cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.9613247
title: Dataset for manuscript "Helpers increase daily survival rate of Southern Lapwing (Vanellus chilensis) nests during the incubation stage"

description: This is the raw data used in the manuscript entitled "Helpers increase daily survival rate of Southern Lapwing (<i>Vanellus chilensis</i>) nests during the incubation stage", published in The Wilson Journal of Ornithology.<br>This dataset contains one .txt file (<b>LapwingNestDSR.txt</b>). In this file, there are seven data columns, as described below:<br>1. <b>FirstFound</b>: The first day a lapwing nest was found within a breeding season.<br>2. <b>LastPresent</b>: The last day the nest was checked when eggs were alive. <br>3. <b>LastChecked</b>: The last day the nest was checked.<br>4. <b>Fate</b>: The fate of the nest (0 = successful, 1 = depredated).<br>5. <b>Freq</b>: The number (frequency) of nests that had this same encounter history. This column only contains '1', as each nest had its own unique encounter history.<br>6. <b>GroupType</b>: The type of breeding group that tended the nest (0 = monogamous pair, 1 = cooperative group).<br>7. <b>AgeDay1</b>: The age of the nest on the first day of the nestingseason. Because the age variable is for the first day of the nesting season, this value will be negative forall the nests in the sample except those that were initiated (started) on or before day 1.<br>All variables have been described following the conventions published in chapter 17 of the Mark book (http://www.phidot.org/software/mark/docs/book/). Days have been standardised within each nesting season (2007/2008; see Mark book section 17.2 for details).
DOI: 10.6084/m9.figshare.9613247.v1
title: Dataset for manuscript "Helpers increase daily survival rate of Southern Lapwing (Vanellus chilensis) nests during the incubation stage"

description: This is the raw data used in the manuscript entitled "Helpers increase daily survival rate of Southern Lapwing (<i>Vanellus chilensis</i>) nests during the incubation stage", published in The Wilson Journal of Ornithology.<br>This dataset contains one .txt file (<b>LapwingNestDSR.txt</b>). In this file, there are seven data columns, as described below:<br>1. <b>FirstFound</b>: The first day a lapwing nest was found within a breeding season.<br>2. <b>LastPresent</b>: The last day the nest was checked when eggs were alive. <br>3. <b>LastChecked</b>: The last day the nest was checked.<br>4. <b>Fate</b>: The fate of the nest (0 = successful, 1 = depredated).<br>5. <b>Freq</b>: The number (frequency) of nests that had this same encounter history. This column only contains '1', as each nest had its own unique encounter history.<br>6. <b>GroupType</b>: The type of breeding group that tended the nest (0 = monogamous pair, 1 = cooperative group).<br>7. <b>AgeDay1</b>: The age of the nest on the first day of the nestingseason. Because the age variable is for the first day of the nesting season, this value will be negative forall the nests in the sample except those that were initiated (started) on or before day 1.<br>All variables have been described following the conventions published in chapter 17 of the Mark book (http://www.phidot.org/software/mark/docs/book/). Days have been standardised within each nesting season (2007/2008; see Mark book section 17.2 for details).
DOI: 10.6084/m9.figshare.9611876
title: Age-associated changes in the response of tendon explants to stress deprivation is sex-dependent

description: <b>Purpose of the Study:</b> The incidence of tendon injuries increases dramatically with age, which presents a major clinical burden. While previous studies have sought to identify age-related changes in extracellular matrix structure and function, few have been able to explain fully why aged tissues are more prone to degeneration and injury. In addition, recent studies have also demonstrated that age-related processes in humans may be sex-dependent, which could be responsible for muddled conclusions in changes with age. In this study, we investigate short-term responses through an ex vivo explant culture model of stress deprivation that specifically questions how age and sex differentially affect the ability of tendons to respond to altered mechanical stimulus. <b>Materials and Methods:</b> We subjected murine flexor explants from young (4 months of age) and aged (22–24 months of age) male and female mice to stress-deprived culture conditions for up to 1 week and investigated changes in viability, cell metabolism and proliferation, matrix biosynthesis and composition, gene expression, and inflammatory responses throughout the culture period. <b>Results and Conclusions</b>: We found that aging did have a significant influence on the response to stress deprivation, demonstrating that aged explants have a less robust response overall with reduced metabolic activity, viability, proliferation, and biosynthesis. However, age-related changes appeared to be sex-dependent. Together, this work demonstrates that the aging process and the subsequent effect of age on the ability of tendons to respond to stress-deprivation are inherently different based on sex, where male explants favor increased activity, apoptosis, and matrix remodeling while female explants favor reduced activity and tissue preservation.
DOI: 10.6084/m9.figshare.9611876.v1
title: Age-associated changes in the response of tendon explants to stress deprivation is sex-dependent

description: <b>Purpose of the Study:</b> The incidence of tendon injuries increases dramatically with age, which presents a major clinical burden. While previous studies have sought to identify age-related changes in extracellular matrix structure and function, few have been able to explain fully why aged tissues are more prone to degeneration and injury. In addition, recent studies have also demonstrated that age-related processes in humans may be sex-dependent, which could be responsible for muddled conclusions in changes with age. In this study, we investigate short-term responses through an ex vivo explant culture model of stress deprivation that specifically questions how age and sex differentially affect the ability of tendons to respond to altered mechanical stimulus. <b>Materials and Methods:</b> We subjected murine flexor explants from young (4 months of age) and aged (22–24 months of age) male and female mice to stress-deprived culture conditions for up to 1 week and investigated changes in viability, cell metabolism and proliferation, matrix biosynthesis and composition, gene expression, and inflammatory responses throughout the culture period. <b>Results and Conclusions</b>: We found that aging did have a significant influence on the response to stress deprivation, demonstrating that aged explants have a less robust response overall with reduced metabolic activity, viability, proliferation, and biosynthesis. However, age-related changes appeared to be sex-dependent. Together, this work demonstrates that the aging process and the subsequent effect of age on the ability of tendons to respond to stress-deprivation are inherently different based on sex, where male explants favor increased activity, apoptosis, and matrix remodeling while female explants favor reduced activity and tissue preservation.
DOI: 10.6084/m9.figshare.9611198
title: kneepaingwas

description: GWAS summary statistics on knee pain from UK Biobank
DOI: 10.6084/m9.figshare.9610067
title: Erratum

description: Erratum
DOI: 10.6084/m9.figshare.9610067.v1
title: Erratum

description: Erratum
DOI: 10.6084/m9.figshare.9610112.v1
title: Data from "Non-linear body size distributions linked to omnivory in stream food webs"

description: Data used in "Non-linear body size distributions linked to omnivory in stream food webs" by Perkins et al. <br><br> Data included in the deposit are specifically designed for the reproduction of the core analyses of this publication. Therefore, researchers interested in using the data for purposes other than replicating our analyses are advised to contact the corresponding author directly, as other useful information from the original data might not be included.
DOI: 10.17028/rd.lboro.9609566
title: Developing a proactive safety performance measurement tool (SPMT) for construction sites. Appendix 4. CD-ROM version of SPMT

description: Files originally stored on CD-ROM attached to thesis: Read me in Rich Text FormatScore Matrix in MS ExcelSPMT in MS AccessTo understand how to operate SPMT effectively, please read the READ ME file first. This version will only enable the user to 'read only' all the files.
DOI: 10.6084/m9.figshare.9609509
title: Supplementary Material for: Coordination of Neuron Production in Mouse and Human Cerebral Cortex by the Homolog of <b><i>Drosophila</i></b> Mastermind Protein

description: The coordination of progenitor self-renewal, neuronal production, and migration is essential to the normal development and evolution of the cerebral cortex. Numerous studies have shown that the Notch, Wnt/beta-catenin, and Neurogenin pathways contribute separately to progenitor expansion, neurogenesis, and neuronal migration, but it is unknown how these signals are coordinated. In vitro studies suggested that the mastermind-like 1 (MAML1) gene, homologue of the <i>Drosophila</i> mastermind, plays a role in coordinating the aforementioned signaling pathways, yet its role during cortical development remains largely unknown. Here we show that ectopic expression of dominant-negative MAML (dnMAML) causes exuberant neuronal production in the mouse cortex without disrupting neuronal migration. Comparing the transcriptional consequences of dnMAML and Neurog2 ectopic expression revealed a complex genetic network controlling the balance of progenitor expansion versus neuronal production. Manipulation of MAML and Neurog2 in cultured human cerebral stem cells exposed interactions with the same set of signaling pathways. Thus, our data suggest that evolutionary changes that affect the timing, tempo, and density of successive neuronal layers of the small lissencephalic rodent and large convoluted primate cerebral cortex depend on similar molecular mechanisms that act from the earliest developmental stages.
DOI: 10.17028/rd.lboro.9609566.v1
title: Developing a proactive safety performance measurement tool (SPMT) for construction sites. Appendix 4. CD-ROM version of SPMT

description: Files originally stored on CD-ROM attached to thesis: Read me in Rich Text FormatScore Matrix in MS ExcelSPMT in MS AccessTo understand how to operate SPMT effectively, please read the READ ME file first. This version will only enable the user to 'read only' all the files.
DOI: 10.6084/m9.figshare.9609422
title: DMBT1 suppresses progression of gallbladder carcinoma through PI3K/AKT signaling pathway by targeting PTEN

description: Gallbladder carcinoma (GBC) is a highly lethal malignancy of the gastrointestinal tract. Despite extensive research, the underlying molecular mechanism of GBC remains largely unclear. Deleted in malignant brain tumors 1 (DMBT1) is low-expression during cancer progression and as a potential tumor-suppressor gene in various types of cancer. However, its role in Gallbladder cancer remains poorly understood. Here, we found that DMBT1 was significantly low-expression and deletion of copy number in GBC tissues by qRT-PCR and Western blot. Overexpression of DMBT1 impaired survival, promoted apoptosis in GBC cells <i>in vitro</i>, and inhibited tumor progression <i>in vivo</i>. Further study of underlying mechanisms demonstrated that DMBT1 combined with PTEN which could stabilize PTEN protein, resulting in inhibiting the activation of PI3K/AKT signaling pathway. Our study revealed a new sight of DMBT1 as a tumor-suppressor gene on the PI3K/AKT pathway in GBC, which may be a potential therapeutic target for improving treatment. Down-regulation of DMBT1 suppresses progression of gallbladder carcinoma through PI3K/AKT signaling pathway activation by targeting PTEN.
DOI: 10.6084/m9.figshare.9609422.v1
title: DMBT1 suppresses progression of gallbladder carcinoma through PI3K/AKT signaling pathway by targeting PTEN

description: Gallbladder carcinoma (GBC) is a highly lethal malignancy of the gastrointestinal tract. Despite extensive research, the underlying molecular mechanism of GBC remains largely unclear. Deleted in malignant brain tumors 1 (DMBT1) is low-expression during cancer progression and as a potential tumor-suppressor gene in various types of cancer. However, its role in Gallbladder cancer remains poorly understood. Here, we found that DMBT1 was significantly low-expression and deletion of copy number in GBC tissues by qRT-PCR and Western blot. Overexpression of DMBT1 impaired survival, promoted apoptosis in GBC cells <i>in vitro</i>, and inhibited tumor progression <i>in vivo</i>. Further study of underlying mechanisms demonstrated that DMBT1 combined with PTEN which could stabilize PTEN protein, resulting in inhibiting the activation of PI3K/AKT signaling pathway. Our study revealed a new sight of DMBT1 as a tumor-suppressor gene on the PI3K/AKT pathway in GBC, which may be a potential therapeutic target for improving treatment. Down-regulation of DMBT1 suppresses progression of gallbladder carcinoma through PI3K/AKT signaling pathway activation by targeting PTEN.
DOI: 10.6084/m9.figshare.9609509.v1
title: Supplementary Material for: Coordination of Neuron Production in Mouse and Human Cerebral Cortex by the Homolog of <b><i>Drosophila</i></b> Mastermind Protein

description: The coordination of progenitor self-renewal, neuronal production, and migration is essential to the normal development and evolution of the cerebral cortex. Numerous studies have shown that the Notch, Wnt/beta-catenin, and Neurogenin pathways contribute separately to progenitor expansion, neurogenesis, and neuronal migration, but it is unknown how these signals are coordinated. In vitro studies suggested that the mastermind-like 1 (MAML1) gene, homologue of the <i>Drosophila</i> mastermind, plays a role in coordinating the aforementioned signaling pathways, yet its role during cortical development remains largely unknown. Here we show that ectopic expression of dominant-negative MAML (dnMAML) causes exuberant neuronal production in the mouse cortex without disrupting neuronal migration. Comparing the transcriptional consequences of dnMAML and Neurog2 ectopic expression revealed a complex genetic network controlling the balance of progenitor expansion versus neuronal production. Manipulation of MAML and Neurog2 in cultured human cerebral stem cells exposed interactions with the same set of signaling pathways. Thus, our data suggest that evolutionary changes that affect the timing, tempo, and density of successive neuronal layers of the small lissencephalic rodent and large convoluted primate cerebral cortex depend on similar molecular mechanisms that act from the earliest developmental stages.
DOI: 10.6084/m9.figshare.9609509.v2
title: Supplementary Material for: Coordination of Neuron Production in Mouse and Human Cerebral Cortex by the Homolog of <b><i>Drosophila</i></b> Mastermind Protein

description: The coordination of progenitor self-renewal, neuronal production, and migration is essential to the normal development and evolution of the cerebral cortex. Numerous studies have shown that the Notch, Wnt/beta-catenin, and Neurogenin pathways contribute separately to progenitor expansion, neurogenesis, and neuronal migration, but it is unknown how these signals are coordinated. In vitro studies suggested that the mastermind-like 1 (MAML1) gene, homologue of the <i>Drosophila</i> mastermind, plays a role in coordinating the aforementioned signaling pathways, yet its role during cortical development remains largely unknown. Here we show that ectopic expression of dominant-negative MAML (dnMAML) causes exuberant neuronal production in the mouse cortex without disrupting neuronal migration. Comparing the transcriptional consequences of dnMAML and Neurog2 ectopic expression revealed a complex genetic network controlling the balance of progenitor expansion versus neuronal production. Manipulation of MAML and Neurog2 in cultured human cerebral stem cells exposed interactions with the same set of signaling pathways. Thus, our data suggest that evolutionary changes that affect the timing, tempo, and density of successive neuronal layers of the small lissencephalic rodent and large convoluted primate cerebral cortex depend on similar molecular mechanisms that act from the earliest developmental stages.
DOI: 10.6084/m9.figshare.9609509.v3
title: Supplementary Material for: Coordination of Neuron Production in Mouse and Human Cerebral Cortex by the Homolog of <b><i>Drosophila</i></b> Mastermind Protein

description: The coordination of progenitor self-renewal, neuronal production, and migration is essential to the normal development and evolution of the cerebral cortex. Numerous studies have shown that the Notch, Wnt/beta-catenin, and Neurogenin pathways contribute separately to progenitor expansion, neurogenesis, and neuronal migration, but it is unknown how these signals are coordinated. In vitro studies suggested that the mastermind-like 1 (MAML1) gene, homologue of the <i>Drosophila</i> mastermind, plays a role in coordinating the aforementioned signaling pathways, yet its role during cortical development remains largely unknown. Here we show that ectopic expression of dominant-negative MAML (dnMAML) causes exuberant neuronal production in the mouse cortex without disrupting neuronal migration. Comparing the transcriptional consequences of dnMAML and Neurog2 ectopic expression revealed a complex genetic network controlling the balance of progenitor expansion versus neuronal production. Manipulation of MAML and Neurog2 in cultured human cerebral stem cells exposed interactions with the same set of signaling pathways. Thus, our data suggest that evolutionary changes that affect the timing, tempo, and density of successive neuronal layers of the small lissencephalic rodent and large convoluted primate cerebral cortex depend on similar molecular mechanisms that act from the earliest developmental stages.
DOI: 10.6084/m9.figshare.9609509.v4
title: Supplementary Material for: Coordination of Neuron Production in Mouse and Human Cerebral Cortex by the Homolog of <b><i>Drosophila</i></b> Mastermind Protein

description: The coordination of progenitor self-renewal, neuronal production, and migration is essential to the normal development and evolution of the cerebral cortex. Numerous studies have shown that the Notch, Wnt/beta-catenin, and Neurogenin pathways contribute separately to progenitor expansion, neurogenesis, and neuronal migration, but it is unknown how these signals are coordinated. In vitro studies suggested that the mastermind-like 1 (MAML1) gene, homologue of the <i>Drosophila</i> mastermind, plays a role in coordinating the aforementioned signaling pathways, yet its role during cortical development remains largely unknown. Here we show that ectopic expression of dominant-negative MAML (dnMAML) causes exuberant neuronal production in the mouse cortex without disrupting neuronal migration. Comparing the transcriptional consequences of dnMAML and Neurog2 ectopic expression revealed a complex genetic network controlling the balance of progenitor expansion versus neuronal production. Manipulation of MAML and Neurog2 in cultured human cerebral stem cells exposed interactions with the same set of signaling pathways. Thus, our data suggest that evolutionary changes that affect the timing, tempo, and density of successive neuronal layers of the small lissencephalic rodent and large convoluted primate cerebral cortex depend on similar molecular mechanisms that act from the earliest developmental stages.
DOI: 10.6084/m9.figshare.9607589
title: data(Establishment of a Diagnostic Model of Coronary Heart Disease for Patients with Diabetic Foot).xlsx

description: This data is used to establish a diagnostic model which has good diagnostic value and provides the basis for preliminary screening for coronary heart disease in patients with diabetic foot.
DOI: 10.6084/m9.figshare.9609509.v5
title: Supplementary Material for: Coordination of Neuron Production in Mouse and Human Cerebral Cortex by the Homolog of <b><i>Drosophila</i></b> Mastermind Protein

description: The coordination of progenitor self-renewal, neuronal production, and migration is essential to the normal development and evolution of the cerebral cortex. Numerous studies have shown that the Notch, Wnt/beta-catenin, and Neurogenin pathways contribute separately to progenitor expansion, neurogenesis, and neuronal migration, but it is unknown how these signals are coordinated. In vitro studies suggested that the mastermind-like 1 (MAML1) gene, homologue of the <i>Drosophila</i> mastermind, plays a role in coordinating the aforementioned signaling pathways, yet its role during cortical development remains largely unknown. Here we show that ectopic expression of dominant-negative MAML (dnMAML) causes exuberant neuronal production in the mouse cortex without disrupting neuronal migration. Comparing the transcriptional consequences of dnMAML and Neurog2 ectopic expression revealed a complex genetic network controlling the balance of progenitor expansion versus neuronal production. Manipulation of MAML and Neurog2 in cultured human cerebral stem cells exposed interactions with the same set of signaling pathways. Thus, our data suggest that evolutionary changes that affect the timing, tempo, and density of successive neuronal layers of the small lissencephalic rodent and large convoluted primate cerebral cortex depend on similar molecular mechanisms that act from the earliest developmental stages.
DOI: 10.6084/m9.figshare.9609509.v6
title: Supplementary Material for: Coordination of Neuron Production in Mouse and Human Cerebral Cortex by the Homolog of <b><i>Drosophila</i></b> Mastermind Protein

description: The coordination of progenitor self-renewal, neuronal production, and migration is essential to the normal development and evolution of the cerebral cortex. Numerous studies have shown that the Notch, Wnt/beta-catenin, and Neurogenin pathways contribute separately to progenitor expansion, neurogenesis, and neuronal migration, but it is unknown how these signals are coordinated. In vitro studies suggested that the mastermind-like 1 (MAML1) gene, homologue of the <i>Drosophila</i> mastermind, plays a role in coordinating the aforementioned signaling pathways, yet its role during cortical development remains largely unknown. Here we show that ectopic expression of dominant-negative MAML (dnMAML) causes exuberant neuronal production in the mouse cortex without disrupting neuronal migration. Comparing the transcriptional consequences of dnMAML and Neurog2 ectopic expression revealed a complex genetic network controlling the balance of progenitor expansion versus neuronal production. Manipulation of MAML and Neurog2 in cultured human cerebral stem cells exposed interactions with the same set of signaling pathways. Thus, our data suggest that evolutionary changes that affect the timing, tempo, and density of successive neuronal layers of the small lissencephalic rodent and large convoluted primate cerebral cortex depend on similar molecular mechanisms that act from the earliest developmental stages.