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The large-sized Tarangaole uranium deposit and its neighboring Daying and Nalinggou deposits, located in the northeastern margin of the Ordos Basin, constitutes a major uranium resource base in northern China. In order to further clarify the sedimentary material source, uranium source and regional sediment–tectonic setting of the uranium-fed clastic rocks (i.e., Zhiluo Formation(J2z)) in the district, this paper carried out whole-rock geochemistry, heavy minerals composition and in situ U-Pb dating of detrital zircons for sandstones from the lower section of the Zhiluo Formation. The results have shown that the average chemical differentiation index (CIA) for the host rocks is 73.16 and the chemical weathering degree is moderate. Heavy minerals are mainly composed of ilmenite, garnet, chlorpyrite, zircon, pyrite, apatite, hematite, etc. The U-Pb dating of detrital zircon generally indicates three age peaks, i.e., 260~Ma, 1850~Ma and 2450~Ma, respectively. In conclusion, the source rocks may have been formed at active continental margins, e.g., in a continental margin arc environment. The sedimentary materials mainly come from khondalite series, TTGs, granulite, and mafic–ultramafic intrusive rocks distributed among the Daqing–Ula Mountains and adjacent areas, etc. The Late Paleozoic U-rich intermediate and acidic magmatic rocks spreading over the eastern part of the Ula–Daqing and Wolf mountains have provided the main uranium sources for the formation of major U deposits in the northern Ordos Basin. [ABSTRACT FROM AUTHOR]

Cerebral ischemia triggers secondary ischemia/reperfusion injury and endoplasmic reticulum stress initiates cell apoptosis. However, the regulatory mechanism of the signaling pathway remains unclear. We hypothesize that the regulatory mechanisms are mediated by the protein kinase-like endoplasmic reticulum kinase/eukaryotic initiation factor 2α in the endoplasmic reticulum stress signaling pathway. To verify this hypothesis, we occluded the middle cerebral artery in rats to establish focal cerebral ischemia/reperfusion model. Results showed that the expression levels of protein kinase-like endoplasmic reticulum kinase and caspase-3, as well as the phosphorylation of eukaryotic initiation factor 2α, were increased after ischemia/reperfusion. Administration of atorvastatin decreased the expression of protein kinase-like endoplasmic reticulum kinase, caspase-3 and phosphorylated eukaryotic initiation factor 2α, reduced the infarct volume and improved ultrastructure in the rat brain. After salubrinal, the specific inhibitor of phosphorylated eukaryotic initiation factor 2α was given into the rats intragastrically, the expression levels of caspase-3 and phosphorylated eukaryotic initiation factor 2α in the were decreased, a reduction of the infarct volume and less ultrastructural damage were observed than the untreated, ischemic brain. However, salubrinal had no impact on the expression of protein kinase-like endoplasmic reticulum kinase. Experimental findings indicate that atorvastatin inhibits endoplasmic reticulum stress and exerts neuroprotective effects. The underlying mechanisms of attenuating ischemia/reperfusion injury are associated with the protein kinase-like endoplasmic reticulum kinase/eukaryotic initiation factor 2α/caspase-3 pathway.

Objective: To investigate the optimal conditions for establishing insulin-resistant 3T3-L1 adipocytes., Methos: Dexamethason (DEX), 3-isobutyl-methylxanthine (IBMX) and different concentrations of insulin (10(-8), 10(-7), and 10(-6) mol·L(-1)) were used to induce 3T3-L1 preadipocytes into mature adipocytes identified by oil red O staining. We established insulin- resistant 3T3-L1 adipocytes cell model (IR-3T3-L1) by exposing the cells to 1µmol·L(-1) DEX, and the changes of glucose concen- tration in the cell culture were determined by glucose oxidase-peroxidase (GOD-POD) assay., Results: Treatment of 3T3-L1 cells with DEX, IBMX and 10(-6) mol·L(-1)) insulin for 9 days resulted in the differentiation of >90% of the cells into mature adipocytes. IR-3T3-L1 cells cultured for 96 h in the culture media containing 1 µmol·L(-1) DEX showed significantly increased glucose consumption (P=0.0003) as compared with the control group at 36 h (P<0.001)., Conclusion: 3T3-L1 cells can be induced into mature adipocytes by exposure to 1 µmol·L(-1) DEX, 0.5 mmol·L(-1) IBMX and 10(-6) mol·L(-1)) insulin. A 96 h exposure to 1 µmol·L(-1) DEX can induce 3T3-L1 adipocytes to acquire insulin resistance that can be maintained for 36 h.