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Background: Cystic echinococcosis (CE) is a worldwide parasitic zoonosis caused by infection of the larval stage of tapeworm Echinococcus granulosus. In human CE, the parasites develop and form cysts in internal organs. The differentiated cysts can be classified into five types based on WHO-IWGE standard CE1-5 representing different developmental stages. Infection with E. granulosus triggers hosts’ humoral and cellular response, displaying elevated serum antibodies and Th1 and Th2 cytokines, which are presumed to be in association with the disease outcome. Identification of immunological markers for evaluation of disease progression has been a growing concern. However, the distinctive profile of cytokines and antibodies associated with the cyst progression has not been ascertained. Methods: To better understand the interaction between host immune response and disease outcome, the present study followed-up four CE patients over three years by yearly measuring serum level of 27 cytokines, total IgG and isotypes, and ultrasound scanning, beginning in year 1 for all patients with CE1 and CE2 cysts before treatment and continued in year 2 with CE4 and in year 3 with CE3-CE5 post-treatment. Results: Nine cytokines including Th1-type IL-2, Th17-type IL-17A, and inflammatory cytokines IL-1β, IL-1Rα and TNF-α, chemokines IL-8, MIP-1α, MIP-1β, and growth factor G-CSF were significantly elevated in patients with cyst type CE1, compared to the normal controls, and then declined to a normal level at CE4 and CE5. Examining the antibody production, we found that serum specific IgG was significantly increased in patients with active and transitional cysts, specifically the total IgG at CE1/CE3/CE4-CE5, IgG4 at CE1 and IgG1 at CE1/CE3 cyst status, in comparison with the normal controls, but showed no significant changes between the cyst stages. Conclusions: Our findings provide new information on the profile of multiplex cytokines and serum antibodies associated with cyst stages in cystic echinococcosis patients through a three-year follow-up, implying that further studies using an approach combining cyst-associated immune parameters may aid in identifying immunological markers for differentiation of disease progression. [ABSTRACT FROM AUTHOR]

The closing time of the Paleo-Asian Ocean and the tectonic evolution of the northern margin of the North China Craton are still controversial. The geochronology and geochemistry of the Zhaojinggou monzogranite pluton provide new constraints on the late Paleozoic tectonic evolution and the closure time of the Paleo-Asian Ocean in the southern Central Asian Orogenic Belt (CAOB). The monzogranite yielded a zircon U-Pb age of 286.7 ± 1.2 Ma. Due to the characteristics of low–moderate Mg# values (25.87–39.21), low Fe2O3T values (1.13–1.72), and A/CNK > 1, we show that the pluton is weak peraluminous, high in potassium calc–alkaline series, and displays the feature of S-type granite. The total REE content is low, the distribution curve is right dipping, and the LREE is enriched; the δEu average value is 1.32 (1.11–1.54). The granite presents relatively high (87Sr/86Sr)i values of 0.712345–0.713723, low εNd(t) values of −8.89–−8.21 (an average value of −8.56), and a TDM2 of 1718–1773 Ma. Furthermore, the zircon in situ Hf isotopic analysis shows 176Hf/177Hf ratios of 0.282342 to 0.282614, low εHf(t) values of −9.27–0.38 (mean −4.74), and a TDM2 of 1275–1887 Ma. Additionally, high field strength elements such as Nb, Ta, and Ti are depleted, and large ion lithophile elements, e.g., Rb, Ba, K, and Sr, are enriched. The above features of the Zhaojinggou monzogranite indicate that the pluton was derived from late Paleoproterozoic to Mesoproterozoic lower crustal mafic materials. By discussing the genesis and tectonic implications of the pluton massif, we propose that the Zhaojinggou monzogranite represents a magmatic event caused by the crustal–mantle interaction during the southward subduction of the eastern Paleo-Asian Ocean in the northern margin of the North China Craton during the Early Permian. [ABSTRACT FROM AUTHOR]