Data_Sheet_1_Teaching programming and computational thinking in early childhood education: a case study of content knowledge and pedagogical knowledge.docx

Programming and computational thinking (CT) have been progressively incorporated into early childhood education to prepare children for the digital age. However, little is known about the content knowledge (CK) and pedagogical knowledge (PK) possessed by early childhood teachers in this domain. To address this gap, we conducted a case study of an early childhood teacher in China who had experience developing and implementing an unplugged programming and CT curriculum. The triangulation of data sources was established to collect evidence from videotaped observations, interviews, and lesson plans. For the CK, analysis of these findings revealed that the teacher had a more robust understanding of CT concepts (e.g., sequences, conditionals, and loops) compared to CT practices (e.g., decomposition, debugging) and CT perspectives (e.g., perseverance, choices of conduct). In terms of PK, the teacher could apply the general pedagogical knowledge but was relatively weak in using content-specific pedagogical knowledge. As the first endeavor to investigate an early childhood teacher’s CK and PK in teaching programming and CT, this study provides significant implications for improving teachers’ professional knowledge and teaching effectiveness in this burgeoning area.</p

Net is down-regulated in pancreatic ductal adenocarcinoma.

<p>(A) Immunohistochemical analysis of Net, c-fos and Ras expression in pancreatic ductal adenocarcinoma tissues (top row) and matched adjacent normal tissue samples (bottom row). a and b is H&E staining with low resolution (×100); c, d denote the expression of Net representative with high resolution (×200); e, f denote the expression of c-fos representative with high resolution (×200); g, h denote the expression of Ras representative with high resolution (×200). (B) Expression of Net was examined at mRNA and protein levels using RT-PCR and western blotting on human pancreatic ductal adenocarcinoma tissues (T) and matched adjacent normal tissue samples (N) (presentive 5 cases of 36). (C) Expression of Net was examined at mRNA and protein levels using RT-PCR and western blotting in pancreatic cancer cell lines (SW1990, PANC-1 and PL45) and human pancreatic cell hTERT-HPNE. PDAT, pancreatic ductal adenocarcinoma tissues; NAT, normal adjacent tissue.</p

Dysbiosis of intestinal microbiota and decrease in paneth cell antimicrobial peptide level during acute necrotizing pancreatitis in rats

<div><p>Objectives</p><p>Intestinal barrier dysfunction plays an important role in acute necrotizing pancreatitis (ANP) and intestinal microbiota dysbiosis was involved in intestinal barrier failure. Paneth cells protect intestinal barrier and are associated with intestinal microbiota. Here, we investigated changes in intestinal microbiota and antimicrobial peptides of Paneth cells in ileum during ANP.</p><p>Methods</p><p>Rats with ANP were established by retrograde injection of 3.5% sodium taurocholate into biliopancreatic duct and sacrificed at 24h and 48h, respectively. Injuries of pancreas and distal ileum were evaluated by histopathological score. Intestinal barrier function was assessed by plasma diamine oxidase activity (DAO) and D-lactate. Systemic and intestinal inflammation was evaluated by TNFα, IL-1β and IL-17A concentration by ELISA, respectively. 16S rRNA high throughput sequencing on fecal samples was used to investigate the changes in intestinal microbiota in the ANP group at 48h. Lysozyme and α-defensin5 were measured by real-time PCR, western blot and immunofluoresence.</p><p>Results</p><p>ANP rats had more severe histopathological injuries in pancreas and distal ileum, injured intestinal barrier and increased expression of TNFα, IL-1β and IL-17A in plasma and distal ileum compared with those of the sham-operated (SO) group. Principal component analysis (PCA) showed structural segregation between the SO and ANP groups. Operational taxonomic unit (OTU) number and ACE index revealed decreased microbiota diversity in the ANP group. Taxonomic analysis showed dysbiosis of intestinal microbiota structure. At phyla level, <i>Saccharibacteria</i> and <i>Tenericutes</i> decreased significantly. At genus level, <i>Escherichia-Shigella</i> and <i>Phascolarctobacterium</i> increased significantly, while <i>Candidatus_Saccharimonas</i>, <i>Prevotellaceae_UCG-001</i>, <i>Lachnospiraceae_UCG-001</i>, <i>Ruminiclostridium_5</i> and <i>Ruminococcaceae_UCG-008</i> decreased significantly. Lysozyme and α-defensin5 mRNA expression levels decreased significantly in ANP group at 48h. Protein expression of lysozyme decreased in ANP groups at 24h and 48h. Meanwhile, the relative abundance of <i>Escherichia-Shigella</i> correlated inversely with the decrease in lysozyme.</p><p>Conclusion</p><p>The disorder in intestinal microbiota and decreases of Paneth cell antimicrobial peptides might participate in the pathogenesis of intestinal barrier dysfunction during ANP.</p></div

The effects of Net expression on tumor growth in vivo.

<p>(A) Tumor size was measured every three days interval in each group. (B) Weight of dissectable xenograft tumors was measured in each group. (C) Expression of Net, c-fos and P21 in mRNA levels in xenograft tissues. (D) Representative H&E staining, histological staining of Net, c-fos and P21, PCNA staining and TUNEL assay in xenogrft tissues. (E) Index of PCNA and apoptosis were accounted in xenograft tumour tissues. *p<0.05, **p<0.01.</p

The possible regulatory model of effect of Net on pancreatic ductal adenocarcinoma.

<p>Net inhibits the growth of pancreatic ductal adenocarcinoma cell by inhibiting the expression of c-fos, subsequently inactivating the transcription activity of AP-1, followed by activation of p21 to antagonize the effects of Cyclin D/CDK4 on cell cycle progression, and ultimately leading to cell death. On the contrary, phosphorylation of Net is activated by intra or extracellular stimulation signals through Ras-MAPKs pathway, which results in downregulation of Net expression and lack of inhibitory ability on c-fos transcription, thus promoting cell proliferation.</p

Additional file 1: Figure S1. of Transcriptional repression of SOCS3 mediated by IL-6/STAT3 signaling via DNMT1 promotes pancreatic cancer growth and metastasis

(A) Normalized band quantization data of pSTAT3 and SOCS3 in Fig. 1c by Image J between matched pancreatic cancer and pericancerous tissues were used to confirm our claim. (B) Normalized band quantization data of pSTAT3 and SOCS3 in Fig. 1d by Image J were evaluated. (C) The CCK8 assay was used to evaluate the proliferation of Panc1 cells after treatment with IL-6 (100 ng/ml) at 0 h, 24 h and 48 h. After seeding Bxpc3 cells for 24 h, we treated Bxpc3 cells with S31-201 (10ΟM). The CCK8 assay was used to evaluate the proliferation of Bxpc3 cells after treatment with S31-201 at 0 h, 24 h and 48 h. (JPG 973 kb