Megafossils of Betulaceae from the Oligocene of Qaidam Basin and their paleoenvironmental and phytogeographic implications.

Understanding the paleoenvironment and phytogeographical history of the Tibetan Plateau, China relies on discovering new plant fossils. The Qaidam Basin has long been regarded as an ideal 'field laboratory' to investigate the paleoclimate and paleobiological evolution of the northern Tibetan Plateau. However, fossil angiosperms from the Qaidam Basin are rare, and our knowledge of its paleovegetation is poor. Here, we report fossil leaves and fruits of Betulaceae found from the Oligocene Shangganchaigou Formation of northwestern Qaidam Basin (Huatugou area). Comparative morphological analysis led us to assign the fruits to the Betula subgenus Betula and the leaves to Carpinus grandis. These findings, together with other reported fossil plants from the same locality, reveal a close floristic linkage between the Qaidam Basin and Europe during the Oligocene. The northern pathway of this floristic exchange may have crossed through the Qaidam Basin during the late Paleogene. This floristic linkage may have been facilitated by the continuous narrowing of the Turgai Strait and stronger westerlies, which transported moisture and provided favorable climatic conditions. Indeed, fossil plants collected from the Qaidam Basin suggest that during the Oligocene this region had warm and humid deciduous broad-leaf forest, which differs from the region's modern vegetation and indicates that the Qaidam Basin may have been a suitable region for these plants to flourish and spread during the Oligocene.

NEAT1 regulates MPP+-induced neuronal injury by targeting miR-124 in neuroblastoma cells.

Long non-coding RNAs (lncRNAs) have been reported to play important roles in Parkinson's disease (PD) pathogenesis. It was indicated that lncRNA nuclear enriched abundant transcript 1 (NEAT1) is involved in PD. However, the underlying mechanism of NEAT1 is still not fully explored. Human neuroblastoma cell line SH-SY5Y was treated with 1-Methyl-4-phenylpyridinium (MPP+) to mimic PD model in vitro. qRT-PCR was employed to detect the expression of NEAT1, IL-1ß, IL-6 and TNF-α. Starbase database, RNA pull-down assay and RNA immunoprecipitation (RIP) assay were performed to verify the relationship between NEAT1 and miR-124. MTT assay and flow cytometry assay were used to detect cell viability and apoptosis. Elisa was introduced to measure the levels of IL-1ß, IL6 and TNF-α in culture media. We found that NEAT1 expression was significantly increased in SH-SY5Y cells after MPP+ treatment in dose- and time- dependent manners. MPP+ induced the expression and secretion of IL-1ß, IL-6 and TNF-α, inhibited cell viability and induced apoptosis while these effects could be rescued by NEAT1 silencing. miR-124 was a target of NEAT1. Anti-miR-124 could reverse the effects caused by NEAT1 knockdown in MPP+ treated SH-SY5Y cells. Therefore, we speculated that NEAT1 may regulate MPP+ induced neuronal injury by targeting miR-124 in SH-SY5Y cells.