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ZrB2-SiC coatings were prepared by spark plasma sintering method. The effect of ZrB2 content ranging from 20wt.% to 80 wt.% on the oxidation behavior of the ZrB2-SiC coatings was investigated at 1973K in air. In the initial oxidation stage (

Additional file 1: Table S1. Primary and secondary antibodies.

Additional file 1: Figure S1. Randomness assessments of the three libraries.

Additional file 5: Table S2. Differentially expressed genes involved in starch and sucrose metabolism during zygotic embryo development of oil palm.

Additional file 4: Fig. S2. scRNAseq analysis shows there are multiple cell types in the proliferating cell cluster and there are 3 types of fibroblasts. A Unsupervised sub-clustering of the cluster containing proliferating cells, represented as an UMAP plot. The proliferating cell cluster contains proliferating T cells, B cells, Na��ve B cells, NK cells and epithelial cells. B Numbers of cells from PK-Ins1-/-;Ins2+/+ (orange) and PK-Ins1-/-;Ins2+/- (green) mice for each cell type. C Violin plot showing the expression level of selected cell type-specific markers for identified cell types within the proliferating cell cluster. D Expression level of the typical markers for identifying M1 macrophages and M2 macrophages for each genotype. E Violin plots showing the expression level of selected markers for inflammatory, myofibroblastic and antigen-presenting fibroblasts. F The differential expression of Reg3a, Reg3b, Reg3d, and Reg3g genes in acinar cells between PK-Ins1-/-;Ins2+/+ and PK-Ins1-/-;Ins2+/- mice.

Additional file 6: Table S3. Differentially expressed genes involved in fatty acid biosynthesis during zygotic embryo development of oil palm.

Additional file 3: Figure S3. GO enrichment classification histogram for the pairwise comparisons of S1 vs S2, S1 vs S3, and S2 vs S3.

Additional file 7: Table S4. Comparing differential expression genes from RNA-seq and qRT-PCR during zygotic embryo development of oil palm.

Additional file 4: Table S1. Differentially expressed genes involved in hormone signaling pathway during zygotic embryo development of oil palm. S1-a. Differentially expressed genes involved in auxin signalling pathway during zygotic embryo development of oil palm. S1-b. Differentially expressed genes involved in IAA biosynthesis during zygotic embryo development of oil palm. S1-c. Differentially expressed genes involved in CTK signal transduction during zygotic embryo development of oil palm. S1-d. Differentially expressed genes involved in CTK biosynthesis during zygotic embryo development of oil palm. S1-e. Differentially expressed genes involved in GA signal transduction during zygotic embryo development of oil palm. S1-f. Differentially expressed genes involved in GA biosynthesis during zygotic embryo development of oil palm. S1-g. Differentially expressed genes involved in ABA signal transduction during zygotic embryo development of oil palm. S1-h. Differentially expressed genes involved in ABA signal transduction during zygotic embryo development of oil palm.

Additional file 2: Figure S2. Sequencing saturation analysis of the three libraries.

Pancreatic ductal adenocarcinoma (PDAC) is the 3rd leading cause of cancer death in Canada and its incidence is increasing, largely driven by the expanding epidemics of PDAC risk factors including obesity and type 2 diabetes (T2D). Hyperinsulinemia is a cardinal feature of obesity and T2D, and is associated with increased PDAC incidence and mortality. Despite epidemiological data linking hyperinsulinemia to PDAC, there was no direct in vivo evidence of a causal role for endogenous insulin in any cancer type before this work. We studied how reduced insulin production or local insulin action affected the development of pancreatic intraepithelial neoplasia (PanIN) precursor lesions in Ptf1aCreER;KrasLSL-G12D mice. We first generated Ptf1aCreER;KrasLSL-G12D;Ins1+/+;Ins2-/- control and Ptf1aCreER;KrasLSL-G12D;Ins1+/-;Ins2-/- experimental mice. We found high fat diet (HFD)-induced hyperinsulinemia was modestly reduced in experimental mice without affecting glucose homeostasis. Genetically reduced insulin production resulted in ~50% suppression of PanIN. However, in this study, only female mice remained normoglycemic and only the gene dosage of rodent-specific Ins1 alleles was tested. Therefore, we then generated Ptf1aCreER;KrasLSL-G12D;Ins1-/-;Ins2+/+ control and Ptf1aCreER;KrasLSL-G12D;Ins1-/-;Ins2+/- experimental mice. Mice with reduced insulin production tended to develop fewer PanIN and acinar-to-ductal metaplasia (ADM) lesions. Using single-cell transcriptomics, we found hyperinsulinemia modulated pathways associated with protein translation, MAPK/ERK signaling and PI3K/AKT/mTOR signaling, which were changed in epithelial cells and subsets of immune cells. Finally, we examined whether hyperinsulinemia contributed to PDAC development directly through insulin receptor (INSR) signaling in KrasG12D carrying pancreatic acinar cells. We generated Ptf1aCreER;LSL-KrasG12D;nTnG mice with an Insrwt/wt, Insrwt/f, or Insrf/f genotype to reduce insulin receptor mRNA by 0%, 50%, or 100% in acinar cells. Loss of insulin receptors from acinar cells did not significantly influence body weight, fasting glucose, or insulin levels. Compared to mice with wild-type INSR expression in acinar cells, mice lacking INSR had a 2.7-fold and 5.3-fold significant reduction in PanIN plus tumor area in males and females, respectively. Collectively, these results indicate that hyperinsulinemia and INSR signaling in acinar cells are important for the early stages of pancreatic cancer. Insulin-lowering interventions such as lifestyle management and therapies targeting insulin receptor signaling may be beneficial in preventing and/or treating pancreatic cancer.

Additional file 3: Fig. S1. Amylase activity and pancreatic area of PK-Ins1-/-;Ins2+/+ and PK-Ins1-/-;Ins2+/- mice and the sex difference in PanIN development. A-B The amylase activity in male (A) and female mice (B) for each genotype. C-D The comparison of percent of total pancreatic area occupied by PanINs and tumor (C) or only PanINs (excluding tumor bearing mice) (D) in male and female PK-Ins1-/-; Ins2+/+ mice (n= 15-22) (dark blue and dark orange dots denote mice that developed tumors). E The comparison of percent of total pancreatic area occupied by only PanINs in male and female PK-Ins1-/-; Ins2+/- mice (n= 10-14). F The comparison of percent of total pancreatic area occupied by ADM in male and female PK-Ins1-/-; Ins2+/+ mice (n= 16-22). G The comparison of percent of total pancreatic area occupied by ADM in male and female PK-Ins1-/-; Ins2+/- mice (n= 10-14). H The total pancreatic area for mice in an Ins2-null background or in an Ins1-null background. I-J Correlations of adipocyte area with PanIN area in non-tumor bearing male (I) and female (J) PK-Ins1-/-;Ins2+/+ (dark colors) and PK-Ins1-/-;Ins2+/- (light colors) mice (n = 10-22). ****p