Presentation1_Karst landslides detection and monitoring with multiple SAR data and multi-dimensional SBAS technique in Shuicheng, Guizhou, China.pdf

Shuicheng District is a karst mountain area, located in Guizhou Province, China. Its fragile stratum and frequent underground mining activities makes it prone to landslides. Owning to its wide coverage and frequent revisit, the InSAR technology has advantages in potential landslide identification and deformation monitor. However, affected by dense vegetation and atmospheric delay, it is much difficult to get sufficient effective targets to derive the deformation in this area. Besides, deformation derived from single orbit SAR data can result in the missing identification of some potential landslides and the misinterpreting of the real kinematics process of landslides. In this study, the multi-source SAR data, atmospheric error correction by quadratic tree image segmentation method, and phase-stacking method were selected to derive the surface deformation of this area. Besides, DS-InSAR and MSBAS method were combined to derive the deformation of Pingdi landslide. First, the potential landslides in this area were identified, surface deformation result, optical remote sensing images and geomorphological features were jointly considered. Then, the landslide distribution characteristics was analyzed in terms of slope, elevation and stratum. After that, the deformation along the LOS direction was acquired using the DS-InSAR method. The MSBAS method was used to retrieve the two-dimensional deformation of Pingdi landslide. Finally, the comprehensive analysis of triggering factors and failure process were conducted according to the spatial-temporal deformation characteristics and field investigation. The results indicated that landslides in Shuicheng district were mostly located in the junction of T1 and P3 stratum and mining related. Mining activity was the main cause of the Pingdi landslide deformation, the precipitation was the driving factor of the landslide instability. The research provides an insight into the explore the unstable slope distribution characteristic and the failure process of the landslides.</p

Supplementary Methods from Metformin Sensitizes EGFR-TKI–Resistant Human Lung Cancer Cells <i>In Vitro</i> and <i>In Vivo</i> through Inhibition of IL-6 Signaling and EMT Reversal

PDF file - 103K</p

Image_1_Molecular Expression Profile of Changes in Rat Acute Spinal Cord Injury.tif

Background: Spinal cord injury (SCI) is a highly lethal and debilitating disease with a variety of etiologies. To date, there is no effective therapeutic modality for a complete cure. The pathological mechanisms of spinal cord injury at the molecular gene and protein expression levels remain unclear.Methods: This study used single-cell transcriptomic analysis and protein microarray analysis to analyzes changes in the gene expression profiles of cells and secretion of inflammatory factors respectively, around the lesion site in a rat SCI model.Results: Single-cell transcriptomic analysis found that three types of glial cells (microglia, astrocyte, and oligodendrocyte) becomes activated after acute injury, with GO exhibiting a variety of inflammatory-related terms after injury, such as metabolic processes, immune regulation, and antigen presentation. Protein microarray results showed that the levels of four inflammatory cytokines favoring SCI repair decreased while the levels of nine inflammatory cytokines hindering SCI repair increased after injury.Conclusion: These findings thus reveal the changes in cellular state from homeostatic to reactive cell type after SCI, which contribute to understand the pathology process of SCI, and the potential relationship between glial cells and inflammatory factors after SCI, and provides new theoretical foundation for further elucidating the molecular mechanisms of secondary SCI.</p

Supplementary Figure Legends from Metformin Sensitizes EGFR-TKI–Resistant Human Lung Cancer Cells <i>In Vitro</i> and <i>In Vivo</i> through Inhibition of IL-6 Signaling and EMT Reversal

PDF file - 119K</p

Supplementary Figures 1 - 18 from Metformin Sensitizes EGFR-TKI–Resistant Human Lung Cancer Cells <i>In Vitro</i> and <i>In Vivo</i> through Inhibition of IL-6 Signaling and EMT Reversal

PDF file - 1625K, Supplementary Figure 1 IC50 values of different cell lines to TKIs under indicated conditions Supplementary Figure 2 BrdU incorporation assay for H1975 cells. Supplementary Figure 3 Expression of OCT-1 and LKB1 in different cell lines used in the current study. Supplementary Figure 4 Metformin decreases invasion and motility of erlotinib-resistant H1650-M3 cells. Supplementary Figure 5 Metformin decreases SNAIL expression in TKI-resistant human lung cancer cells. Supplementary Figure 6 Quantification of blots shown in Fig. 2E. Supplementary Figure 7 Metformin decreases IL-6 gene transcription in TKI-resistant cell lines. Supplementary Figure 8 Metformin reverses TKI resistance in IL-6 overexpressing PC-9psb cells. Supplementary Figure 9 Inhibition of IL-6 signaling is essential for metformin to overcome erlotinib resistance in H1650-M3 cells. Supplementary Figure 10 Body weight of PC-9GR xenografts Supplementary Figure 11 Serum insulin levels and glucose levels from xenografts established by PC-9GR cells. Supplementary Figure 12 Metformin in combination with gefitinib suppresses tumor growth in PC-9 xenografts Supplementary Figure 13 Metformin in combination with gefitinib increased the expression of E-cadherin and decreased the expression of Vimentin in tumor sections of PC-9 xenografts. Supplementary Figure 14 Quantification of blots in Fig. 6D. Supplementary Figure 15 Western blotting analysis of the expression of indicated markers on protein extracts obtained from harvested tumors of the gefitinib group and gefitinib+metformin group. Supplementary Figure 16 Metformin in combination with gefitinib decreases expression of phosphorylation of AKT and STAT3 in xenografts established by PC-9GR cells. Supplemental Figure 17 Metformin overcomes TKI resistance through EMT reversal and IL-6 signaling inhibition. Supplemental Figure 18 Metformin disrupts the evil axis of TGFbeta/IL-6, EMT, CSCs and TKI resistance.</p

Data_Sheet_2_Molecular Expression Profile of Changes in Rat Acute Spinal Cord Injury.xlsx

Background: Spinal cord injury (SCI) is a highly lethal and debilitating disease with a variety of etiologies. To date, there is no effective therapeutic modality for a complete cure. The pathological mechanisms of spinal cord injury at the molecular gene and protein expression levels remain unclear.Methods: This study used single-cell transcriptomic analysis and protein microarray analysis to analyzes changes in the gene expression profiles of cells and secretion of inflammatory factors respectively, around the lesion site in a rat SCI model.Results: Single-cell transcriptomic analysis found that three types of glial cells (microglia, astrocyte, and oligodendrocyte) becomes activated after acute injury, with GO exhibiting a variety of inflammatory-related terms after injury, such as metabolic processes, immune regulation, and antigen presentation. Protein microarray results showed that the levels of four inflammatory cytokines favoring SCI repair decreased while the levels of nine inflammatory cytokines hindering SCI repair increased after injury.Conclusion: These findings thus reveal the changes in cellular state from homeostatic to reactive cell type after SCI, which contribute to understand the pathology process of SCI, and the potential relationship between glial cells and inflammatory factors after SCI, and provides new theoretical foundation for further elucidating the molecular mechanisms of secondary SCI.</p

Data_Sheet_1_Molecular Expression Profile of Changes in Rat Acute Spinal Cord Injury.xls

Background: Spinal cord injury (SCI) is a highly lethal and debilitating disease with a variety of etiologies. To date, there is no effective therapeutic modality for a complete cure. The pathological mechanisms of spinal cord injury at the molecular gene and protein expression levels remain unclear.Methods: This study used single-cell transcriptomic analysis and protein microarray analysis to analyzes changes in the gene expression profiles of cells and secretion of inflammatory factors respectively, around the lesion site in a rat SCI model.Results: Single-cell transcriptomic analysis found that three types of glial cells (microglia, astrocyte, and oligodendrocyte) becomes activated after acute injury, with GO exhibiting a variety of inflammatory-related terms after injury, such as metabolic processes, immune regulation, and antigen presentation. Protein microarray results showed that the levels of four inflammatory cytokines favoring SCI repair decreased while the levels of nine inflammatory cytokines hindering SCI repair increased after injury.Conclusion: These findings thus reveal the changes in cellular state from homeostatic to reactive cell type after SCI, which contribute to understand the pathology process of SCI, and the potential relationship between glial cells and inflammatory factors after SCI, and provides new theoretical foundation for further elucidating the molecular mechanisms of secondary SCI.</p

Figure S2 from Combination of Metformin and Gefitinib as First-Line Therapy for Nondiabetic Advanced NSCLC Patients with EGFR Mutations: A Randomized, Double-Blind Phase II Trial

Kaplan-Meier analyses of PFS for patients with normal and elevated ({greater than or equal to}7 pg/ml) baseline IL-6 levels.</p

Figure S3 from Combination of Metformin and Gefitinib as First-Line Therapy for Nondiabetic Advanced NSCLC Patients with EGFR Mutations: A Randomized, Double-Blind Phase II Trial

Impact of the IL-6 cutoff level on progression-free survival (A) and overall survival (B).</p

Figure S1 from Combination of Metformin and Gefitinib as First-Line Therapy for Nondiabetic Advanced NSCLC Patients with EGFR Mutations: A Randomized, Double-Blind Phase II Trial

Kaplan-Meier curves for progression-free survival in subgroups.</p