Topological Susceptibility under Gradient Flow

We study the impact of the Gradient Flow on the topology in various models of lattice field theory. The topological susceptibility $\chi_{\rm t}$ is measured directly, and by the slab method, which is based on the topological content of sub-volumes ("slabs") and estimates $\chi_{\rm t}$ even when the system remains trapped in a fixed topological sector. The results obtained by both methods are essentially consistent, but the impact of the Gradient Flow on the characteristic quantity of the slab method seems to be different in 2-flavour QCD and in the 2d O(3) model. In the latter model, we further address the question whether or not the Gradient Flow leads to a finite continuum limit of the topological susceptibility (rescaled by the correlation length squared, $\xi^{2}$). This ongoing study is based on direct measurements of $\chi_{\rm t}$ in $L \times L$ lattices, at $L/\xi \simeq 6$.Comment: 8 pages, LaTex, 5 figures, talk presented at the 35th International Symposium on Lattice Field Theory, June 18-24, 2017, Granada, Spai

Additional file 1 of DNA methylation and expression profiles of placenta and umbilical cord blood reveal the characteristics of gestational diabetes mellitus patients and offspring

Additional file1: Fig. S1 Placenta shows genome-wide methylation alteration associated with glucose metabolism in GDM patients. Unique mapping ratio of placenta and blood samples for A RRBS data and B RNA-seq data. C Genomic distribution of DMRs in placenta. GO pathway enrichment result of placenta for D hyper-DMGs and E hypo-DMGs. The number in brackets represents the number of enriched genes. Fig. S2 Methylation contributes to expression change of genes associated with insulin signaling pathway. A KEGG pathway enrichment analysis of down-DMGs in placenta. B “Cortisol synthesis and secretion” C “Adherens junction,” D “Insulin resistance” and E “Type I diabetes mellitus” pathway enrichment result of placenta expression profile GSEA analysis. F GSEA analysis of placenta DMGs to placenta expression profile. Fig. S3 Alterations for umbilical cord blood were related to insulin secretion and resistance A Genomic distribution of DMRs in umbilical cord blood. B Differences of DMRs mean methylation levels between GDM and control umbilical cord blood samples. Yellow box represents GDM samples and green box represents control samples. *** P value < 0.001, Wilcoxon rank-sum test. Fig. S4 Differential characteristics of primary bile acid synthesis and autophagy between GDM and control samples. Total bile acid concentration between GDM and control sample in A 24 gestational week and B 40 gestational week. Wilcoxon rank-sum test. C ‘primary bile acid biosynthesis’ and D ‘Autophagy’ pathway enrichment result of placenta expression profile GSEA analysis

Additional file 2 of DNA methylation and expression profiles of placenta and umbilical cord blood reveal the characteristics of gestational diabetes mellitus patients and offspring

Additional file2: Table S1.1 Quality control table of placenta RRBS data. Table S1.2 Quality control table of umbilical cord blood RRBS data. Table S1.3 Quality control table of placenta RNA-seq data. Table S1.4 Quality control table of umbilical cord blood RNA-seq data. Table S2 The 2779 differential methylation regions of placenta. Table S3 GO pathway enrichment of hyper-DMGs of placenta. Table S4 KEGG pathway enrichment of hyper-DMGs of placenta. Table S5 GO pathway enrichment of hypo-DMGs of placenta. Table S6 KEGG pathway enrichment of hypo-DMGs of placenta. Table S7 Up-regulated differentially expressed genes of placenta. Table S8 Down-regulated differentially expressed genes of placenta. Table S9 GO pathway enrichment of UP-DEGs of placenta. Table S10 KEGG pathway enrichment of UP-DEGs of placenta. Table S11 GO pathway enrichment of DN-DEGs of placenta. Table S12 KEGG pathway enrichment of DN-DEGs of placenta. Table S13 Positive enriched pathways of GSEA for placenta gene expression profile. Table S14 Negative enriched pathways of GSEA for placenta gene expression profile. Table S15 Up-regulated differentially expressed genes of umbilical cord blood. Table S16 Down-regulated differentially expressed genes of umbilical cord blood. Table S17 Positive enriched pathways of GSEA for umbilical cord blood gene expression profile. Table S18 Negative enriched pathways of GSEA for umbilical cord blood gene expression profile

Peripheral arterial occlusive disease: Global gene expression analyses suggest a major role for immune and inflammatory responses-2

a Venn diagram. B, C. Heatmap representation of commonly up-regulated genes (B) and commonly down-regulated genes (C) in overlapping genes, respectively. Samples are displayed in columns and genes in rows. Gene expression is represented as a color, normalized across each row, with brighter red for higher values and brighter green for lower values. Gene symbols are listed to the right. N (Normal control group), Int (intermediate lesions group), Ad (advanced lesions group).<p><b>Copyright information:</b></p><p>Taken from "Peripheral arterial occlusive disease: Global gene expression analyses suggest a major role for immune and inflammatory responses"</p><p>http://www.biomedcentral.com/1471-2164/9/369</p><p>BMC Genomics 2008;9():369-369.</p><p>Published online 1 Aug 2008</p><p>PMCID:PMC2529314.</p><p></p

Peripheral arterial occlusive disease: Global gene expression analyses suggest a major role for immune and inflammatory responses-5

Ption factors (AP-1 and CREB) were significantly enriched in disease progression (q-value <p><b>Copyright information:</b></p><p>Taken from "Peripheral arterial occlusive disease: Global gene expression analyses suggest a major role for immune and inflammatory responses"</p><p>http://www.biomedcentral.com/1471-2164/9/369</p><p>BMC Genomics 2008;9():369-369.</p><p>Published online 1 Aug 2008</p><p>PMCID:PMC2529314.</p><p></p

Peripheral arterial occlusive disease: Global gene expression analyses suggest a major role for immune and inflammatory responses-7

S illustrated with significantly regulated genes highlighted.<p><b>Copyright information:</b></p><p>Taken from "Peripheral arterial occlusive disease: Global gene expression analyses suggest a major role for immune and inflammatory responses"</p><p>http://www.biomedcentral.com/1471-2164/9/369</p><p>BMC Genomics 2008;9():369-369.</p><p>Published online 1 Aug 2008</p><p>PMCID:PMC2529314.</p><p></p

Peripheral arterial occlusive disease: Global gene expression analyses suggest a major role for immune and inflammatory responses-0

8 um cryostat sections were stained with hematoxylin and eosin, dehydrated in graded alcohol, and cover-slipped with permanent mounting solution after xylene clearing. Three representative samples are listed: normal artery (A, B, C), intermediate lesions (D, E, F), and advanced lesions (G, H, I).<p><b>Copyright information:</b></p><p>Taken from "Peripheral arterial occlusive disease: Global gene expression analyses suggest a major role for immune and inflammatory responses"</p><p>http://www.biomedcentral.com/1471-2164/9/369</p><p>BMC Genomics 2008;9():369-369.</p><p>Published online 1 Aug 2008</p><p>PMCID:PMC2529314.</p><p></p

Peripheral arterial occlusive disease: Global gene expression analyses suggest a major role for immune and inflammatory responses-9

8 um cryostat sections were stained with hematoxylin and eosin, dehydrated in graded alcohol, and cover-slipped with permanent mounting solution after xylene clearing. Three representative samples are listed: normal artery (A, B, C), intermediate lesions (D, E, F), and advanced lesions (G, H, I).<p><b>Copyright information:</b></p><p>Taken from "Peripheral arterial occlusive disease: Global gene expression analyses suggest a major role for immune and inflammatory responses"</p><p>http://www.biomedcentral.com/1471-2164/9/369</p><p>BMC Genomics 2008;9():369-369.</p><p>Published online 1 Aug 2008</p><p>PMCID:PMC2529314.</p><p></p

Peripheral arterial occlusive disease: Global gene expression analyses suggest a major role for immune and inflammatory responses-3

To three major clusters by visual inspection. Clustering method: Average linking; Similarity measure: Euclidean distance. Samples are displayed in columns and genes in rows. Gene expression is represented as a color, normalized across each row, with brighter red for higher values and brighter green for lower values. N (Normal control group), Int (intermediate lesions group), Ad (advanced lesions group). The list of differentially expressed genes in disease progression is provided [see Additional file ].<p><b>Copyright information:</b></p><p>Taken from "Peripheral arterial occlusive disease: Global gene expression analyses suggest a major role for immune and inflammatory responses"</p><p>http://www.biomedcentral.com/1471-2164/9/369</p><p>BMC Genomics 2008;9():369-369.</p><p>Published online 1 Aug 2008</p><p>PMCID:PMC2529314.</p><p></p

Peripheral arterial occlusive disease: Global gene expression analyses suggest a major role for immune and inflammatory responses-4

descending triangle) were determined by real-time PCR and presented as a ratio to GAPDH mRNA. mRNA abundance in intermediate lesions or advanced lesions was differentially expressed (*P < 0.05, and **P < 0.01, respectively) when normal samples were used for comparison.<p><b>Copyright information:</b></p><p>Taken from "Peripheral arterial occlusive disease: Global gene expression analyses suggest a major role for immune and inflammatory responses"</p><p>http://www.biomedcentral.com/1471-2164/9/369</p><p>BMC Genomics 2008;9():369-369.</p><p>Published online 1 Aug 2008</p><p>PMCID:PMC2529314.</p><p></p