Spatial transcriptomics is an omics technology that realizes the determination of cell spatial location information on the basis of single cell RNA sequencing. This technology overcomes the problem of losing the spatial information of cells in the tissue during the single-cell isolation of single cell RNA sequencing. Spatial transcriptomics can provide both transcriptome information and spatial location information of research objects in tissues. Spatial transcriptomics plays an important role in the study of cell lineage generation, regulation mechanism and interaction between cells, and is an important development direction and hot spot of omics technology research. In recent years, spatial transcriptomics technology has developed rapidly, new detection methods have been continuously produced, and technical indicators such as detection sensitivity, resolution and detection throughput have been continuously improved. According to the different principles of obtaining spatial information, this paper classifies the commonly used spatial transcriptomics techniques, and summarizes the detection principles, representative technical methods and technical indicators. Then, the application of spatial transcriptomics technology in neuroscience is expounded from two aspects: differentiation of brain cell types and construction of cell layer maps, and analysis of characteristics of diseases and biomarker related to nervous systems. Finally, we summarize the current problems of spatial transcriptomics technology and give an outlook on its future development direction.

OBJECTIVETo investigate the clinical features of unexpected sudden death (SUD) clustered in families in Yunnan province.

METHODSThis retrospective study analyzed the clinical features of SUD occurred between July to September 2005 in 7 families in Yunnan province.

RESULTSAll 16 SUD patients shared common clinical features such as fatigue and repeated syncope and one group of SUD patients (n = 8 from 4 families) presented with the gastric intestinal tract manifestations including nausea, vomiting, abdominal pain and diarrhea with suspected dietary history and abnormal laboratory enzyme findings (GOT/GPT, CK/CKMB, LDH/LDH1 etc.). In SUD patients without gastric intestinal tract manifestations (n = 8 from 3 families), there were no clear symptoms before death and repeated ventricular tachycardia and ventricular fibrillation were recorded in one survivor. There was no clear evidence for the involvements of hereditary and infectious factors for observed SUD.

CONCLUSIONThe reason for the unexpected sudden death clustered in 7 families in Yunnan remains unclear. Repeated syncope and fatigue served as the common clinical features in the presence or absence of gastric intestinal tract manifestations in all SUD cases. Further studies are needed to clarify the pathology and detailed clinical manifestations of SUD occurred in this area.

Adolescent ; Adult ; Bias ; Cause of Death ; Child ; China ; epidemiology ; Death, Sudden ; epidemiology ; Family ; Female ; Humans ; Male ; Middle Aged ; Retrospective Studies ; Young Adult

In the original publication, Figure 4G was incorrectly published. The correct version of Figure 4G is presented in this correction. This correction does not affect the conclusions of the paper.

The present study was designed to examine the therapeutic effects of Botulinum neurotoxin A (BoNT/A) on depression-like behaviors in mice and to explore the potential mechanisms. These results revealed that a single facial injection of BoNT/A induced a rapid and prolonged improvement of depression-like behaviors in naïve and space-restriction-stressed (SRS) mice, reflected by a decreased duration of immobility in behavioral despair tests. BoNT/A significantly increased the 5-hydroxytryptamine (5-HT) levels in several brain regions, including the hippocampus and hypothalamus, in SRS mice. BoNT/A increased the expression of the N-methyl-D-aspartate receptor subunits NR1 and NR2B in the hippocampus, which were significantly decreased in SRS mice. Furthermore, BoNT/A significantly increased the expression of brain-derived neurotrophic factor (BDNF) in the hippocampus, hypothalamus, prefrontal cortex, and amygdala, which were decreased in SRS mice. Finally, BoNT/A transiently increased the levels of phosphorylated extracellular signal-regulated kinase (p-ERK) and cAMP-response element binding protein (p-CREB), which were suppressed in the hippocampus of SRS mice. Collectively, these results demonstrated that BoNT/A treatment has anti-depressant-like activity in mice, and this is associated with increased 5-HT levels and the activation of BDNF/ERK/CREB pathways in the hippocampus, supporting further investigation of BoNT/A therapy in depression.