cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.4551520.v1
title: Rapid Diagnostic Assay to Detect Herbicide Resistance in Annual Bluegrass

description: Data and statistical analysis files used in developing a rapid diagnostic assay to detect herbicide resistance in several annual bluegrass phenotypes.
DOI: 10.6084/m9.figshare.4551517.v1
title: Working Memory Trial Data

description: This database contains cognitive testing data from healthy young adults (aged 18-40) who participated in a randomized trial of online working memory training compared to both active and passive control groups. All participants are English speaking, and data were collected at the University of Calgary, Calgary, Alberta, Canada, between 2015 and 2016. <br>Participants were recruited via printed advertisements distributed throughout the community. Study involvement included completing cognitive tests of general intelligence, fluid intelligence, and working memory both before and after approximately 6 weeks of online working memory training, processing speed training (active control condition), or no contact with experimenters. Participants also completed several questionnaires regarding demographic and psychological variables. Functional and structural neuroimaging data was also collected before and after the training period for those assigned to the working memory training group and the processing speed active control group. Of the 107 participants that consented to participate, a total of 76 were included in the final analyses. <br>The University of Calgary Conjoint Faculties Research Ethics Board approved this study, and all participants provided written informed consent.
DOI: 10.6084/m9.figshare.4551520.v2
title: Rapid Diagnostic Assay to Detect Herbicide Resistance in Annual Bluegrass

description: Data and statistical analysis files used in developing a rapid diagnostic assay to detect herbicide resistance in several annual bluegrass phenotypes.
DOI: 10.6084/m9.figshare.4551520.v4
title: Diagnostic Assay to Detect Herbicide Resistance in Annual Bluegrass

description: Data and statistical analysis files used in developing a diagnostic assay to detect herbicide resistance in several annual bluegrass phenotypes.
DOI: 10.6084/m9.figshare.4551520.v3
title: Rapid Diagnostic Assay to Detect Herbicide Resistance in Annual Bluegrass

description: Data and statistical analysis files used in developing a rapid diagnostic assay to detect herbicide resistance in several annual bluegrass phenotypes.
DOI: 10.6084/m9.figshare.4551421
title: Deletion of <i>PRKAA</i> triggers mitochondrial fission by inhibiting the autophagy-dependent degradation of DNM1L

description: PRKAA (protein kinase, AMP-activated, α catalytic subunit) regulates mitochondrial biogenesis, function, and turnover. However, the molecular mechanisms by which PRKAA regulates mitochondrial dynamics remain poorly characterized. Here, we report that PRKAA regulated mitochondrial fission via the autophagy-dependent degradation of DNM1L (dynamin 1-like). Deletion of <i>Prkaa1</i>/AMPKα1 or <i>Prkaa2</i>/AMPKα2 resulted in defective autophagy, DNM1L accumulation, and aberrant mitochondrial fragmentation in the mouse aortic endothelium. Furthermore, autophagy inhibition by chloroquine treatment or <i>ATG7</i> small interfering RNA (siRNA) transfection, upregulated DNM1L expression and triggered DNM1L-mediated mitochondrial fragmentation. In contrast, autophagy activation by overexpression of ATG7 or chronic administration of rapamycin, the MTOR inhibitor, promoted DNM1L degradation and attenuated mitochondrial fragmentation in <i>Prkaa2</i>-deficient (<i>prkaa2</i><sup>−/−</sup>) mice, suggesting that defective autophagy contributes to enhanced DNM1L expression and mitochondrial fragmentation. Additionally, the autophagic receptor protein SQSTM1/p62, which bound to DNM1L and led to its translocation into the autophagosome, was involved in DNM1L degradation by the autophagy-lysosome pathway. Gene silencing of <i>SQSTM1</i> markedly reduced the association between SQSTM1 and DNM1L, impaired the degradation of DNM1L, and enhanced mitochondrial fragmentation in PRKAA-deficient endothelial cells. Finally, the genetic (<i>DNM1L</i> siRNA) or pharmacological (mdivi-1) inhibition of DNMA1L ablated mitochondrial fragmentation in the mouse aortic endothelium and prevented the acetylcholine-induced relaxation of isolated mouse aortas. This suggests that aberrant DNM1L is responsible for enhanced mitochondrial fragmentation and endothelial dysfunction in <i>prkaa</i> knockout mice. Overall, our results show that PRKAA deletion promoted mitochondrial fragmentation in vascular endothelial cells by inhibiting the autophagy-dependent degradation of DNM1L.
DOI: 10.6084/m9.figshare.4551418
title: A sperm-specific proteome-scale metabolic network model identifies non-glycolytic genes for energy deficiency in asthenozoospermia

description: About 15% of couples experience difficulty in conceiving a child, of which half of the cases are thought to be male-related. Asthenozoospermia, or low sperm motility, is one of the frequent types of male infertility. Although energy metabolism is suggested to be central to the etiology of asthenozoospermia, very few attempts have been made to identify its underlying metabolic pathways. Here, we reconstructed SpermNet, the first proteome-scale model of the sperm cell by using whole-proteome data and the mCADRE algorithm. The reconstructed model was then analyzed using the COBRA toolbox. Genes were knocked-out in the model to investigate their effect on ATP production. A total of 78 genes elevated ATP production rate considerably of which most encode components of oxidative phosphorylation, fatty acid oxidation, the Krebs cycle, and members of the solute carrier 25 family. Among them, we identified 11 novel genes which have previously not been associated with sperm cell energy metabolism and may thus be implicated in asthenozoospermia. We further examined the reconstructed model by <i>in silico</i> knock out of currently known asthenozoospermia implicated-genes that were not predicted by our model. The pathways affected by knocking out these genes were also related to energy metabolism, confirming previous findings. Therefore, our model not only predicts the known pathways, it also identifies several non-glycolytic genes for deficient energy metabolism in asthenozoospermia. Finally, this model supports the notion that metabolic pathways besides glycolysis such as oxidative phosphorylation and fatty acid oxidation are essential for sperm energy metabolism and if validated, may form a basis for fertility recovery. <b>Abbreviations</b>: mCADRE: metabolic context-specificity assessed by deterministic reaction evaluation; ATP: adenosine triphosphate; RNA: ribonucleic acid; FBA: flux balance analysis; FVA: flux variability analysis; DAVID: database for annotation, visualization and integrated discovery; OXPHOS: oxidative phosphorylation; ETC: electron transfer chain; SLC: solute carrier; DLD: dihydrolypoamide dehydrogenase; DLST: dihydrolypoamide S-succinyl transferase; OGDH: oxoglutarate dehydrogenase; CS: citrate synthase; FH: fumarate hydratase; IDH: isocitrate dehydrogenase; SUCLG1: succinate-CoA ligase; SD: succinate dehydrogenase; HADHA: hydroxyacyl-CoA dehydrogenase/3-ketoacyl-CoA thiolase/enoyl-CoA hydratase, subunit A; HADHB: hydroxyacyl-CoA dehydrogenase/3-ketoacyl-CoA thiolase/enoyl-CoA hydratase, subunit B; PPA2: pyrophosphatase (inorganic) 2; PP<sub>i</sub>: inorganic phosphate; GALT: galactose-1-phosphate uridylyltransferase
DOI: 10.6084/m9.figshare.4551421.v1
title: Deletion of <i>PRKAA</i> triggers mitochondrial fission by inhibiting the autophagy-dependent degradation of DNM1L

description: PRKAA (protein kinase, AMP-activated, α catalytic subunit) regulates mitochondrial biogenesis, function, and turnover. However, the molecular mechanisms by which PRKAA regulates mitochondrial dynamics remain poorly characterized. Here, we report that PRKAA regulated mitochondrial fission via the autophagy-dependent degradation of DNM1L (dynamin 1-like). Deletion of <i>Prkaa1</i>/AMPKα1 or <i>Prkaa2</i>/AMPKα2 resulted in defective autophagy, DNM1L accumulation, and aberrant mitochondrial fragmentation in the mouse aortic endothelium. Furthermore, autophagy inhibition by chloroquine treatment or <i>ATG7</i> small interfering RNA (siRNA) transfection, upregulated DNM1L expression and triggered DNM1L-mediated mitochondrial fragmentation. In contrast, autophagy activation by overexpression of ATG7 or chronic administration of rapamycin, the MTOR inhibitor, promoted DNM1L degradation and attenuated mitochondrial fragmentation in <i>Prkaa2</i>-deficient (<i>prkaa2</i><sup>−/−</sup>) mice, suggesting that defective autophagy contributes to enhanced DNM1L expression and mitochondrial fragmentation. Additionally, the autophagic receptor protein SQSTM1/p62, which bound to DNM1L and led to its translocation into the autophagosome, was involved in DNM1L degradation by the autophagy-lysosome pathway. Gene silencing of <i>SQSTM1</i> markedly reduced the association between SQSTM1 and DNM1L, impaired the degradation of DNM1L, and enhanced mitochondrial fragmentation in PRKAA-deficient endothelial cells. Finally, the genetic (<i>DNM1L</i> siRNA) or pharmacological (mdivi-1) inhibition of DNMA1L ablated mitochondrial fragmentation in the mouse aortic endothelium and prevented the acetylcholine-induced relaxation of isolated mouse aortas. This suggests that aberrant DNM1L is responsible for enhanced mitochondrial fragmentation and endothelial dysfunction in <i>prkaa</i> knockout mice. Overall, our results show that PRKAA deletion promoted mitochondrial fragmentation in vascular endothelial cells by inhibiting the autophagy-dependent degradation of DNM1L.
DOI: 10.6084/m9.figshare.4551418.v1
title: A sperm-specific proteome-scale metabolic network model identifies non-glycolytic genes for energy deficiency in asthenozoospermia

description: About 15% of couples experience difficulty in conceiving a child, of which half of the cases are thought to be male-related. Asthenozoospermia, or low sperm motility, is one of the frequent types of male infertility. Although energy metabolism is suggested to be central to the etiology of asthenozoospermia, very few attempts have been made to identify its underlying metabolic pathways. Here, we reconstructed SpermNet, the first proteome-scale model of the sperm cell by using whole-proteome data and the mCADRE algorithm. The reconstructed model was then analyzed using the COBRA toolbox. Genes were knocked-out in the model to investigate their effect on ATP production. A total of 78 genes elevated ATP production rate considerably of which most encode components of oxidative phosphorylation, fatty acid oxidation, the Krebs cycle, and members of the solute carrier 25 family. Among them, we identified 11 novel genes which have previously not been associated with sperm cell energy metabolism and may thus be implicated in asthenozoospermia. We further examined the reconstructed model by <i>in silico</i> knock out of currently known asthenozoospermia implicated-genes that were not predicted by our model. The pathways affected by knocking out these genes were also related to energy metabolism, confirming previous findings. Therefore, our model not only predicts the known pathways, it also identifies several non-glycolytic genes for deficient energy metabolism in asthenozoospermia. Finally, this model supports the notion that metabolic pathways besides glycolysis such as oxidative phosphorylation and fatty acid oxidation are essential for sperm energy metabolism and if validated, may form a basis for fertility recovery. <b>Abbreviations</b>: mCADRE: metabolic context-specificity assessed by deterministic reaction evaluation; ATP: adenosine triphosphate; RNA: ribonucleic acid; FBA: flux balance analysis; FVA: flux variability analysis; DAVID: database for annotation, visualization and integrated discovery; OXPHOS: oxidative phosphorylation; ETC: electron transfer chain; SLC: solute carrier; DLD: dihydrolypoamide dehydrogenase; DLST: dihydrolypoamide S-succinyl transferase; OGDH: oxoglutarate dehydrogenase; CS: citrate synthase; FH: fumarate hydratase; IDH: isocitrate dehydrogenase; SUCLG1: succinate-CoA ligase; SD: succinate dehydrogenase; HADHA: hydroxyacyl-CoA dehydrogenase/3-ketoacyl-CoA thiolase/enoyl-CoA hydratase, subunit A; HADHB: hydroxyacyl-CoA dehydrogenase/3-ketoacyl-CoA thiolase/enoyl-CoA hydratase, subunit B; PPA2: pyrophosphatase (inorganic) 2; PP<sub>i</sub>: inorganic phosphate; GALT: galactose-1-phosphate uridylyltransferase
DOI: 10.6084/m9.figshare.4551373
title: Tianmuthredo davei Taeger and Kramp, 2017, paratype, photos and videos

description: Tianmuthredo davei Taeger and Kramp, 2017<br><br>Taeger, A. & Kramp, K. (2017): Tianmuthredo davei (Hymenoptera:Tenthredinidae), a New Species from the Russian Far East. – Proceedings of the Entomological Society of Washington, 119(Special Issue): 864-878.<br>
DOI: 10.6084/m9.figshare.4551373.v1
title: Tianmuthredo davei Taeger and Kramp, 2017, paratype, photos and videos

description: Tianmuthredo davei Taeger and Kramp, 2017<br><br>Taeger, A. & Kramp, K. (2017): Tianmuthredo davei (Hymenoptera:Tenthredinidae), a New Species from the Russian Far East. – Proceedings of the Entomological Society of Washington, 119(Special Issue): 864-878.<br>
DOI: 10.6084/m9.figshare.4551142
title: Outsourcing in place: Should a retailer sell its store-brand factory?

description: Several major grocery chains in the United States own factories that produce some of their store-brand products. Historically, these store-brand products have been the low-price, lower-quality alternatives to higher-priced national brands, but the quality and consumer acceptance of store brands have increased markedly in recent years. Although demand for store-brand products has grown, managing the associated factories can be costly for retailers, leading some to consider selling the factories to third parties. We study the impact of selling a retailer’s existing capacity-limited factory to a third party when a store-brand product competes with a similar national-brand product. We examine the equilibrium dynamics between two external suppliers and show how the outcome changes with respect to prices, capacity limitations, the distribution of profits, and the sequencing of pricing decisions. Among other things, we show that, surprisingly, the national brand’s equilibrium wholesale price may fall when the factory is sold. We also show that the retailer may be strictly better off if he sells the factory, with these benefits being above and beyond any savings in fixed ownership and operating costs. Taken together, these results imply that when the store-brand factory has tight capacity, the adverse effects due to double marginalization on the store-brand product from selling the factory to a third party may be partially or fully offset by a reduction in the national brand’s wholesale price.
DOI: 10.6084/m9.figshare.4551142.v1
title: Outsourcing in place: Should a retailer sell its store-brand factory?

description: Several major grocery chains in the United States own factories that produce some of their store-brand products. Historically, these store-brand products have been the low-price, lower-quality alternatives to higher-priced national brands, but the quality and consumer acceptance of store brands have increased markedly in recent years. Although demand for store-brand products has grown, managing the associated factories can be costly for retailers, leading some to consider selling the factories to third parties. We study the impact of selling a retailer’s existing capacity-limited factory to a third party when a store-brand product competes with a similar national-brand product. We examine the equilibrium dynamics between two external suppliers and show how the outcome changes with respect to prices, capacity limitations, the distribution of profits, and the sequencing of pricing decisions. Among other things, we show that, surprisingly, the national brand’s equilibrium wholesale price may fall when the factory is sold. We also show that the retailer may be strictly better off if he sells the factory, with these benefits being above and beyond any savings in fixed ownership and operating costs. Taken together, these results imply that when the store-brand factory has tight capacity, the adverse effects due to double marginalization on the store-brand product from selling the factory to a third party may be partially or fully offset by a reduction in the national brand’s wholesale price.
DOI: 10.6084/m9.figshare.4550713
title: MicroRNA-432 targeting <i>E2F3</i> and <i>P55PIK</i> inhibits myogenesis through PI3K/AKT/mTOR signaling pathway

description: Skeletal muscle is the dominant executant in locomotion and regulator in energy metabolism. Embryonic myogenesis and postnatal muscle growth are controlled by a cascade of transcription factors and epigenetic regulatory mechanisms. MicroRNAs (miRNAs), a family of non-coding RNA of 22 nucleotides in length, post-transcriptionally regulates expression of mRNA by pairing the seed sequence to 3′ UTR of target mRNA. Increasing evidence has demonstrated that miRNAs are important regulators in diverse myogenic processes. The profiling of miRNA expression revealed that miR-432 is more enriched in the <i>longissimus dorsi</i> of 35-day-old piglets than that of adult pigs. Our gain of function study showed that miR-432 can negatively regulate both myoblast proliferation and differentiation. Mechanically, we found that miR-432 is able to down-regulate E2F transcription factor 3 (E2F3) to inactivate the expression of cell cycle and myogenic genes. We also identified that phosphatidylinositol 3-kinase regulatory subunit (P55PIK) is another target gene of miR-432 in muscle cells. downregulation of P55PIK by miR-432 leads to inhibition of P55PIK-mediated PI3K/AKT/mTOR signaling pathway during differentiation. The blocking effect of miR-432 on this pathway can be rescued by insulin treatment. Taken together, our findings identified microRNA-432 as a potent inhibitor of myogenesis which functions by targeting E2F3 and P55PIK in muscle cells.
DOI: 10.6084/m9.figshare.4550713.v1
title: MicroRNA-432 targeting <i>E2F3</i> and <i>P55PIK</i> inhibits myogenesis through PI3K/AKT/mTOR signaling pathway

description: Skeletal muscle is the dominant executant in locomotion and regulator in energy metabolism. Embryonic myogenesis and postnatal muscle growth are controlled by a cascade of transcription factors and epigenetic regulatory mechanisms. MicroRNAs (miRNAs), a family of non-coding RNA of 22 nucleotides in length, post-transcriptionally regulates expression of mRNA by pairing the seed sequence to 3′ UTR of target mRNA. Increasing evidence has demonstrated that miRNAs are important regulators in diverse myogenic processes. The profiling of miRNA expression revealed that miR-432 is more enriched in the <i>longissimus dorsi</i> of 35-day-old piglets than that of adult pigs. Our gain of function study showed that miR-432 can negatively regulate both myoblast proliferation and differentiation. Mechanically, we found that miR-432 is able to down-regulate E2F transcription factor 3 (E2F3) to inactivate the expression of cell cycle and myogenic genes. We also identified that phosphatidylinositol 3-kinase regulatory subunit (P55PIK) is another target gene of miR-432 in muscle cells. downregulation of P55PIK by miR-432 leads to inhibition of P55PIK-mediated PI3K/AKT/mTOR signaling pathway during differentiation. The blocking effect of miR-432 on this pathway can be rescued by insulin treatment. Taken together, our findings identified microRNA-432 as a potent inhibitor of myogenesis which functions by targeting E2F3 and P55PIK in muscle cells.
DOI: 10.6084/m9.figshare.4549531
title: Mutations in <i>DZIP1</i> and <i>XYLT1</i> are associated with nonsyndromic early onset high myopia in the Korean population

description: Mutations in <i>DZIP1</i> and <i>XYLT1</i> are associated with nonsyndromic early onset high myopia in the Korean population
DOI: 10.6084/m9.figshare.4549531.v1
title: Mutations in <i>DZIP1</i> and <i>XYLT1</i> are associated with nonsyndromic early onset high myopia in the Korean population

description: Mutations in <i>DZIP1</i> and <i>XYLT1</i> are associated with nonsyndromic early onset high myopia in the Korean population
DOI: 10.6084/m9.figshare.4547374
title: Bonath,Incera&Mclennan - Dataset.xlsx

description: We examined whether memory load affects participants’ ratings of native and foreign accents. The influence of memory load emerged for the high load condition in foreign speakers, but had no significant effect on the ratings of the native-accented speakers. These results have important theoretical and practical implications.
DOI: 10.6084/m9.figshare.4547374.v1
title: Bonath,Incera&Mclennan - Dataset.xlsx

description: We examined whether memory load affects participants’ ratings of native and foreign accents. The influence of memory load emerged for the high load condition in foreign speakers, but had no significant effect on the ratings of the native-accented speakers. These results have important theoretical and practical implications.
DOI: 10.6084/m9.figshare.4547338
title: Supplementary Table 1: GTF Field and PCR raw data.xlsx; Development and application of an eDNA method to detect the critically endangered Trinidad golden tree frog (Phytotriades auratus) in bromeliad phytotelmata

description: This supplementary table provides all of the GPS coordinates, heights of bromeliads sampled, environmental data (Temperature, collection times, humidity) and notes the samples that gave positive PCR results in two replicates of the eDNA assay developed for the publication.
DOI: 10.6084/m9.figshare.4547293
title: Antioxidant molecular targets of wheat bran fermented by white rot fungi and its potential modulation of antioxidative status in broiler chickens

description: 1. The study focused on antioxidant molecular targets of wheat bran fermented by white rot fungi (WRF) in poultry. After solid-state fermentation of wheat bran by WRF for 12 d, scanning electron microscopy found that the lignocellulose structure showed degradation and fragmentation. 2. A total of 300 1-d-old broilers were evenly divided by gender and randomly allocated into the following treatments: (1) maize–soybean meal (control group), (2) 10% of wheat bran replacing maize (10% WB group) or (3) 10% of fermented wheat bran replacing maize (10% FWB group). 3. The results indicated that the antioxidant gene expression, such as haem oxygenase-1 and glutathione-S-transferase of chicken peripheral blood mononuclear cells, of the 10% FWB group was significantly higher than that of the control group at d 35. For genes of Nicotinamide adenine dinucleotide phosphate oxygenase 1 and reactive oxygen species modulator protein 1, the expression of the 10% FWB group was lower than that of the control group at d 21 and 35. 4. In conclusion, wheat bran fermented by WRF could increase lignocellulolytic enzyme activities and the levels of active components that further regulate the expression of antioxidant molecular targets in poultry.