Search

Based on the combination of core observation, experimental analysis and testingand geological analysis, the main controlling factors of shale oil enrichment in the Lower Permian Fengcheng Formation in the Mahu Sag of the Junggar Basin are clarified, and a shale oil enrichment model is established. The results show that the enrichment of shale oil in the Fengcheng Formation in the Mahu Sag is controlled by the organic abundance, organic type, reservoir capacity and the amount of migration hydrocarbon in shale. The abundance of organic matter provides the material basis for shale oil enrichment, and the shales containing types I and II organic matters have good oil content. The reservoir capacity controls shale oil enrichment. Macropores are the main space for shale oil enrichment in the Fengcheng Formation, and pore size and fracture scale directly control the degree of shale oil enrichment. The migration of hydrocarbons in shale affects shale oil enrichment. The shale that has expelled hydrocarbons has poor oil content, while the shale that has received hydrocarbons migrated from other strata has good oil content. Lithofacies reflect the hydrocarbon generation and storage capacity comprehensively. The laminated felsic shale, laminated lime-dolomitic shale and thick-layered felsic shale have good oil content, and they are favorable lithofacies for shale oil enrichment. Under the control of these factors, relative migration of hydrocarbons occurred within the Fengcheng shale, which leads to the the difference in the enrichment process of shale oil. Accordingly, the enrichment mode of shale oil in Fengcheng Formation is established as “in-situ enrichment” and “migration enrichment”. By superimposing favorable lithofacies and main controlling factors of enrichment, the sweet spot of shale oil in the Fengcheng Formation can be selected which has great significance for the exploration and development of shale oil.

Primary Sjögren’s syndrome (pSS) is characterized by a panel of autoantibodies, while it is not clear whether B cells and autoantibodies play an essential role in pathogenesis of the disease. Here, we report a novel mouse model for pSS which is induced by immunization with the Ro60_316-335 peptide containing a predominant T cell epitope. After immunization, mice developed several symptoms mimicking pSS, including a decreased secretion of tears, lymphocytic infiltration into the lacrimal glands, autoantibodies, and increased levels of inflammatory cytokines. Disease susceptibility to this novel mouse model varies among strains, where C3H/HeJ (H2-k) and C3H/HeN (H2-k) are susceptible while DBA/1 (H2-q) and C57BL/6 (H2-b) are resistant. Depletion of B cells using anti-CD20 monoclonal antibodies prevented C3H/HeN mice from development of the pSS-like disease. In addition, HLA-DRB1*0803, a pSS risk allele, was predicted to bind to the hRo60_308-328 which contains a predominant T cell epitope of human Ro60. Therefore, this study provides a novel mouse model for pSS and reveals an indispensable role of B cells in this model. Moreover, it suggests that T cell epitope within Ro60 antigen is potentially pathogenic for pSS.