Revisiting the mechanisms of mid-Tertiary uplift of the NE Tibetan Plateau.

Contrasting views exist on timing and mechanisms of Tertiary crustal uplift in the NE Tibetan Plateau based on different approaches, with many models attributing surface uplift to crustal shortening. We carry out a comprehensive investigation of mid-Tertiary stratigraphy, sedimentology, and volcanism in the West Qinling, Hoh Xil and Qaidam basin, and the results challenge previous views. It was held that the discordance between Oligocene and Miocene strata is an angular unconformity in the West Qinling, but our field observations show that it is actually a disconformity, indicative of vertical crustal uplifting rather than crustal shortening at the Oligocene to Miocene transition. Widespread occurrence of synsedimentary normal faults in mid-Tertiary successions implicates supracrustal stretching. Miocene potassic-ultrapassic and mafic-ultramafic volcanics in the Hoh Xil and West Qinling suggest a crucial role of deep thermomechanical processes in generating crust- and mantle-sourced magmatism. Also noticeable are the continuity of mid-Tertiary successions and absence of volcanics in the Qaidam basin. Based on a holistic assessment of stratigraphic-sedimentary processes, volcanic petrogenesis, and spatial variations of lithospheric thicknesses, we speculate that small-sale mantle convection might have been operating beneath northeast Tibet in the mid-Tertiary. It is assumed that northward asthenospheric flow was impeded by thicker cratonic lithosphere of the Qaidam and Alxa blocks, thereby leading to edge convection. The edge-driven convection could bring about surface uplift, induce supracrustal stretching, and trigger vigorous volcanism in the Hoh Xil and West Qinling in the mid-Tertiary period. This mechanism satisfactorily explains many key geologic phenomena that are hardly reconciled by previous models.

Low dinosaur biodiversity in central China 2 million years prior to the end-Cretaceous mass extinction.

Whether or not nonavian dinosaur biodiversity declined prior to the end-Cretaceous mass extinction remains controversial as the result of sampling biases in the fossil record, differences in the analytical approaches used, and the rarity of high-precision geochronological dating of dinosaur fossils. Using magnetostratigraphy, cyclostratigraphy, and biostratigraphy, we establish a high-resolution geochronological framework for the fossil-rich Late Cretaceous sedimentary sequence in the Shanyang Basin of central China. We have found only three dinosaurian eggshell taxa (Macroolithus yaotunensis, Elongatoolithus elongatus, and Stromatoolithus pinglingensis) representing two clades (Oviraptoridae and Hadrosauridae) in sediments deposited between ∼68.2 and ∼66.4 million y ago, indicating sustained low dinosaur biodiversity, and that assessment is consistent with the known skeletal remains in the Shanyang and surrounding basins of central China. Along with the dinosaur eggshell records from eastern and southern China, we find a decline in dinosaur biodiversity from the Campanian to the Maastrichtian. Our results support a long-term decline in global dinosaur biodiversity prior to 66 million y ago, which likely set the stage for the end-Cretaceous nonavian dinosaur mass extinction.

Development of a screening system for DNA damage and repair of potential carcinogens based on dual luciferase assay in human HepG2 cell.

At present, different methods are used for the detection of early biological effects of DNA-damaging agents in environment. Some sensitive testing methods employing DNA damage-inducing genes RNR3, RAD51, RAD54 or growth-arrested and DNA damage-inducible gene 153 (Gadd 153) are used to detect the DNA damage. The host cell reactivation (HCR) assay is a functional assay that is based on the independent transfection of cells with either damaged or undamaged plasmid DNA and allows the identification of the genes responsible for DNA repair-deficient syndromes. In this study, we combined the gadd153-luc test system and HCR assay to measure the DNA damage and DNA repair by dual luciferase assay. We used 16 DNA-damaging agents all of which were detected by a positive dual luciferase reporter test system. The sensitivity of the dual luciferase assay system to detect DNA damage/repair was same as the gadd153-luc test system and/or the HCR assay. Since DNA repair is important to maintain genetic stability, DNA damage and repair have been good biomarkers of early biological effects of DNA-damaging agents. Accordingly, the measurement of DNA repair capacity should be a valued tool in molecular epidemiology studies. The dual luciferase assay described in this study is rapid, convenient, stable and standard.

[The effects of the cadmium chloride on the DNA damage and the expression level of gadd gene in HepG2 cell line].

OBJECTIVE: To investigate the effects of the cadmium chloride on the DNA damage and the expression of the gadd153 and gadd45beta promoter and mRNA in HepG2 cells. METHODS: DNA damage induced by cadmium chloride was detected by comet assay. The plasmids (pGADD153-Luc and pG45-Luc) containing DNA damage and repair inducible gene 153 and 45 (gadd153 and gadd45beta) promoter and luciferase and gadd45beta reporter gene were constructed. The activity of gadd153 and gadd45beta promoter were represented by the luciferase activity, the inducible luciferase activities was detected by bioluminescence. The expression of gadd153 and gadd45beta mRNA was detected by RT-PCR. RESULTS: The results of comet assay indicated that Olive Tail Moment induced by the cadmium chloride increased significantly at the dose of 100, 300 micromol/L, compared with the control (P < 0.05). The luciferase activity analysis showed that the expression levels of gadd153 promoter increased significantly in 1, 5, 10 micromol/L treatment group, compared with the control (P < 0.05). The expression levels of gadd45beta promoter in 5, 10 micromol/L treatment group were significantly higher than that in control group (P < 0.05). The expression levels of gadd153 mRNA induced by cadmium chloride at the doses of 1, 5, 10 micromol/L and the expression levels of gadd45beta mRNA induced at the doses of 5, 10 micromol/L were significantly higher than thoae in control group (P < 0.05). CONCLUSION: The cadmium chloride can induce the DNA damage and increase the expression levels of the gadd153 and gadd45beta promoters in HepG2 cells.