes (IRGs) and 42 immune pathways in HPC. The results of immune infiltration analysis showed that the differential immune cells in HPC were effector memory T (Tem) cells. The correlation of immune-related DEGs (IDEGs) and immune cells further analysis showed that NPY, BLNK, OXTR, and FGF12, were moderately correlated with Tem cells. Functional pathway analysis indicated that these four genes might affect Tem by regulating the PI3K-AKT pathway and the neuroactive ligand-receptor interaction pathway. The receiver operating characteristic curve (ROC) analysis results indicated that these four genes had a high diagnostic ability (AUC=95.19%). Finally, the disease animal model was successfully replicated, and further validation was conducted using the real-time PCR and the western blot. These results showed that these gene expression changes were consistent with our previous expression profiling. In conclusion, our findings suggested that HPC in SZ may be more closely related to immune disorders and modulate immune function through Tem, PI3K-Akt pathway, and neuroactive ligand-binding receptor interactions. To the best of our knowledge, the Immucell AI tool has been applied for the first time to analyze immune infiltration in SZ, contributing to a better understanding of the role of immune dysfunction in SZ from a new perspective. [ABSTRACT FROM AUTHOR]

Background: The outbreak of coronavirus disease 2019 (COVID-19) that occurred in Wuhan, China, has become a global public health threat. It is necessary to identify indicators that can be used as optimal predictors for clinical outcomes of COVID-19 patients. Methods: The clinical information from 126 patients diagnosed with COVID-19 were collected from Wuhan Fourth Hospital. Specific clinical characteristics, laboratory findings, treatments and clinical outcomes were analyzed from patients hospitalized for treatment from 1 February to 15 March 2020, and subsequently died or were discharged. A random forest (RF) algorithm was used to predict the prognoses of COVID-19 patients and identify the optimal diagnostic predictors for patients' clinical prognoses. Results: Seven of the 126 patients were excluded for losing endpoints, 103 of the remaining 119 patients were discharged (alive) and 16 died in the hospital. A synthetic minority over-sampling technique (SMOTE) was used to correct the imbalanced distribution of clinical patients. Recursive feature elimination (RFE) was used to select the optimal subset for analysis. Eleven clinical parameters, Myo, CD8, age, LDH, LMR, CD45, Th/Ts, dyspnea, NLR, D-Dimer and CK were chosen with AUC approximately 0.9905. The RF algorithm was built to predict the prognoses of COVID-19 patients based on the best subset, and the area under the ROC curve (AUC) of the test data was 100%. Moreover, two optimal clinical risk predictors, lactate dehydrogenase (LDH) and Myoglobin (Myo), were selected based on the Gini index. The univariable logistic analysis revealed a substantial increase in the risk for in-hospital mortality when Myo was higher than 80 ng/ml (OR = 7.54, 95% CI [3.42-16.63]) and LDH was higher than 500 U/L (OR = 4.90, 95% CI [2.13-11.25]). Conclusion: We applied an RF algorithm to predict the mortality of COVID-19 patients with high accuracy and identified LDH higher than 500 U/L and Myo higher than 80 ng/ml to be potential risk factors for the prognoses of COVID-19 patients in the early stage of the disease. [ABSTRACT FROM AUTHOR]

Background: Studies have confirmed that the thalamus and the primary somatosensory cortex (SI) are associated with cognitive function. These two brain regions are closely related in structure and function. The interactions between SI and the thalamus are of crucial significance for the cognitive process. Patients with major depressive disorder (MDD) have significant cognitive impairment. Based on these observations, we used resting-state functional magnetic resonance imaging (rs-fMRI) to investigate whether there is an abnormality in the SI-thalamic functional connection in MDD. Furthermore, we explored the clinical symptoms related to this abnormality. Methods: We included 31 patients with first-episode major depressive disorder and 28 age-, gender-, and education-matched healthy controls (HC). The SI-thalamic functional connectivity was compared between the MDD and HC groups. The correlation analyses were performed between areas with abnormal connectivity and clinical characteristics. Results: Compared with healthy subjects, the MDD patients had enhanced functional connectivity between the thalamus and SI (p < 0.05, corrected). Brain areas with significantly different levels of connectivity had a negative correlation with the Assessment of Neuropsychological Status total score (r = - 0.383, p = 0.033), delayed memory score (r = - 0.376, p = 0.037) and two-digit continuous operation test score (r = - 0.369, p = 0.041) in MDD patients. Conclusions: These results demonstrate that SI-thalamic functional connectivity is abnormal and associated with the core clinical symptoms in MDD. The SI-thalamic functional connectivity functions as a neurobiological feature and potential biomarker for MDD. [ABSTRACT FROM AUTHOR]

Previous studies have demonstrated that dysregulation of micro (mi)RNAs is associated with the etiology of various neuropsychiatric disorders, including depression and schizophrenia. Cerebralcare GranuleR (CG) is a Chinese herbal medicine, which has been reported to have an ameliorative effect on brain injury by attenuating blood.brain barrier disruption and improving hippocampal neural function. The present study aimed to evaluate the cognitive behavior of rats continuously overexpressing miRNA.30e (lenti.miRNA.30e), prior to and following the administration of CG. In addition, the mechanisms underlying the ameliorative effects of CG were investigated. The cognitive ability of the rats was assessed using an open.field test and a Morris water maze spatial reference/ working memory test. A terminal deoxynucleotidyl transferase dUTP nick end labeling assay was used to detect neuronal apoptosis in the dentate gyrus of the hippocampus. Immunohistochemical analysis and western blotting were conducted to detect the expression levels of B.cell lymphoma 2 (BCL.2) and ubiquitin.conjugating enzyme 9 (UBC9), in order to examine neuronal apoptosis. The lenti.miRNA.30e rats exhibited increased signs of anxiety, depression, hyperactivity and schizophrenia, which resulted in a severe impairment in cognitive ability. Furthermore, in the dentate gyrus of these rats, the expression levels of BCL.2 and UBC9 were reduced and apoptosis was increased. The administration of CG alleviated cognitive impairment, enhanced the expression levels of BCL.2 and UBC9, and reduced apoptosis in the dentate gyrus in the lenti.miRNA.30e rats. No significant differences were detected in behavioral indicators between the lenti.miRNA.30e rats treated with CG and the normal controls. These findings suggested that CG exerts a potent therapeutic effect, conferred by its ability to enhance the expression levels of BCL.2 and UBC9, which inhibits the apoptotic process in neuronal cells. Therefore, CG may be considered a potential therapeutic strategy for the treatment of cognitive impairment in mental disorders. [ABSTRACT FROM AUTHOR]