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29 result(s) for "Ju, MingLiang"
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Stage-dependent patterns of cognitive network connectivity in early psychosis
Cognitive impairments in early psychosis are common, yet prior studies have focused mainly on domain-specific deficits rather than inter-domain relationships. Analyzing cognitive network connectivity may uncover insights into early psychosis mechanisms. Cognitive functions were assessed from 2,518 participants, including 988 first-episode schizophrenia (FES), 767 clinical high-risk (CHR), and 763 healthy controls (HC), using the Chinese version of the Measurement and Treatment Research to Improve Cognition in Schizophrenia Consensus Cognitive Battery (MCCB). Results revealed a stage-dependent “dedifferentiation” pattern: mean inter-domain correlation increased from HC (0.28) to CHR (0.33) to FES (0.40). Confirmatory factor analysis revealed a common “g” factor across groups, with significantly reduced strength in FES compared to CHR and HC. The reduction in the “g” factor was associated with increased connectivity and stronger inter-domain correlations. These findings highlight cognitive network dedifferentiation and “g” factor decline as key features of early psychosis. This study reveals stage-dependent cognitive network dedifferentiation in early psychosis, with increasing inter-domain correlations from healthy controls to clinical high risk to first-episode schizophrenia, linked to reduced general intelligence.
Transplantation of gut microbiota derived from patients with schizophrenia induces schizophrenia-like behaviors and dysregulated brain transcript response in mice
Schizophrenia (SCZ), as a neurodevelopmental disorder and devastating disease, affects approximately 1% of the world population. Although numerous studies have attempted to elucidate the causes of SCZ occurrence, it is not clearly understood. Recently, the emerging roles of the gut microbiota in a range of brain disorders, including SCZ, have attracted much attention. While the molecular mechanism of gut microbiota in regulating the pathogenesis of SCZ is still lacking. Here, we first confirmed the difference of gut microbiome between SCZ patients and healthy controls, and then, we performed fecal microbiota transplantation (FMT) to clarify the roles of SCZ patients-derived microbiota in a specific pathogen free (SPF) mice model. 16 S rDNA sequencing confirmed that a significant difference of gut microbiome was present between two groups of FMT mice, which has a similar trend with the above human gut microbiome. Furthermore, we found that transplantation of fecal microbiota from SCZ patients into SPF mice was sufficient to induce schizophrenia-like (SCZ-like) symptoms, such as deficits in sociability and hyperactivity. Furthermore, the brains of mice colonized with SCZ microbiota displayed dysregulated transcript response and alternative splicing of SCZ-relevant genes. Moreover, 10 key genes were identified to be correlated with SCZ by an integrative transcriptome data analysis. Finally, 4 key genes were identified to be correlated with the 12 differential genera between two groups of FMT mice. Our results thus demonstrated that the gut microbiome might modify the transcriptomic profile in the brain, thereby modulating social behavior, and our present study can help better understand the link between gut microbiota and SCZ pathogenesis through the gut-brain axis.
Distribution of borderline personality disorder related impulsivity types in psychiatric clinical populations
Background Impulsivity is a core feature of Borderline Personality Disorder (BPD), yet its prevalence and variations across demographics and diagnoses in clinical populations are underexplored. This study aims to investigate the frequency and distribution of impulsive behaviors related to BPD among a large clinical sample, considering gender, age, and diagnostic categories. Methods A total of 2862 participants were consecutively sampled from psychiatric and psycho-counseling clinics. BPD traits and symptoms were assessed using the Personality Diagnostic Questionnaire 4th Edition Plus (PDQ-4plus), a concise and well-structured self-report questionnaire. Impulsive behaviors, including overspending, casual sex, excessive drinking, drug use, overeating, and reckless behavior, were evaluated based on item 106 of the PDQ-4plus. Results Overall frequencies show that 36.10% engaged in overspending, 10.30% in casual sex, 20.00% in excessive drinking, 7.30% in using drugs, 38.70% in overeating, and 15.60% in reckless behavior. Significant gender differences were observed, with men reporting higher rates of casual sex ( χ² = 13.868, p  < 0.001) and excessive drinking ( χ² = 35.331, p  < 0.001), while women reported higher rates of overeating ( χ² = 27.320, p  < 0.001). Age analysis revealed that younger adults exhibited higher impulsivity, particularly in overspending and reckless behavior. Diagnostic analysis showed that psychotic and mood disorders were associated with higher rates of overspending and overeating. Conclusions The study underscores the importance of considering demographic and diagnostic variations when addressing impulsive behaviors in BPD. These findings can inform the development of targeted interventions. Clinical trial number Not applicable.
Multiple Factor Analysis of Depression and/or Anxiety in Patients with Acute Exacerbation Chronic Obstructive Pulmonary Disease
Objective: To reveal the risk factors, the symptom distribution characteristics, the clinical values of white blood cell counts (WBC counts), red blood cell distribution width (RDW), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR) and monocyte-tolymphocyte ratio (MLR) in hospitalized patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) combined with depression and/or anxiety. Methods: The study included prospective cross-sectional and case-control studies, and was executed in the Affiliated Hospital of Zunyi Medical University, Guizhou, China. Previously diagnosed chronic obstructive pulmonary disease (COPD) patients who admitted to the hospital with AECOPD, patients with depression and/or anxiety, and healthy people were enrolled in the study. The Hamilton Rating Scales were used to assess all subjects, and the complete blood counts (CBC) were collected. Baseline data and clinical measurement data [spirometry, arterial blood gas analysis, and COPD evaluation test (the CAT scale)] from patients with AECOPD were collected. Results: Of the 307 patients with AECOPD included, 63.5% (N=195) had depressive and/or anxiety symptoms, and 36.5% (N=112) had no symptoms. Sex, respiratory failure, number of comorbidities, number of acute exacerbations in the previous year and the CAT score were closely related to AECOPD combined with depression and/or anxiety (p<0.05). The CAT scale score were the independent risk factor (OR=6.576, 95% CI 3.812-11.342) and significant predictor of AECOPD with depression and/or anxiety (AUC=0.790,95% CI 0.740-0.834); the patients with depression and/or anxiety were more severe and characteristic than the patients with AECOPD combined with depression and/or anxiety; RDW was associated with AECOPD with depression and/or anxiety (p=0.020, OR1.212,95% CI1.03-1.426), and had certain clinical diagnostic value (AUC=0.570,95% CI 0.531-0.626). Conclusion: Depression and anxiety should not be ignored in patients with AECOPD. The severity and quality of life of COPD were closely related to the occurrence of depression and/or anxiety symptoms. In most cases, perhaps depression and anxiety in AECOPD are only symptoms and not to the extents of the diseases. RDW had clinical diagnostic value in AECOPD combined with depression and/or anxiety. NLR, PLR, MLR, and RDW may become the novel indicators for evaluating the degree of inflammation of AECOPD and deserve further research. Keywords: AECOPD, anxiety, depression, comorbidities, Hamilton Rating Scale, inflammatory markers, symptomatology
Longitudinal investigation of the T helper (Th)1-Th2 balance and complement system in clinical high risk for psychosis cohort
The T Helper (Th)1-Th2 imbalance has been observed during the transition from the clinical high-risk (CHR) state to psychosis. However, it remains unclear whether the complement system influences this imbalance during psychosis onset. This study aimed to investigate the dynamic interplay between complement activation and the Th1-Th2 balance during the progression of psychosis. A prospective case-control study was conducted to evaluate the Th1-Th2 balance, as indicated by interleukin(IL)-1Beta and IL-6 levels, in 49 individuals at CHR for psychosis and 26 age- and sex-matched healthy controls(HC). Based on the Th1-Th2 balance, the samples were divided into two groups: Th1 > Th2 and Th1 < Th2. Additionally, the levels of thirteen complement proteins (C1q, C2, C3, C3b, C4, C4b, C5, C5a, factor B, D, I, H, and Mannose-Binding Lectin) were measured at baseline. Correlations between cytokines and complement factors were examined, and longitudinal changes were assessed through a 1-year follow-up period. At baseline, significant differences were observed in complement characteristics (C4, C4b, C5, and B) between Th1 > Th2 and Th1 < Th2 balance states, highlighting variations in complement factors between the CHR and HC groups. In the CHR group, a negative association was noted between Th1-Th2 balance and complement factors, with significant correlations observed for components C4b, C5, I, C3, C4, and B. However, no significant correlation was found in the HC group. At follow-up, the Th1 < Th2 group exhibited a higher proportion of CHR individuals who converted to psychosis compared to the Th1 > Th2 group, indicating a significant association between Th1-Th2 balance and the onset of psychosis ( χ 2  = 12.09, p  = 0.001). This shift in balance was notably linked to baseline complement C4b and C4 levels. Our study reveals a complex interplay between complement and inflammatory factor balance in psychosis onset, highlighting the potential role of complement, particularly associated with baseline C4b and C4 levels, in modulating Th1-Th2 balance and contributing to the pathogenesis of psychosis.
Cytokine changes in clinical high risk for psychosis population following antipsychotic medication
Serum cytokine alterations are associated with the usage of antipsychotic medications (AP). However, few studies have been designed to longitudinally measure cytokine changes during AP exposure in individuals at clinical high risk (CHR) for psychosis. This study aimed to assess changes in levels of cytokines after initiating AP in the prodromal phase. This longitudinal study involved individuals with CHR who completed the 1-year follow-up reassessment. Individuals with CHR were grouped into those treated with AP (AP + group) and those without (AP- group). Levels of vascular endothelial growth factor (VEGF), granulocyte-macrophage colony-stimulating factor (GM-CSF), tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, 2, 6, 8, and 10 were measured at baseline and 1 year after completion of the clinical assessment. This study included 88 CHR individuals (median age, 18 years and 40.9% [n = 36] women; AP- group: n = 28, AP + group: n = 60). The baseline serum levels of IL-6 were higher in the AP- group than in the AP + group ( z  = −2.577, p  = 0.010). Self-controlled comparisons showed that VEGF ( z  = 3.826, p  < 0.001), TNF-α ( z  = 2.642, p  = 0.008), IL-8 ( z  = 2.300, p  = 0.021), and GM-CSF ( z  = 2.346, p  = 0.019) levels were significantly increased in the AP- group. In the AP + group, IL-6 ( z  = 3.512, p  < 0.001) was significantly increased, IL-1β ( z  = 2.563, p  = 0.010), and GM-CSF ( z  = 2.095, p  = 0.036) were significantly decreased. Repeated-measures analysis of variance revealed a significant group × visit effect on VEGF ( F  = 20.348, p  < 0.001), GM-CSF ( F  = 7.042, p  = 0.013), and IL-1β( F  = 4.670, p  = 0.040). The findings revealed significant differences in trajectories between individuals with CHR who were and were not taking AP. There is an association between AP use in CHR individuals and differences in inflammatory and neurotrophic factor trajectories.
Metformin in the Treatment of Amisulpride-Induced Hyperprolactinemia: A Clinical Trial
To evaluate the efficacy and safety of metformin in the treatment of amisulpride-induced hyperprolactinemia.ObjectiveTo evaluate the efficacy and safety of metformin in the treatment of amisulpride-induced hyperprolactinemia.A total of 86 schizophrenic patients who developed hyperprolactinemia after taking amisulpride were screened and randomly assigned to the metformin group (42 patients) and placebo group (44 patients) and followed up for eight weeks. The patients' serum prolactin levels, blood glucose and lipids were measured at the baseline and the end of the intervention. The treatment emergent symptom scale (TESS) was also assessed.MethodsA total of 86 schizophrenic patients who developed hyperprolactinemia after taking amisulpride were screened and randomly assigned to the metformin group (42 patients) and placebo group (44 patients) and followed up for eight weeks. The patients' serum prolactin levels, blood glucose and lipids were measured at the baseline and the end of the intervention. The treatment emergent symptom scale (TESS) was also assessed.After eight weeks of intervention, serum prolactin levels in the metformin group decreased from (1737.360 ± 626.918) mIU/L at baseline to (1618.625 ± 640.865) mIU/L, whereas serum prolactin levels in the placebo group increased from (2676.470 ± 1269.234) mIU/L at baseline to (2860.933 ± 1317.376) mIU/L. There was a significant difference in prolactin changes (Fcovariance = 9.982, P = 0.002) between the two groups. There was no significant difference in the incidence of adverse drug reactions (P > 0.05) between the two groups.ResultsAfter eight weeks of intervention, serum prolactin levels in the metformin group decreased from (1737.360 ± 626.918) mIU/L at baseline to (1618.625 ± 640.865) mIU/L, whereas serum prolactin levels in the placebo group increased from (2676.470 ± 1269.234) mIU/L at baseline to (2860.933 ± 1317.376) mIU/L. There was a significant difference in prolactin changes (Fcovariance = 9.982, P = 0.002) between the two groups. There was no significant difference in the incidence of adverse drug reactions (P > 0.05) between the two groups.Metformin is able to improve amisulpride-induced hyperprolactinemia with its safety.ConclusionMetformin is able to improve amisulpride-induced hyperprolactinemia with its safety.
A case of antipsychotic-induced psychomotor seizure
A seizure is one of the most uncommon severe adverse side effects of antipsychotics. Clinical recognition rates for it are low, especially for psychomotor seizures. The authors present a case of psychomotor seizure caused by amisulpride to treat schizophrenia. A 60-year-old male patient in our hospital experienced a recent onset of repetitive, stereotyped involuntary and unconscious movements that began with amisulpride use. All of the symptoms disappeared following amisulpride withdrawal. His Naranjo Adverse Drug Reactions Probability Scale Score was 5 points. The case sheds light on the clinical risk of seizures related to antipsychotics.
Identifying neurobiological heterogeneity in clinical high-risk psychosis: a data-driven biotyping approach using resting-state functional connectivity
To explore the neurobiological heterogeneity within the Clinical High-Risk (CHR) for psychosis population, this study aimed to identify and characterize distinct neurobiological biotypes within CHR using features from resting-state functional networks. A total of 239 participants from the Shanghai At Risk for Psychosis (SHARP) program were enrolled, consisting of 151 CHR individuals and 88 matched healthy controls (HCs). Functional connectivity (FC) features that were correlated with symptom severity were subjected to the single-cell interpretation through multikernel learning (SIMLR) algorithm in order to identify latent homogeneous subgroups. The cognitive function, clinical symptoms, FC patterns, and correlation with neurotransmitter systems of biotype profiles were compared. Three distinct CHR biotypes were identified based on 646 significant ROI-ROI connectivity features, comprising 29.8%, 19.2%, and 51.0% of the CHR sample, respectively. Despite the absence of overall FC differences between CHR and HC groups, each CHR biotype demonstrated unique FC abnormalities. Biotype 1 displayed augmented somatomotor connection, Biotype 2 shown compromised working memory with heightened subcortical and network-specific connectivity, and Biotype 3, characterized by significant negative symptoms, revealed extensive connectivity reductions along with increased limbic-subcortical connectivity. The neurotransmitter correlates differed across biotypes. Biotype 2 revealed an inverse trend to Biotype 3, as increased neurotransmitter concentrations improved functional connectivity in Biotype 2 but reduced it in Biotype 3. The identification of CHR biotypes provides compelling evidence for the early manifestation of heterogeneity within the psychosis spectrum, suggesting that distinct pathophysiological mechanisms may underlie these subgroups.
How psychiatrists coordinate treatment for COVID‐19: a retrospective study and experience from China
Background Patients with COVID‐19 are at high risk of developing mental health problems; however, the prevalence and management of mental disorders and how psychiatrists coordinate the treatment are unclear. Aims We aimed to investigate the mental health problems of patients infected with COVID‐19 and to identify the role of psychiatrists in the clinical treatment team during the pandemic. We also share the experience of psychiatric consultations of patients with COVID‐19 in Shanghai, China. Methods We analysed data from the psychiatric medical records of 329 patients with COVID‐19 in the Shanghai Public Health Clinical Center from 20 January to 8 March 2020. We collected information including sociodemographic characteristics, whether patients received psychiatric consultation, mental health symptoms, psychiatric diagnoses, psychiatric treatments and severity level of COVID‐19. Results Psychiatric consultations were received by 84 (25.5%) patients with COVID‐19. The most common symptoms of mental health problems were sleep disorders (75%), anxiety (58.3%) and depressive symptoms (11.9%). The psychiatric consultation rate was highest in critically ill patients (69.2%), with affective symptoms or disturbed behaviour as their main mental health problems. Psychiatric diagnoses for patients who received consultation included acute stress reaction (39.3%), sleep disorders (33.3%), anxiety (15.5%), depression (7.1%) and delirium (4.8%). In terms of psychiatric treatments, 86.9% of patients who received psychiatric consultation were treated with psychotropic medications, including non‐benzodiazepine sedative‐hypnotic agents (54.8%), antidepressants (26.2%), benzodiazepines (22.6%) and antipsychotics (10.7%). Among the 76 patients who were discharged from the hospital, 79% had recovered from mental health problems and were not prescribed any psychotropic medications. The symptoms of the remaining 21% of patients had improved and they were prescribed medications to continue the treatment. Conclusions This is the first study to report psychiatric consultations for patients with COVID‐19. Our study indicated that a considerable proportion of patients with COVID‐19, especially critically ill cases, experienced mental health problems. Given the remarkable effect of psychiatric treatments, we recommend that psychiatrists be timely and actively involved in the treatment of COVID‐19.