Frequency-dependent alterations of global signal topography in patients with major depressive disorder.

BACKGROUND: Major depressive disorder (MDD) is associated not only with disorders in multiple brain networks but also with frequency-specific brain activities. The abnormality of spatiotemporal networks in patients with MDD remains largely unclear. METHODS: We investigated the alterations of the global spatiotemporal network in MDD patients using a large-sample multicenter resting-state functional magnetic resonance imaging dataset. The spatiotemporal characteristics were measured by the variability of global signal (GS) and its correlation with local signals (GSCORR) at multiple frequency bands. The association between these indicators and clinical scores was further assessed. RESULTS: The GS fluctuations were reduced in patients with MDD across the full frequency range (0-0.1852 Hz). The GSCORR was also reduced in the MDD group, especially in the relatively higher frequency range (0.0728-0.1852 Hz). Interestingly, these indicators showed positive correlations with depressive scores in the MDD group and relative negative correlations in the control group. CONCLUSION: The GS and its spatiotemporal effects on local signals were weakened in patients with MDD, which may impair inter-regional synchronization and related functions. Patients with severe depression may use the compensatory mechanism to make up for the functional impairments.

SSH3 promotes pancreatic cancer proliferation and migration by activating the notch signaling pathway.

Recent studies have indicated that the dual-specificity phosphatases (DUSP) family may play a role in the advancement of pancreatic cancer. Exploring the role of the DUSP family in pancreatic cancer development and discovering novel therapeutic targets are crucial for pancreatic cancer therapy. A critical subset of 20 genes exhibiting differential expression was identified, with particular emphasis on four key genes: DUSP10, PTP4A2, SSH3, and CDKN3 by multivariate Cox proportional hazards analysis. These genes were integral to developing a novel risk model for PC, which has been independently validated as a prognostic factor for patients. To provide help for clinical treatment, we performed tumor immune analysis and predicted potential chemical drugs. Notably, our research unveiled elevated expression levels of SSH3 in human PC cells and tissues. Intriguingly, SSH3 expression correlates with the patient grade, staging, and T stage in PC. Additional studies reveal SSH3's role in enhancing PC cell proliferation and migration, intricately linked to the activation of the Notch signaling pathway. These insights provide a deeper understanding of PC pathophysiology and pave the way for novel therapeutic interventions.