Abstract Background: Biomarkers play an important role in accurate diagnosis of traumatic brain injury (TBI). Due to the complexity and diversity of TBI, it is likely that a single biomarker will not be used for exactly diagnose. Amyloid-beta (Aβ) protein is generated by sequential cleavage of amyloid precursor protein (APP) by β- and γ-secretase, which may exert its toxic effects by increasing reactive oxygen species and neuroinflammation in the brain as damage factor of TBI. Its use in diagnosis for TBI is becoming more widespread. Neuroglobin (NGB) protein is great potential to diminish neuronal damage. Most epidemiological evidence suggested that Aβ and NGB may be used as biomarkers on brainstem (BS) following TBI. The aim of this study was to investigate the trend of Aβ and NGB on BS of rats with TBI and to analyze comprehensively them as potential biomarkers. Methods: Adult male Sprague-Dawley rats were subjected to the modified weight-drop model of closed TBI. Biologic behavior observation, histopathological assessments and western blot assay were performed. Aβ and NGB expression indicated temporal changes in BS after TBI. Their accuracy and efficiency of performing these tasks were calculated and statistical comparisons performed.Results: The results of Aβ enable us to speculate that the time points of 3 h, 6 h and 12 h may be crucial points for the diagnosis of TBI. NGB expression in the injured had obvious difference versus the control, the points of 1 h and 3 h were apparently higher than the control, and the groups of 12 h and 48 h were two peaks in the present study. Furthermore, the immunofluorescence assay results supported that Aβ and NGB co-localization in the neuros of BS, and the NGB specific expression in the BS of neurons.Conclusions: Therefore, the expression and change rules of Aβ and NBG in the BS may provide an important foundation for the diagnosis of TBI, damage assessment and therapeutic intervention.

Background Circular RNAs (circRNAs) have been reported to exert critical functions in tumorigenesis and development. However, the underlying mechanism by which circRNAs regulate melanoma progression remain to be elucidated. Methods The differentially expressed circRNAs were first identified by circRNA-seq, and circRNAs were validated via qRT-PCR and Sanger sequencing. Then, the impact of circRPS5, miR-151a and NPTX1 expression on the progression of melanoma cell were determined by gain- and loss-of-function assays. The relationship between circRPS5, miR-151a, and NPTX1 was predicted by StarBase website and authenticated by luciferase reporter assay. The melanoma cells-derived exosomes were characterized using nanoparticle tracking analysis (NTA) and western blot. Results CircRPS5 was significantly downregulated in melanoma tissues and cell lines. Functionally, circRPS5 suppressed the proliferation, migration, and invasion of melanoma cells, and induced cell cycle arrest and apoptosis in vitro. Mechanistically, circRPS5 harbor miR-151a, acting as miRNA sponge, and then miR-151a targeted the 3’-UTR of NPTX1. Finally, circRPS5 was mainly incorporated into exosomes to inhibit the progression of melanoma cells. Conclusions This finding reveal circRPS5 suppressed the progression of melanoma through miR-151a/NPTX1 pathway, and may provide a promising therapeutic strategies for melanoma.