Shanghai Mental Health Center (simplified Chinese: 上海市精神卫生中心; traditional Chinese: 上海市精神衛生中心; pinyin: Shànghǎishì Jīngshén Wèishēng Zhōngxīn), also known as Shanghai Psychological Consultative Center, is a hospital in Shanghai focusing on treating mental disorders. It was founded in 1935, as Puci Rehabilitation Hospital. It was formerly called Shanghai Psychiatric Hospital. Since May 2006, the hospital has been affiliated to School of Medicine of Shanghai Jiao Tong University.
Psychiatric comorbidity is clinically significant yet challenging due to the complexity of multiple co-occurring disorders. To address this, we develop a novel approach integrating synthetic patient electronic medical record (EMR) construction and multi-agent diagnostic dialogue generation. We create 502 synthetic EMRs for common comorbid conditions using a pipeline that ensures clinical relevance and diversity. Our multi-agent framework transfers the clinical interview protocol into a hierarchical state machine and context tree, supporting over 130 diagnostic states while maintaining clinical standards. Through this rigorous process, we construct the first large-scale dialogue dataset supporting comorbidity, containing 3,000 multi-turn diagnostic dialogues validated by psychiatrists. This dataset enhances diagnostic accuracy and treatment planning, offering a valuable resource for psychiatric comorbidity research. Compared to real-world clinical transcripts, PsyCoTalk exhibits high structural and linguistic fidelity in terms of dialogue length, token distribution, and diagnostic reasoning strategies. Licensed psychiatrists confirm the realism and diagnostic validity of the dialogues. This dataset enables the development and evaluation of models capable of multi-disorder psychiatric screening in a single conversational pass.
OBJECTIVE:Sublobectomy is a modified surgical paradigm based on anatomical lobectomy, incorporating functional boundaries to extend resection safely, particularly for glioblastoma, a highly aggressive brain tumor. This study aimed to evaluate the efficacy and safety of sublobectomy and its prognostic value within the Response Assessment in Neuro-Oncology (RANO) categories for extent of resection. METHODS:Building on their clinical practice, the authors established a sublobectomy standard defined by lobe-specific anatomical boundaries complemented by functional mapping limits and applied it across the frontal, temporal, parietal, and occipital lobes. In this retrospective single-center study, 989 IDH-wildtype glioblastoma cases were analyzed, and 401 met the anatomical criteria for sublobectomy. After excluding cases with residual contrast-enhancing (CE) tumor or incomplete postoperative chemoradiotherapy, 331 cases were included. Propensity score matching (PSM) and inverse probability of treatment weighting (IPTW) were used to minimize confounding biases. Survival outcomes were assessed using Kaplan-Meier survival analysis and Cox proportional hazards models, while functional outcomes were evaluated using Karnofsky Performance Status, Boston Diagnostic Aphasia Examination, and Eastern Cooperative Oncology Group scores. RESULTS:Sublobectomy significantly improved overall survival (OS) and progression-free survival (PFS) compared to CE tumor resection (median OS: 25.6 vs 18.1 months [p < 0.001], median PFS: 17.0 vs 12.0 months [p < 0.001]). These findings remained consistent after IPTW and PSM analyses. Functional assessments showed no additional risks to quality of life, physical performance, or language function. In RANO class 1 patients, sublobectomy also significantly improved OS and PFS. Subgroup analyses revealed greater survival benefits in patients with TERTp mutations or MGMTp methylation. Maximal safe edema resection emerged as a key factor for improved outcomes. CONCLUSIONS:Sublobectomy is a functionally optimized supramaximal resection strategy with favorable safety and significant survival benefits for glioblastoma patients.
IntroductionChinese expatriate oilfield employees working in Iraq are exposed to multiple occupational and psychosocial stressors, yet evidence on sleep disturbance and its correlates in this workforce remains limited.MethodsA cross-sectional survey was conducted among 917 employees. 826 (90.1%) were included after excluding incomplete or invalid responses. Sleep quality and related concern was assessed using the Pittsburgh Sleep Quality Index (PSQI) and the second item of the General Health Questionnaire-12 (GHQ-12). Depression, anxiety, occupational stress, burnout dimensions, Iraq-specific environmental stress, and perceived social support were measured using validated instruments and context-specific questionnaires. Multivariable linear regression and regularized partial correlation network analyses were performed.ResultsThe median global PSQI score was 3 (IQR 1–6). Sleep disturbance prevalence was 11.9% (95% CI 9.7%–14.3%) using PSQI > 7 and 25.2% (95% CI 22.3%–28.3%) using PSQI > 5, while 61.3% (95% CI 57.9%–64.7%) reported sleep-related concern on the GHQ-12. In the fully adjusted regression model (adjusted R2 = 0.522), poorer sleep quality was independently associated with higher educational attainment (high school or junior college: β = 0.68, p = 0.012; bachelor degree or above: β = 0.89, p = 0.011), more depressive symptoms (β = 0.25, p < 0.001), higher occupational stress (β = 0.03, p = 0.022), greater emotional exhaustion (β = 0.90, p < 0.001), and greater environmental stress (β = 0.57, p = 0.002). In the global network, PSQI had direct edges with depressive symptoms, anxiety symptoms, emotional exhaustion, and environmental stress and showed moderate centrality (strength = 0.69; expected influence = 0.61), with good stability of strength (CS-coefficient = 0.75). In the component network, subjective sleep quality and daytime dysfunction had the highest centrality among PSQI domains.ConclusionAlthough overall self-reported sleep quality was relatively good among Chinese expatriate employees in Iraq, subclinical sleep problems and sleep-related concern were common. Poorer sleep quality was more consistently linked to depressive symptoms, work-related stress and exhaustion, and environmental stressors, while subjective sleep quality and daytime dysfunction emerged as key sleep domains. These findings may help inform priorities for improving sleep health in this expatriate oilfield workforce.
Background Forced running often triggers discomfort and stress, leading to poor adherence; those compelled to exercise frequently choose to quit rather than persist. However, the neural mechanisms mediating this negative experience and ultimately leading to exercise abandonment remain unclear. The nucleus accumbens (NAc) plays a crucial role in motivation and aversion responses, but how specific neuronal subpopulations adapt to forced running is not fully elucidated. In this study, we investigated the region-specific mechanisms by which D2-MSNs in the nucleus accumbens regulate forced treadmill running. Methods Adult male D2R-eGFP mice were randomly divided into a sedentary control group (Ctrl-Sed) and an exercise group (Treadmill). We established a forced treadmill running model and used immunofluorescence staining and whole-cell patch-clamp recordings to examine the effects of forced treadmill running on the activation and plasticity of D2-MSNs in the nucleus accumbens. Furthermore, by chemogenetically modulating D2-MSNs in the nucleus accumbens core of D2R-Cre mice, we validated the regulatory role of nucleus accumbens core D2-MSNs in forced treadmill running performance. Results Immunofluorescence staining revealed that the Treadmill group exhibited increased c-fos expression in D2-MSNs within the nucleus accumbens, and that forced treadmill running recruited D2-MSNs to varying levels across the two subregions of the nucleus accumbens. Whole-cell patch-clamp recordings indicated that D2-MSNs in the nucleus accumbens core exhibited plastic changes in the Treadmill group, manifested as increased intrinsic excitability and enhanced excitatory synaptic transmission. Chemogenetic manipulation revealed that the activity of D2-MSNs in the nucleus accumbens core significantly influences performance during forced running. Conclusion Our data indicate that forced treadmill running specifically activates D2-MSNs in the nucleus accumbens core, and that this neuronal activation may act as a central “braking signal” leading to an earlier termination of forced running.
