What was retained? The assessment of the training for the peer trainers' course on short and long term basis

<p>Abstract</p> <p>Background</p> <p>In Turkey, the studies have reported that the age at which sexual intercourse and sexual activity starts has been steadily declining. There is an urgent need to increase social and health services for young people in order to provide them with a healthy life by changing their risky behaviors, avoiding unwanted pregnancies and sexually transmitted diseases (STDs). Sexual and reproductive health training particularly for adolescents warrants special attention and consideration.</p> <p>The objective of our study is to find out the short and long term effectiveness of a training course on peer education.</p> <p>Methods</p> <p>The study was conducted on 237 students who participated in a 40 hour Peer Trainer Training course. We utilized two types of evaluation methods to measure the effectiveness of the training on students' knowledge and attitude. The first method consisted of administering 3 tests comprised of the same 45 questions at 3 separate time intervals. Prior to the training a pre-test was given to obtain a measurement of base knowledge, and then an immediate post-test was given to evaluate the change in the knowledge and opinion of the participants.</p> <p>Finally, 6 months later the same test was administered to measure the retention of knowledge by the students. In the second type of evaluation, the participants' assessment of the training itself was sought by asking them to complete a Short Course Evaluation Form. We utilized SPSS 12.0 for descriptive analysis, and the Wilcoxon two related sample t-test were run.</p> <p>Results</p> <p>According to the pre and immediate post-test results, the training resulted in an increase in knowledge learned by an average of 21.6% (p < 0.05). Whereas, according to the immediate post test and the late post-test which was given six month later, there was a 1.8% decrease in the knowledge and attitude of the participants (p > 0.05). Participants thought that they had fun during training, and they became aware of what they knew and what they did not know.</p> <p>Conclusion</p> <p>Peer trainers with the training methods utilized, the knowledge and counseling acquired during training sessions will be able to provide counseling to their peers on reproductive health.</p

Retrospective evaluation of whole exome and genome mutation calls in 746 cancer samples

Funder: NCI U24CA211006Abstract: The Cancer Genome Atlas (TCGA) and International Cancer Genome Consortium (ICGC) curated consensus somatic mutation calls using whole exome sequencing (WES) and whole genome sequencing (WGS), respectively. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2,658 cancers across 38 tumour types, we compare WES and WGS side-by-side from 746 TCGA samples, finding that ~80% of mutations overlap in covered exonic regions. We estimate that low variant allele fraction (VAF < 15%) and clonal heterogeneity contribute up to 68% of private WGS mutations and 71% of private WES mutations. We observe that ~30% of private WGS mutations trace to mutations identified by a single variant caller in WES consensus efforts. WGS captures both ~50% more variation in exonic regions and un-observed mutations in loci with variable GC-content. Together, our analysis highlights technological divergences between two reproducible somatic variant detection efforts

<span style="font-size:20.0pt;mso-bidi-font-size:14.0pt; line-height:115%;font-family:"Times New Roman","serif";mso-fareast-font-family: "Times New Roman";color:black;mso-ansi-language:EN-US;mso-fareast-language: EN-US;mso-bidi-language:AR-SA">Depurination of ribosomal RNA and inhibition of viral RNA translation by an antiviral protein of <i><span style="font-size:20.5pt;mso-bidi-font-size:14.5pt;line-height:115%;font-family: "Times New Roman","serif";mso-fareast-font-family:"Times New Roman";color:black; mso-ansi-language:EN-US;mso-fareast-language:EN-US;mso-bidi-language:AR-SA">Celosia cristata</span></i></span>

1195-1197<span style="font-size: 14.0pt;mso-bidi-font-size:8.0pt;font-family:" times="" new="" roman","serif";="" color:black"="">An antiviral protein (25 kD) isolated from leaves of Celosia cristata <span style="font-size:14.0pt; mso-bidi-font-size:8.0pt;font-family:" times="" new="" roman","serif";color:black"="">(CCP 25) was tested for depurination study on ribosomal RNA from yeast. Ribosomal RNA yielded 360 nucleotide base fragment after treatment with CCP 25 indicating that CCP 25 was a ribosome inactivating protein. CCP 25 also inhibited translation of brome mosaic virus (BMV) and pokeweed mosaic virus (PMV) RNAs in rabbit reticulocyte translation system. The radioactive assay showed that incorporation <span style="font-size: 14.0pt;mso-bidi-font-size:8.0pt;font-family:" times="" new="" roman","serif";="" color:black"="">of  [35S]-methionine was less in translation proteins of BMV nucleic acid when CCP 25 was added to translation system. This indicated that antiviral protein from Celosia cristata <span style="font-size:14.0pt; mso-bidi-font-size:8.0pt;font-family:" times="" new="" roman","serif";color:black"="">not only depurinated ribosomal RNA but also inhibited translation of  viral RNA <span style="font-size: 14.5pt;mso-bidi-font-size:8.5pt;font-family:" times="" new="" roman","serif";="" color:black"="">in vitro. </span

Sex differences in oncogenic mutational processes

Funder: Canadian Network for Research and Innovation in Machining Technology, Natural Sciences and Engineering Research Council of Canada (NSERC Canadian Network for Research and Innovation in Machining Technology); doi: https://doi.org/10.13039/501100002790Funder: Genome Canada (Génome Canada); doi: https://doi.org/10.13039/100008762Funder: Canada Foundation for Innovation (Fondation canadienne pour l'innovation); doi: https://doi.org/10.13039/501100000196Funder: Terry Fox Research Institute (Institut de Recherche Terry Fox); doi: https://doi.org/10.13039/501100004376Abstract: Sex differences have been observed in multiple facets of cancer epidemiology, treatment and biology, and in most cancers outside the sex organs. Efforts to link these clinical differences to specific molecular features have focused on somatic mutations within the coding regions of the genome. Here we report a pan-cancer analysis of sex differences in whole genomes of 1983 tumours of 28 subtypes as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium. We both confirm the results of exome studies, and also uncover previously undescribed sex differences. These include sex-biases in coding and non-coding cancer drivers, mutation prevalence and strikingly, in mutational signatures related to underlying mutational processes. These results underline the pervasiveness of molecular sex differences and strengthen the call for increased consideration of sex in molecular cancer research

Sex differences in oncogenic mutational processes

Sex differences have been observed in multiple facets of cancer epidemiology, treatment and biology, and in most cancers outside the sex organs. Efforts to link these clinical differences to specific molecular features have focused on somatic mutations within the coding regions of the genome. Here we report a pan-cancer analysis of sex differences in whole genomes of 1983 tumours of 28 subtypes as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium. We both confirm the results of exome studies, and also uncover previously undescribed sex differences. These include sex-biases in coding and non-coding cancer drivers, mutation prevalence and strikingly, in mutational signatures related to underlying mutational processes. These results underline the pervasiveness of molecular sex differences and strengthen the call for increased consideration of sex in molecular cancer research.Sex differences have been observed in multiple facets of cancer epidemiology, treatment and biology, and in most cancers outside the sex organs. Efforts to link these clinical differences to specific molecular features have focused on somatic mutations within the coding regions of the genome. Here we report a pan-cancer analysis of sex differences in whole genomes of 1983 tumours of 28 subtypes as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium. We both confirm the results of exome studies, and also uncover previously undescribed sex differences. These include sex-biases in coding and non-coding cancer drivers, mutation prevalence and strikingly, in mutational signatures related to underlying mutational processes. These results underline the pervasiveness of molecular sex differences and strengthen the call for increased consideration of sex in molecular cancer research.Peer reviewe

Retrospective evaluation of whole exome and genome mutation calls in 746 cancer samples

Funder: NCI U24CA211006Abstract: The Cancer Genome Atlas (TCGA) and International Cancer Genome Consortium (ICGC) curated consensus somatic mutation calls using whole exome sequencing (WES) and whole genome sequencing (WGS), respectively. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2,658 cancers across 38 tumour types, we compare WES and WGS side-by-side from 746 TCGA samples, finding that ~80% of mutations overlap in covered exonic regions. We estimate that low variant allele fraction (VAF < 15%) and clonal heterogeneity contribute up to 68% of private WGS mutations and 71% of private WES mutations. We observe that ~30% of private WGS mutations trace to mutations identified by a single variant caller in WES consensus efforts. WGS captures both ~50% more variation in exonic regions and un-observed mutations in loci with variable GC-content. Together, our analysis highlights technological divergences between two reproducible somatic variant detection efforts

Retrospective evaluation of whole exome and genome mutation calls in 746 cancer samples

The Cancer Genome Atlas (TCGA) and International Cancer Genome Consortium (ICGC) curated consensus somatic mutation calls using whole exome sequencing (WES) and whole genome sequencing (WGS), respectively. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2,658 cancers across 38 tumour types, we compare WES and WGS side-by-side from 746 TCGA samples, finding that ~80% of mutations overlap in covered exonic regions. We estimate that low variant allele fraction (VAF < 15%) and clonal heterogeneity contribute up to 68% of private WGS mutations and 71% of private WES mutations. We observe that ~30% of private WGS mutations trace to mutations identified by a single variant caller in WES consensus efforts. WGS captures both ~50% more variation in exonic regions and un-observed mutations in loci with variable GC-content. Together, our analysis highlights technological divergences between two reproducible somatic variant detection efforts.The Cancer Genome Atlas (TCGA) and International Cancer Genome Consortium (ICGC) curated consensus somatic mutation calls using whole exome sequencing (WES) and whole genome sequencing (WGS), respectively. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2,658 cancers across 38 tumour types, we compare WES and WGS side-by-side from 746 TCGA samples, finding that -80% of mutations overlap in covered exonic regions. We estimate that low variant allele fraction (VAFPeer reviewe