cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.8325434
title: DNA methyltransferase inhibition reduces inflammation-induced colon tumorigenesis

description: Chronic inflammation is strongly associated with an increased risk of developing colorectal cancer. DNA hypermethylation of CpG islands alters the expression of genes in cancer cells and plays an important role in carcinogenesis. Chronic inflammation is also associated with DNA methylation alterations and in a mouse model of inflammation-induced colon tumorigenesis, we previously demonstrated that inflammation-induced tumours have 203 unique regions with DNA hypermethylation compared to uninflamed epithelium. To determine if altering inflammation-induced DNA hypermethylation reduces tumorigenesis, we used the same mouse model and treated mice with the DNA methyltransferase (DNMT) inhibitor decitabine (DAC) throughout the tumorigenesis time frame. DAC treatment caused a significant reduction in colon tumorigenesis. The tumours that did form after DAC treatment had reduced inflammation-specific DNA hypermethylation and alteration of expression of associated candidate genes. When compared, inflammation-induced tumours from control (PBS-treated) mice were enriched for cell proliferation associated gene expression pathways whereas inflammation-induced tumours from DAC-treated mice were enriched for interferon gene signatures. To further understand the altered tumorigenesis, we derived tumoroids from the different tumour types. Interestingly, tumoroids derived from inflammation-induced tumours from control mice maintained many of the inflammation-induced DNA hypermethylation alterations and had higher levels of DNA hypermethylation at these regions than tumoroids from DAC-treated mice. Importantly, tumoroids derived from inflammation-induced tumours from the DAC-treated mice proliferated more slowly than those derived from the inflammation-induced tumours from control mice. These studies suggest that inhibition of inflammation-induced DNA hypermethylation may be an effective strategy to reduce inflammation-induced tumorigenesis.
DOI: 10.6084/m9.figshare.8325533.v1
title: AIRS

description: AIRS
DOI: 10.6084/m9.figshare.8325533.v3
title: AIRS-D2

description: AIRS
DOI: 10.6084/m9.figshare.8325434.v2
title: DNA methyltransferase inhibition reduces inflammation-induced colon tumorigenesis

description: Chronic inflammation is strongly associated with an increased risk of developing colorectal cancer. DNA hypermethylation of CpG islands alters the expression of genes in cancer cells and plays an important role in carcinogenesis. Chronic inflammation is also associated with DNA methylation alterations and in a mouse model of inflammation-induced colon tumorigenesis, we previously demonstrated that inflammation-induced tumours have 203 unique regions with DNA hypermethylation compared to uninflamed epithelium. To determine if altering inflammation-induced DNA hypermethylation reduces tumorigenesis, we used the same mouse model and treated mice with the DNA methyltransferase (DNMT) inhibitor decitabine (DAC) throughout the tumorigenesis time frame. DAC treatment caused a significant reduction in colon tumorigenesis. The tumours that did form after DAC treatment had reduced inflammation-specific DNA hypermethylation and alteration of expression of associated candidate genes. When compared, inflammation-induced tumours from control (PBS-treated) mice were enriched for cell proliferation associated gene expression pathways whereas inflammation-induced tumours from DAC-treated mice were enriched for interferon gene signatures. To further understand the altered tumorigenesis, we derived tumoroids from the different tumour types. Interestingly, tumoroids derived from inflammation-induced tumours from control mice maintained many of the inflammation-induced DNA hypermethylation alterations and had higher levels of DNA hypermethylation at these regions than tumoroids from DAC-treated mice. Importantly, tumoroids derived from inflammation-induced tumours from the DAC-treated mice proliferated more slowly than those derived from the inflammation-induced tumours from control mice. These studies suggest that inhibition of inflammation-induced DNA hypermethylation may be an effective strategy to reduce inflammation-induced tumorigenesis.
DOI: 10.6084/m9.figshare.8325443.v2
title: Avian influenza H9N2 subtype in Ghana: virus characterization and evidence of co-infection

description: Between November 2017 and February 2018, Ghanaian poultry producers reported to animal health authorities a dramatic increase in mortality rate and a relevant drop in egg production in several layer hen farms. Laboratory investigations revealed that the farms had been infected by the H9N2 influenza subtype. Virological and molecular characterization of the viruses identified in Ghana is described here for the first time. Whole genome analysis showed that the viruses belong to the G1-lineage and cluster with viruses identified in North and West Africa. The low pathogenicity of the virus was confirmed by the intravenous pathogenicity index assay. Further investigations revealed co-infection with infectious bronchitis virus of the GI-19 lineage, which very likely explained the severity of the disease observed during the outbreaks. The H9N2 outbreaks in Ghana highlight the importance of performing a differential diagnosis and an in-depth characterization of emerging viruses. In addition, the detection of a potentially zoonotic subtype, such as the H9N2, in a region where highly pathogenic avian influenza H5Nx is currently circulating highlights the urgency of implementing enhanced monitoring strategies and supporting improved investments in regional diagnostic technologies. <b>RESEARCH HIGHLIGHTS</b>Influenza A H9N2 subtype was detected in layer hens in Ghana in 2017–2018Whole genome characterization of seven H9N2 viruses was performedPhylogenetic trees revealed that the H9N2 viruses belong to the G1 lineageThe HA protein possesses the amino acid mutations 226L and 155TCo-infection with infectious bronchitis virus of the GI-19 lineage was identified Influenza A H9N2 subtype was detected in layer hens in Ghana in 2017–2018 Whole genome characterization of seven H9N2 viruses was performed Phylogenetic trees revealed that the H9N2 viruses belong to the G1 lineage The HA protein possesses the amino acid mutations 226L and 155T Co-infection with infectious bronchitis virus of the GI-19 lineage was identified
DOI: 10.6084/m9.figshare.8325434.v1
title: DNA methyltransferase inhibition reduces inflammation-induced colon tumorigenesis

description: Chronic inflammation is strongly associated with an increased risk of developing colorectal cancer. DNA hypermethylation of CpG islands alters the expression of genes in cancer cells and plays an important role in carcinogenesis. Chronic inflammation is also associated with DNA methylation alterations and in a mouse model of inflammation-induced colon tumorigenesis, we previously demonstrated that inflammation-induced tumours have 203 unique regions with DNA hypermethylation compared to uninflamed epithelium. To determine if altering inflammation-induced DNA hypermethylation reduces tumorigenesis, we used the same mouse model and treated mice with the DNA methyltransferase (DNMT) inhibitor decitabine (DAC) throughout the tumorigenesis time frame. DAC treatment caused a significant reduction in colon tumorigenesis. The tumours that did form after DAC treatment had reduced inflammation-specific DNA hypermethylation and alteration of expression of associated candidate genes. When compared, inflammation-induced tumours from control (PBS-treated) mice were enriched for cell proliferation associated gene expression pathways whereas inflammation-induced tumours from DAC-treated mice were enriched for interferon gene signatures. To further understand the altered tumorigenesis, we derived tumoroids from the different tumour types. Interestingly, tumoroids derived from inflammation-induced tumours from control mice maintained many of the inflammation-induced DNA hypermethylation alterations and had higher levels of DNA hypermethylation at these regions than tumoroids from DAC-treated mice. Importantly, tumoroids derived from inflammation-induced tumours from the DAC-treated mice proliferated more slowly than those derived from the inflammation-induced tumours from control mice. These studies suggest that inhibition of inflammation-induced DNA hypermethylation may be an effective strategy to reduce inflammation-induced tumorigenesis.
DOI: 10.6084/m9.figshare.8325533.v2
title: AIRS-D1

description: AIRS
DOI: 10.6084/m9.figshare.8325443.v1
title: Avian influenza H9N2 subtype in Ghana: virus characterization and evidence of co-infection

description: Between November 2017 and February 2018, Ghanaian poultry producers reported to animal health authorities a dramatic increase in mortality rate and a relevant drop in egg production in several layer hen farms. Laboratory investigations revealed that the farms had been infected by the H9N2 influenza subtype. Virological and molecular characterization of the viruses identified in Ghana is described here for the first time. Whole genome analysis showed that the viruses belong to the G1-lineage and cluster with viruses identified in North and West Africa. The low pathogenicity of the virus was confirmed by the intravenous pathogenicity index assay. Further investigations revealed co-infection with infectious bronchitis virus of the GI-19 lineage, which very likely explained the severity of the disease observed during the outbreaks. The H9N2 outbreaks in Ghana highlight the importance of performing a differential diagnosis and an in-depth characterization of emerging viruses. In addition, the detection of a potentially zoonotic subtype, such as the H9N2, in a region where highly pathogenic avian influenza H5Nx is currently circulating highlights the urgency of implementing enhanced monitoring strategies and supporting improved investments in regional diagnostic technologies. RESEARCH HIGHLIGHTSInfluenza A H9N2 subtype was detected in layer hens in Ghana in 2017–2018Whole genome characterization of seven H9N2 viruses was performedPhylogenetic trees revealed that the H9N2 viruses belong to the G1 lineageThe HA protein possesses the amino acid mutations 226L and 155TCo-infection with infectious bronchitis virus of the GI-19 lineage was identified Influenza A H9N2 subtype was detected in layer hens in Ghana in 2017–2018 Whole genome characterization of seven H9N2 viruses was performed Phylogenetic trees revealed that the H9N2 viruses belong to the G1 lineage The HA protein possesses the amino acid mutations 226L and 155T Co-infection with infectious bronchitis virus of the GI-19 lineage was identified
DOI: 10.6084/m9.figshare.8325389
title: Supplementary Material for: The Specific Organism: Not Bacterial Gram Type: Drives the Inflammatory Response in Septic Shock

description: <b><i>Background and Hypothesis:</i></b> The inflammatory response was targeted by unsuccessful therapies but ignored pathogen. We hypothesized that the inflammatory response differs according to organism in human septic shock. <b><i>Materials and Methods:</i></b> We measured 39 cytokines at baseline and 24 h in patients (<i>n</i> = 363) in the Vasopressin and Septic Shock Trial (VASST). We compared cytokine profiles (cytokine functional class) at baseline and at 24 h by organism and used hierarchical clustering to classify cytokines according to 28-day outcomes. <b><i>Results:</i></b> In 363 patients, 88 and 176 patients had at least 1 species isolated from blood and other sites, respectively. Cytokine levels differed significantly according to organism: <i>Neisseria meningitidis</i> and <i>Streptococcus pneumoniae</i> had the highest (baseline and at 24 h), while <i>Enterococcus faecalis</i> (blood) had the lowest mean cytokine levels. <i>N. meningitidis</i> and <i>Klebsiella pneumoniae</i> had significantly higher cytokine levels at baseline versus 24 h (<i>p</i> = 0.01 and 0.02, respectively); <i>E. faecalis</i> had significantly higher cytokine levels at 24 h versus baseline. Hierarchical clustering heat maps showed that pathogens elicited similar cytokine responses not related to the functional cytokine class. <b><i>Conclusion:</i></b> The organism type induces different cytokine profiles in septic shock. Specific gram-positive and gram-negative pathogens stimulated similar plasma cytokine-level patterns.
DOI: 10.6084/m9.figshare.8325362
title: Supplementary Material for: Evaluation of Electrocardiographic Parameters Predicting Cardiovascular Events in Patients with End-Stage Renal Disease before and after Transplantation

description: <b><i>Background and Objectives:</i></b> Cardiovascular (CV) mortality represents the leading cause of death in patients with end-stage renal disease (ESRD). Efficient screening is required to detect CV disease at an early stage, but the best diagnostic work-up is uncertain. The aim of this study was to identify electrocardiographic parameters in dialysis patients associated with an increased frequency of CV events. <b><i>Methods:</i></b> A 12-lead electrocardiogram was performed in 139 patients who were on the renal transplant waiting list and who subsequently received a kidney transplant. CV events were analyzed from the day of listing for kidney transplantation until 1 year after renal transplantation. <b><i>Results:</i></b> Multivariate Cox regression analysis showed that an elevated T:R ratio in anterior and inferior leads was independently associated with CV events (T:R ratio of anterior leads hazard ratio [HR] 1.32 [95% CI 1.09–1.59; <i>p</i> = 0.004] and inferior leads HR 2.15 [95% CI 1.23–3.77; <i>p</i> = 0.008]). In particular, a T:R ratio in inferior leads exceeding 0.6 was associated with CV events in a Kaplan-Meier analysis. <b><i>Conclusions:</i></b> Taken together, we found an increased T:R ratio in ESRD patients to be a predictive marker for CV events.
DOI: 10.6084/m9.figshare.8325362.v1
title: Supplementary Material for: Evaluation of Electrocardiographic Parameters Predicting Cardiovascular Events in Patients with End-Stage Renal Disease before and after Transplantation

description: <b><i>Background and Objectives:</i></b> Cardiovascular (CV) mortality represents the leading cause of death in patients with end-stage renal disease (ESRD). Efficient screening is required to detect CV disease at an early stage, but the best diagnostic work-up is uncertain. The aim of this study was to identify electrocardiographic parameters in dialysis patients associated with an increased frequency of CV events. <b><i>Methods:</i></b> A 12-lead electrocardiogram was performed in 139 patients who were on the renal transplant waiting list and who subsequently received a kidney transplant. CV events were analyzed from the day of listing for kidney transplantation until 1 year after renal transplantation. <b><i>Results:</i></b> Multivariate Cox regression analysis showed that an elevated T:R ratio in anterior and inferior leads was independently associated with CV events (T:R ratio of anterior leads hazard ratio [HR] 1.32 [95% CI 1.09–1.59; <i>p</i> = 0.004] and inferior leads HR 2.15 [95% CI 1.23–3.77; <i>p</i> = 0.008]). In particular, a T:R ratio in inferior leads exceeding 0.6 was associated with CV events in a Kaplan-Meier analysis. <b><i>Conclusions:</i></b> Taken together, we found an increased T:R ratio in ESRD patients to be a predictive marker for CV events.
DOI: 10.6084/m9.figshare.8325347
title: Additional file 3.xls

description: Interproscan domains in <i>Aspergillus flavus </i>TERIBR1
DOI: 10.6084/m9.figshare.8325338
title: Additional file 1.xls

description: Length of scaffolds in genomic assembly of <i>A. flavus</i> TERIBR1
DOI: 10.6084/m9.figshare.8325347.v1
title: Additional file 3.xls

description: Interproscan domains in <i>Aspergillus flavus </i>TERIBR1
DOI: 10.6084/m9.figshare.8325335
title: Additional file 2.xls

description: <i>Aspergillus flavus</i> genome completeness statistics based on 248 CEGs.
DOI: 10.6084/m9.figshare.8325338.v1
title: Additional file 1.xls

description: Length of scaffolds in genomic assembly of <i>A. flavus</i> TERIBR1
DOI: 10.6084/m9.figshare.8325335.v1
title: Additional file 2.xls

description: <i>Aspergillus flavus</i> genome completeness statistics based on 248 CEGs.
DOI: 10.6084/m9.figshare.8325206
title: Supplementary Material for: HPV Infection Downregulates the Expression of Autophagy-Related Genes in Condylomata Acuminata

description: <b><i>Background:</i></b> Condylomata acuminata are benign anogenital warts caused by human papillomavirus (HPV) infection with a high recurrence rate. Autophagy plays an important role in maintaining internal environmental stability. However, the role of autophagy regulation in the anogenital warts caused by HPV infection remains unknown. <b><i>Objective:</i></b> A multigroup case-control study was designed to identify the autophagy gene fingerprint involved in anogenital warts arising from infections with different HPV genotypes. <b><i>Methods:</i></b> Human autophagy PCR arrays were performed on the initial 18 participants grouped by their different HPV genotypes for gene expression-profiling analysis. The negative control was skin samples collected during plastic surgery on the chest from a group of individuals who showed none of the clinical symptoms or evidence of HPV infection. Real-time polymerase chain reaction (qPCR) was performed to validate the microarray results in another 24 individuals. <b><i>Results:</i></b> Out of 84 genes involved in autophagy, different autophagic responses were found among the 29 genes that encode autophagy machinery components, and expression levels of 13 of these genes were downregulated. Finally, we verified that the expression levels of 2 key genes that participate in the formation of autophagosomes, ATG3 and ­BECLIN1, were downregulated in the HPV infection groups independently of genotype compared with the control group. <b><i>Conclusions:</i></b> These findings showed that HPV infection downregulated the expression of ATGs in CA. Additionally, there were no differences in the expression of ATGs between the different HPV genotype infection groups. This study provided new insights into the autophagic response to HPV infection.
DOI: 10.6084/m9.figshare.8325182
title: Supplementary Material for: Extract of<b><i> Helicobacter pylori</i></b> Ameliorates Parameters of Airway Inflammation and Goblet Cell Hyperplasia following Repeated Allergen Exposure

description: <b><i>Background:</i></b> An inverse relation between <i>Helicobacter pylori</i> infection and asthma has been shown in epidemiological studies. Infection with <i>H. pylori</i>, or application of an extract of it before or after sensitization, inhibits allergic airway disease in mice. <b><i>Objectives:</i></b> The aim of this study was to investigate the effect of an extract of <i>H. pylori</i> on allergic airway disease induced by repeated allergen exposure in mice that were sensitized and challenged prior to extract application. <b><i>Method:</i></b> C57BL/6 mice were intranasally (i.n.) sensitized and challenged with house dust mite (HDM). After a minimum of 4 weeks, mice received the <i>H. pylori</i> extract intraperitoneally and were rechallenged i.n. with HDM. Allergen-specific antibodies were measured by ELISA. Cells present in the bronchoalveolar lavage fluid and dendritic cell (DC) subsets in the lung tissue were analyzed by flow cytometry. Tissue inflammation and goblet cell hyperplasia were assessed by histology. Cells of the mediastinal lymph node (mLN) were isolated and in vitro restimulated with HDM or <i>H. pylori</i> extract. <b><i>Results:</i></b> Treatment with <i>H. pylori</i> extract before rechallenge reduced allergen-specific IgE, the DC numbers in the tissue, and goblet cell hyperplasia. Cells isolated from mLN of mice treated with the extract produced significantly more IL-10 and IL-17 after in vitro restimulation with HDM. mLN cells of <i>H. pylori-</i>treated mice that were re-exposed to the <i>H. pylori</i> extract produced significantly more interferon gamma. <b><i>Conclusions:</i></b> An extract of <i>H. pylori</i> is effective in reducing mucus production and various features of inflammation in HDM rechallenged mice.
DOI: 10.6084/m9.figshare.8325206.v1
title: Supplementary Material for: HPV Infection Downregulates the Expression of Autophagy-Related Genes in Condylomata Acuminata

description: <b><i>Background:</i></b> Condylomata acuminata are benign anogenital warts caused by human papillomavirus (HPV) infection with a high recurrence rate. Autophagy plays an important role in maintaining internal environmental stability. However, the role of autophagy regulation in the anogenital warts caused by HPV infection remains unknown. <b><i>Objective:</i></b> A multigroup case-control study was designed to identify the autophagy gene fingerprint involved in anogenital warts arising from infections with different HPV genotypes. <b><i>Methods:</i></b> Human autophagy PCR arrays were performed on the initial 18 participants grouped by their different HPV genotypes for gene expression-profiling analysis. The negative control was skin samples collected during plastic surgery on the chest from a group of individuals who showed none of the clinical symptoms or evidence of HPV infection. Real-time polymerase chain reaction (qPCR) was performed to validate the microarray results in another 24 individuals. <b><i>Results:</i></b> Out of 84 genes involved in autophagy, different autophagic responses were found among the 29 genes that encode autophagy machinery components, and expression levels of 13 of these genes were downregulated. Finally, we verified that the expression levels of 2 key genes that participate in the formation of autophagosomes, ATG3 and ­BECLIN1, were downregulated in the HPV infection groups independently of genotype compared with the control group. <b><i>Conclusions:</i></b> These findings showed that HPV infection downregulated the expression of ATGs in CA. Additionally, there were no differences in the expression of ATGs between the different HPV genotype infection groups. This study provided new insights into the autophagic response to HPV infection.
DOI: 10.6084/m9.figshare.8325110
title: 01. Komposisi Responden

description: Pada tahun ini, Creative Commons Indonesia (CCID) sudah menginjak tahun kedelapan sebagai salah satu perwakilan lokal resmi Creative Commons International (CC HQ). Hingga saat ini, terhitung sebanyak 34 lokakarya telah terselenggara dan lebih dari 500.000 konten (termasuk artikel-artikel Wikipedia Bahasa Indonesia) yang menerapkan lisensi Creative Commons (CC) di Indonesia. Kami ingin mengetahui kaitan angka-angka tersebut dengan pengetahuan hak cipta dan lisensi CC, khususnya bagi pengguna internet di Indonesia. <br>Survei ini merupakan cara kami untuk memperoleh gambaran awal perilaku dan ukuran tingkat pengetahuan dari para pengguna internet di Indonesia terkait hal-hal tersebut, serta mengetahui apakah respon-respon dalam survei memiliki keterkaitan dengan statistik jumlah ciptaan yang ada.
DOI: 10.6084/m9.figshare.8325107
title: 03. Penjelasan Pengetahuan Tentang Lisensi CC oleh Responden

description: Pada tahun ini, Creative Commons Indonesia (CCID) sudah menginjak tahun kedelapan sebagai salah satu perwakilan lokal resmi Creative Commons International (CC HQ). Hingga saat ini, terhitung sebanyak 34 lokakarya telah terselenggara dan lebih dari 500.000 konten (termasuk artikel-artikel Wikipedia Bahasa Indonesia) yang menerapkan lisensi Creative Commons (CC) di Indonesia. Kami ingin mengetahui kaitan angka-angka tersebut dengan pengetahuan hak cipta dan lisensi CC, khususnya bagi pengguna internet di Indonesia. <br>Survei ini merupakan cara kami untuk memperoleh gambaran awal perilaku dan ukuran tingkat pengetahuan dari para pengguna internet di Indonesia terkait hal-hal tersebut, serta mengetahui apakah respon-respon dalam survei memiliki keterkaitan dengan statistik jumlah ciptaan yang ada.