cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.5755308
title: Institutional transparency improves public perceptions of lab animal technicians and support for animal research

description: The use of animals in research is controversial and often takes place under a veil of secrecy. Lab animal technicians responsible for the care of animals at research institutions are sometimes described as performing ‘dirty work’ (i.e. professions that are viewed as morally tainted), and may be stigmatized by negative perceptions of their job.<i> </i>This study assessed if transparency affects public perceptions of lab animal technicians and support for animal research. Participants (n=550) were randomly assigned to one of six scenarios (using a 3x2 design) that described identical research varying only the transparency of the facility (low, high) and the species used (mice, dogs, cows). Participants provided Likert-type and open-ended responses to questions about the personal characteristics (warmth, competence) of a hypothetical lab technician ‘Cathy’ and their support for the described research. Quantitative analysis showed participants in the low-transparency condition perceived Cathy to be less warm and were less supportive of the research regardless of animal species. Qualitative responses varied greatly, with some participants expressing support for both Cathy and the research. These results suggest that increasing transparency in lab animal institutions could result in a more positive perception of lab animal researchers and the work that they do.
DOI: 10.6084/m9.figshare.5755308.v1
title: Institutional transparency improves public perceptions of lab animal technicians and support for animal research

description: The use of animals in research is controversial and often takes place under a veil of secrecy. Lab animal technicians responsible for the care of animals at research institutions are sometimes described as performing ‘dirty work’ (i.e. professions that are viewed as morally tainted), and may be stigmatized by negative perceptions of their job.<i> </i>This study assessed if transparency affects public perceptions of lab animal technicians and support for animal research. Participants (n=550) were randomly assigned to one of six scenarios (using a 3x2 design) that described identical research varying only the transparency of the facility (low, high) and the species used (mice, dogs, cows). Participants provided Likert-type and open-ended responses to questions about the personal characteristics (warmth, competence) of a hypothetical lab technician ‘Cathy’ and their support for the described research. Quantitative analysis showed participants in the low-transparency condition perceived Cathy to be less warm and were less supportive of the research regardless of animal species. Qualitative responses varied greatly, with some participants expressing support for both Cathy and the research. These results suggest that increasing transparency in lab animal institutions could result in a more positive perception of lab animal researchers and the work that they do.
DOI: 10.6084/m9.figshare.5754120
title: T-DNA database

description: This file is a database, containing all <i>Agrobacterium</i>'s genes, found in different types of T-DNA.The head of each sequences contains names of the gen, strain, species, and an Acs.number.
DOI: 10.6084/m9.figshare.5753391
title: DataSet S1 from Unique perceptuomotor control of stone hammers in wild monkeys

description: Joint angles.
DOI: 10.6084/m9.figshare.5753391.v1
title: DataSet S1 from Unique perceptuomotor control of stone hammers in wild monkeys

description: Joint angles.
DOI: 10.6084/m9.figshare.5753331
title: Supplementary Data for Upload.xlsx from Stresses and strains on the human foetal skeleton during development

description: Mechanical forces generated by foetal kicks and movements result in stimulation of the foetal skeleton in the form of stress and strain. This stimulation is known to be critical for prenatal musculoskeletal development; indeed, abnormal or absent movements have been implicated in multiple congenital disorders. However, the mechanical stress and strain experienced by the developing human skeleton <i>in utero</i> have never before been characterized. Here, we quantify the biomechanics of foetal movements during the second half of gestation by modelling foetal movements captured using novel cine-MRI technology. By tracking these movements, quantifying foetal kick and muscle forces, and applying them to three-dimensional geometries of the foetal skeleton, we test the hypothesis that stress and strain change over ontogeny. We find that foetal kick force increases significantly from 20 to 30 weeks gestation, before decreasing towards term. However, stress and strain in the foetal skeleton rises significantly over the latter half of gestation. This increasing trend with gestational age is important because changes in foetal movement patterns in late pregnancy have been linked to poor foetal outcomes and musculoskeletal malformations. This research represents the first quantification of kick force and mechanical stress and strain due to foetal movements in the human skeleton <i>in utero</i>, thus advancing our understanding of the biomechanical environment of the uterus. Further, by revealing a potential link between foetal biomechanics and skeletal malformations, our work will stimulate future research in tissue engineering and mechanobiology.
DOI: 10.6084/m9.figshare.5753331.v1
title: Supplementary Data for Upload.xlsx from Stresses and strains on the human foetal skeleton during development

description: Mechanical forces generated by foetal kicks and movements result in stimulation of the foetal skeleton in the form of stress and strain. This stimulation is known to be critical for prenatal musculoskeletal development; indeed, abnormal or absent movements have been implicated in multiple congenital disorders. However, the mechanical stress and strain experienced by the developing human skeleton <i>in utero</i> have never before been characterized. Here, we quantify the biomechanics of foetal movements during the second half of gestation by modelling foetal movements captured using novel cine-MRI technology. By tracking these movements, quantifying foetal kick and muscle forces, and applying them to three-dimensional geometries of the foetal skeleton, we test the hypothesis that stress and strain change over ontogeny. We find that foetal kick force increases significantly from 20 to 30 weeks gestation, before decreasing towards term. However, stress and strain in the foetal skeleton rises significantly over the latter half of gestation. This increasing trend with gestational age is important because changes in foetal movement patterns in late pregnancy have been linked to poor foetal outcomes and musculoskeletal malformations. This research represents the first quantification of kick force and mechanical stress and strain due to foetal movements in the human skeleton <i>in utero</i>, thus advancing our understanding of the biomechanical environment of the uterus. Further, by revealing a potential link between foetal biomechanics and skeletal malformations, our work will stimulate future research in tissue engineering and mechanobiology.
DOI: 10.6084/m9.figshare.5753274
title: NIH Basic Behavioral and Social Science Research Opportunity Network (OppNet) Program R Scripts

description: R scripts used for <b>A Bibliometric Comparison of NIH R01 and R21 Awards: A Case Study Using Basic Behavioral and Social Science Research Awards.</b><b><br></b><b>Abbreviations</b>:<b>BSSR</b>: behavioral and social science research<b>bBSSR</b>: basic behavioral and social science research<b>BSSR-only</b>: awards that are BSSR but not bBSSR<br><b>The following R scripts are contained in this fileset: </b><b>1. BSSR.analyses.R</b>: statistical analyses for BSSR-only and bBSSR awards and publicationsStatistics include: * Number of publications and citations by activity code (R01 vs R21) * Time to first publication * Time to first citation<br><b>2. OppNet.analyses.R</b>: statistical analyses for OppNet awards and publicationsStatistics include: * Number of publications and citations by activity code * Number of awards by group (bBSSR vs BSSR-only) and activity code (R01 vs R21) * Time to first publication * Time to first citation * Total costs by group and activity code<br>Contact Xueying Han (xhan@ida.org) if you have any questions.
DOI: 10.6084/m9.figshare.5753274.v1
title: NIH Basic Behavioral and Social Science Research Opportunity Network (OppNet) Program R Scripts

description: R scripts used for <b>A Bibliometric Comparison of NIH R01 and R21 Awards: A Case Study Using Basic Behavioral and Social Science Research Awards.</b><b><br></b><b>Abbreviations</b>:<b>BSSR</b>: behavioral and social science research<b>bBSSR</b>: basic behavioral and social science research<b>BSSR-only</b>: awards that are BSSR but not bBSSR<br><b>The following R scripts are contained in this fileset: </b><b>1. BSSR.analyses.R</b>: statistical analyses for BSSR-only and bBSSR awards and publicationsStatistics include: * Number of publications and citations by activity code (R01 vs R21) * Time to first publication * Time to first citation<br><b>2. OppNet.analyses.R</b>: statistical analyses for OppNet awards and publicationsStatistics include: * Number of publications and citations by activity code * Number of awards by group (bBSSR vs BSSR-only) and activity code (R01 vs R21) * Time to first publication * Time to first citation * Total costs by group and activity code<br>Contact Xueying Han (xhan@ida.org) if you have any questions.
DOI: 10.5281/zenodo.3968534
title: An algorithm to quantify intratumor heterogeneity based on alterations of gene expression profiles: Data availability

description: DEPTH evaluates the tumor heterogeneity level of each tumor sample based on gene expression profiles Heterogeneity score.
DOI: 10.6084/m9.figshare.5753082
title: TGFB1 is secreted through an unconventional pathway dependent on the autophagic machinery and cytoskeletal regulators

description: TGFB1 (transforming growth factor beta 1) is a potent cytokine playing a driving role in development, fibrosis and cancer. It is synthesized as prodomain-growth factor complex that requires tethering to LTBP (latent transforming growth factor beta binding protein) for efficient secretion into the extracellular space. Upon release, this large latent complex is sequestered by anchorage to extracellular matrix (ECM) networks, from which the mature growth factor needs to be activated in order to reach its receptors and initiate signaling. Here, we uncovered a novel intracellular secretion pathway by which the latent TGFB1 complex reaches the plasma membrane and is released from fibroblasts, the key effector cells during tissue repair, fibrosis and in the tumor stroma. We show that secretion of latent TGFB1, but not of other selected cytokines or of bulk cargo, is regulated by fibroblast-ECM communication through ILK (integrin linked kinase) that restricts RHOA activity by interacting with ARHGAP26/GRAF1. Latent TGFB1 interacts with GORASP2/GRASP55 and is detected inside MAP1LC3-positive autophagosomal intermediates that are secreted by a RAB8A-dependent pathway. Interestingly, TGFB1 secretion is fully abrogated in human and murine fibroblasts and macrophages that lack key components of the autophagic machinery. Our data demonstrate an unconventional secretion mode of TGFB1 adding another level of control of its bioavailability and activity in order to effectively orchestrate cellular programs prone to dysregulation as seen in fibrosis and cancer.
DOI: 10.6084/m9.figshare.5753082.v1
title: TGFB1 is secreted through an unconventional pathway dependent on the autophagic machinery and cytoskeletal regulators

description: TGFB1 (transforming growth factor beta 1) is a potent cytokine playing a driving role in development, fibrosis and cancer. It is synthesized as prodomain-growth factor complex that requires tethering to LTBP (latent transforming growth factor beta binding protein) for efficient secretion into the extracellular space. Upon release, this large latent complex is sequestered by anchorage to extracellular matrix (ECM) networks, from which the mature growth factor needs to be activated in order to reach its receptors and initiate signaling. Here, we uncovered a novel intracellular secretion pathway by which the latent TGFB1 complex reaches the plasma membrane and is released from fibroblasts, the key effector cells during tissue repair, fibrosis and in the tumor stroma. We show that secretion of latent TGFB1, but not of other selected cytokines or of bulk cargo, is regulated by fibroblast-ECM communication through ILK (integrin linked kinase) that restricts RHOA activity by interacting with ARHGAP26/GRAF1. Latent TGFB1 interacts with GORASP2/GRASP55 and is detected inside MAP1LC3-positive autophagosomal intermediates that are secreted by a RAB8A-dependent pathway. Interestingly, TGFB1 secretion is fully abrogated in human and murine fibroblasts and macrophages that lack key components of the autophagic machinery. Our data demonstrate an unconventional secretion mode of TGFB1 adding another level of control of its bioavailability and activity in order to effectively orchestrate cellular programs prone to dysregulation as seen in fibrosis and cancer.
DOI: 10.6084/m9.figshare.5753079
title: IL4 (interleukin 4) induces autophagy in B cells leading to exacerbated asthma

description: Allergic asthma is a common airway inflammatory disease in which B cells play important roles through IgE production and antigen presentation. SNP (single nucleotide polymorphism) analysis showed that <i>Atg</i> (autophagy-related) allele mutations are involved in asthma. It has been demonstrated that macroautophagy/autophagy is essential for B cell survival, plasma cell differentiation and immunological memory maintenance. However, whether B cell autophagy participates in asthma pathogenesis remains to be investigated. In this report, we found that autophagy was enhanced in pulmonary B cells from asthma-prone mice. Autophagy deficiency in B cells led to attenuated immunopathological symptoms in asthma-prone mice. Further investigation showed that IL4 (interleukin 4), a key effector Th2 cytokine in allergic asthma, was critical for autophagy induction in B cells both in vivo and in vitro, which further sustained B cell survival and enhanced antigen presentation by B cells. Moreover, IL4-induced autophagy depended on JAK signaling via an MTOR-independent, PtdIns3K-dependent pathway. Together, our data indicate that B cell autophagy aggravates experimental asthma through multiple mechanisms.
DOI: 10.6084/m9.figshare.5753079.v1
title: IL4 (interleukin 4) induces autophagy in B cells leading to exacerbated asthma

description: Allergic asthma is a common airway inflammatory disease in which B cells play important roles through IgE production and antigen presentation. SNP (single nucleotide polymorphism) analysis showed that <i>Atg</i> (autophagy-related) allele mutations are involved in asthma. It has been demonstrated that macroautophagy/autophagy is essential for B cell survival, plasma cell differentiation and immunological memory maintenance. However, whether B cell autophagy participates in asthma pathogenesis remains to be investigated. In this report, we found that autophagy was enhanced in pulmonary B cells from asthma-prone mice. Autophagy deficiency in B cells led to attenuated immunopathological symptoms in asthma-prone mice. Further investigation showed that IL4 (interleukin 4), a key effector Th2 cytokine in allergic asthma, was critical for autophagy induction in B cells both <i>in vivo</i> and <i>in vitro</i>, which further sustained B cell survival and enhanced antigen presentation by B cells. Moreover, IL4-induced autophagy depended on JAK signaling via an MTOR-independent, PtdIns3K-dependent pathway. Together, our data indicate that B cell autophagy aggravates experimental asthma through multiple mechanisms.
DOI: 10.6084/m9.figshare.5753079.v2
title: IL4 (interleukin 4) induces autophagy in B cells leading to exacerbated asthma

description: Allergic asthma is a common airway inflammatory disease in which B cells play important roles through IgE production and antigen presentation. SNP (single nucleotide polymorphism) analysis showed that <i>Atg</i> (autophagy-related) allele mutations are involved in asthma. It has been demonstrated that macroautophagy/autophagy is essential for B cell survival, plasma cell differentiation and immunological memory maintenance. However, whether B cell autophagy participates in asthma pathogenesis remains to be investigated. In this report, we found that autophagy was enhanced in pulmonary B cells from asthma-prone mice. Autophagy deficiency in B cells led to attenuated immunopathological symptoms in asthma-prone mice. Further investigation showed that IL4 (interleukin 4), a key effector Th2 cytokine in allergic asthma, was critical for autophagy induction in B cells both in vivo and in vitro, which further sustained B cell survival and enhanced antigen presentation by B cells. Moreover, IL4-induced autophagy depended on JAK signaling via an MTOR-independent, PtdIns3K-dependent pathway. Together, our data indicate that B cell autophagy aggravates experimental asthma through multiple mechanisms.
DOI: 10.6084/m9.figshare.5753049
title: Figure 2.csv

description: Data for Figure 2 of Raymond and Hamilton to LOL<br>The alkalinity data are provided by the New Orleans water treatment facilities (Carrollton Street Sewage and Water Engineering Plant in New Orleans LA and the Algiers Water Treatment Plant in Algiers, LA). The data prior to 2005 are presented and explained in Raymond et al. 2008. The newer data are publicly available. The discharge reconstruction for annual discharge prior to 2005 are also presented in Raymond et al. 2008 and are publicly available. For this study the monthly Mississippi River Basin flow was summed from the USGS stations “Mississippi River at Tarbert Landing” and “Old River Outflow” for the water years 1967-2015. It was found that for the period of 1968-1990 the Raymond et al. 2008 paper underestimated discharge by 3%, and these years were adjusted. For years prior to 1968 data from Raymond et al. were used. <br><br>Raymond, P. A., N. H. Oh, R. E. Turner, and W. Broussard. 2008. Anthropogenically enhanced fluxes of water and carbon from the Mississippi River. Nature 451: 449-452.<br>
DOI: 10.6084/m9.figshare.5753049.v2
title: Figure 2.csv

description: Data for Figure 2 of Raymond and Hamilton to LOL<br>The alkalinity data are provided by the New Orleans water treatment facilities (Carrollton Street Sewage and Water Engineering Plant in New Orleans LA and the Algiers Water Treatment Plant in Algiers, LA). The data prior to 2005 are presented and explained in Raymond et al. 2008. The newer data are publicly available. The discharge reconstruction for annual discharge prior to 2005 are also presented in Raymond et al. 2008 and are publicly available. For this study the monthly Mississippi River Basin flow was summed from the USGS stations “Mississippi River at Tarbert Landing” and “Old River Outflow” for the water years 1967-2015. It was found that for the period of 1968-1990 the Raymond et al. 2008 paper underestimated discharge by 3%, and these years were adjusted. For years prior to 1968 data from Raymond et al. were used. <br><br>Raymond, P. A., N. H. Oh, R. E. Turner, and W. Broussard. 2008. Anthropogenically enhanced fluxes of water and carbon from the Mississippi River. Nature 451: 449-452.<br>
DOI: 10.6084/m9.figshare.5752965
title: Supplementary Material for: Human Malformation Syndromes of Defective GLI: Opposite Phenotypes of 2q14.2 (GLI2) and 7p14.2 (GLI3) Microdeletions and a GLIA/R Balance Model

description: GLI family zinc finger proteins are transcriptional effectors of the sonic hedgehog signaling pathway. GLI regulates gene expression and repression at various phases of embryonic morphogenesis. In humans, 4 <i>GLI</i> genes are known, and <i>GLI2</i> (2q14.2) and <i>GLI3</i> (7p14.1) mutations cause different syndromes. Here, we present 2 distinctive cases with a chromosomal microdeletion in one of these genes. Patient 1 is a 14-year-old girl with Culler-Jones syndrome. She manifested short stature, cleft palate, and mild intellectual/social disability caused by a 6.6-Mb deletion of 2q14.1q14.3. Patient 2 is a 2-year-old girl with Greig cephalopolysyndactyly contiguous gene deletion syndrome. She manifested macrocephaly, preaxial polysyndactyly, psychomotor developmental delay, cerebral cavernous malformations, and glucose intolerance due to a 6.2-Mb deletion of 7p14.1p12.3 which included <i>GLI3</i>, <i>GCK</i>, and <i>CCM2</i>. Each patient manifests a different phenotype which is associated with different functions of each <i>GLI</i> gene and different effects of the chromosomal contiguous gene deletion. We summarize the phenotypic extent of GLI2/3 syndromes in the literature and determine that these 2 syndromes manifest opposite features to a certain extent, such as midface hypoplasia or macrocephaly, and anterior or posterior side of polydactyly. We propose a GLIA/R balance model that may explain these findings.
DOI: 10.6084/m9.figshare.5752908
title: COPO Demo Files

description: Demo files for testing COPO ENA upload capabillity.
DOI: 10.6084/m9.figshare.5752908.v1
title: COPO Demo Files

description: Demo files for testing COPO ENA upload capabillity.
DOI: 10.6084/m9.figshare.5752908.v2
title: COPO Demo Files

description: Demo files for testing COPO ENA upload capabillity.
DOI: 10.6084/m9.figshare.5752908.v4
title: COPO Demo Files

description: Demo files for testing COPO ENA upload capabillity.
DOI: 10.6084/m9.figshare.5752908.v3
title: COPO Demo Files

description: Demo files for testing COPO ENA upload capabillity.
DOI: 10.6084/m9.figshare.5752884
title: Estimating scale economies in non-convex production models

description: The literature on nonparametric frontier technologies lacks a method for the measurement of scale economies in non-convex settings. This paper proposes a general procedure which is based on the minimization of the ray average cost and requires the solution of a single programming problem. Our approach allows for multiple optima to introduce the case of global sub-constant scale economies, and it also permits the estimation of scale economies at a local level. The empirical application investigates the role of replicability and the relationship between global and local indicators. It also points out the managerial implications for companies operating in the Italian public transit industry.
DOI: 10.6084/m9.figshare.5752884.v1
title: Estimating scale economies in non-convex production models

description: The literature on nonparametric frontier technologies lacks a method for the measurement of scale economies in non-convex settings. This paper proposes a general procedure which is based on the minimization of the ray average cost and requires the solution of a single programming problem. Our approach allows for multiple optima to introduce the case of global sub-constant scale economies, and it also permits the estimation of scale economies at a local level. The empirical application investigates the role of replicability and the relationship between global and local indicators. It also points out the managerial implications for companies operating in the Italian public transit industry.