cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.1296110.v1
title: The St. John’s Hospital Cemetery and Environs, Cambridge: Contextualizing the Medieval Urban Dead

description: The excavation of four hundred complete and partial <i>in situ</i> burials from the Hospital of St. John the Evangelist, Cambridge, represented one of the largest medieval hospital osteoarchaeological assemblages from the British Isles. The significance of the group is enhanced by the detailed investigation of a carefully maintained network of pathways associated with the cemetery, the archaeological sequence that pre- and post-dated its use and a number of contemporary properties that were situated immediately outside its bounds. This evidence allows the cemetery to be placed within its urban context in a way that is rarely possible. The overwhelming majority of the burials were extended west-east aligned supine inhumations without grave-goods. Atypical burials included examples aligned east-west and south-north, a double burial, a prone burial and individuals buried with a jet crucifix and a brooch. Other significant finds included a nearby pit with four bodies in it, an anthropomorphic bone handle and a reused cruciform horse harness pendant. The proportion of males and females in the burial population is similar, whilst individuals who died under the age of sixteen are relatively uncommon and individuals aged under five are completely absent.
DOI: 10.6084/m9.figshare.1296151.v2
title: Data from: Molecular evolution and island colonisation

description: For details of the contents of the fileset, please see the README file.
DOI: 10.6084/m9.figshare.1296151.v3
title: Data from: Molecular evolution and island colonisation

description: For details of the contents of the fileset, please see the README file.
DOI: 10.6084/m9.figshare.1295991
title: University of Bath APCs 2014

description: This spreadsheet contains details of article processing charges (APCs) paid by the University of Bath during 2014. The data is being collected as part of Jisc's APC data collection project to address the Total Cost of Ownership of scholarly communication (https://www.jisc-collections.ac.uk/Jisc-Monitor/APC-data-collection/) and has been released with permission of the University of Bath Library.
DOI: 10.6084/m9.figshare.1295987
title: The influence of handwriting style in writer identification

description: This data is public as PLOS ONE required.
DOI: 10.6084/m9.figshare.1295949
title: plos one "Optogenetic Activation of CA1 Pyramidal Neurons at the Dorsal and Ventral Hippocampus Evokes Distinct Brain-wide Responses Revealed by Mouse fMRI"

description: post-processed fMRI time series image files
DOI: 10.6084/m9.figshare.1295991.v1
title: University of Bath APCs 2014

description: This spreadsheet contains details of article processing charges (APCs) paid by the University of Bath during 2014. The data is being collected as part of Jisc's APC data collection project to address the Total Cost of Ownership of scholarly communication (https://www.jisc-collections.ac.uk/Jisc-Monitor/APC-data-collection/) and has been released with permission of the University of Bath Library.
DOI: 10.6084/m9.figshare.1295936
title: Mr

description: This data is used to determine the prevealence and pridectors of Mental distress among University students in Northwest Ethiopia.. The data were collected by self administer questionnaire (SRQ-20)
DOI: 10.6084/m9.figshare.1295949.v1
title: plos one "Optogenetic Activation of CA1 Pyramidal Neurons at the Dorsal and Ventral Hippocampus Evokes Distinct Brain-wide Responses Revealed by Mouse fMRI"

description: post-processed fMRI time series image files
DOI: 10.6084/m9.figshare.1295586
title: OmpA redesign phage tests

description: Raw data for Supplemental Figure 2 of 2015 OmpA redesign paper. Photographs of phage susceptibility plates. On each plate are spotted eight successive tenfold dilutions of K3 phage solution. Two identical sets were spotted on each plate.
DOI: 10.6084/m9.figshare.1295516
title: Epigenetic analysis of sporadic and Lynch-associated ovarian cancers reveals histology-specific patterns of DNA methylation

description: Diagnosis and treatment of epithelial ovarian cancer is challenging due to the poor understanding of the pathogenesis of the disease. Our aim was to investigate epigenetic mechanisms in ovarian tumorigenesis and, especially, whether tumors with different histological subtypes or hereditary background (Lynch syndrome) exhibit differential susceptibility to epigenetic inactivation of growth regulatory genes. Gene candidates for epigenetic regulation were identified from the literature and by expression profiling of ovarian and endometrial cancer cell lines treated with demethylating agents. Thirteen genes were chosen for methylation-specific multiplex ligation-dependent probe amplification assays on 104 (85 sporadic and 19 Lynch syndrome-associated) ovarian carcinomas. Increased methylation (i.e., hypermethylation) of variable degree was characteristic of ovarian carcinomas relative to the corresponding normal tissues, and hypermethylation was consistently more prominent in non-serous than serous tumors for individual genes and gene sets investigated. Lynch syndrome-associated clear cell carcinomas showed the highest frequencies of hypermethylation. Among endometrioid ovarian carcinomas, lower levels of promoter methylation of <i>RSK4</i>, <i>SPARC</i>, and <i>HOXA9</i> were significantly associated with higher tumor grade; thus, the methylation patterns showed a shift to the direction of high-grade serous tumors. In conclusion, we provide evidence of a frequent epigenetic inactivation of <i>RSK4</i>, <i>SPARC</i>, <i>PROM1</i>, <i>HOXA10</i>, <i>HOXA9</i>, <i>WT1-AS</i>, <i>SFRP2</i>, <i>SFRP5</i>, <i>OPCML</i>, and MIR34B in the development of non-serous ovarian carcinomas of Lynch and sporadic origin, as compared to serous tumors. Our findings shed light on the role of epigenetic mechanisms in ovarian tumorigenesis and identify potential targets for translational applications.
DOI: 10.6084/m9.figshare.1295987.v2
title: The influence of handwriting style in writer identification

description: This data is public as PLOS ONE required.
DOI: 10.6084/m9.figshare.1295515
title: Overexpression of HOX genes is prevalent in Ewing sarcoma and is associated with altered epigenetic regulation of developmental transcription programs

description: The polycomb proteins BMI-1 and EZH2 are highly overexpressed by Ewing sarcoma (ES), a tumor of stem cell origin that is driven by EWS-ETS fusion oncogenes, most commonly EWS-FLI1. In the current study we analyzed expression of transcription programs that are controlled by polycomb proteins during embryonic development to determine if they are abnormal in ES. Our results show that polycomb target gene expression in ES deviates from normal tissues and stem cells and that, as expected, most targets are relatively repressed. However, we also discovered a paradoxical up regulation of numerous polycomb targets and these were highly enriched for homeobox (HOX) genes. Comparison of HOX profiles between malignant and non-malignant tissues revealed a distinctive HOX profile in ES, which was characterized by overexpression of posterior HOXD genes. In addition, ectopic expression of EWS-FLI1 during stem cell differentiation led to aberrant up regulation of posterior HOXD genes. Mechanistically, this up regulation was associated with altered epigenetic regulation. Specifically, ES and EWS-FLI1+ stem cells displayed a relative loss of polycomb-dependent H3K27me3 and gain of trithorax-dependent H3K4me3 at the promoters of posterior HOXD genes and also at the HOXD11.12 polycomb response element. In addition, a striking correlation was evident between <i>HOXD13</i> and other genes whose regulation is coordinately regulated during embryonic development by distal enhancer elements. Together, these studies demonstrate that epigenetic regulation of polycomb target genes, in particular HOXD genes, is altered in ES and that these changes are mediated downstream of EWS-FLI1.
DOI: 10.6084/m9.figshare.1295585
title: Properties of the elements

description: The raw file (RData binary format, use R's load() function to open) contains the properties of the elements, scraped from periodictable.com. The element-data.rda contains cleaned-up database of elemental properties, easily accessible for anyone with a working R install. The blog post in the link below describes how to use this file (see the MWE section). The csv files are ascii-formatted versions of the rda file's content.
DOI: 10.6084/m9.figshare.1295586.v1
title: OmpA redesign phage tests

description: Raw data for Supplemental Figure 2 of 2015 OmpA redesign paper. Photographs of phage susceptibility plates. On each plate are spotted eight successive tenfold dilutions of K3 phage solution. Two identical sets were spotted on each plate.
DOI: 10.6084/m9.figshare.1295987.v1
title: he influence of handwriting style in writer identification

description: T
DOI: 10.6084/m9.figshare.1295512
title: <i>OASIS/CREB3L1</i> is epigenetically silenced in human bladder cancer facilitating tumor cell spreading and migration <i>in vitro</i>

description: <i>CREB3L1</i> has been recently proposed as a novel metastasis suppressor gene in breast cancer. Our current study highlights CREB3L1 expression, regulation, and function in bladder cancer. We demonstrate a significant downregulation of <i>CREB3L1</i> mRNA expression (n = 64) in primary bladder cancer tissues caused by tumor-specific <i>CREB3L1</i> promoter hypermethylation (n = 51). Based on pyrosequencing <i>CREB3L1</i> methylation was shown to be potentially associated with a more aggressive phenotype of bladder cancer. These findings were verified by an independent public data set containing data from 184 bladder tumors. In addition, immunohistochemical evaluation showed that CREB3L1 protein expression is decreased in bladder cancer tissues as well. Interestingly, protein loss is predominately observed in the nuclei of aggressive tumor cells. Based on <i>in vitro</i> models we clearly show that CREB3L1 re-expression mediates suppression of tumor cell migration and colony growth of high grade and invasive bladder cancer cells. The candidate tumor suppressor and TGF-β signaling inhibitor HTRA3 was furthermore identified as putative target gene of CREB3L1 in both invasive J82 bladder cells and primary bladder tumors. Hence, our data provide for the first time evidence that the transcription factor CREB3L1 may have an important role as a putative tumor suppressor in bladder cancer.
DOI: 10.6084/m9.figshare.1295513
title: Aberrant CpG methylation of the <i>TFAP2A</i> gene constitutes a mechanism for loss of <i>TFAP2A</i> expression in human metastatic melanoma

description: Metastatic melanoma is a deadly treatment-resistant form of skin cancer whose global incidence is on the rise. During melanocyte transformation and melanoma progression the expression profile of many genes changes. Among these, a gene implicated in several steps of melanocyte development, <i>TFAP2A</i>, is frequently silenced; however, the molecular mechanism of <i>TFAP2A</i> silencing in human melanoma remains unknown. In this study, we measured <i>TFAP2A</i> mRNA expression in primary human melanocytes compared to 11 human melanoma samples by quantitative real-time RT-PCR. In addition, we assessed CpG DNA methylation of the <i>TFAP2A</i> promoter in these samples using bisulfite sequencing. Compared to primary melanocytes, which showed high <i>TFAP2A</i> mRNA expression and no promoter methylation, human melanoma samples showed decreased <i>TFAP2A</i> mRNA expression and increased promoter methylation. We further show that increased CpG methylation correlates with decreased <i>TFAP2A</i> mRNA expression. Using The Cancer Genome Atlas, we further identified <i>TFAP2A</i> as a gene displaying among the most decreased expression in stage 4 melanomas vs. non-stage 4 melanomas, and whose CpG methylation was frequently associated with lack of mRNA expression. Based on our data, we conclude that <i>TFAP2A</i> expression in human melanomas can be silenced by aberrant CpG methylation of the <i>TFAP2A</i> promoter. We have identified aberrant CpG DNA methylation as an epigenetic mark associated with TFAP2A silencing in human melanoma that could have significant implications for the therapy of human melanoma using epigenetic modifying drugs.
DOI: 10.6084/m9.figshare.1295516.v2
title: Epigenetic analysis of sporadic and Lynch-associated ovarian cancers reveals histology-specific patterns of DNA methylation

description: Diagnosis and treatment of epithelial ovarian cancer is challenging due to the poor understanding of the pathogenesis of the disease. Our aim was to investigate epigenetic mechanisms in ovarian tumorigenesis and, especially, whether tumors with different histological subtypes or hereditary background (Lynch syndrome) exhibit differential susceptibility to epigenetic inactivation of growth regulatory genes. Gene candidates for epigenetic regulation were identified from the literature and by expression profiling of ovarian and endometrial cancer cell lines treated with demethylating agents. Thirteen genes were chosen for methylation-specific multiplex ligation-dependent probe amplification assays on 104 (85 sporadic and 19 Lynch syndrome-associated) ovarian carcinomas. Increased methylation (i.e., hypermethylation) of variable degree was characteristic of ovarian carcinomas relative to the corresponding normal tissues, and hypermethylation was consistently more prominent in non-serous than serous tumors for individual genes and gene sets investigated. Lynch syndrome-associated clear cell carcinomas showed the highest frequencies of hypermethylation. Among endometrioid ovarian carcinomas, lower levels of promoter methylation of <i>RSK4</i>, <i>SPARC</i>, and <i>HOXA9</i> were significantly associated with higher tumor grade; thus, the methylation patterns showed a shift to the direction of high-grade serous tumors. In conclusion, we provide evidence of a frequent epigenetic inactivation of <i>RSK4</i>, <i>SPARC</i>, <i>PROM1</i>, <i>HOXA10</i>, <i>HOXA9</i>, <i>WT1-AS</i>, <i>SFRP2</i>, <i>SFRP5</i>, <i>OPCML</i>, and MIR34B in the development of non-serous ovarian carcinomas of Lynch and sporadic origin, as compared to serous tumors. Our findings shed light on the role of epigenetic mechanisms in ovarian tumorigenesis and identify potential targets for translational applications.
DOI: 10.6084/m9.figshare.1295516.v1
title: Epigenetic analysis of sporadic and Lynch-associated ovarian cancers reveals histology-specific patterns of DNA methylation

description: Diagnosis and treatment of epithelial ovarian cancer is challenging due to the poor understanding of the pathogenesis of the disease. Our aim was to investigate epigenetic mechanisms in ovarian tumorigenesis and, especially, whether tumors with different histological subtypes or hereditary background (Lynch syndrome) exhibit differential susceptibility to epigenetic inactivation of growth regulatory genes. Gene candidates for epigenetic regulation were identified from the literature and by expression profiling of ovarian and endometrial cancer cell lines treated with demethylating agents. Thirteen genes were chosen for methylation-specific multiplex ligation-dependent probe amplification assays on 104 (85 sporadic and 19 Lynch syndrome-associated) ovarian carcinomas. Increased methylation (i.e., hypermethylation) of variable degree was characteristic of ovarian carcinomas relative to the corresponding normal tissues, and hypermethylation was consistently more prominent in non-serous than serous tumors for individual genes and gene sets investigated. Lynch syndrome-associated clear cell carcinomas showed the highest frequencies of hypermethylation. Among endometrioid ovarian carcinomas, lower levels of promoter methylation of <i>RSK4</i>, <i>SPARC</i>, and <i>HOXA9</i> were significantly associated with higher tumor grade; thus, the methylation patterns showed a shift to the direction of high-grade serous tumors. In conclusion, we provide evidence of a frequent epigenetic inactivation of <i>RSK4</i>, <i>SPARC</i>, <i>PROM1</i>, <i>HOXA10</i>, <i>HOXA9</i>, <i>WT1-AS</i>, <i>SFRP2</i>, <i>SFRP5</i>, <i>OPCML</i>, and MIR34B in the development of non-serous ovarian carcinomas of Lynch and sporadic origin, as compared to serous tumors. Our findings shed light on the role of epigenetic mechanisms in ovarian tumorigenesis and identify potential targets for translational applications.
DOI: 10.6084/m9.figshare.1295515.v2
title: Overexpression of HOX genes is prevalent in Ewing sarcoma and is associated with altered epigenetic regulation of developmental transcription programs

description: The polycomb proteins BMI-1 and EZH2 are highly overexpressed by Ewing sarcoma (ES), a tumor of stem cell origin that is driven by EWS-ETS fusion oncogenes, most commonly EWS-FLI1. In the current study we analyzed expression of transcription programs that are controlled by polycomb proteins during embryonic development to determine if they are abnormal in ES. Our results show that polycomb target gene expression in ES deviates from normal tissues and stem cells and that, as expected, most targets are relatively repressed. However, we also discovered a paradoxical up regulation of numerous polycomb targets and these were highly enriched for homeobox (HOX) genes. Comparison of HOX profiles between malignant and non-malignant tissues revealed a distinctive HOX profile in ES, which was characterized by overexpression of posterior HOXD genes. In addition, ectopic expression of EWS-FLI1 during stem cell differentiation led to aberrant up regulation of posterior HOXD genes. Mechanistically, this up regulation was associated with altered epigenetic regulation. Specifically, ES and EWS-FLI1+ stem cells displayed a relative loss of polycomb-dependent H3K27me3 and gain of trithorax-dependent H3K4me3 at the promoters of posterior HOXD genes and also at the HOXD11.12 polycomb response element. In addition, a striking correlation was evident between <i>HOXD13</i> and other genes whose regulation is coordinately regulated during embryonic development by distal enhancer elements. Together, these studies demonstrate that epigenetic regulation of polycomb target genes, in particular HOXD genes, is altered in ES and that these changes are mediated downstream of EWS-FLI1.
DOI: 10.6084/m9.figshare.1295515.v1
title: Overexpression of HOX genes is prevalent in Ewing sarcoma and is associated with altered epigenetic regulation of developmental transcription programs

description: The polycomb proteins BMI-1 and EZH2 are highly overexpressed by Ewing sarcoma (ES), a tumor of stem cell origin that is driven by EWS-ETS fusion oncogenes, most commonly EWS-FLI1. In the current study we analyzed expression of transcription programs that are controlled by polycomb proteins during embryonic development to determine if they are abnormal in ES. Our results show that polycomb target gene expression in ES deviates from normal tissues and stem cells and that, as expected, most targets are relatively repressed. However, we also discovered a paradoxical up regulation of numerous polycomb targets and these were highly enriched for homeobox (HOX) genes. Comparison of HOX profiles between malignant and non-malignant tissues revealed a distinctive HOX profile in ES, which was characterized by overexpression of posterior HOXD genes. In addition, ectopic expression of EWS-FLI1 during stem cell differentiation led to aberrant up regulation of posterior HOXD genes. Mechanistically, this up regulation was associated with altered epigenetic regulation. Specifically, ES and EWS-FLI1+ stem cells displayed a relative loss of polycomb-dependent H3K27me3 and gain of trithorax-dependent H3K4me3 at the promoters of posterior HOXD genes and also at the HOXD11.12 polycomb response element. In addition, a striking correlation was evident between <i>HOXD13</i> and other genes whose regulation is coordinately regulated during embryonic development by distal enhancer elements. Together, these studies demonstrate that epigenetic regulation of polycomb target genes, in particular HOXD genes, is altered in ES and that these changes are mediated downstream of EWS-FLI1.
DOI: 10.6084/m9.figshare.1295512.v2
title: <i>OASIS/CREB3L1</i> is epigenetically silenced in human bladder cancer facilitating tumor cell spreading and migration <i>in vitro</i>

description: <i>CREB3L1</i> has been recently proposed as a novel metastasis suppressor gene in breast cancer. Our current study highlights CREB3L1 expression, regulation, and function in bladder cancer. We demonstrate a significant downregulation of <i>CREB3L1</i> mRNA expression (n = 64) in primary bladder cancer tissues caused by tumor-specific <i>CREB3L1</i> promoter hypermethylation (n = 51). Based on pyrosequencing <i>CREB3L1</i> methylation was shown to be potentially associated with a more aggressive phenotype of bladder cancer. These findings were verified by an independent public data set containing data from 184 bladder tumors. In addition, immunohistochemical evaluation showed that CREB3L1 protein expression is decreased in bladder cancer tissues as well. Interestingly, protein loss is predominately observed in the nuclei of aggressive tumor cells. Based on <i>in vitro</i> models we clearly show that CREB3L1 re-expression mediates suppression of tumor cell migration and colony growth of high grade and invasive bladder cancer cells. The candidate tumor suppressor and TGF-β signaling inhibitor HTRA3 was furthermore identified as putative target gene of CREB3L1 in both invasive J82 bladder cells and primary bladder tumors. Hence, our data provide for the first time evidence that the transcription factor CREB3L1 may have an important role as a putative tumor suppressor in bladder cancer.
DOI: 10.6084/m9.figshare.1295513.v2
title: Aberrant CpG methylation of the <i>TFAP2A</i> gene constitutes a mechanism for loss of <i>TFAP2A</i> expression in human metastatic melanoma

description: Metastatic melanoma is a deadly treatment-resistant form of skin cancer whose global incidence is on the rise. During melanocyte transformation and melanoma progression the expression profile of many genes changes. Among these, a gene implicated in several steps of melanocyte development, <i>TFAP2A</i>, is frequently silenced; however, the molecular mechanism of <i>TFAP2A</i> silencing in human melanoma remains unknown. In this study, we measured <i>TFAP2A</i> mRNA expression in primary human melanocytes compared to 11 human melanoma samples by quantitative real-time RT-PCR. In addition, we assessed CpG DNA methylation of the <i>TFAP2A</i> promoter in these samples using bisulfite sequencing. Compared to primary melanocytes, which showed high <i>TFAP2A</i> mRNA expression and no promoter methylation, human melanoma samples showed decreased <i>TFAP2A</i> mRNA expression and increased promoter methylation. We further show that increased CpG methylation correlates with decreased <i>TFAP2A</i> mRNA expression. Using The Cancer Genome Atlas, we further identified <i>TFAP2A</i> as a gene displaying among the most decreased expression in stage 4 melanomas vs. non-stage 4 melanomas, and whose CpG methylation was frequently associated with lack of mRNA expression. Based on our data, we conclude that <i>TFAP2A</i> expression in human melanomas can be silenced by aberrant CpG methylation of the <i>TFAP2A</i> promoter. We have identified aberrant CpG DNA methylation as an epigenetic mark associated with TFAP2A silencing in human melanoma that could have significant implications for the therapy of human melanoma using epigenetic modifying drugs.