cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.1248827
title: Degradation of benzotrifluoride via the dioxygenase pathway in <i>Rhodococcus</i> sp. 065240

description: We previously isolated <i>Rhodococcus</i> sp. 065240, which catalyzes the defluorination of benzotrifluoride (BTF). In order to investigate the mechanism of this degradation of BTF, we performed proteomic analysis of cells grown with or without BTF. Three proteins, which resemble dioxygenase pathway enzymes responsible for isopropylbenzene degradation from <i>Rhodococcus erythropolis</i> BD2, were induced by BTF. Genomic PCR and DNA sequence analysis revealed that the <i>Rhodococcus</i> sp. 065240 carries the gene cluster, <i>btf</i>, which is highly homologous to the <i>ipb</i> gene cluster from <i>R. erythropolis</i> BD2. A mutant strain, which could not catalyze BTF defluorination, was isolated from 065240 strain by UV mutagenesis. The mutant strain had one mutation in the <i>btfT</i> gene, which encodes a response regulator of the two component system. The defluorinating ability of the mutant strain was recovered by complementation of <i>btfT</i>. These results suggest that the <i>btf</i> gene cluster is responsible for degradation of BTF.
DOI: 10.6084/m9.figshare.1247703
title: Action Potential Modulation in CA1 Pyramidal Neuron Axons Facilitates OLM Interneuron Activation in Recurrent Inhibitory Microcircuits of Rat Hippocampus

description: Kim S (2014) Action Potential Modulation in CA1 Pyramidal Neuron Axons Facilitates OLM Interneuron Activation in Recurrent Inhibitory Microcircuits of Rat Hippocampus. PLoS ONE 9(11): e113124. doi:10.1371/journal.pone.0113124
DOI: 10.6084/m9.figshare.1247673
title: Baseline values of experimental groups at day 0

description: The table includes the baseline values of both experimental groups (Bx and Ctrl) at day 0.
DOI: 10.6084/m9.figshare.1247689
title: TRAMA AMIANTO

description: AMIANTO SUSTANCIA PELIGROSA
DOI: 10.6084/m9.figshare.1247689.v1
title: TRAMA AMIANTO

description: AMIANTO SUSTANCIA PELIGROSA
DOI: 10.6084/m9.figshare.1247703.v1
title: Action Potential Modulation in CA1 Pyramidal Neuron Axons Facilitates OLM Interneuron Activation in Recurrent Inhibitory Microcircuits of Rat Hippocampus

description: Kim S (2014) Action Potential Modulation in CA1 Pyramidal Neuron Axons Facilitates OLM Interneuron Activation in Recurrent Inhibitory Microcircuits of Rat Hippocampus. PLoS ONE 9(11): e113124. doi:10.1371/journal.pone.0113124
DOI: 10.6084/m9.figshare.1248827.v1
title: Degradation of benzotrifluoride via the dioxygenase pathway in <i>Rhodococcus</i> sp. 065240

description: We previously isolated <i>Rhodococcus</i> sp. 065240, which catalyzes the defluorination of benzotrifluoride (BTF). In order to investigate the mechanism of this degradation of BTF, we performed proteomic analysis of cells grown with or without BTF. Three proteins, which resemble dioxygenase pathway enzymes responsible for isopropylbenzene degradation from <i>Rhodococcus erythropolis</i> BD2, were induced by BTF. Genomic PCR and DNA sequence analysis revealed that the <i>Rhodococcus</i> sp. 065240 carries the gene cluster, <i>btf</i>, which is highly homologous to the <i>ipb</i> gene cluster from <i>R. erythropolis</i> BD2. A mutant strain, which could not catalyze BTF defluorination, was isolated from 065240 strain by UV mutagenesis. The mutant strain had one mutation in the <i>btfT</i> gene, which encodes a response regulator of the two component system. The defluorinating ability of the mutant strain was recovered by complementation of <i>btfT</i>. These results suggest that the <i>btf</i> gene cluster is responsible for degradation of BTF.
DOI: 10.6084/m9.figshare.1247673.v1
title: Baseline values of experimental groups at day 0

description: The table includes the baseline values of both experimental groups (Bx and Ctrl) at day 0.
DOI: 10.6084/m9.figshare.1248827.v3
title: Degradation of benzotrifluoride via the dioxygenase pathway in <i>Rhodococcus</i> sp. 065240

description: We previously isolated <i>Rhodococcus</i> sp. 065240, which catalyzes the defluorination of benzotrifluoride (BTF). In order to investigate the mechanism of this degradation of BTF, we performed proteomic analysis of cells grown with or without BTF. Three proteins, which resemble dioxygenase pathway enzymes responsible for isopropylbenzene degradation from <i>Rhodococcus erythropolis</i> BD2, were induced by BTF. Genomic PCR and DNA sequence analysis revealed that the <i>Rhodococcus</i> sp. 065240 carries the gene cluster, <i>btf</i>, which is highly homologous to the <i>ipb</i> gene cluster from <i>R. erythropolis</i> BD2. A mutant strain, which could not catalyze BTF defluorination, was isolated from 065240 strain by UV mutagenesis. The mutant strain had one mutation in the <i>btfT</i> gene, which encodes a response regulator of the two component system. The defluorinating ability of the mutant strain was recovered by complementation of <i>btfT</i>. These results suggest that the <i>btf</i> gene cluster is responsible for degradation of BTF.
DOI: 10.6084/m9.figshare.1247659
title: Restoration of CFTR function in patients with cystic fibrosis carrying the F508del-CFTR mutation

description: Restoration of BECN1/Beclin 1-dependent autophagy and depletion of SQSTM1/p62 by genetic manipulation or autophagy-stimulatory proteostasis regulators, such as cystamine, have positive effects on mouse models of human cystic fibrosis (CF). These measures rescue the functional expression of the most frequent pathogenic CFTR mutant, F508del, at the respiratory epithelial surface and reduce lung inflammation in <i>Cftr<sup>F508del</sup></i> homozygous mice. Cysteamine, the reduced form of cystamine, is an FDA-approved drug. Here, we report that oral treatment with cysteamine greatly reduces the mortality rate and improves the phenotype of newborn mice bearing the <i>F508del-CFTR</i> mutation. Cysteamine was also able to increase the plasma membrane expression of the F508del-CFTR protein in nasal epithelial cells from <i>F508del</i> homozygous CF patients, and these effects persisted for 24 h after cysteamine withdrawal. Importantly, this cysteamine effect after washout was further sustained by the sequential administration of epigallocatechin gallate (EGCG), a green tea flavonoid, both <i>in vivo</i>, in mice, and <i>in vitro</i>, in primary epithelial cells from CF patients. In a pilot clinical trial involving 10 <i>F508del-CFTR</i> homozygous CF patients, the combination of cysteamine and EGCG restored BECN1, reduced SQSTM1 levels and improved CFTR function from nasal epithelial cells <i>in vivo</i>, correlating with a decrease of chloride concentrations in sweat, as well as with a reduction of the abundance of <i>TNF/TNF-alpha (tumor necrosis factor)</i> and <i>CXCL8</i> (<i>chemokine [C-X-C motif] ligand 8</i>) transcripts in nasal brushing and TNF and CXCL8 protein levels in the sputum. Altogether, these results suggest that optimal schedules of cysteamine plus EGCG might be used for the treatment of CF caused by the <i>F508del-CFTR</i> mutation.
DOI: 10.6084/m9.figshare.1248827.v2
title: Degradation of benzotrifluoride via the dioxygenase pathway in <i>Rhodococcus</i> sp. 065240

description: We previously isolated <i>Rhodococcus</i> sp. 065240, which catalyzes the defluorination of benzotrifluoride (BTF). In order to investigate the mechanism of this degradation of BTF, we performed proteomic analysis of cells grown with or without BTF. Three proteins, which resemble dioxygenase pathway enzymes responsible for isopropylbenzene degradation from <i>Rhodococcus erythropolis</i> BD2, were induced by BTF. Genomic PCR and DNA sequence analysis revealed that the <i>Rhodococcus</i> sp. 065240 carries the gene cluster, <i>btf</i>, which is highly homologous to the <i>ipb</i> gene cluster from <i>R. erythropolis</i> BD2. A mutant strain, which could not catalyze BTF defluorination, was isolated from 065240 strain by UV mutagenesis. The mutant strain had one mutation in the <i>btfT</i> gene, which encodes a response regulator of the two component system. The defluorinating ability of the mutant strain was recovered by complementation of <i>btfT</i>. These results suggest that the <i>btf</i> gene cluster is responsible for degradation of BTF.
DOI: 10.6084/m9.figshare.1247641
title: RNA shotgun metagenomic sequencing of northern California mosquitoes uncovers viruses, bacteria, and fungi

description: See the README file for details
DOI: 10.6084/m9.figshare.1247639
title: README File

description: Describes all the other files in this project
DOI: 10.6084/m9.figshare.1247659.v1
title: Restoration of CFTR function in patients with cystic fibrosis carrying the F508del-CFTR mutation

description: Restoration of BECN1/Beclin 1-dependent autophagy and depletion of SQSTM1/p62 by genetic manipulation or autophagy-stimulatory proteostasis regulators, such as cystamine, have positive effects on mouse models of human cystic fibrosis (CF). These measures rescue the functional expression of the most frequent pathogenic CFTR mutant, F508del, at the respiratory epithelial surface and reduce lung inflammation in <i>Cftr<sup>F508del</sup></i> homozygous mice. Cysteamine, the reduced form of cystamine, is an FDA-approved drug. Here, we report that oral treatment with cysteamine greatly reduces the mortality rate and improves the phenotype of newborn mice bearing the <i>F508del-CFTR</i> mutation. Cysteamine was also able to increase the plasma membrane expression of the F508del-CFTR protein in nasal epithelial cells from <i>F508del</i> homozygous CF patients, and these effects persisted for 24 h after cysteamine withdrawal. Importantly, this cysteamine effect after washout was further sustained by the sequential administration of epigallocatechin gallate (EGCG), a green tea flavonoid, both <i>in vivo</i>, in mice, and <i>in vitro</i>, in primary epithelial cells from CF patients. In a pilot clinical trial involving 10 <i>F508del-CFTR</i> homozygous CF patients, the combination of cysteamine and EGCG restored BECN1, reduced SQSTM1 levels and improved CFTR function from nasal epithelial cells <i>in vivo</i>, correlating with a decrease of chloride concentrations in sweat, as well as with a reduction of the abundance of <i>TNF/TNF-alpha (tumor necrosis factor)</i> and <i>CXCL8</i> (<i>chemokine [C-X-C motif] ligand 8</i>) transcripts in nasal brushing and TNF and CXCL8 protein levels in the sputum. Altogether, these results suggest that optimal schedules of cysteamine plus EGCG might be used for the treatment of CF caused by the <i>F508del-CFTR</i> mutation.
DOI: 10.6084/m9.figshare.1247639.v1
title: README File

description: Describes all the other files in this project
DOI: 10.6084/m9.figshare.1247634
title: SMASH – semi-automatic muscle analysis using segmentation of histology: a MATLAB application

description: SMASH is composed of a set of functions enabling the user analyze aspects of histological muscle sections. Image segmentation: identifies potential muscle fibers. Fiber filter: removes non fiber elements. Fiber properties computes parameters related to fiber size. Fiber type: determines which fibers are positively stained within an image. Central nucleation: determines which fibers have central nuclei within an image. Object counter: identifies non fiber objects within an image. SMASH Stand Alone requires MATLAB Compiler Runtime (MCR) version R2014a (8.3) which is freely available from Mathworks (http://www.mathworks.com/products/compiler/mcr/). SMASH App requires MATLAB version R2014a (8.3) or later with the Image Processing Toolbox.
DOI: 10.6084/m9.figshare.1247636
title: Human Disturbance and Its Effect on Plant Biodiversity within Local Powerline Field

description: Local powerine was studied to see the effects of human disturbances on plant biodiversity.
DOI: 10.6084/m9.figshare.1247636.v1
title: Human Disturbance and Its Effect on Plant Biodiversity within Local Powerline Field

description: Local powerine was studied to see the effects of human disturbances on plant biodiversity.
DOI: 10.6084/m9.figshare.1247659.v2
title: Restoration of CFTR function in patients with cystic fibrosis carrying the F508del-CFTR mutation

description: Restoration of BECN1/Beclin 1-dependent autophagy and depletion of SQSTM1/p62 by genetic manipulation or autophagy-stimulatory proteostasis regulators, such as cystamine, have positive effects on mouse models of human cystic fibrosis (CF). These measures rescue the functional expression of the most frequent pathogenic CFTR mutant, F508del, at the respiratory epithelial surface and reduce lung inflammation in <i>Cftr<sup>F508del</sup></i> homozygous mice. Cysteamine, the reduced form of cystamine, is an FDA-approved drug. Here, we report that oral treatment with cysteamine greatly reduces the mortality rate and improves the phenotype of newborn mice bearing the <i>F508del-CFTR</i> mutation. Cysteamine was also able to increase the plasma membrane expression of the F508del-CFTR protein in nasal epithelial cells from <i>F508del</i> homozygous CF patients, and these effects persisted for 24 h after cysteamine withdrawal. Importantly, this cysteamine effect after washout was further sustained by the sequential administration of epigallocatechin gallate (EGCG), a green tea flavonoid, both <i>in vivo</i>, in mice, and <i>in vitro</i>, in primary epithelial cells from CF patients. In a pilot clinical trial involving 10 <i>F508del-CFTR</i> homozygous CF patients, the combination of cysteamine and EGCG restored BECN1, reduced SQSTM1 levels and improved CFTR function from nasal epithelial cells <i>in vivo</i>, correlating with a decrease of chloride concentrations in sweat, as well as with a reduction of the abundance of <i>TNF/TNF-alpha (tumor necrosis factor)</i> and <i>CXCL8</i> (<i>chemokine [C-X-C motif] ligand 8</i>) transcripts in nasal brushing and TNF and CXCL8 protein levels in the sputum. Altogether, these results suggest that optimal schedules of cysteamine plus EGCG might be used for the treatment of CF caused by the <i>F508del-CFTR</i> mutation.
DOI: 10.6084/m9.figshare.1247634.v4
title: SMASH – semi-automatic muscle analysis using segmentation of histology: a MATLAB application

description: SMASH is composed of a set of functions enabling the user analyze aspects of histological muscle sections. Image segmentation: identifies potential muscle fibers. Fiber filter: removes non fiber elements. Fiber properties computes parameters related to fiber size. Fiber type: determines which fibers are positively stained within an image. Central nucleation: determines which fibers have central nuclei within an image. Object counter: identifies non fiber objects within an image. SMASH Stand Alone requires MATLAB Compiler Runtime (MCR) version R2014a (8.3) which is freely available from Mathworks (http://www.mathworks.com/products/compiler/mcr/). SMASH App requires MATLAB version R2014a (8.3) or later with the Image Processing Toolbox.
DOI: 10.6084/m9.figshare.1247641.v1
title: RNA shotgun metagenomic sequencing of northern California mosquitoes uncovers viruses, bacteria, and fungi

description: Draft Abstract
DOI: 10.6084/m9.figshare.1247629
title: Stress Heterogeneities in Sheared Type-I Collagen Networks Revealed by Boundary Stress Microscopy

description: These are the data for the PLOS one manuscript by Arevalo et al.
DOI: 10.6084/m9.figshare.1247628
title: Coastal land

description: Coastal land management - property rights restrictions and responsibilities in the coastal zone and high water mark
DOI: 10.6084/m9.figshare.1247659.v3
title: Restoration of CFTR function in patients with cystic fibrosis carrying the F508del-CFTR mutation

description: Restoration of BECN1/Beclin 1-dependent autophagy and depletion of SQSTM1/p62 by genetic manipulation or autophagy-stimulatory proteostasis regulators, such as cystamine, have positive effects on mouse models of human cystic fibrosis (CF). These measures rescue the functional expression of the most frequent pathogenic CFTR mutant, F508del, at the respiratory epithelial surface and reduce lung inflammation in <i>Cftr<sup>F508del</sup></i> homozygous mice. Cysteamine, the reduced form of cystamine, is an FDA-approved drug. Here, we report that oral treatment with cysteamine greatly reduces the mortality rate and improves the phenotype of newborn mice bearing the <i>F508del-CFTR</i> mutation. Cysteamine was also able to increase the plasma membrane expression of the F508del-CFTR protein in nasal epithelial cells from <i>F508del</i> homozygous CF patients, and these effects persisted for 24 h after cysteamine withdrawal. Importantly, this cysteamine effect after washout was further sustained by the sequential administration of epigallocatechin gallate (EGCG), a green tea flavonoid, both <i>in vivo</i>, in mice, and <i>in vitro</i>, in primary epithelial cells from CF patients. In a pilot clinical trial involving 10 <i>F508del-CFTR</i> homozygous CF patients, the combination of cysteamine and EGCG restored BECN1, reduced SQSTM1 levels and improved CFTR function from nasal epithelial cells <i>in vivo</i>, correlating with a decrease of chloride concentrations in sweat, as well as with a reduction of the abundance of <i>TNF/TNF-alpha (tumor necrosis factor)</i> and <i>CXCL8</i> (<i>chemokine [C-X-C motif] ligand 8</i>) transcripts in nasal brushing and TNF and CXCL8 protein levels in the sputum. Altogether, these results suggest that optimal schedules of cysteamine plus EGCG might be used for the treatment of CF caused by the <i>F508del-CFTR</i> mutation.
DOI: 10.6084/m9.figshare.1247628.v1
title: Coastal land

description: Coastal land management - property rights restrictions and responsibilities in the coastal zone and high water mark
DOI: 10.6084/m9.figshare.1247641.v2
title: RNA shotgun metagenomic sequencing of northern California mosquitoes uncovers viruses, bacteria, and fungi

description: See the README file for details
DOI: 10.6084/m9.figshare.1247659.v5
title: Restoration of CFTR function in patients with cystic fibrosis carrying the F508del-CFTR mutation

description: Restoration of BECN1/Beclin 1-dependent autophagy and depletion of SQSTM1/p62 by genetic manipulation or autophagy-stimulatory proteostasis regulators, such as cystamine, have positive effects on mouse models of human cystic fibrosis (CF). These measures rescue the functional expression of the most frequent pathogenic CFTR mutant, F508del, at the respiratory epithelial surface and reduce lung inflammation in <i>Cftr<sup>F508del</sup></i> homozygous mice. Cysteamine, the reduced form of cystamine, is an FDA-approved drug. Here, we report that oral treatment with cysteamine greatly reduces the mortality rate and improves the phenotype of newborn mice bearing the <i>F508del-CFTR</i> mutation. Cysteamine was also able to increase the plasma membrane expression of the F508del-CFTR protein in nasal epithelial cells from <i>F508del</i> homozygous CF patients, and these effects persisted for 24 h after cysteamine withdrawal. Importantly, this cysteamine effect after washout was further sustained by the sequential administration of epigallocatechin gallate (EGCG), a green tea flavonoid, both <i>in vivo</i>, in mice, and <i>in vitro</i>, in primary epithelial cells from CF patients. In a pilot clinical trial involving 10 <i>F508del-CFTR</i> homozygous CF patients, the combination of cysteamine and EGCG restored BECN1, reduced SQSTM1 levels and improved CFTR function from nasal epithelial cells <i>in vivo</i>, correlating with a decrease of chloride concentrations in sweat, as well as with a reduction of the abundance of <i>TNF/TNF-alpha (tumor necrosis factor)</i> and <i>CXCL8</i> (<i>chemokine [C-X-C motif] ligand 8</i>) transcripts in nasal brushing and TNF and CXCL8 protein levels in the sputum. Altogether, these results suggest that optimal schedules of cysteamine plus EGCG might be used for the treatment of CF caused by the <i>F508del-CFTR</i> mutation.
DOI: 10.6084/m9.figshare.1247629.v1
title: PLOS One

description: These are the data for the PLOS one manuscript by Arevalo et al.
DOI: 10.6084/m9.figshare.1247659.v4
title: Restoration of CFTR function in patients with cystic fibrosis carrying the F508del-CFTR mutation

description: Restoration of BECN1/Beclin 1-dependent autophagy and depletion of SQSTM1/p62 by genetic manipulation or autophagy-stimulatory proteostasis regulators, such as cystamine, have positive effects on mouse models of human cystic fibrosis (CF). These measures rescue the functional expression of the most frequent pathogenic CFTR mutant, F508del, at the respiratory epithelial surface and reduce lung inflammation in <i>Cftr<sup>F508del</sup></i> homozygous mice. Cysteamine, the reduced form of cystamine, is an FDA-approved drug. Here, we report that oral treatment with cysteamine greatly reduces the mortality rate and improves the phenotype of newborn mice bearing the <i>F508del-CFTR</i> mutation. Cysteamine was also able to increase the plasma membrane expression of the F508del-CFTR protein in nasal epithelial cells from <i>F508del</i> homozygous CF patients, and these effects persisted for 24 h after cysteamine withdrawal. Importantly, this cysteamine effect after washout was further sustained by the sequential administration of epigallocatechin gallate (EGCG), a green tea flavonoid, both <i>in vivo</i>, in mice, and <i>in vitro</i>, in primary epithelial cells from CF patients. In a pilot clinical trial involving 10 <i>F508del-CFTR</i> homozygous CF patients, the combination of cysteamine and EGCG restored BECN1, reduced SQSTM1 levels and improved CFTR function from nasal epithelial cells <i>in vivo</i>, correlating with a decrease of chloride concentrations in sweat, as well as with a reduction of the abundance of <i>TNF/TNF-alpha (tumor necrosis factor)</i> and <i>CXCL8</i> (<i>chemokine [C-X-C motif] ligand 8</i>) transcripts in nasal brushing and TNF and CXCL8 protein levels in the sputum. Altogether, these results suggest that optimal schedules of cysteamine plus EGCG might be used for the treatment of CF caused by the <i>F508del-CFTR</i> mutation.
DOI: 10.6084/m9.figshare.1247629.v3
title: Stress Heterogeneities in Sheared Type-I Collagen Networks Revealed by Boundary Stress Microscopy

description: These are the data for the PLOS one manuscript by Arevalo et al.
DOI: 10.6084/m9.figshare.1247641.v3
title: RNA shotgun metagenomic sequencing of northern California mosquitoes uncovers viruses, bacteria, and fungi

description: See the README file for details
DOI: 10.6084/m9.figshare.1247629.v2
title: PLOS One

description: These are the data for the PLOS one manuscript by Arevalo et al.
DOI: 10.6084/m9.figshare.1247641.v4
title: RNA shotgun metagenomic sequencing of northern California mosquitoes uncovers viruses, bacteria, and fungi

description: See the README file for details
DOI: 10.6084/m9.figshare.1247500
title: Gaussian Job Archive for F2I6

description: Archive of work produced using the resources of the Imperial College High Performance Computing Service.
DOI: 10.6084/m9.figshare.1247641.v5
title: RNA shotgun metagenomic sequencing of northern California mosquitoes uncovers viruses, bacteria, and fungi

description: See the README file for details
DOI: 10.6084/m9.figshare.1247500.v1
title: Gaussian Job Archive for F2I6

description: Archive of work produced using the resources of the Imperial College High Performance Computing Service.
DOI: 10.6084/m9.figshare.1247220
title: BASTI stellar model grid

description: BASTI stellar model grids. This data is stored here in order to be downloaded by the 'isochrones' python package upon installation.
DOI: 10.6084/m9.figshare.1247208
title: Dartmouth stellar models triangulation

description: A python pickle file of a Qhull triangulation of mass, age, and metallicity of the Dartmouth stellar models. This file is meant to be downloaded and used by the 'isochrones' python module.
DOI: 10.6084/m9.figshare.1247204
title: Padova stellar model grid

description: Padova stellar model grid to be used by 'isochrones' python module (by automatic download).