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The Yangtze Platform preserves relatively thick carbonate successions and excellent fossil records across the Ediacaran–Cambrian boundary interval. The intensely studied Meishucun section in East Yunnan was one of the Global Stratotype Section candidates for the Precambrian–Cambrian boundary. However, depositional breaks were suspected in the section and the first appearance of small shelly fossils could not be verified. The Laolin section located in NE Yunnan is more continuous and shows great potential for global correlation of carbon isotope features across the Precambrian–Cambrian boundary. However, the stratigraphic framework and correlations were controversial. We studied and systematically sampled the Laolin section and present here new carbon isotope data for this section. The Laolin section consists of, in ascending order, the Baiyanshao dolostone of the Dengying Formation, the Daibu siliceous dolostone, Zhongyicun dolomitic phosphorite, lower Dahai dolostone and upper Dahai limestone of the Zhujiaqing Formation, and the black siltstone of the Shiyantou Formation. Our data reveal a large negative δ13C excursion (−7.2‰, L1′) in the Daibu Member, which matches the previously published data for the Laolin section, and a large positive excursion (+3.5‰, L4) in the Dahai Member, which was not shown in the published data. The excursion L1′ correlates well with the similarly large negative excursion near the first appearance of small shelly fossils in Siberia and Mongolia. Similar magnitude excursions are also known from Morocco and Oman, for which there are no robust fossil constraints but from where volcanic ash beds have been dated precisely at 542 Ma, thus confirming a global biogeochemical event near the Ediacaran–Cambrian boundary. Our data also indicate that deposition was more continuous at the Laolin section compared with the Meishucun section, where there are no records of a comparable negative excursion near the Ediacaran–Cambrian boundary, nor any comparable positive excursion in the Dahai Member. Therefore, the Laolin section has proven potential to be a supplementary Global Stratotype Section for the Ediacaran–Cambrian boundary on the Yangtze Platform.

BackgroundImpaired wound healing frequently occurs in diabetes mellitus (DM) and is implicated in impaired angiogenesis. Long non-coding RNA (lncRNA) H19 has been reported as being reduced in DM and played a critical role in inducing angiogenesis. Thus, we hypothesized that H19 may affect impaired wound healing in streptozotocin (STZ)-induced diabetic mice transfused with autologous blood preserved in standard preservative fluid or modified preservative fluid.MethodsFibroblasts in injured skin were isolated and cultured in vitro. After location of H19 in fibroblasts using fluorescence in situ hybridization (FISH), RNA-pull down, RNA immunoprecipitation (RIP), chromatin immunoprecipitation (ChIP), Co immunoprecipitation (COIP) and dual luciferase reporter gene assay were used to verify the binding of H19 to HIF-1α.ResultsThe modified preservative fluid preserved autologous blood increased the H19 expression in fibroblasts, and maintained better oxygen-carrying and oxygen release capacities as well as coagulation function. Furthermore, H19 promoted HIF-1α histone H3K4me3 methylation and increased HIF-1α expression by recruiting EZH2. H19 promoted fibroblast activation by activating HIF-1α signaling pathway in fibroblasts and enhanced wound healing in diabetic mice.ConclusionsTaken together, H19 accelerated fibroblast activation by recruiting EZH2-mediated histone methylation and modulating the HIF-1α signaling pathway, whereby augmenting the process of modified preservative fluid preserved autologous blood enhancing the postoperative wound healing in diabetic mice.

This is a repository copy of Seawater carbon and strontium isotope variations through the late Ediacaran to late Cambrian in the Tarim Basin.

Impaired wound healing is a debilitating complication of diabetes. The long non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) has been recognized to be differentially expressed in various diseases. However, its underlying mechanism in diabetes has not been fully understood. Notably, we aim to examine the expression of MALAT1 in diabetic mice and its role in wound healing involving the hypoxia-inducible factor-1α (HIF-1α) signaling pathway with a modified autologous blood preservative solution reported. A mouse model of diabetes was established. MALAT1 was identified to promote the activation of the HIF-1α signaling pathway and to be enriched in autologous blood through modified preservation, which might facilitate the improvement of physiological function of blood cells. Through gain- or loss-of-function approaches, viability of fibroblasts cultured in high glucose, wound healing of mice, and collagen expression in wound areas were enhanced by MALAT1 and HIF-1α. Taken together, the present study demonstrated that the physiological status of mouse blood was effectively improved by modified autologous blood preservation, which exhibited upregulated MALAT1, thereby accelerating the fibroblast activation and wound healing in diabetic mice via the activation of the HIF-1α signaling pathway. The upregulation of MALAT1 activating the HIF-1α signaling pathway provides a novel insight into drug targets against diabetes.

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