The northwest striking Qishan‐Mazhao fault (QMF) accommodates complex deformation in the Tibet‐Ordos transition zone. We studied the geologic and geomorphic expression of the QMF using interpretations of high‐resolution satellite images and structure‐from‐motion models combined with detailed field investigations. Displaced loess tablelands, stream channels, and fluvial terraces show that the QMF is predominately a left‐lateral strike‐slip fault with a minor normal component. The magnetic susceptibility and optically stimulated luminescence ages of offset fluvial terraces yield left‐lateral slip rates ranging from 0.5 to 1.0 mm/year. Regionally, the QMF and the Haiyuan fault (HYF) form a large right step, in which the Liupanshan Mountains are located. The QMF shares a similar orientation and sense of motion to the HYF, suggesting that the left‐lateral slip of the HYF is not completely absorbed as crustal shortening across the Liupanshan Mountains but is partially transferred to slip along the QMF.

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The quantification of the geometry and kinematics of the boundary faults of an active orogenic belt is key to exploring its deformation pattern. The Kashihe fault (KSHF), which bounds the northern margin of the Ili Basin and is more than 400 km long, is a WNW-striking fault in the northern Tian Shan. Although the KSHF displays active faulting and is the seismogenic fault of the 1812 Ms 8 Nilka earthquake, the quantitative slip rate and its role in regional strain accommodation have not been reported. Here, we quantify the late Quaternary activity of the KSHF based on high-resolution remote sensing image interpretations and detailed field investigations. Six field observation sites along a~270 km active fault in the Chinese Tian Shan indicate that the KSHF is characterized by dextral strike-slip faulting and N-S thrusting. Based on the surveying of offset geomorphic surfaces with an unmanned drone and the dating of late Quaternary sediments using optically stimulated luminescence (OSL) and radiocarbon methods, we estimated a late Quaternary right-lateral strike-slip rate across the fault of 2.39 ± 0.55 mm/yr and a shortening rate of 0.62 ± 0.30 mm/yr. Analysis of field investigations and fault section exposing indicated that a young paleoearthquake event occurred on the western segment of the KSHF. Active tectonics around the Ili Basin imply that the rigid Ili block extrudes westward along its boundary strike-slip faults and rotates counterclockwise. We propose that this block rotation driven by dextral faulting accommodates regional N-S convergence and sinistral shearing.

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Background: To investigate the effect of vascular endothelial growth factor (VEGF) on tumor angiogenesis in gallbladder carcinoma. Methods: Fifty one patients with gallbladder carcinoma were enrolled as observation group. Thirty healthy people were included as control group. Chemically synthesized siRNA sequences targeting VEGF was transfected with VEGF-siRNA. A blank group (group B), a negative control group (transfected with independent sequence, group C), and an inhibition group (transfected with VEGF siRNA, group D) were established. Physiological saline was set as group A. The expression of VEGF was detected by qRT-PCR. The expression of VEGF protein was detected by Western blot. MVD was used to measure microvessel density. CCK-8, Transwell and flow cytometry were used to detect cell proliferation, invasion and apoptosis. Results: The tumor volume of nude mice and VEGF mRNA expression in group D was significantly smaller than that in group B and C (P<0.05). The MVD density in group B and C was significantly higher than that in group D (P<0.01). The proliferation of cells was detected from the 3rd day, and the proliferation of cells in the blank and negative control groups was faster than that of the inhibition group (P<0.05). The apoptosis rate of the blank group and the negative control group was lower than that of the inhibition group (P<0.001). Conclusion: VEGF is highly expressed in serum of patients with cholangiocarcinoma, it promotes angiogenesis, proliferation and invasion of gallbladder cancer cells, and inhibits apoptosis of tumor cells.