Data_Sheet_1_Coexistence mechanisms of sympatric ungulates: Behavioral and physiological adaptations of blue sheep (Pseudois nayaur) and red deer (Cervus elaphus alxaicus) in Helan Mountains, China.zip

Studying the coexistence mechanisms of sympatric wildlife helps to shed light on why the earth has so many different species. When ungulates share ranges, food and habitat requirements may partially or fully overlap. Therefore, the aim of this study was to determine how sympatric ungulates share limited resources. Carcasses of 27 adult blue sheep (Pseudois nayaur) and three adult red deer (Cervus elaphus alxaicus) were collected in the Helan Mountains, China. Nutritive indices of plant species foraged and morphometric measurements of the digestive system of the two sympatric ungulates were determined. In addition, 120 passive, infrared motion-triggered cameras recorded spatial overlap and temporal overlap between the two species. Camera trapping revealed relatively limited spatial overlap and significantly different activity rhythms between blue sheep and red deer. Differences were also observed in stomach weight, surface enlargement factor of the rumen, and intestine length between the two species. However, the combined relative weight of the stomach and intestine was not different between species. The low spatiotemporal overlap decreased opportunities for encounters between sympatric blue sheep and red deer, and significant differences in digestive systems allowed the two species to consume different plant species or different parts of the same species. Thus, the two sympatric ungulates coexist harmoniously in the Helan Mountains because of long-term evolutionary behavioral and physiological adaptations that eliminate negative effects on the survival of the other species.</p

MOESM2 of Hepatocellular carcinoma with hilar bile duct tumor thrombus versus hilar Cholangiocarcinoma on enhanced computed tomography: a diagnostic challenge

Additional file 2: Figure S2. A patient with hepatocellular carcinoma (a-d). Intrahepatic HCC lesion (black arrows) and HBDTT (white arrow heads) show hyperattenuation in plain CT image (a). The HCC lesion show relative isoattenuation in arterial phase (b) and hypoattenuation in portal venous phase(c). The HBDTT show hypoattenustion without enhancement in both two phase (b-c). The spleen is about nine rib elements (a-c). d (HE stain, original magnification×200) The HCC is moderately differentiated trabecular type, grade II, and part of the lesion was clear cell type

MOESM1 of Hepatocellular carcinoma with hilar bile duct tumor thrombus versus hilar Cholangiocarcinoma on enhanced computed tomography: a diagnostic challenge

Additional file 1: Figure S1. A patient with hepatocellular carcinoma (a-e). HBDTT (white arrow heads) appeared like irregular bile duct wall thickening, show hypoattenuation in plain CT image (a), enhancement with relative hyperattenuation in arterial phase (b) and heterogeneous hypoattenuation in portal venous phase (c). d A coronal image shows the connection of the intrahepatic HCC lesion (white arrow) and HBDTT (white arrow head), both show hypoattenuation in portal venous phase. Intrahepatic biliary dilation could be found (a-c). e (HE stain, original magnification×40) The thrombi do not adhere to the bile duct wall, without bile duct infiltration and mainly consisted of tumor nests

Additional file 1 of Preoperative assessment of peripheral vascular invasion of pancreatic ductal adenocarcinoma based on high-resolution MRI

Additional File 1: Non-HR-MRI scan sequence and parameters

MOESM3 of Hepatocellular carcinoma with hilar bile duct tumor thrombus versus hilar Cholangiocarcinoma on enhanced computed tomography: a diagnostic challenge

Additional file 3: Figure S3. A patient with hepatocellular carcinoma (a-d). HBDTT (white arrows) show hypoattenuation in plain and postcontrast CT images with increased CT value (a-c). The spleen is more than seven rib elements (a-c). d (HE stain, original magnification×40) The HCC is moderately differentiated trabecular type, grade II

Healing the Buried Cavities and Defects in Quasi-2D Perovskite Films by Self-Generated Methylamine Gas

Perovskites with grain size comparable to film thickness are intensively pursued for high-efficiency solar cells. Geometrically, large grains with high crystallinity tend to form polyhedral shapes that have difficulty forming compact and smooth films. When quasi-two-dimensional RP perovskite films adopt a downward growth mode, defective contacts tend to form at their bottom interfaces with many nanocavities. This is attributed to the angular growing fronts of RP perovskite grains adopting [111] (or/and [101]) growth directions. Self-generated methylamine gas, by a replacement reaction in solution, is introduced to in situ heal these irregular nanocavities that are deeply buried in perovskite films during crystallization processes. The amount of self-generated methylamine gas should be adequately controlled to avoid the homogeneous nucleation of perovskites from a liquid perovskite-amine intermediate phase, which is a key to avoid ruining the grain size and film composition. This in situ healing strategy offers significantly enhanced charge collection efficiency and device working stability

MOESM1 of Constructing an experiential education model in undergraduate radiology education by the utilization of the picture archiving and communication system (PACS)

Additional file 1. Self-assessment radiologic skills questionnaire (English language version)

MOESM2 of Constructing an experiential education model in undergraduate radiology education by the utilization of the picture archiving and communication system (PACS)

Additional file 2. Learner satisfaction questionnaire (English language version)

DataSheet_3_ROBO1 p.E280* Loses the Inhibitory Effects on the Proliferation and Angiogenesis of Wild-Type ROBO1 in Cholangiocarcinoma by Interrupting SLIT2 Signal.docx

BackgroundCholangiocarcinoma (CCA) remains one of the most lethal malignancies with an increasing incidence globally. Through whole-exome sequencing of 67 CCA tissues, we identified new mutated genes in CCA, including MACF1, METTL14, ROBO1, and so on. The study was designed to explore the effects and mechanism of ROBO1 wild type (ROBO1WT) and ROBO1E280* mutation on the progression of CCA.MethodsWhole-exome sequencing was performed to identify novel mutations in CCAs. In vitro and in vivo experiments were used to examine the function and mechanism of ROBO1WT and ROBO1E280* in cholangiocarcinoma. A tissue microarray including 190 CCA patients and subsequent analyses were performed to indicate the clinical significance of ROBO1.ResultsThrough whole-exome sequencing, we identified a novel CCA-related mutation, ROBO1E280*. ROBO1 was downregulated in CCA tissues, and the downregulation of ROBO1 was significantly correlated with poor prognosis. ROBO1WT suppressed the proliferation and angiogenesis of CCA in vitro and in vivo, while ROBO1E280* lost the inhibitory effects. Mechanically, ROBO1E280* translocated from the cytomembrane to the cytoplasm and interrupted the interaction between SLIT2 and ROBO1. We identified OLFML3 as a potential target of ROBO1 by conducting RNA-Seq assays. OLFML3 expression was downregulated by ROBO1WT and recovered by ROBO1E280*. Functionally, the silence of OLFML3 inhibited CCA proliferation and angiogenesis and was sufficient to repress the loss-of-function role of ROBO1E280*.ConclusionsThese results suggest that ROBO1 may act as a tumor suppressor and potential prognostic marker for CCA. ROBO1E280* mutation is a loss-of-function mutation, and it might serve as a candidate therapeutic target for CCA patients.</p

Additional file 1 of Hypoxia-induced SKA3 promoted cholangiocarcinoma progression and chemoresistance by enhancing fatty acid synthesis via the regulation of PAR-dependent HIF-1a deubiquitylation

Additional file 1: Fig. S1. (A) SKA3 was upregulated in various types of tumours in the Cancer Genome Atlas (TCGA) database. (B) TCGA database showed that SKA3 was upregulated in CCA.  (C) The Gene Expression Omnibus dataset (GSE107943) indicated that SKA3 was upregulated in CCA tissues. (D-E) Adjust batch effect of TCGA and GSE107943. (F) RT-qPCR and (G) Western blot analysis showed the expression level of SKA3 in CCA cell lines. Fig. S2. (A)SKA3 expression was detected under hypoxic and normoxic conditions. (B) SKA3 knockdown and overexpression cells was established in CCA cells. (C) Heatmap and (D) Volcano plot of differential expressed genes, which transfected in NC sequence compared with Si-SKA3 sequence. (E) Statistical and quantitative results of Fig. 3E *p<0.05; **p<0.01; ***p<0.001. Fig. S3. (A) CCK8 assays and (B) Clone formation assays showed FASN, ACLY, SCD, ACACA reversed the proliferation of CCA induced by SKA3 under hypoxic conditions. (C) Nile red staining and (D) Cellular triglycerides detection showed FASN, ACLY, SCD and ACACA reversed the fatty acid synthesis of CCA under hypoxic conditions. (E) The ATP concentration in QBC939 cells were tested by ATP Assay Kit. *p<0.05;**p<0.01;***p<0.001. Fig. S4. (A) Statistical and quantitative results of Fig. 4A. (B) The mRNA level of HIF-1a was detected in SKA3 knockdown and overexpression cells under hypoxic conditions. (C) Statistical and quantitative results of Fig. 4E. (D) Statistical and quantitative results of Fig. 4F. (E) Statistical and quantitative results of Fig. 4G. (F) Statistical and quantitative results of Fig. 4D. (G) Western blot analysis showed the expression of HIF-1a under hypoxic conditions with the increasing concentration of PARG inhibitor. *p<0.05; **p<0.01; ***p<0.001. Fig. S5. Statistical and quantitative results of (A) Fig. 5E, (B) Fig. 5K, (C) Fig. 5L, (D) Fig. 6B, (E) Fig. 6C, (F) Fig. 6D, (G) Fig. 6E, (H) Fig.5F and (G) Fig. 6G. *p<0.05; **p<0.01;***p<0.001. Fig. S6. (A) The proliferation of HIF-1a knockdown and overexpression cells under hypoxic conditions was determined by CCK8 assays 0, 24, 48, 72, and 96h . (B) The colony formation number of HIF-1a knockdown and overexpression cells under hypoxic conditions was count. (C) Flow cytometry analyzed cell cycle of CCA cell transfected with Si-HIF-1a or HIF-1a overexpression. *p<0.05; **p<0.01; ***p<0.001. Fig. S7. EdU staining assays showed HIF-1a promoted the proliferation of CCA under hypoxic conditions.Fig. S8. (A) Cellular neutral lipids were measured in HuCCT1 cells by double staining with Nile Red and DAPI. (B) Cellular triglycerides were measured in HuCCT1 cells, which normalized by NC group. (C) The ATP concentration in HuCCT1 and QBC939 cells were tested by ATP Assay Kit. (D) Western bolt analysis was used to detect the expression of HIF-1a in SKA3 knockdown and overexpression CCA cells under hypoxic conditions.*p<0.05; **p<0.01; ***p<0.001.Fig. S9. (A-B) TCGA database showed that PARP1 was oncogenic in various of tumours including CCA. (C) CCK8 assays, and (D) Clone formation assays showed PARP1 promoted the proliferation of CCA under hypoxic conditions.Fig. S10. (A) Cell cycle assays and (B) EdU staining assays showed PARP1 enhanced the proliferation of CCA under hypoxic conditions. Fig. S11. (A) Nile red staining, (B) Cellular triglycerides detection, and  (C)  Western blot analysis showed PARP1 promoted the fatty acid synthesis of CCA under hypoxic conditions. Fig. S12. (A) CCK8 assays, (B) Clone formation assays, (C) Cell cycle analysis, (D) EdU staining assays detected the proliferation of CCA cells. (E) Statistical and quantitative results of Fig. 7F. (F) Nile red staining, (G) Cellular triglycerides detection, and (H) Western blot analysis showed PARP1 or HIF-1a overexpression reversed the increase of fatty acid synthesis in SKA3 Knockdown CCA cells under hypoxic conditions. (I) The ATP concentration in QBC939 cells were tested by ATP Assay Kit