cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.6220217.v1
title: Activation of Class I histone deacetylases contributes to mitochondrial dysfunction in cardiomyocytes with altered complex activities

description: Histone deacetylases (HDACs) play vital roles in the pathophysiology of heart failure, which is associated with mitochondrial dysfunction. Tumor necrosis factor-α (TNF-α) contributes to the genesis of heart failure and impairs mitochondria. This study evaluated the role of HDACs in TNF-α-induced mitochondrial dysfunction and investigated their therapeutic potential and underlying mechanisms. We measured mitochondrial oxygen consumption rate (OCR) and ATP production using Seahorse XF24 extracellular flux analyzer and bioluminescent assay in control and TNF-α (10 ng/ml, 24 h)-treated HL-1 cells with or without HDAC inhibition. TNF-α increased Class I and II (but not Class IIa) HDAC activities (assessed by Luminescent) with enhanced expressions of Class I (HDAC1, HDAC2, HDAC3, and HDAC8) but not Class IIb HDAC (HDAC6 and HDAC10) proteins in HL-1 cells. TNF-α induced mitochondrial dysfunction with impaired basal, ATP-linked, and maximal respiration, decreased cellular ATP synthesis, and increased mitochondrial superoxide production (measured by MitoSOX red fluorescence), which were rescued by inhibiting HDACs with MPT0E014 (1 μM, a Class I and IIb inhibitor), or MS-275 (1 μM, a Class I inhibitor). MPT0E014 reduced TNF-α-decreased complex I and II enzyme (but not III or IV) activities (by enzyme activity microplate assays). Our results suggest that Class I HDAC actions contribute to TNF-α-induced mitochondrial dysfunction in cardiomyocytes with altered complex I and II enzyme regulation. HDAC inhibition improves dysfunctional mitochondrial bioenergetics with attenuation of TNF-α-induced oxidative stress, suggesting the therapeutic potential of HDAC inhibition in cardiac dysfunction.
DOI: 10.6084/m9.figshare.6220214
title: Robust prediction of gene regulation in colorectal cancer tissues from DNA methylation profiles

description: DNA methylation is recognized as one of several epigenetic regulators of gene expression and as potential driver of carcinogenesis through gene-silencing of tumor suppressors and activation of oncogenes. However, abnormal methylation, even of promoter regions, does not necessarily alter gene expression levels, especially if the gene is already silenced, leaving the exact mechanisms of methylation unanswered. Using a large cohort of matching DNA methylation and gene expression samples of colorectal cancer (CRC; n = 77) and normal adjacent mucosa tissues (n = 108), we investigated the regulatory role of methylation on gene expression. We show that on a subset of genes enriched in common cancer pathways, methylation is significantly associated with gene regulation through gene-specific mechanisms. We built two classification models to infer gene regulation in CRC from methylation differences of tumor and normal tissues, taking into account both gene-silencing and gene-activation effects through hyper- and hypo-methylation of CpGs. The classification models result in high prediction performances in both training and independent CRC testing cohorts (0.92HMGA1 as consistently associated with methylation across cancers, suggesting a potential candidate for DNA methylation targeting cancer therapy.
DOI: 10.6084/m9.figshare.6220214.v1
title: Robust prediction of gene regulation in colorectal cancer tissues from DNA methylation profiles

description: DNA methylation is recognized as one of several epigenetic regulators of gene expression and as potential driver of carcinogenesis through gene-silencing of tumor suppressors and activation of oncogenes. However, abnormal methylation, even of promoter regions, does not necessarily alter gene expression levels, especially if the gene is already silenced, leaving the exact mechanisms of methylation unanswered. Using a large cohort of matching DNA methylation and gene expression samples of colorectal cancer (CRC; n = 77) and normal adjacent mucosa tissues (n = 108), we investigated the regulatory role of methylation on gene expression. We show that on a subset of genes enriched in common cancer pathways, methylation is significantly associated with gene regulation through gene-specific mechanisms. We built two classification models to infer gene regulation in CRC from methylation differences of tumor and normal tissues, taking into account both gene-silencing and gene-activation effects through hyper- and hypo-methylation of CpGs. The classification models result in high prediction performances in both training and independent CRC testing cohorts (0.92HMGA1 as consistently associated with methylation across cancers, suggesting a potential candidate for DNA methylation targeting cancer therapy.
DOI: 10.6084/m9.figshare.6220211
title: Novel imprinted single CpG sites found by global DNA methylation analysis in human parthenogenetic induced pluripotent stem cells

description: Genomic imprinting is the process of epigenetic modification whereby genes are expressed in a parent-of-origin dependent manner; it plays an important role in normal growth and development. Parthenogenetic embryos contain only the maternal genome. Parthenogenetic embryonic stem cells could be useful for studying imprinted genes. In humans, mature cystic ovarian teratomas originate from parthenogenetic activation of oocytes; they are composed of highly differentiated mature tissues containing all three germ layers. To establish human parthenogenetic induced pluripotent stem cell lines (PgHiPSCs), we generated parthenogenetic fibroblasts from ovarian teratoma tissues. We compared global DNA methylation status of PgHiPSCs with that of biparental human induced pluripotent stem cells by using Illumina Infinium HumanMethylation450 BeadChip array. This analysis identified novel single imprinted CpG sites. We further tested DNA methylation patterns of two of these sites using bisulfite sequencing and described novel candidate imprinted CpG sites. These results confirm that PgHiPSCs are a powerful tool for identifying imprinted genes and investigating their roles in human development and diseases.
DOI: 10.6084/m9.figshare.6220211.v1
title: Novel imprinted single CpG sites found by global DNA methylation analysis in human parthenogenetic induced pluripotent stem cells

description: Genomic imprinting is the process of epigenetic modification whereby genes are expressed in a parent-of-origin dependent manner; it plays an important role in normal growth and development. Parthenogenetic embryos contain only the maternal genome. Parthenogenetic embryonic stem cells could be useful for studying imprinted genes. In humans, mature cystic ovarian teratomas originate from parthenogenetic activation of oocytes; they are composed of highly differentiated mature tissues containing all three germ layers. To establish human parthenogenetic induced pluripotent stem cell lines (PgHiPSCs), we generated parthenogenetic fibroblasts from ovarian teratoma tissues. We compared global DNA methylation status of PgHiPSCs with that of biparental human induced pluripotent stem cells by using Illumina Infinium HumanMethylation450 BeadChip array. This analysis identified novel single imprinted CpG sites. We further tested DNA methylation patterns of two of these sites using bisulfite sequencing and described novel candidate imprinted CpG sites. These results confirm that PgHiPSCs are a powerful tool for identifying imprinted genes and investigating their roles in human development and diseases.
DOI: 10.6084/m9.figshare.6220196
title: contraceptives.dta

description: The data was collected in the field and STATA version 13.1 was used to create the data file.
DOI: 10.6084/m9.figshare.6220142
title: Transcriptome profiling to identify key mediators of granulosa cell proliferation upon FSH stimulation in the goose (<i>Anser cygnoides</i>)

description: 1. The low reproductive performance of geese has seriously hampered the development of the industry. Reproductive performance, particularly the egg laying rate mainly depends on the development of the follicle. Previous studies have shown that follicle-stimulating hormone (FSH) plays an important role in the process of follicular development, but the exact underlying mechanism remains unclear. 2. This study showed that FSH stimulated granulosa cell proliferation in a dose-dependent manner. The effect of FSH treatment on granulosa cell proliferation was greatest at a dose of 100 mIU/ml FSH for 24 h. 3. Secondly, the effect of different concentrations of FSH on goose granulosa cell proliferation was investigated, and <i>de novo</i> transcriptome assembly and gene expression analysis performed using short-read sequencing technology (Illumina). High-throughput sequencing results yielded 62.61 M reads and 7.8 G base pairs from granulosa cells treated with 100 mIU/ml FSH. These reads were assembled into 65,757 unigenes (mean length: 705 bp) with an N50 of 903 bp. A total of 110 upregulated and 510 downregulated differentially expressed genes (DEGs) were identified by RNA-seq. 4. Functional analysis by gene ontology (GO) and KEGG pathway annotation indicated that hormone biosynthesis (GO:0042446), positive regulation of hormone secretion (GO:0046887), steroid biosynthesis, oxidative phosphorylation and carbon metabolism pathways were involved in FSH-mediated proliferation of goose granulosa cells. 5. After screening, a group of key responsive genes including superoxide dismutase 1, fatty acyl-CoA reductase 1, transforming growth factor-beta receptor-associated protein 1 and follistatin were tested by real-time reverse transcription PCR to confirm differential expression in granulosa cells stimulated by FSH. 6. FSH-stimulated goose granulosa cells and DEG profiling data provided comprehensive gene expression information at the transcriptional level that could promote better understanding of the molecular mechanisms underlying follicle development in response to FSH stimulation.
DOI: 10.6084/m9.figshare.6220142.v1
title: Transcriptome profiling to identify key mediators of granulosa cell proliferation upon FSH stimulation in the goose (Anser cygnoides)

description: 1. The low reproductive performance of geese has seriously hampered the development of the industry. Reproductive performance, particularly the egg laying rate mainly depends on the development of the follicle. Previous studies have shown that follicle-stimulating hormone (FSH) plays an important role in the process of follicular development, but the exact underlying mechanism remains unclear. 2. This study showed that FSH-stimulated granulosa cell proliferation in a dose-dependent manner. The effect of FSH treatment on granulosa cell proliferation was greatest at a dose of 100 mIU/ml FSH for 24 h. 3. Secondly, the effect of different concentrations of FSH on goose granulosa cell proliferation was investigated, and <i>de novo</i> transcriptome assembly and gene expression analysis performed using short-read sequencing technology (Illumina). High-throughput sequencing results yielded 62.61 M reads and 7.8 G base pairs from granulosa cells treated with 100 mIU/ml FSH. These reads were assembled into 65,757 unigenes (mean length: 705 bp) with an N50 of 903 bp. A total of 110 upregulated and 510 downregulated differentially expressed genes (DEGs) were identified by RNA-seq. 4. Functional analysis by gene ontology (GO) and KEGG pathway annotation indicated that hormone biosynthesis (GO: 0042446), positive regulation of hormone secretion (GO: 0046887), steroid biosynthesis, oxidative phosphorylation and carbon metabolism pathways were involved in FSH-mediated proliferation of goose granulosa cells. 5. After screening, a group of key responsive genes including superoxide dismutase 1 (SOD1), fatty acyl-CoA reductase 1 (FAR1), transforming growth factor-beta receptor-associated protein 1 (TGFBRAP1) and follistatin were tested by real-time reverse transcription PCR to confirm differential expression in granulosa cells stimulated by FSH. 6. FSH-stimulated goose granulosa cells and DEG profiling data provided comprehensive gene expression information at the transcriptional level that could promote better understanding of the molecular mechanisms underlying follicle development in response to FSH stimulation.
DOI: 10.6084/m9.figshare.6220142.v3
title: Transcriptome profiling to identify key mediators of granulosa cell proliferation upon FSH stimulation in the goose (<i>Anser cygnoides</i>)

description: 1. The low reproductive performance of geese has seriously hampered the development of the industry. Reproductive performance, particularly the egg laying rate mainly depends on the development of the follicle. Previous studies have shown that follicle-stimulating hormone (FSH) plays an important role in the process of follicular development, but the exact underlying mechanism remains unclear. 2. This study showed that FSH stimulated granulosa cell proliferation in a dose-dependent manner. The effect of FSH treatment on granulosa cell proliferation was greatest at a dose of 100 mIU/ml FSH for 24 h. 3. Secondly, the effect of different concentrations of FSH on goose granulosa cell proliferation was investigated, and <i>de novo</i> transcriptome assembly and gene expression analysis performed using short-read sequencing technology (Illumina). High-throughput sequencing results yielded 62.61 M reads and 7.8 G base pairs from granulosa cells treated with 100 mIU/ml FSH. These reads were assembled into 65,757 unigenes (mean length: 705 bp) with an N50 of 903 bp. A total of 110 upregulated and 510 downregulated differentially expressed genes (DEGs) were identified by RNA-seq. 4. Functional analysis by gene ontology (GO) and KEGG pathway annotation indicated that hormone biosynthesis (GO:0042446), positive regulation of hormone secretion (GO:0046887), steroid biosynthesis, oxidative phosphorylation and carbon metabolism pathways were involved in FSH-mediated proliferation of goose granulosa cells. 5. After screening, a group of key responsive genes including superoxide dismutase 1, fatty acyl-CoA reductase 1, transforming growth factor-beta receptor-associated protein 1 and follistatin were tested by real-time reverse transcription PCR to confirm differential expression in granulosa cells stimulated by FSH. 6. FSH-stimulated goose granulosa cells and DEG profiling data provided comprehensive gene expression information at the transcriptional level that could promote better understanding of the molecular mechanisms underlying follicle development in response to FSH stimulation.
DOI: 10.6084/m9.figshare.6220142.v2
title: Transcriptome profiling to identify key mediators of granulosa cell proliferation upon FSH stimulation in the goose (<i>Anser cygnoides</i>)

description: 1. The low reproductive performance of geese has seriously hampered the development of the industry. Reproductive performance, particularly the egg laying rate mainly depends on the development of the follicle. Previous studies have shown that follicle-stimulating hormone (FSH) plays an important role in the process of follicular development, but the exact underlying mechanism remains unclear. 2. This study showed that FSH stimulated granulosa cell proliferation in a dose-dependent manner. The effect of FSH treatment on granulosa cell proliferation was greatest at a dose of 100 mIU/ml FSH for 24 h. 3. Secondly, the effect of different concentrations of FSH on goose granulosa cell proliferation was investigated, and <i>de novo</i> transcriptome assembly and gene expression analysis performed using short-read sequencing technology (Illumina). High-throughput sequencing results yielded 62.61 M reads and 7.8 G base pairs from granulosa cells treated with 100 mIU/ml FSH. These reads were assembled into 65,757 unigenes (mean length: 705 bp) with an N50 of 903 bp. A total of 110 upregulated and 510 downregulated differentially expressed genes (DEGs) were identified by RNA-seq. 4. Functional analysis by gene ontology (GO) and KEGG pathway annotation indicated that hormone biosynthesis (GO:0042446), positive regulation of hormone secretion (GO:0046887), steroid biosynthesis, oxidative phosphorylation and carbon metabolism pathways were involved in FSH-mediated proliferation of goose granulosa cells. 5. After screening, a group of key responsive genes including superoxide dismutase 1, fatty acyl-CoA reductase 1, transforming growth factor-beta receptor-associated protein 1 and follistatin were tested by real-time reverse transcription PCR to confirm differential expression in granulosa cells stimulated by FSH. 6. FSH-stimulated goose granulosa cells and DEG profiling data provided comprehensive gene expression information at the transcriptional level that could promote better understanding of the molecular mechanisms underlying follicle development in response to FSH stimulation.
DOI: 10.6084/m9.figshare.6220088
title: bow shock breakout

description: bow shock breakout<br>
DOI: 10.6084/m9.figshare.6220088.v1
title: bow shock breakout

description: bow shock breakout<br>
DOI: 10.6084/m9.figshare.6217478
title: Crockford_Data from Chimpanzee quiet hoo variants differ according to context

description: All data used in this publication
DOI: 10.6084/m9.figshare.6217478.v1
title: Crockford_Data from Chimpanzee quiet hoo variants differ according to context

description: All data used in this publication
DOI: 10.6084/m9.figshare.6217463
title: Crockford_simulation from Chimpanzee quiet hoo variants differ according to context

description: Code used for simulation
DOI: 10.6084/m9.figshare.6217463.v1
title: Crockford_simulation from Chimpanzee quiet hoo variants differ according to context

description: Code used for simulation
DOI: 10.6084/m9.figshare.6217460
title: Crockford_code from Chimpanzee quiet hoo variants differ according to context

description: Code used for statistical analyses
DOI: 10.6084/m9.figshare.6217460.v1
title: Crockford_code from Chimpanzee quiet hoo variants differ according to context

description: Code used for statistical analyses
DOI: 10.6084/m9.figshare.6217415
title: Climatic variation across a latitudinal gradient affect phenology and group size, but not social complexity in small carpenter bees

description: Greater social complexity at lower latitudes have been observed in a variety of arthropods from termites to spiders. Social behavior in the small carpenter bees, <i>Ceratina,</i> has been shown to vary widely both between species and across geographic range. Our goal was to determine how social plasticity of three populations of <i>Ceratina </i>species, <i>C. calcarata</i> and <i>C. strenua</i>, vary across a latitudinal gradient. The data files contain 1) Climate data for the three collection sites: New Hampshire, Missouri and Georgia. 2) The nest collection and adult measurements for the three sites 3) The brood measurements and development rates from the three sites.
DOI: 10.6084/m9.figshare.6217361
title: Dataset for: Computational modeling highlights disordered Formin Homology 1 domain's role in profilin-actin transfer

description: Formins accelerate actin polymerization, assumed to occur through flexible FH1 domain mediated transfer of profilin-actin to the barbed end. To study FH1 properties and address sequence effects including varying length/distribution of profilin-binding proline-rich motifs, we performed all-atom simulations of mouse mDia1, mDia2; budding yeast Bni1, Bnr1; fission yeast Cdc12, For3, and Fus1 FH1s. We find FH1 has flexible regions between high propensity polyproline helix regions. A coarse-grained model retaining sequence-specificity, assuming rigid polyproline segments, describes their size. Multiple bound profilins or profilin-actin complexes expand mDia1-FH1, which may be important in cells. Simulations of the barbed end bound to Bni1-FH1-FH2 dimer show the leading FH1 can better transfer profilin or profilin-actin, having decreasing probability with increasing distance from FH2.
DOI: 10.6084/m9.figshare.6217361.v1
title: Dataset for: Computational modeling highlights disordered Formin Homology 1 domain's role in profilin-actin transfer

description: Formins accelerate actin polymerization, assumed to occur through flexible FH1 domain mediated transfer of profilin-actin to the barbed end. To study FH1 properties and address sequence effects including varying length/distribution of profilin-binding proline-rich motifs, we performed all-atom simulations of mouse mDia1, mDia2; budding yeast Bni1, Bnr1; fission yeast Cdc12, For3, and Fus1 FH1s. We find FH1 has flexible regions between high propensity polyproline helix regions. A coarse-grained model retaining sequence-specificity, assuming rigid polyproline segments, describes their size. Multiple bound profilins or profilin-actin complexes expand mDia1-FH1, which may be important in cells. Simulations of the barbed end bound to Bni1-FH1-FH2 dimer show the leading FH1 can better transfer profilin or profilin-actin, having decreasing probability with increasing distance from FH2.
DOI: 10.6084/m9.figshare.6217337
title: bow shock breakout

description: bow shock breakout
DOI: 10.6084/m9.figshare.6217337.v1
title: bow shock breakout

description: bow shock breakout
DOI: 10.6084/m9.figshare.6217319
title: Estimating geographic patterns of ophidism risk in Ecuador

description: The species richness of venomous snakes in Ecuador (~39 species) is among the highest in the world. However, until now no information exists regarding geographic patterns of ophidism. In this study, we present a detailed spatial snakebite risk map which was built by stacking weighted ecological niche models of the 19 snake species responsible for the majority of Ecuador’s envenomation cases. Our weights were based on the proportion of cases reported for each species on local epidemiological studies. Based on our analyses, we identify 184 densely populated rural communities with high snakebite risk that should be monitored by health organizations. We also identified three densely populated rural locations (Palora Metzera, Sangay and Shell) that may require special attention because they had much higher snakebite risk values than the rest.
DOI: 10.6084/m9.figshare.6217319.v1
title: Estimating geographic patterns of ophidism risk in Ecuador

description: The species richness of venomous snakes in Ecuador (~39 species) is among the highest in the world. However, until now no information exists regarding geographic patterns of ophidism. In this study, we present a detailed spatial snakebite risk map which was built by stacking weighted ecological niche models of the 19 snake species responsible for the majority of Ecuador’s envenomation cases. Our weights were based on the proportion of cases reported for each species on local epidemiological studies. Based on our analyses, we identify 184 densely populated rural communities with high snakebite risk that should be monitored by health organizations. We also identified three densely populated rural locations (Palora Metzera, Sangay and Shell) that may require special attention because they had much higher snakebite risk values than the rest.
DOI: 10.6084/m9.figshare.6217268
title: 1-D stress-strain calculation code in VBA from A mathematical model for fitting and predicting relaxation modulus and simulating viscoelastic responses

description: txt
DOI: 10.6084/m9.figshare.6217268.v1
title: 1-D stress-strain calculation code in VBA from A mathematical model for fitting and predicting relaxation modulus and simulating viscoelastic responses

description: txt
DOI: 10.6084/m9.figshare.6217265
title: Fortran subroutine for building viscoelastic stiffness matrix from A mathematical model for fitting and predicting relaxation modulus and simulating viscoelastic responses

description: txt
DOI: 10.6084/m9.figshare.6217265.v1
title: Fortran subroutine for building viscoelastic stiffness matrix from A mathematical model for fitting and predicting relaxation modulus and simulating viscoelastic responses

description: txt
DOI: 10.6084/m9.figshare.6217262
title: Model fitting prediction and 1-D stress analysis from A mathematical model for fitting and predicting relaxation modulus and simulating viscoelastic responses

description: xlsm