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Additional file 8.

Additional file 1.

Additional file 3: Table S1. Detailed clinical and pathologic information of TCGA entire set. Table S2. Detailed clinical and pathologic information of CRA001160 dataset. Table S3. The imaging channels for each antibody and antibody incubation information in tissue microenvironment landscape imaging. Table S4. Immune-related genes obtained from the ImmPort database.

Additional file 1: Figure S1. Flowchart of the whole study. Figure S2. The mutation status of the seven hub IRGs in TCGA dataset (A) and ICGC dataset (B). Figure S3. Representative images of hub IRGs expression status except CXCL10 and LIFR in normal pancreas and PC tissues. (The expression information of CXCL10 and LIFR was unavailable in HPA database). Figure S4. Independence of the risk signature and the other clinical variables, including, age, tumor grade, AJCC_stage and gender. (A, C, E) Univariate Cox regression analyses in the training set, testing set and entire set. (B, D, F) Multivariate Cox regression analyses in the training set testing set and entire set. Figure S5. Stratification analyses of all patients using the risk signature. (A-C) The Kaplan-Meier analysis of the younger stratum (age ≤ 65, n=88), older stratum (age >65, n=78) and all patients with PC (n=166). (D-F) The Kaplan-Meier analysis of the male stratum (n=90), female stratum n=76) and all patients with PC (n=166). (G-I) The Kaplan-Meier analysis of the Grade I/II stratum (n=117), Grade III/IV stratum (n=49) and all patients with PC (n=166). (J-L) The Kaplan-Meier analysis of the T1+T2 stratum (n=27), T3+T4 stratum (n=139) and all patients with PC (n=166). Figure S6. The mutation profiles of patients in S100A14 high expression group. Figure S7. The mutation profiles of patients in S100A14 low expression group. Figure S8. Correlation analysis of S100A14 and CD3E in the Bailey P. et al. cohort.

Additional file 2.

Additional file 8: Figure S4. Validation of the nomogram in training set, testing set and entire set. (A–C) Time-dependent ROC analysis of the risk signature in training set, testing set and entire set. (D–L) The calibration plot of the nomogram for agreement test between 1-, 2- and 3-year OS prediction and actual outcome in the training set, testing set and entire set.

Additional file 6: Figure S2. Stratification analyses of all patients using the risk signature. (A–C) The Kaplan–Meier plot of the younger stratum (age ≤ 65, n = 91), older stratum (age > 65, n = 80) and entire patients with PC (n = 171). (D–F) The Kaplan–Meier plot of the male stratum (n = 93), female stratum n = 78) and entire patients with PC (n = 171). (G–I) The Kaplan–Meier plot of the Grade I/II stratum (n = 121), Grade III/IV stratum (n = 50) and entire patients with PC (n = 171). (J–L) The Kaplan–Meier plot of the T1 + T2 stratum (n = 30), T3 + T4 stratum (n = 141) and entire patients with PC (n = 171).

Additional file 12: Figure S8. Differential gene expression in the high- and low-risk group compared with the normal group. (A) Heatmap of DEGs (Top50) between the low-risk pancreatic cancer group and the normal group. (B) Volcanic map of the DEGs between the low-risk pancreatic cancer group and the normal group. (C) Heatmap of DEGs (Top50) between the high-risk pancreatic cancer group and the normal group. (D) Volcanic map of the DEGs between the high-risk pancreatic cancer group and the normal group

Additional file 11: Figure S7. Gene Set Enrichment Analysis (GSEA) based on all genes between low and high risk groups. The top 3 GO enrichments (A) and KEGG enrichments (B) are displayed on the top respectively.

Additional file 7. Supplementary figures and tables.

Additional file 5: Figure S1. Further validation of the risk signature for the survival prediction in testing set, the entire TCGA set and the GSE57495 set. (A–C) Heatmap of the four genes expression, the risk scores distribution and survival status of the patients in the testing set, entire TCGA set and GSE57495 set.

Additional file 9: Figure S5. The mutations status and mechanisms of function of DPY30, CBX8, CENPT and PADI1. (A) Mutation information of DPY30, CBX8, CENPT and PADI1 from the cBioPortal database. (B–E) Interaction of DPY30, CBX8, CENPT and PADI1 with other proteins obtained from STRING database and validation in the TCGA entire set.

Aldol condensation between furfural (FA) and MIBK is used to synthesize branched bio-jet-fuel precursors. It remains difficult to design hybrid solid bases to efficiently promote this reaction, because only strong basic sites can activate MIBK. Different basic species were immobilized into zirconia/carbon hybrid supports by thermal decomposition of GO/UiO materials loaded with corresponding alkane (earth) nitrides. Only Cs immobilized zirconia/carbon (CsZC) could efficiently promote this reaction, while counterparts with Li, Mg and Ca species showed little activity over condensation between MIBK and FA. Optimized CsZC showed excellent FA conversion and selectivity towards desired products (88.6% in yields of FMIBK in 6 h at 130 °C). Two indirect proofs were provided to check the influence of basic strength on the catalytic performance, and only Cs samples had enough strong basic sites to accelerate the reaction. After modified with octyl groups, hydrophobic CsZC were reused for 4th cycle while retaining most of its original activity. Functionalization with organosilanes increased the hydrophobicity of the surface, which had dramatical promotion on activity, selectivity, and stability. It was the first time to run recycling experiments for this reaction, to afford the demands for chemical sustainability.

The cyclic adenosine monophosphate-inducible basic helix-loop-helix (bHLH) domain containing class-B2 transcriptional factor BHLHB2 is differentially expressed in a number of human malignancies. In the present study, the expression, regulation, functions and prognostic impact of BHLHB2 in pancreatic cancer were investigated.Expression analyses were carried out in tissues of the normal pancreas (n=10) and pancreatic ductal adenocarcinoma (n=77) as well as in eight pancreatic cancer cell lines using quantitative RT-PCR, semiquantitative immunohistochemistry, and immunoblot analyses. In vitro functional experiments were conducted using siRNA transfection, hypoxia, serum starvation, apoptosis induction with gemcitabine and actinomycin-D, and invasion assays. Survival analysis was performed using the Kaplan-Meier method. Prognostic factors were determined in a multivariable analysis using a Cox proportional hazards model.BHLHB2 mRNA and protein expressions were strongly induced by hypoxia and by serum starvation in pancreatic cancer cell lines. BHLHB2 silencing with RNAi had no significant effects on growth and invasion but increased apoptosis resistance against gemcitabine by reducing caspace-3 cleavage. In BHLHB2 silenced cells the ED50 of gemcitabine increased from 13.95 ± 1.353 to 38.70 ± 5.262 nM (p0.05). Ex vivo, the weak/absent nuclear staining in normal pancreatic ducts and acinar cells was replaced by moderate to strong nuclear/cytoplasmic staining in PanIN lesions and pancreatic cancer cells. Patients with weak/absent nuclear BHLHB2 staining had significantly worse median survival compared to those with strong staining (13 months vs. 27 months, p=0.03). In a multivariable analysis, BHLHB2 staining was an independent prognostic factor (Hazard-Ratio=2.348, 95% CI=1.250-4.411, p=0.008).Hypoxia-inducible BHLHB2 expression is a novel independent prognostic marker in pancreatic cancer patients and indicates increased chemosensitivity towards gemcitabine.

To establish stable methods for detecting plasma endotoxin level and endotoxin inactivation capacity in a normal population and general surgical patients and evaluate their perioperative changes. 50 healthy people and 50 patients receiving gastrointestinal operation were enrolled, their plasma endotoxin levels and plasma endotoxin inactivation capacity were assayed. Our results showed that plasma endotoxin levels were 0.044 +/- 0.009 EU/ml in the normal population and 0.044 +/- 0.023 EU/ml in the preoperative patients. Endotoxin level peaked 3 h after the operation (0.223 +/- 0.041 EU/ml), and then decreased rapidly on the first day after the operation (0.134 +/- 0.164 EU/ml). Endotoxin inactivation capacity also had the same time course as endotoxin level. Systemic inflammatory response syndrome and infection induced another elevation in the time course. It is concluded that establishing the endotoxin standard curve by using pyrogenic free water is better than by using plasma. Plasma endotoxin inactivation capacity can be used as an indirect indicator of postoperative immune depression. Plasma endotoxin level and endotoxin inactivation capacity peaked shortly after operation, indicating surgical stress is closely related with the changes.

Seventy-eight patients with neoplasm (74 cases) or pancreatitis (4 cases) were treated with pylorus-preserving pancreatoduodenectomy (PPPD) from 1984 to 1994. One postoperative death occurred. Follow-up studies were performed in 35 patients who had been treated by PPPD or the standard Whipple procedure beyond 1 year post operation; they were questioned carefully concerning clinical symptoms. Further studies were performed in 20 patients with or without pylorus preservation (10 patients each). Nutritional status and gastrointestinal digestive and absorptive function were evaluated by determination of serum components, gastric analysis, barium emptying time, D-xylose absorptive test, CO2 breath test, p-aminobenzoic acid (PABA), and other methods. The results demonstrated malnutrition and postgastrectomy syndromes in some patients after the conventional Whipple procedure, but not in those with PPPD; the quality of life was better in the latter. Pylorus preservation may be the main reason for this difference. Delayed gastric emptying in the early postoperative period was a complication in some patients (22%). We recommend PPPD for pancreatoduodenectomy.