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In general, aragonite exists as a metastable carbonate mineral under near-surface conditions, and is commonly transformed into calcite under the subsurface and during diagenesis. It is thus seldom found in sedimentary rocks, but aragonite is common in the Paleogene lacustrine shales in the Jiyang Depression in eastern China. Dissolution experiments were conducted on the Paleogene aragonite-enriched and calcite-enriched shales at different temperatures, pressures and acetic acid concentrations, and in different types of solution. The results show that aragonite is insoluble in thein situformation water but dissolved more readily under acetic acid conditions than calcite with the degree of dissolution increasing with increasing temperature, pressure and acetic acid concentrations. During the shallow burial diagenesis of the Paleogene sediment sequence in the Jiyang Depression, aragonite was relatively stable and was not dissolved by the connate pore water in the shales. Increasing burial (temperature) and maturity of the organic matter produced large amounts of organic acids that accelerated the dissolution of aragonite. In the late stage, as the organic matter became over-matured, the pore water changed from acidic to alkaline, and calcite precipitated from the carbonate-rich solution. Therefore, the conditions provided by organic acids enabled the conversion of aragonite to calcite during sedimentary diagenesis in the Paleogene lacustrine shales in the Jiyang Depression. This transformation corresponded to the thermal evolution of the organic matter within the shale sequence. [ABSTRACT FROM AUTHOR]

Background: The current study was undertaken to investigate the time course of gastric ischemia-reperfusion (GI-R)-induced gastric mucosal injury and repair and whether extracellular signal-regulated kinase 1/2 (ERK1/2) were involved in GI-R-induced gastric mucosal injury and repair.Methods: Immunohistochemistry and Western blot analyses were used.Results: Gastric mucosal injury induced by ischemia alone was mild. However, the injury worsened after reperfusion, reaching a maximum at 1 h, and was accompanied by increased apoptotic cells and decreased proliferative cells. Then, the gastric mucosal cells began to repair the injury by enhanced proliferation, which peaked at 24 h after reperfusion, and by 72 h the damaged gastric mucosa was mostly repaired. The ERK1/2 (nonactivated ERK1/2) protein expression level and distribution profile showed no significant changes during the entire reperfusion phase, but the p-ERK1/2 (activated ERK1/2) level changed dramatically. The p-ERK1/2 protein level was decreased at 0.5 h after reperfusion began, and then gradually increased, peaking after 3 h of reperfusion; these changes in p-ERK1/2 occurred simultaneously in the cytoplasm and nucleus. On the other hand, inhibition of the activation of ERK1/2, induced by PD98059, a specific ERK1/2 upstream inhibitor, aggravated the gastric mucosal injury, and apoptosis was increased and proliferation was reduced in the gastric mucosal cells after the same duration of reperfusion.Conclusions: Serious gastric mucosal damage involving apoptotic cells occurred rapidly at an early stage of reperfusion and was closely related to the suppression of ERK1/2 activation. The activated ERK1/2 signaling transduction pathway played an important role. Activated ERK1/2 participated in the regulation of gastric mucosal injury and repair induced by GI-R, and might be mediated by the inhibition of apoptosis and the promotion of proliferation in gastric mucosal cells. [ABSTRACT FROM AUTHOR]