Electronic Design Automation (EDA) plays a crucial role in classical chip design and significantly influences the development of quantum chip design. However, traditional EDA tools cannot be directly applied to quantum chip design due to vast differences compared to the classical realm. Several EDA products tailored for quantum chip design currently exist, yet they only cover partial stages of the quantum chip design process instead of offering a fully comprehensive solution. Additionally, they often encounter issues such as limited automation, steep learning curves, challenges in integrating with actual fabrication processes, and difficulties in expanding functionality. To address these issues, we developed a full-stack EDA tool specifically for quantum chip design, called EDA-Q. The design workflow incorporates functionalities present in existing quantum EDA tools while supplementing critical design stages such as device mapping and fabrication process mapping, which users expect. EDA-Q utilizes a unique architecture to achieve exceptional scalability and flexibility. The integrated design mode guarantees algorithm compatibility with different chip components, while employing a specialized interactive processing mode to offer users a straightforward and adaptable command interface. Application examples demonstrate that EDA-Q significantly reduces chip design cycles, enhances automation levels, and decreases the time required for manual intervention. Multiple rounds of testing on the designed chip have validated the effectiveness of EDA-Q in practical applications.

Neuroimaging studies have suggested the presence of abnormalities in the prefrontal-thalamic-cerebellar circuit in schizophrenia (SCH) and depression (DEP). However, the common and distinct structural and causal connectivity abnormalities in this circuit between the two disorders are still unclear. In the current study, structural and resting-state functional magnetic resonance imaging (fMRI) data were acquired from 20 patients with SCH, 20 depressive patients and 20 healthy controls (HC). Voxel-based morphometry analysis was first used to assess gray matter volume (GMV). Granger causality analysis, seeded at regions with altered GMVs, was subsequently conducted. To discover the differences between the groups, ANCOVA and post hoc tests were performed. Then, the relationships between the structural changes, causal connectivity and clinical variables were investigated. Finally, a leave-one-out resampling method was implemented to test the consistency. Statistical analyses showed the GMV and causal connectivity changes in the prefrontal-thalamic-cerebellar circuit. Compared with HC, both SCH and DEP exhibited decreased GMV in middle frontal gyrus (MFG), and a lower GMV in MFG and medial prefrontal cortex (MPFC) in SCH than DEP. Compared with HC, both patient groups showed increased causal flow from the right cerebellum to the MPFC (common causal connectivity abnormalities). And distinct causal connectivity abnormalities (increased causal connectivity from the left thalamus to the MPFC in SCH than HC and DEP, and increased causal connectivity from the right cerebellum to the left thalamus in DEP than HC and SCH). In addition, the structural deficits in the MPFC and its causal connectivity from the cerebellum were associated with the negative symptom severity in SCH. This study found common/distinct structural deficits and aberrant causal connectivity patterns in the prefrontal-thalamic-cerebellar circuit in SCH and DEP, which may provide a potential direction for understanding the convergent and divergent psychiatric pathological mechanisms between SCH and DEP. Furthermore, concomitant structural and causal connectivity deficits in the MPFC may jointly contribute to the negative symptoms of SCH.