10 research outputs found
Supersymmetric dS/CFT
We put forward new explicit realisations of dS/CFT that relate
supersymmetric Euclidean vector models with reversed spin-statistics in three
dimensions to specific supersymmetric Vasiliev theories in four-dimensional de
Sitter space. The partition function of the free supersymmetric vector model
deformed by a range of low spin deformations that preserve supersymmetry
appears to specify a well-defined wave function with asymptotic de Sitter
boundary conditions in the bulk. In particular we find the wave function is
globally peaked at undeformed de Sitter space, with a low amplitude for strong
deformations. This suggests that supersymmetric de Sitter space is stable in
higher-spin gravity and in particular free from ghosts. We speculate this is a
limiting case of the de Sitter realizations in exotic string theories.Comment: V2: references and comments added, typos corrected, version published
in JHEP; 27 pages, 3 figures, 1 tabl
Additional file 5 of Complex regulation of ADAR-mediated RNA-editing across tissues
Figure S5. A-to-I editing frequency at 575 sites across nineteen tissue samples, represented as a heatmap. These sites were selected on the basis of having at least 10X coverage and an editing frequency >0.4 in at least one tissue. Tissues for which the coverage was < 10X at a site appear as cyan. Very few sites are highly edited across all nine tissues. Most sites that are edited in only one tissue are often not expressed (insufficient read coverage) in the other tissues. (PDF 373 kb
Additional file 7 of Complex regulation of ADAR-mediated RNA-editing across tissues
Figure S7. The variability in editing frequency per site across tissues in the human Illumina Body Map 2 dataset. Only samples with ≥ 10X coverage at these sites are plotted. Three sites where the RDD encodes a non-synonymous change were selected and presented here (Tmem63b, Flnb, and Copa). (PDF 5 kb
Additional file 1 of Complex regulation of ADAR-mediated RNA-editing across tissues
Figure S2. The ratio of reads mapping to introns versus exons in each sample. (PDF 5 kb
Additional file 5: Figure S5. of Massively parallel nanowell-based single-cell gene expression profiling
Percentage of mitochondrial transcripts plotted against total number of detected transcripts for mouse Ba/F3 cells (a), human cell lines (b), mouse cell lines (c), and pancreatic islets (d). Dashed lines indicate the minimum number of detected transcripts required as a cell QC filter for each data set. (PDF 409 kb
Additional file 4: Figure S4. of Massively parallel nanowell-based single-cell gene expression profiling
Heatmaps illustrating the total number of detected transcripts for each well selected for downstream processing. Data are for three microchips, each with 5184 wells arranged in a 72 × 72 square layout. Microchips 72,618 and 72,598 were used for profiling human and mouse cell lines (names of cell lines indicated in the plot). Microchip 72,625 was used for profiling pancreatic islets. For microchips with multiple dispensed samples, the dispense area for each sample is indicated. (PDF 93 kb
Additional file 2: Figure S2. of Massively parallel nanowell-based single-cell gene expression profiling
Checkerboard assay. (a) Image of a microchip where the right half contains negative control master mix (NTC wells, n = 2520) and the left half contains lambda DNA master mix master (Positive wells, n = 1024) and negative control master mix (Test wells, n = 1496) in a checkerboard pattern. (b) Number of Test wells with signal, number of NTC wells with signal, and calculated misalignment rate for 11 MSNDs and 19 microchips. (PDF 1288 kb
Additional file 1: Table S1a. of Comprehensive genomic analysis identifies pathogenic variants in maturity-onset diabetes of the young (MODY) patients in South India
Sample information and clinical characteristics. Table S1b. Summary of clinical characteristics of MODY patient samples. Table S2a. Sequencing statistics of combined exome and WGS. Table S2b. Sequencing statistics of targeted exome samples. Table S3. Targeted gene panel. Table S4. Candidate variants identified in MODY samples. Table S5. Differentially expressed genes - NKX6–1 (XLS 292 kb
Additional file 2: Figure S1. of Comprehensive genomic analysis identifies pathogenic variants in maturity-onset diabetes of the young (MODY) patients in South India
Box plot showing (a) fasting plasma glucose, (b) fasting insulin, (c) C-peptide fasting, (d) C-peptide stimulated and (e) creatinine in MODY and control samples. The median value is shown as a line with the whiskers extending from the highest value within 1.5 * IQR of the third quartile to the lowest value within 1.5 * IQR of the first quartile where IQR is the inter-quartile range. Figure S2. Heatmap depicting the genotype based identity of the discovery and validation MODY cohort and control samples. Genomic regions for which we obtained data for the validation cohort samples and corresponding regions from the discovery set samples using GATK joint-variant caller. The sample identity was computed based on the high-confidence set of single nucleotide variants (SNVs) that passed GATK Hard-Filtering criteria. Figure S3. Expression level of mouse Nkx6–1 (top) or human NKX6–1 (bottom) following induction in cells stably expressing the indicated variant or wildtype. Figure S4. Western blot showing the expression of NKX6–1 48 h post dox induction. Hsp90 was used as a loading control. (ZIP 5136 kb