The neurobiological mechanism of post-traumatic stress disorder (PTSD) is poorly understood. The inhibition of GABA neurons, especially in the amygdala, is crucial for the precise regulation of the consolidation, expression, and extinction of fear conditioning. The GABAergic system is involved in the pathophysiological process of PTSD, with several studies demonstrating that the function of the GABAergic system decreases in PTSD patients. This paper reviews the preclinical and clinical studies, neuroimaging techniques, and pharmacological studies of the GABAergic system in PTSD and summarizes the role of the GABAergic system in PTSD. Understanding the role of the GABAergic system in PTSD and searching for new drug targets will be helpful in the treatment of PTSD.

In this study, we analyzed the status and research trends of the GABAergic system in depression from 2004 to 2020 to provide a reference for further research. The Web of Science database was used as the data source and 1,658 publishments were included. Using two visualization analysis software, CiteSpace and VOSviewer, we analyzed the publishing years, countries, institutions, authors, journals, categories, keywords, and research frontiers in depression. The publishments revealed an upward trend from 2004 to 2020; the most prolific country and institutions were the United States and INSERM, respectively. The journal of Neuroscience was the most published and cited journal. The most relevant category was neurosciences. The hot topics in this field were GABAergic research in Gaba(a) receptor; the research frontier was depressive model. These analysis results provide a new perspective for researchers to conduct studies on related topics in the future and guidance for scientists to identify potential collaborators and research cooperation institutions.

Midbrain dopamine (DA) neurons are essential for regulating movement, emotion, and reward, with their dysfunction closely linked to Parkinson’s disease (PD). While DA neurons in the substantia nigra pars compacta (SNc) and ventral tegmental area (VTA) have known overlapping roles in behaviors such as depression and reward, their distinct contributions to subtle spontaneous behaviors remain insufficiently understood. In this study, we utilized a 3D behavioral analysis platform powered by machine learning to explore motor and nuanced behavioral changes in a subacute MPTP mouse model of PD. This investigative approach was combined with cell-type-specific genetic ablation of DA neurons in both the SNc and VTA. Our findings highlight significant deficits in rearing, walking, and hunching behaviors correlated with the loss of SNc DA neurons, but not VTA DA neurons, alongside increased overall movement, reduced movement precision, and pronounced right-sided lateralization. These subtle features, particularly rearing deficits and lateralization, emerge as critical behavioral biomarkers of SNc DA neuron loss, thereby enhancing the translational relevance of PD models.

Ovarian mature cystic teratomas with malignant transformation are rare, and squamous cell carcinoma is the most common pathological entity. Among these malignant transformations, urothelial cell carcinoma is rare. We report a woman presenting with a huge pelvic cystic mass, favoring a right ovarian mature cystic teratoma with malignant transformation, based on magnetic resonance imaging, who was successfully treated with surgery. The final pathology confirmed concomitant malignant transformation of urothelial carcinoma.

Photodynamic therapy (PDT) has emerged as a prominent strategy for the treatment of breast cancer, which is prevalent among women globally. Organelles targeted photosensitizers have brought great promise for enhancing the PDT efficiency. Photosensitizers possessing mitochondria and nuclei dual-targeting, especially those multipled with type I/II reactive oxygen species (ROS) generation and aggregation-induced emission (AIE) characteristics are urgently needed to improve the PDT efficiency. Herein, a new amphiphilic compound, 2-(2-(5-(7-(4-((4-butylphenyl)(4-(7-(5-formylthiophen-2-yl)benzo[c] [1,2,5]thiadiazol-4-yl)phenyl)amino)phenyl)benzo[c][1,2,5]thiadiazol-4-yl)thiophen-2-yl)vinyl)-3-methylbenzo[d]thiazol-3-ium iodide (SgTBB), is introduced. SgTBB exhibits bright emission at 731 nm in solution and it redshifts to 930 nm in solid state. Interestingly, SgTBB generates singlet oxygen (¹O₂, type II ROS) and •OH/O₂⁻• (type I ROS) simultaneously when exposed to light irradiation. In vitro experiments show that SgTBB NPs can light up the cells and exhibit light-driven mitochondria-to-nuclei cascade targeting. Under light irradiation, decrease of mitochondrial membrane potential (MMP), obvious mitochondria damage, upregulation of cleaved caspase-3 expression as well as severe DNA damage are observed, which further cause cell apoptosis and immunogenic cell death (ICD), then promote the antitumor activity. Furthermore, SgTBB NPs used as a phototheranostic agent can effectively inhibit tumor growth in mice. Our research demonstrates that SgTBB NPs can be used as a potent photosensitizer for imaging-guided PDT, and the work here presents a wonderful route for the creation of multi-organelles targeted photosensitizers with special type I/II ROS generation capability.