Additional file 1: Figures S1–S5. of Widespread activation of antisense transcription of the host genome during herpes simplex virus 1 infection

Figure S1 Coverage profiles of antisense transcripts. Figure S2 Validation of antisense transcripts. Figure S3 Antisense transcripts with PAA, knockout virus, and HSV-2 infection [67]. Figure S4 Antisense transcript promoters are already poised for transcription. Figure S5 Ectopically expressed BBC3as localizes outside the nucleus. (PDF 4275 kb

The utility of short-course radiotherapy in a watch-and-wait strategy for rectal cancer – the need to measure the interval to tumour response assessment from the radiation start

The utility of short-course radiotherapy in a watch-and-wait strategy for rectal cancer – the need to measure the interval to tumour response assessment from the radiation star

The literature-selected SNPs significant associations with AD, CRC or PCa, considering allelic and additive models.

<p>Bold denotes significant association (<i>p</i>-value_cor<0.05). MA; minor allele (+) strand, G1 vs. G2; compared groups of cases and controls, respectively, OR; odds ratio, CI; confidence interval, N; control, PCa; prostate cancer, AD; adenoma, CRC; colorectal cancer, F; female, M; male.</p>a<p>^/SNP identifier based on NCBI SNP database;</p>b<p>^/NCBI ID of genes localized in proximity to the SNPs of interest (source: HapMap).</p

Group statistics of the GWAS and the replication study cohorts.

<p>The GWAS validation panel indicates numbers of patients (N) enrolled in the GWAS, after excluding microarrays that did not meet quality control criteria based on the PCA results. The ‘Range’ and ‘Median’ values regard age of cases and controls in respective groups. Both GWAS validation and replication analyses were done using respective individual patient TaqMan® genotyping. The TaqMan® genotyping data was subjected to a quality filtration using the 5% threshold of per-individual maximum genotype missingness (see ‘<i>Statistical analyses – individual genotyping</i>’).</p

Meta-analysis of previously reported PCa and CRC associations including replication results from the present study.

a<p>^/SNP identifier based on NCBI SNP database;</p>b<p>^/meta-analysis was done for minor allele (MA).</p

The GWAS-selected SNPs association with AD, CRC or PCa, considering allelic and additive models.

<p>Bold denotes significant association (<i>p</i><0.05). G1 vs. G2; compared groups of cases and controls, respectively, MA; minor allele (+) strand, F1, F2; frequency of MA in the case and control groups, respectively, OR; odds ratio, CI; confidence interval, N; control, PCa; prostate cancer, AD; adenoma, CRC; colorectal cancer, F; female, M; male.</p>a<p>^/SNP identifier based on NCBI SNP database;</p>b<p>^/NCBI ID of genes localized in proximity to the SNPs of interest (source: HapMap).</p

A – Closure of cutaneous wounds in the HO-1^+/+ wild type and HO-1^Tg mice.

<p>Each bar represents mean+SD. N = 10 animals per group. * P<0.05, ** P<0.01, *** P<0.001 in comparison to HO-1^+/+ mice. B – Representative pictures demonstrating CD31 staining of endothelial cells in the wounded skin (3 days after wounding) in the 3-month old mice of different genotypes. Scale bar = 100 µm. C – Number of vessels in wounded skin (3 days after wounding, CD31 staining) in the 3-month old mice of different genotypes. Each bar represents analysis of samples from 5–8 animals. Data are presented as mean+SD. * P<0.05 in comparison to HO-1^+/+ animals.</p

Effect of SnPPIX (10 µmol/L) on time of gap closure by HaCaT cells cultured <i>in vitro</i> in the presence of hydroxyurea (10 mmol/L).

<p>Scratch assay. A – Quantitative data. Each point represents mean±SD of 3 experiments done in duplicates. * P<0.05 in comparison to control. B – representative pictures. Scale bar = 200 µm.</p

Effect of HO-1 transgene delivery on wounds.

<p>A – Effect of HO-1 transgene delivery on wound closure in the db/db diabetic mice. Adenoviral vectors (2.3×10⁷ IU in 100 µL of PBS) were injected subcutaneously near the wound immediately after injury. Control animal were injected with the same amount of AdGFP carriers. Each bar represents mean+SD; N = 5–8 animals per group. * P<0.05 in comparison to control, AdGFP treated mice. B – representative pictures showing blood vessels in the wounded skin of db/db mice injected with AdHO-1 or AdGFP vectors. CD31 staining of the skin cross-section. Scale bar = 100 µm. C – Number of vessels in wounded skin in the db/db mice injected with AdHO-1 or AdGFP, on the 3^rd and 14^th days after wounding. Analysis of specimens stained for CD31 to visualize endothelial cells. Each bar represents mean+SD values for 5–8 animals. * P<0.05 in comparison to control, AdGFP injected animals.</p

Pooled-DNA allelotyping GWAS and technical validation of GWAS selections using individual patient TaqMan genotyping.

<p>Technical validation was performed by individual typing of DNA samples from the same study cohorts used for pooled-DNA GWAS. The allele frequency distribution and χ²-test <i>p</i>-values were taken into account. G1 vs. G2; compared groups of cases and controls, respectively, MA; minor allele (+) strand, F1, F2; frequency of MA in the case and control groups, respectively, OR; odds ratio, CI; confidence interval, N; control, PCa; prostate cancer, AD; adenoma, CRC; colorectal cancer, F; female, M; male.</p>a<p>^/SNP identifier based on NCBI SNP database;</p>b<p>^/SNP identified in two independent comparisons.</p