cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.1385003.v2
title: data of "When a silhouette appears male: Observer's own physical fitness governs social categorization of sexually ambiguous stimuli"

description: Categorization bias in social cognition is widely observed, as it is more beneficial to commit low-risk biases in order to reduce high-risk biases. In this context, a short age of the capacity to protect oneself when at high risk of approaching potentially harmful others, and hence, physical load and low physical fitness, are considered to be disadvantageous in self-protection. Thus, we hypothesized that a low capacity to self-protect leads to a biased social categorization of others as harmful. To examine this hypothesis, silhouettes of the human body, which had a sexually dimorphic cue (waist-to-hip ratio), were presented, and participants categorized the stimuli as female or male. Participants’ basic physical fitness was measured, and we manipulated physical load by a heavy or light backpack. Physical load did not significantly influence categorization. In contrast, only female participants tended to categorize the stimuli as male as basic physical fitness increased, suggesting that basic physical fitness, not physical load, affects sex categorization for females. Our findings shed new light on the effect of fitness factors on social cognition.
DOI: 10.6084/m9.figshare.1384885
title: DYSREGULATION OF AUTONOMIC NERVOUS SYSTEM IN CHAGAS’ HEART DISEASE IS ASSOCIATED WITH ALTERED ADIPOCYTOKINE LEVELS

description: This file is the full dataset from the manuscript: DYSREGULATION OF AUTONOMIC NERVOUS SYSTEM IN CHAGAS’ HEART DISEASE IS ASSOCIATED WITH ALTERED ADIPOCYTOKINE LEVELS
DOI: 10.6084/m9.figshare.1384884
title: GitHub users in Spain: an geospatial analysis

description: Measuring and ranking the free software developers in a particular geographical space is a way<br>of knowing the existing community and also allows assessing the impact of certain policies in<br>the dynamics of such a community. Besides, it is interesting to try and find out why there are<br>differences from one place to the next and how these differences evolve with time. In this paper,<br>our main interest is to measure and rank the community of free software developers in Spain and<br>also check its geographical distribution. This paper measures differences by province, providing a<br>classification of provinces according to the number and type of developers present in each place.
DOI: 10.6084/m9.figshare.1384897.v1
title: Gaussian Job Archive for C6H6Br10

description: Archive of work produced using the resources of the Imperial College High Performance Computing Service.
DOI: 10.6084/m9.figshare.1384949.v1
title: PLOS_ONE_PONE-D-14-52198R1

description: seven UCI datasets
DOI: 10.6084/m9.figshare.1384883
title: Data from directed remembering in visual working memory replication

description: Dataset form replication of directed remembering in visual working memory.
DOI: 10.6084/m9.figshare.1384885.v1
title: DYSREGULATION OF AUTONOMIC NERVOUS SYSTEM IN CHAGAS’ HEART DISEASE IS ASSOCIATED WITH ALTERED ADIPOCYTOKINE LEVELS

description: This file is the full dataset from the manuscript: DYSREGULATION OF AUTONOMIC NERVOUS SYSTEM IN CHAGAS’ HEART DISEASE IS ASSOCIATED WITH ALTERED ADIPOCYTOKINE LEVELS
DOI: 10.6084/m9.figshare.1384857
title: E2F1 and E2F2 induction in response to DNA damage preserves genomic stability in neuronal cells

description: E2F transcription factors regulate a wide range of biological processes, including the cellular response to DNA damage. In the present study, we examined whether E2F family members are transcriptionally induced following treatment with several genotoxic agents, and have a role on the cell DNA damage response. We show a novel mechanism, conserved among diverse species, in which <i>E2F1</i> and <i>E2F2</i>, the latter specifically in neuronal cells, are transcriptionally induced after DNA damage. This upregulation leads to increased E2F1 and E2F2 protein levels as a consequence of <i>de novo</i> protein synthesis. Ectopic expression of these E2Fs in neuronal cells reduces the level of DNA damage following genotoxic treatment, while ablation of E2F1 and E2F2 leads to the accumulation of DNA lesions and increased apoptotic response. Cell viability and DNA repair capability in response to DNA damage induction are also reduced by the E2F1 and E2F2 deficiencies. Finally, E2F1 and E2F2 accumulate at sites of oxidative and UV-induced DNA damage, and interact with γH2AX DNA repair factor. As previously reported for E2F1, E2F2 promotes Rad51 foci formation, interacts with GCN5 acetyltransferase and induces histone acetylation following genotoxic insult. The results presented here unveil a new mechanism involving E2F1 and E2F2 in the maintenance of genomic stability in response to DNA damage in neuronal cells.
DOI: 10.6084/m9.figshare.1384883.v1
title: Data from directed remembering in visual working memory replication

description: Dataset form replication of directed remembering in visual working memory.
DOI: 10.6084/m9.figshare.1384885.v2
title: DYSREGULATION OF AUTONOMIC NERVOUS SYSTEM IN CHAGAS’ HEART DISEASE IS ASSOCIATED WITH ALTERED ADIPOCYTOKINE LEVELS

description: This file is the full dataset from the manuscript: DYSREGULATION OF AUTONOMIC NERVOUS SYSTEM IN CHAGAS’ HEART DISEASE IS ASSOCIATED WITH ALTERED ADIPOCYTOKINE LEVELS
DOI: 10.6084/m9.figshare.1384857.v1
title: E2F1 and E2F2 induction in response to DNA damage preserves genomic stability in neuronal cells

description: E2F transcription factors regulate a wide range of biological processes, including the cellular response to DNA damage. In the present study, we examined whether E2F family members are transcriptionally induced following treatment with several genotoxic agents, and have a role on the cell DNA damage response. We show a novel mechanism, conserved among diverse species, in which <i>E2F1</i> and <i>E2F2</i>, the latter specifically in neuronal cells, are transcriptionally induced after DNA damage. This upregulation leads to increased E2F1 and E2F2 protein levels as a consequence of <i>de novo</i> protein synthesis. Ectopic expression of these E2Fs in neuronal cells reduces the level of DNA damage following genotoxic treatment, while ablation of E2F1 and E2F2 leads to the accumulation of DNA lesions and increased apoptotic response. Cell viability and DNA repair capability in response to DNA damage induction are also reduced by the E2F1 and E2F2 deficiencies. Finally, E2F1 and E2F2 accumulate at sites of oxidative and UV-induced DNA damage, and interact with γH2AX DNA repair factor. As previously reported for E2F1, E2F2 promotes Rad51 foci formation, interacts with GCN5 acetyltransferase and induces histone acetylation following genotoxic insult. The results presented here unveil a new mechanism involving E2F1 and E2F2 in the maintenance of genomic stability in response to DNA damage in neuronal cells.
DOI: 10.6084/m9.figshare.1384885.v3
title: DYSREGULATION OF AUTONOMIC NERVOUS SYSTEM IN CHAGAS’ HEART DISEASE IS ASSOCIATED WITH ALTERED ADIPOCYTOKINE LEVELS

description: This file is the full dataset from the manuscript: DYSREGULATION OF AUTONOMIC NERVOUS SYSTEM IN CHAGAS’ HEART DISEASE IS ASSOCIATED WITH ALTERED ADIPOCYTOKINE LEVELS
DOI: 10.6084/m9.figshare.1384885.v5
title: DYSREGULATION OF AUTONOMIC NERVOUS SYSTEM IN CHAGAS’ HEART DISEASE IS ASSOCIATED WITH ALTERED ADIPOCYTOKINE LEVELS

description: This file is the full dataset from the manuscript: DYSREGULATION OF AUTONOMIC NERVOUS SYSTEM IN CHAGAS’ HEART DISEASE IS ASSOCIATED WITH ALTERED ADIPOCYTOKINE LEVELS
DOI: 10.6084/m9.figshare.1384857.v2
title: E2F1 and E2F2 induction in response to DNA damage preserves genomic stability in neuronal cells

description: E2F transcription factors regulate a wide range of biological processes, including the cellular response to DNA damage. In the present study, we examined whether E2F family members are transcriptionally induced following treatment with several genotoxic agents, and have a role on the cell DNA damage response. We show a novel mechanism, conserved among diverse species, in which <i>E2F1</i> and <i>E2F2</i>, the latter specifically in neuronal cells, are transcriptionally induced after DNA damage. This upregulation leads to increased E2F1 and E2F2 protein levels as a consequence of <i>de novo</i> protein synthesis. Ectopic expression of these E2Fs in neuronal cells reduces the level of DNA damage following genotoxic treatment, while ablation of E2F1 and E2F2 leads to the accumulation of DNA lesions and increased apoptotic response. Cell viability and DNA repair capability in response to DNA damage induction are also reduced by the E2F1 and E2F2 deficiencies. Finally, E2F1 and E2F2 accumulate at sites of oxidative and UV-induced DNA damage, and interact with γH2AX DNA repair factor. As previously reported for E2F1, E2F2 promotes Rad51 foci formation, interacts with GCN5 acetyltransferase and induces histone acetylation following genotoxic insult. The results presented here unveil a new mechanism involving E2F1 and E2F2 in the maintenance of genomic stability in response to DNA damage in neuronal cells.
DOI: 10.6084/m9.figshare.1384885.v4
title: DYSREGULATION OF AUTONOMIC NERVOUS SYSTEM IN CHAGAS’ HEART DISEASE IS ASSOCIATED WITH ALTERED ADIPOCYTOKINE LEVELS

description: This file is the full dataset from the manuscript: DYSREGULATION OF AUTONOMIC NERVOUS SYSTEM IN CHAGAS’ HEART DISEASE IS ASSOCIATED WITH ALTERED ADIPOCYTOKINE LEVELS
DOI: 10.6084/m9.figshare.1384855
title: SMAD signaling and redox imbalance cooperate to induce prostate cancer cell dormancy

description: Metastasis involves the dissemination of single or small clumps of cancer cells through blood or lymphatic vessels and their extravasation into distant organs. Despite the strong regulation of metastases development by a cell dormancy phenomenon, the dormant state of cancer cells remains poorly characterized due to the difficulty of <i>in vivo</i> studies. We have recently shown <i>in vitro</i> that clonogenicity of prostate cancer cells is regulated by a dormancy phenomenon that is strongly induced when cells are cultured both at low cell density and in a slightly hypertonic medium. Here, we characterized by RT-qPCR a genetic expression signature of this dormant state which combines the presence of both stemness and differentiation markers. We showed that both TFGβ/BMP signaling and redox imbalance are required for the full induction of this dormancy signature and cell quiescence. Moreover, reconstruction experiments showed that TFGβ/BMP signaling and redox imbalance are sufficient to generate a pattern of genetic expression displaying all characteristic features of the dormancy signature. Finally, we observed that low cell density was sufficient to activate TGFβ/BMP signaling and to generate a slight redox imbalance thus priming cells for dormancy that can be attained with a co-stimulus like hypertonicity, most likely through an increased redox imbalance. The identification of a dual regulation of dormancy provides a framework for the interpretation of previous reports showing a restricted ability of BMP signaling to regulate cancer cell dormancy <i>in vivo</i> and draws attention on the role of oxidative stress in the metastatic process.
DOI: 10.6084/m9.figshare.1384857.v3
title: E2F1 and E2F2 induction in response to DNA damage preserves genomic stability in neuronal cells

description: E2F transcription factors regulate a wide range of biological processes, including the cellular response to DNA damage. In the present study, we examined whether E2F family members are transcriptionally induced following treatment with several genotoxic agents, and have a role on the cell DNA damage response. We show a novel mechanism, conserved among diverse species, in which <i>E2F1</i> and <i>E2F2</i>, the latter specifically in neuronal cells, are transcriptionally induced after DNA damage. This upregulation leads to increased E2F1 and E2F2 protein levels as a consequence of <i>de novo</i> protein synthesis. Ectopic expression of these E2Fs in neuronal cells reduces the level of DNA damage following genotoxic treatment, while ablation of E2F1 and E2F2 leads to the accumulation of DNA lesions and increased apoptotic response. Cell viability and DNA repair capability in response to DNA damage induction are also reduced by the E2F1 and E2F2 deficiencies. Finally, E2F1 and E2F2 accumulate at sites of oxidative and UV-induced DNA damage, and interact with γH2AX DNA repair factor. As previously reported for E2F1, E2F2 promotes Rad51 foci formation, interacts with GCN5 acetyltransferase and induces histone acetylation following genotoxic insult. The results presented here unveil a new mechanism involving E2F1 and E2F2 in the maintenance of genomic stability in response to DNA damage in neuronal cells.
DOI: 10.6084/m9.figshare.12921407
title: In-tube condensation data of R454B in a horizontal 4.7 mm ID tube

description: The attached data was collected at Oregon State University in the Thermal Energy Systems and Transport (TEST) Laboratory during flow condensation experiments for refrigerants R454B. The experiments were conducted in a horizontal circular copper tube of 4.7 mm internal diameter. Water, flowing in the annulus, was used as the coolant. The local condensation heat transfer coefficients and the associated qualities for each refrigerant are reported at varying mass fluxes (100 to 500 kg m^(-2) s^(-1)) and saturation temperatures of 40, 50 and 60 degrees Celsius.<br>The test section was divided into 7 segments. Exact length of each section is recorded below and attached figure shows visual representation of a segment. Water inlet and outlet temperature and the copper tube surface temperature are measured in each segment. The surface temperatures were measured at the center of each section using self-adhesive surface thermocouples. Using these measurements, local heat transfer coefficients and thermodynamic qualities were evaluated for each segment. This was accomplished by performing energy balances on the coolant side to determine the heat duties transferred in each section.<br>Summaries of the average measured values and the calculated variables are presented in the remaining sheets of this document. For more details regarding the experiments, results, and conclusions, please see cited references.
DOI: 10.6084/m9.figshare.1384857.v5
title: E2F1 and E2F2 induction in response to DNA damage preserves genomic stability in neuronal cells

description: E2F transcription factors regulate a wide range of biological processes, including the cellular response to DNA damage. In the present study, we examined whether E2F family members are transcriptionally induced following treatment with several genotoxic agents, and have a role on the cell DNA damage response. We show a novel mechanism, conserved among diverse species, in which <i>E2F1</i> and <i>E2F2</i>, the latter specifically in neuronal cells, are transcriptionally induced after DNA damage. This upregulation leads to increased E2F1 and E2F2 protein levels as a consequence of <i>de novo</i> protein synthesis. Ectopic expression of these E2Fs in neuronal cells reduces the level of DNA damage following genotoxic treatment, while ablation of E2F1 and E2F2 leads to the accumulation of DNA lesions and increased apoptotic response. Cell viability and DNA repair capability in response to DNA damage induction are also reduced by the E2F1 and E2F2 deficiencies. Finally, E2F1 and E2F2 accumulate at sites of oxidative and UV-induced DNA damage, and interact with γH2AX DNA repair factor. As previously reported for E2F1, E2F2 promotes Rad51 foci formation, interacts with GCN5 acetyltransferase and induces histone acetylation following genotoxic insult. The results presented here unveil a new mechanism involving E2F1 and E2F2 in the maintenance of genomic stability in response to DNA damage in neuronal cells.
DOI: 10.6084/m9.figshare.1384857.v4
title: E2F1 and E2F2 induction in response to DNA damage preserves genomic stability in neuronal cells

description: E2F transcription factors regulate a wide range of biological processes, including the cellular response to DNA damage. In the present study, we examined whether E2F family members are transcriptionally induced following treatment with several genotoxic agents, and have a role on the cell DNA damage response. We show a novel mechanism, conserved among diverse species, in which <i>E2F1</i> and <i>E2F2</i>, the latter specifically in neuronal cells, are transcriptionally induced after DNA damage. This upregulation leads to increased E2F1 and E2F2 protein levels as a consequence of <i>de novo</i> protein synthesis. Ectopic expression of these E2Fs in neuronal cells reduces the level of DNA damage following genotoxic treatment, while ablation of E2F1 and E2F2 leads to the accumulation of DNA lesions and increased apoptotic response. Cell viability and DNA repair capability in response to DNA damage induction are also reduced by the E2F1 and E2F2 deficiencies. Finally, E2F1 and E2F2 accumulate at sites of oxidative and UV-induced DNA damage, and interact with γH2AX DNA repair factor. As previously reported for E2F1, E2F2 promotes Rad51 foci formation, interacts with GCN5 acetyltransferase and induces histone acetylation following genotoxic insult. The results presented here unveil a new mechanism involving E2F1 and E2F2 in the maintenance of genomic stability in response to DNA damage in neuronal cells.
DOI: 10.6084/m9.figshare.1384855.v1
title: SMAD signaling and redox imbalance cooperate to induce prostate cancer cell dormancy

description: Metastasis involves the dissemination of single or small clumps of cancer cells through blood or lymphatic vessels and their extravasation into distant organs. Despite the strong regulation of metastases development by a cell dormancy phenomenon, the dormant state of cancer cells remains poorly characterized due to the difficulty of <i>in vivo</i> studies. We have recently shown <i>in vitro</i> that clonogenicity of prostate cancer cells is regulated by a dormancy phenomenon that is strongly induced when cells are cultured both at low cell density and in a slightly hypertonic medium. Here, we characterized by RT-qPCR a genetic expression signature of this dormant state which combines the presence of both stemness and differentiation markers. We showed that both TFGβ/BMP signaling and redox imbalance are required for the full induction of this dormancy signature and cell quiescence. Moreover, reconstruction experiments showed that TFGβ/BMP signaling and redox imbalance are sufficient to generate a pattern of genetic expression displaying all characteristic features of the dormancy signature. Finally, we observed that low cell density was sufficient to activate TGFβ/BMP signaling and to generate a slight redox imbalance thus priming cells for dormancy that can be attained with a co-stimulus like hypertonicity, most likely through an increased redox imbalance. The identification of a dual regulation of dormancy provides a framework for the interpretation of previous reports showing a restricted ability of BMP signaling to regulate cancer cell dormancy <i>in vivo</i> and draws attention on the role of oxidative stress in the metastatic process.
DOI: 10.6084/m9.figshare.1384855.v2
title: SMAD signaling and redox imbalance cooperate to induce prostate cancer cell dormancy

description: Metastasis involves the dissemination of single or small clumps of cancer cells through blood or lymphatic vessels and their extravasation into distant organs. Despite the strong regulation of metastases development by a cell dormancy phenomenon, the dormant state of cancer cells remains poorly characterized due to the difficulty of <i>in vivo</i> studies. We have recently shown <i>in vitro</i> that clonogenicity of prostate cancer cells is regulated by a dormancy phenomenon that is strongly induced when cells are cultured both at low cell density and in a slightly hypertonic medium. Here, we characterized by RT-qPCR a genetic expression signature of this dormant state which combines the presence of both stemness and differentiation markers. We showed that both TFGβ/BMP signaling and redox imbalance are required for the full induction of this dormancy signature and cell quiescence. Moreover, reconstruction experiments showed that TFGβ/BMP signaling and redox imbalance are sufficient to generate a pattern of genetic expression displaying all characteristic features of the dormancy signature. Finally, we observed that low cell density was sufficient to activate TGFβ/BMP signaling and to generate a slight redox imbalance thus priming cells for dormancy that can be attained with a co-stimulus like hypertonicity, most likely through an increased redox imbalance. The identification of a dual regulation of dormancy provides a framework for the interpretation of previous reports showing a restricted ability of BMP signaling to regulate cancer cell dormancy <i>in vivo</i> and draws attention on the role of oxidative stress in the metastatic process.
DOI: 10.6084/m9.figshare.1384855.v3
title: SMAD signaling and redox imbalance cooperate to induce prostate cancer cell dormancy

description: Metastasis involves the dissemination of single or small clumps of cancer cells through blood or lymphatic vessels and their extravasation into distant organs. Despite the strong regulation of metastases development by a cell dormancy phenomenon, the dormant state of cancer cells remains poorly characterized due to the difficulty of <i>in vivo</i> studies. We have recently shown <i>in vitro</i> that clonogenicity of prostate cancer cells is regulated by a dormancy phenomenon that is strongly induced when cells are cultured both at low cell density and in a slightly hypertonic medium. Here, we characterized by RT-qPCR a genetic expression signature of this dormant state which combines the presence of both stemness and differentiation markers. We showed that both TFGβ/BMP signaling and redox imbalance are required for the full induction of this dormancy signature and cell quiescence. Moreover, reconstruction experiments showed that TFGβ/BMP signaling and redox imbalance are sufficient to generate a pattern of genetic expression displaying all characteristic features of the dormancy signature. Finally, we observed that low cell density was sufficient to activate TGFβ/BMP signaling and to generate a slight redox imbalance thus priming cells for dormancy that can be attained with a co-stimulus like hypertonicity, most likely through an increased redox imbalance. The identification of a dual regulation of dormancy provides a framework for the interpretation of previous reports showing a restricted ability of BMP signaling to regulate cancer cell dormancy <i>in vivo</i> and draws attention on the role of oxidative stress in the metastatic process.
DOI: 10.6084/m9.figshare.1384846
title: Covariance Partition Priors: A Bayesian Approach to Simultaneous Covariance Estimation for Longitudinal Data

description: The estimation of the covariance matrix is a key concern in the analysis of longitudinal data. When data consists of multiple groups, it is often assumed the covariance matrices are either equal across groups or are completely distinct. We seek methodology to allow borrowing of strength across potentially similar groups to improve estimation. To that end, we introduce a covariance partition prior which proposes a partition of the groups at each measurement time. Groups in the same set of the partition share dependence parameters for the distribution of the current measurement given the preceding ones, and the sequence of partitions is modeled as a Markov chain to encourage similar structure at nearby measurement times. This approach additionally encourages a lower-dimensional structure of the covariance matrices by shrinking the parameters of the Cholesky decomposition toward zero. We demonstrate the performance of our model through two simulation studies and the analysis of data from a depression study. This article includes Supplementary Material available online.