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Background: Schizophrenia, bipolar disorder and major depressive disorder are increasingly being conceptualized as a transdiagnostic continuum. Disruption of white matter is a common alteration in these psychiatric disorders, but the molecular mechanisms underlying the disruption remain unclear. Neuregulin 1 (NRG1) is genetically linked with susceptibility to schizophrenia, bipolar disorder and major depressive disorder, and it is also related to white matter. Methods: Using a transdiagnostic approach, we aimed to identify white matter differences associated with NRG1 and their relationship to transdiagnostic symptoms and cognitive function. We examined the white matter of 1051 participants (318 healthy controls and 733 patients with major psychiatric disorders: 254 with schizophrenia, 212 with bipolar disorder and 267 with major depressive disorder) who underwent diffusion tensor imaging. We measured the plasma NRG1-[beta]1 levels of 331 participants. We also evaluated clinical symptoms and cognitive function. Results: In the patient group, abnormal white matter was negatively associated with NRG1-[beta]1 levels in the genu of the corpus callosum, right uncinate fasciculus, bilateral inferior fronto-occipital fasciculus, right external capsule, fornix, right optic tract, left straight gyrus white matter and left olfactory radiation. These NRG1-associated white matter abnormalities were also associated with depression and anxiety symptoms and executive function in patients with a major psychiatric disorder. Furthermore, across the 3 disorders we observed analogous alterations in white matter, NRG1-[beta]1 levels and clinical manifestations. Limitations: Medication status, the wide age range and our cross-sectional findings were limitations of this study. Conclusion: This study is the first to provide evidence for an association between NRG1, white matter abnormalities, clinical symptoms and cognition in a transdiagnostic psychiatric cohort. These findings provide further support for an understanding of the molecular mechanisms that underlie the neuroimaging substrates of major psychiatric disorders and their clinical implications., Introduction Schizophrenia, bipolar disorder and major depressive disorder have been separate diagnoses since the time of Kraepelin in the 1920s. (1) However, diagnostic categories based on presenting signs and symptoms [...]

Background: White matter network alterations have increasingly been implicated in major depressive disorder, bipolar disorder and schizophrenia. The aim of this study was to identify shared and distinct white matter network alterations among the 3 disorders. Methods: We used analysis of covariance, with age and gender as covariates, to investigate white matter network alterations in 123 patients with schizophrenia, 123 with bipolar disorder, 124 with major depressive disorder and 209 healthy controls. Results: We found significant group differences in global network efficiency (F = 3.386, p = 0.018), nodal efficiency (F = 8.015, p < 0.001 corrected for false discovery rate [FDR]) and nodal degree (F = 5.971, [p.sub.FDR] < 0.001) in the left middle occipital gyrus, as well as nodal efficiency (F = 6.930, [p.sub.FDR] < 0.001) and nodal degree (F = 5.884, [p.sub.FDR] < 0.001) in the left postcentral gyrus. We found no significant alterations in patients with major depressive disorder. Post hoc analyses revealed that compared with healthy controls, patients in the schizophrenia and bipolar disorder groups showed decreased global network efficiency, nodal efficiency and nodal degree in the left middle occipital gyrus. Furthermore, patients in the schizophrenia group showed decreased nodal efficiency and nodal degree in the left postcentral gyrus compared with healthy controls. Limitations: Our findings could have been confounded in part by treatment differences. Conclusion: Our findings implicate graded white matter network alterations across the 3 disorders, enhancing our understanding of shared and distinct pathophysiological mechanisms across diagnoses and providing vital insights into neuroimaging-based methods for diagnosis and research., Introduction Schizophrenia, bipolar disorder and major depressive disorder (MDD) are among the most common diseases in psychiatric nosology. There is increasing evidence for shared features among these disorders with respect [...]

Background: Previous studies of atypical antipsychotic effects on cortical structures in schizophrenia (SZ) and bipolar disorder (BD) have findings that vary between the short and long term. In particular, there has not been a study exploring the effects of atypical antipsychotics on age-related cortical structural changes in SZ and BD. This study aimed to determine whether mid- to long-term atypical antipsychotic treatment (mean duration = 20 months) is associated with cortical structural changes and whether age-related cortical structural changes are affected by atypical antipsychotics. Methods: Structural magnetic resonance imaging images were obtained from 445 participants consisting of 88 medicated patients (67 with SZ, 21 with BD), 84 unmedicated patients (50 with SZ, 34 with BD), and 273 healthy controls (HC). Surface-based analyses were employed to detect differences in thickness and area among the three groups. We examined the age-related effects of atypical antipsychotics after excluding the potential effects of illness duration. Results: Significant differences in cortical thickness were observed in the frontal, temporal, parietal, and insular areas and the isthmus of the cingulate gyrus. The medicated group showed greater cortical thinning in these regions than the unmediated group and HC; furthermore, there were age-related differences in the effects of atypical antipsychotics, and these effects did not relate to illness duration. Moreover, cortical thinning was significantly correlated with lower symptom scores and Wisconsin Card Sorting Test (WCST) deficits in patients. After false discovery rate correction, cortical thinning in the right middle temporal gyrus in patients was significantly positively correlated with lower HAMD scores. The unmedicated group showed only greater frontotemporal thickness than the HC group. Conclusion: Mid- to long-term atypical antipsychotic use may adversely affect cortical thickness over the course of treatment and ageing and may also result in worsening cognitive function. [ABSTRACT FROM AUTHOR]

Background Bipolar depression (BD) is easily misdiagnosed as unipolar depression (UD) or major depressive disorder (MDD) because the depressive symptoms can overlap. Regional homogeneity (ReHo), a measure commonly used for analyzing resting-state fMRI data, has been applied to the study of various neuropsychiatric disorders. However, to date, studies directly comparing BD and UD using ReHo have been relatively scarce. Further investigation is needed to study the latent pathophysiological mechanisms of BD and UD. Methods Fifty-five patients with BD and 76 patients with UD, as well as 113 healthy controls (HC), underwent resting-state functional magnetic resonance imaging (fMRI). We compared the voxel-wise ReHo across the whole brain for subjects in each of the three groups. Results Significant differences were found in the left frontal cluster (LFC) across the three groups. There were differences between BD and UD in the LFC and left temporal cluster (LTC). In addition, differences between UD and HC existed in the LFC and the occipital cluster (OC). When comparing BD subjects with HC subjects, significant differences were found in all three clusters. No correlations were observed between the 17-item Hamilton Depression Rating Scale (HDRS-17) scores or sub-scores and the ReHo values of BD or UD patients. Conclusion ReHo values in the LFC differed significantly among BD, UD, and HC subjects. ReHo in the LTC showed significant differences between BD and UD that might serve as neuroimaging markers of BD. Further, BD and UD shared ReHo changes in the cuneus, suggesting that the cuneus might provide a depressive state neuroimaging marker of BD and UD patients. [ABSTRACT FROM AUTHOR]

Aiming at the status of muscle and joint damage caused on surgeons keeping surgical posture for a long time, this paper designs a medical multi-position auxiliary support exoskeleton with multi-joint mechanism by analyzing the surgical postures and conducting conformational studies on different joints respectively. Then by establishing a human-machine static model, this study obtains the joint torque and joint force before and after the human body wears the exoskeleton, and calibrates the strength of the exoskeleton with finite element analysis software. The results show that the maximum stress of the exoskeleton is less than the material strength requirements, the overall deformation is small, and the structural strength of the exoskeleton meets the use requirements. Finally, in this study, subjects were selected to participate in the plantar pressure test and biomechanical simulation with the man-machine static model, and the results were analyzed in terms of plantar pressure, joint torque and joint force, muscle force and overall muscle metabolism to assess the exoskeleton support performance. The results show that the exoskeleton has better support for the whole body and can reduce the musculoskeletal burden. The exoskeleton mechanism in this study better matches the actual working needs of surgeons and provides a new paradigm for the design of medical support exoskeleton mechanism.