cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.1460843.v2
title: Thyroid hormone induction of mitochondrial activity is coupled to mitophagy via ROS-AMPK-ULK1 signaling

description: Currently, there is limited understanding about hormonal regulation of mitochondrial turnover. Thyroid hormone (T<sub>3</sub>) increases oxidative phosphorylation (OXPHOS), which generates reactive oxygen species (ROS) that damage mitochondria. However, the mechanism for maintenance of mitochondrial activity and quality control by this hormone is not known. Here, we used both in vitro and in vivo hepatic cell models to demonstrate that induction of mitophagy by T<sub>3</sub> is coupled to oxidative phosphorylation and ROS production. We show that T<sub>3</sub> induction of ROS activates CAMKK2 (calcium/calmodulin-dependent protein kinase kinase 2, β) mediated phosphorylation of PRKAA1/AMPK (5′ AMP-activated protein kinase), which in turn phosphorylates ULK1 (unc-51 like autophagy activating kinase 1) leading to its mitochondrial recruitment and initiation of mitophagy. Furthermore, loss of ULK1 in T<sub>3</sub>-treated cells impairs both mitophagy as well as OXPHOS without affecting T<sub>3</sub> induced general autophagy/lipophagy. These findings demonstrate a novel ROS-AMPK-ULK1 mechanism that couples T<sub>3</sub>-induced mitochondrial turnover with activity, wherein mitophagy is necessary not only for removing damaged mitochondria but also for sustaining efficient OXPHOS.
DOI: 10.6084/m9.figshare.1460836.v1
title: iCCM Central Uganda Minimal Data Set Household Survey

description: Between July 2010 and December 2012 a pre-post quasi-experimental study in eight districts with iCCM was conducted; 3 districts without iCCM served as controls. A two-stage household cluster survey at baseline (n=1036 and 1042) and end line (n = 3890 and 3844) was done in the intervention and comparison groups respectively. Changes in treatment coverage and timeliness were assessed using difference in differences analysis (DID). This is the Stata database that contains the endline and household cluster survey data that was used. See data dictionary for variable coding and questionnaire to understand where variables were obtained. Note wealth quintile was calculated based on assests, interaction term was added for Differences of differences analysis.
DOI: 10.6084/m9.figshare.1460812.v1
title: The German Economy during World War II and Allied Air Bombing

description: Student paper about Germany and Allied air bombing during WWII
DOI: 10.6084/m9.figshare.1460843.v3
title: Thyroid hormone induction of mitochondrial activity is coupled to mitophagy via ROS-AMPK-ULK1 signaling

description: Currently, there is limited understanding about hormonal regulation of mitochondrial turnover. Thyroid hormone (T<sub>3</sub>) increases oxidative phosphorylation (OXPHOS), which generates reactive oxygen species (ROS) that damage mitochondria. However, the mechanism for maintenance of mitochondrial activity and quality control by this hormone is not known. Here, we used both in vitro and in vivo hepatic cell models to demonstrate that induction of mitophagy by T<sub>3</sub> is coupled to oxidative phosphorylation and ROS production. We show that T<sub>3</sub> induction of ROS activates CAMKK2 (calcium/calmodulin-dependent protein kinase kinase 2, β) mediated phosphorylation of PRKAA1/AMPK (5′ AMP-activated protein kinase), which in turn phosphorylates ULK1 (unc-51 like autophagy activating kinase 1) leading to its mitochondrial recruitment and initiation of mitophagy. Furthermore, loss of ULK1 in T<sub>3</sub>-treated cells impairs both mitophagy as well as OXPHOS without affecting T<sub>3</sub> induced general autophagy/lipophagy. These findings demonstrate a novel ROS-AMPK-ULK1 mechanism that couples T<sub>3</sub>-induced mitochondrial turnover with activity, wherein mitophagy is necessary not only for removing damaged mitochondria but also for sustaining efficient OXPHOS.
DOI: 10.6084/m9.figshare.1460781
title: Test data for heatmaps

description: Test data for heatmaps
DOI: 10.6084/m9.figshare.1460843.v4
title: Thyroid hormone induction of mitochondrial activity is coupled to mitophagy via ROS-AMPK-ULK1 signaling

description: Currently, there is limited understanding about hormonal regulation of mitochondrial turnover. Thyroid hormone (T<sub>3</sub>) increases oxidative phosphorylation (OXPHOS), which generates reactive oxygen species (ROS) that damage mitochondria. However, the mechanism for maintenance of mitochondrial activity and quality control by this hormone is not known. Here, we used both in vitro and in vivo hepatic cell models to demonstrate that induction of mitophagy by T<sub>3</sub> is coupled to oxidative phosphorylation and ROS production. We show that T<sub>3</sub> induction of ROS activates CAMKK2 (calcium/calmodulin-dependent protein kinase kinase 2, β) mediated phosphorylation of PRKAA1/AMPK (5′ AMP-activated protein kinase), which in turn phosphorylates ULK1 (unc-51 like autophagy activating kinase 1) leading to its mitochondrial recruitment and initiation of mitophagy. Furthermore, loss of ULK1 in T<sub>3</sub>-treated cells impairs both mitophagy as well as OXPHOS without affecting T<sub>3</sub> induced general autophagy/lipophagy. These findings demonstrate a novel ROS-AMPK-ULK1 mechanism that couples T<sub>3</sub>-induced mitochondrial turnover with activity, wherein mitophagy is necessary not only for removing damaged mitochondria but also for sustaining efficient OXPHOS.
DOI: 10.6084/m9.figshare.1460765
title: new fileset

description: Previous studies have shown improved external chest compression (ECC) quality and delayed rescuer fatigue when the dominant hand (DH) was in contact with the sternum. However, many rescuers prefer placing the non-dominant hand (NH) in contact with the sternum during ECC. We aimed to investigate the effects of up-down hand position switch on the quality of ECC and the fatigue of rescuers during cardiopulmonary resuscitation (CPR). After completion of a review of the standard adult basic life support (BLS) course, every candidate performed 10 cycles of single adult CPR twice on an adult manikin with either a constant hand position (CH) or a switched hand position (SH) in random order at 7-day intervals. The rescuers’ general characteristics, hand positions, physiological signs, fatigue appearance and ECC qualities were recorded. Our results showed no significant differences in chest compression quality for the DH position rescuers between the CH and SH sessions (p&gt;0.05, resp.). And also no significant differences were found for Borg score (p=0.437) or cycle number (p=0.127) of fatigue appearance after chest compressions between the two sessions. However, for NH position rescuers, the appearance of fatigue was delayed (p=0.046), with a lower Borg score in the SH session (12.67 ± 2.03) compared to the CH session (13.33 ± 1.95) (p=0.011). Moreover, the compression depth was significantly greater in the SH session (39.3 ± 7.2 mm) compared to the CH session (36.3 ± 8.1 mm) (p=0.015). Our data suggest that the up-down hand position switch during CPR may delay the fatigue of non-dominant hand position rescuers and improve the quality of chest compressions.
DOI: 10.6084/m9.figshare.1460766
title: Bayesian model selection: The steepest mountain to climb

description: Capture-mark-recapture and individual body<br>size data on the noble pen shell (Pinna nobilis) used to illustrate methods in the paper.
DOI: 10.6084/m9.figshare.1460781.v1
title: Test data for heatmaps

description: Test data for heatmaps
DOI: 10.6084/m9.figshare.1460747
title: blast output format 6 lesson

description: This file includes blast output after performing filtering steps
DOI: 10.6084/m9.figshare.1460765.v1
title: new fileset

description: Previous studies have shown improved external chest compression (ECC) quality and delayed rescuer fatigue when the dominant hand (DH) was in contact with the sternum. However, many rescuers prefer placing the non-dominant hand (NH) in contact with the sternum during ECC. We aimed to investigate the effects of up-down hand position switch on the quality of ECC and the fatigue of rescuers during cardiopulmonary resuscitation (CPR). After completion of a review of the standard adult basic life support (BLS) course, every candidate performed 10 cycles of single adult CPR twice on an adult manikin with either a constant hand position (CH) or a switched hand position (SH) in random order at 7-day intervals. The rescuers’ general characteristics, hand positions, physiological signs, fatigue appearance and ECC qualities were recorded. Our results showed no significant differences in chest compression quality for the DH position rescuers between the CH and SH sessions (p&gt;0.05, resp.). And also no significant differences were found for Borg score (p=0.437) or cycle number (p=0.127) of fatigue appearance after chest compressions between the two sessions. However, for NH position rescuers, the appearance of fatigue was delayed (p=0.046), with a lower Borg score in the SH session (12.67 ± 2.03) compared to the CH session (13.33 ± 1.95) (p=0.011). Moreover, the compression depth was significantly greater in the SH session (39.3 ± 7.2 mm) compared to the CH session (36.3 ± 8.1 mm) (p=0.015). Our data suggest that the up-down hand position switch during CPR may delay the fatigue of non-dominant hand position rescuers and improve the quality of chest compressions.
DOI: 10.6084/m9.figshare.1460766.v1
title: Bayesian model selection: The steepest mountain to climb

description: Capture-mark-recapture and individual body<br>size data on the noble pen shell (Pinna nobilis) used to illustrate methods in the paper.
DOI: 10.6084/m9.figshare.1460736
title: Example BAM file

description: This is a subset of the reads aligning to the first 100kb of the chromosome 1 of from sample Col0_C1 of experiment MTAB-3279 (http://www.ebi.ac.uk/arrayexpress/experiments/E-MTAB-3279). Full data can be found here: http://www.ebi.ac.uk/arrayexpress/files/E-MTAB-3279/E-MTAB-3279.Col0_C1.snp.concordant_uniq.sorted.bam The corresponding SAM file can be found here: http://figshare.com/articles/Example_SAM_file/1460716
DOI: 10.6084/m9.figshare.1460737
title: Fastq sample dataset

description: sample data for data carpentry genomics https://github.com/plijnzaad/elixir-cloud-genomics/
DOI: 10.6084/m9.figshare.1460735
title: Example BAI file

description: Index file corresponding to BAM file http://figshare.com/articles/Example_BAM_file/1460736
DOI: 10.6084/m9.figshare.1460843.v5
title: Thyroid hormone induction of mitochondrial activity is coupled to mitophagy via ROS-AMPK-ULK1 signaling

description: Currently, there is limited understanding about hormonal regulation of mitochondrial turnover. Thyroid hormone (T<sub>3</sub>) increases oxidative phosphorylation (OXPHOS), which generates reactive oxygen species (ROS) that damage mitochondria. However, the mechanism for maintenance of mitochondrial activity and quality control by this hormone is not known. Here, we used both in vitro and in vivo hepatic cell models to demonstrate that induction of mitophagy by T<sub>3</sub> is coupled to oxidative phosphorylation and ROS production. We show that T<sub>3</sub> induction of ROS activates CAMKK2 (calcium/calmodulin-dependent protein kinase kinase 2, β) mediated phosphorylation of PRKAA1/AMPK (5′ AMP-activated protein kinase), which in turn phosphorylates ULK1 (unc-51 like autophagy activating kinase 1) leading to its mitochondrial recruitment and initiation of mitophagy. Furthermore, loss of ULK1 in T<sub>3</sub>-treated cells impairs both mitophagy as well as OXPHOS without affecting T<sub>3</sub> induced general autophagy/lipophagy. These findings demonstrate a novel ROS-AMPK-ULK1 mechanism that couples T<sub>3</sub>-induced mitochondrial turnover with activity, wherein mitophagy is necessary not only for removing damaged mitochondria but also for sustaining efficient OXPHOS.
DOI: 10.6084/m9.figshare.1460728
title: Blast output format lesson

description: This file includes blast output (format 6) of de novo sequncing annotation
DOI: 10.6084/m9.figshare.1460735.v1
title: Example BAI file

description: Index file corresponding to BAM file http://figshare.com/articles/Example_BAM_file/1460736
DOI: 10.6084/m9.figshare.1460722
title: Modest reproducibility success: a reanalysis of two early branching Metazoa datasets using ReproPhylo

description: This is an html file of the blog post "Modest reproducibility success: a reanalysis of two early branching Metazoa datasets using ReproPhylo" as in the link below.
DOI: 10.6084/m9.figshare.1460737.v1
title: Fastq sample dataset

description: sample data for data carpentry genomics https://github.com/plijnzaad/elixir-cloud-genomics/
DOI: 10.6084/m9.figshare.1460728.v2
title: Blast output format lesson

description: This file includes blast output (format 6) of de novo sequncing annotation
DOI: 10.6084/m9.figshare.1460719
title: University of Liverpool APCs 2015 (January-June)

description: This spreadsheet contains details of the article processing charges (APCs) paid by the University of Liverpool from 01 January 2015 to 22 June 2015. The data is being collected as part of Jisc's APC data collection project to address the Total Cost of Ownership of scholarly communication (https://www.jisc-collections.ac.uk/Jisc-Monitor/APC-data-collection/).
DOI: 10.6084/m9.figshare.1460843.v6
title: Thyroid hormone induction of mitochondrial activity is coupled to mitophagy via ROS-AMPK-ULK1 signaling

description: Currently, there is limited understanding about hormonal regulation of mitochondrial turnover. Thyroid hormone (T<sub>3</sub>) increases oxidative phosphorylation (OXPHOS), which generates reactive oxygen species (ROS) that damage mitochondria. However, the mechanism for maintenance of mitochondrial activity and quality control by this hormone is not known. Here, we used both in vitro and in vivo hepatic cell models to demonstrate that induction of mitophagy by T<sub>3</sub> is coupled to oxidative phosphorylation and ROS production. We show that T<sub>3</sub> induction of ROS activates CAMKK2 (calcium/calmodulin-dependent protein kinase kinase 2, β) mediated phosphorylation of PRKAA1/AMPK (5′ AMP-activated protein kinase), which in turn phosphorylates ULK1 (unc-51 like autophagy activating kinase 1) leading to its mitochondrial recruitment and initiation of mitophagy. Furthermore, loss of ULK1 in T<sub>3</sub>-treated cells impairs both mitophagy as well as OXPHOS without affecting T<sub>3</sub> induced general autophagy/lipophagy. These findings demonstrate a novel ROS-AMPK-ULK1 mechanism that couples T<sub>3</sub>-induced mitochondrial turnover with activity, wherein mitophagy is necessary not only for removing damaged mitochondria but also for sustaining efficient OXPHOS.
DOI: 10.6084/m9.figshare.1460717
title: Distribution of alternative start codons for each microbial Refseq genome

description: Distributions of alternative start codons for each microbial Refseq genome.
DOI: 10.6084/m9.figshare.1460718
title: Changes in the spatial patterns of human appropriation of net primary production (HANPP) in Europe 1990–2006

description: Changes in patterns of land use intesification (HANPP) in Europe between 1990 and 2006. Dataset used in Plutzar et al. (2015) Changes in the spatial patterns of human appropriation of net primary production (HANPP) in Europe 1990–2006. Regional Environmental Change. DOI 10.1007/s10113-015-0820-3 The global dataset is available here: https://www.uni-klu.ac.at/socec/inhalt/1191.htm
DOI: 10.6084/m9.figshare.1460728.v1
title: Blast output format lesson

description: This file includes blast output (format 6) of de novo sequncing annotation
DOI: 10.6084/m9.figshare.1460843.v8
title: Thyroid hormone induction of mitochondrial activity is coupled to mitophagy via ROS-AMPK-ULK1 signaling

description: Currently, there is limited understanding about hormonal regulation of mitochondrial turnover. Thyroid hormone (T<sub>3</sub>) increases oxidative phosphorylation (OXPHOS), which generates reactive oxygen species (ROS) that damage mitochondria. However, the mechanism for maintenance of mitochondrial activity and quality control by this hormone is not known. Here, we used both in vitro and in vivo hepatic cell models to demonstrate that induction of mitophagy by T<sub>3</sub> is coupled to oxidative phosphorylation and ROS production. We show that T<sub>3</sub> induction of ROS activates CAMKK2 (calcium/calmodulin-dependent protein kinase kinase 2, β) mediated phosphorylation of PRKAA1/AMPK (5′ AMP-activated protein kinase), which in turn phosphorylates ULK1 (unc-51 like autophagy activating kinase 1) leading to its mitochondrial recruitment and initiation of mitophagy. Furthermore, loss of ULK1 in T<sub>3</sub>-treated cells impairs both mitophagy as well as OXPHOS without affecting T<sub>3</sub> induced general autophagy/lipophagy. These findings demonstrate a novel ROS-AMPK-ULK1 mechanism that couples T<sub>3</sub>-induced mitochondrial turnover with activity, wherein mitophagy is necessary not only for removing damaged mitochondria but also for sustaining efficient OXPHOS.
DOI: 10.6084/m9.figshare.1460716
title: Example SAM file

description: This is a subset of the reads aligning to the first 100kb of the chromosome 1 of from sample Col0_C1 of experiment MTAB-3279 (http://www.ebi.ac.uk/arrayexpress/experiments/E-MTAB-3279). Full data can be found here: http://www.ebi.ac.uk/arrayexpress/files/E-MTAB-3279/E-MTAB-3279.Col0_C1.snp.concordant_uniq.sorted.bam
DOI: 10.6084/m9.figshare.1460843.v7
title: Thyroid hormone induction of mitochondrial activity is coupled to mitophagy via ROS-AMPK-ULK1 signaling

description: Currently, there is limited understanding about hormonal regulation of mitochondrial turnover. Thyroid hormone (T<sub>3</sub>) increases oxidative phosphorylation (OXPHOS), which generates reactive oxygen species (ROS) that damage mitochondria. However, the mechanism for maintenance of mitochondrial activity and quality control by this hormone is not known. Here, we used both in vitro and in vivo hepatic cell models to demonstrate that induction of mitophagy by T<sub>3</sub> is coupled to oxidative phosphorylation and ROS production. We show that T<sub>3</sub> induction of ROS activates CAMKK2 (calcium/calmodulin-dependent protein kinase kinase 2, β) mediated phosphorylation of PRKAA1/AMPK (5′ AMP-activated protein kinase), which in turn phosphorylates ULK1 (unc-51 like autophagy activating kinase 1) leading to its mitochondrial recruitment and initiation of mitophagy. Furthermore, loss of ULK1 in T<sub>3</sub>-treated cells impairs both mitophagy as well as OXPHOS without affecting T<sub>3</sub> induced general autophagy/lipophagy. These findings demonstrate a novel ROS-AMPK-ULK1 mechanism that couples T<sub>3</sub>-induced mitochondrial turnover with activity, wherein mitophagy is necessary not only for removing damaged mitochondria but also for sustaining efficient OXPHOS.
DOI: 10.6084/m9.figshare.1460719.v2
title: University of Liverpool APCs 2015 (January-June)

description: This spreadsheet contains details of the article processing charges (APCs) paid by the University of Liverpool from 01 January 2015 to 22 June 2015. The data is being collected as part of Jisc's APC data collection project to address the Total Cost of Ownership of scholarly communication (https://www.jisc-collections.ac.uk/Jisc-Monitor/APC-data-collection/).
DOI: 10.6084/m9.figshare.1457787
title: Reanimating the Signature from the Ashes: On Who There Is

description: The chapter "Reanimating the Signature from the Ashes: On Who There Is" from the dissertation entitled "Creation, Resistance, and Refacement: Postfuturist Storytelling, Cultural Flows, and the Remix." The paper "Mothership : (M)otherness and Authorship in <em>Tainted Love</em> by Stewart Home" presented at the conference<em> Motherhood and Creative Practice: Maternal Structures in Creative</em> <em>Work</em> held on 1-2 June 2015 at London South Bank University is based on this chapter.
DOI: 10.6084/m9.figshare.1460719.v1
title: University of Manchester APCs 2015 (January-June)

description: This spreadsheet contains details of the article processing charges (APCs) paid by the University of Liverpool from 01 January 2015 to 22 June 2015. The data is being collected as part of Jisc's APC data collection project to address the Total Cost of Ownership of scholarly communication (https://www.jisc-collections.ac.uk/Jisc-Monitor/APC-data-collection/).
DOI: 10.6084/m9.figshare.1456362
title: Example smFRET data files in Photon-HDF5 format

description: A few smFRET example data files in Photon-HDF5 format. <br>This work was partially supported by NIH Grant R01-GM95904.
DOI: 10.6084/m9.figshare.1456299
title: Structural Investigation of a Putative Phosphoserine Aminotransferase from C.hutchinsonii

description: Figures
DOI: 10.6084/m9.figshare.1456313
title: us-ALEX smFRET data

description: An example smFRET us-ALEX measurement in Photon-HDF5 format.
DOI: 10.6084/m9.figshare.1456296
title: MDH Coupled Assay

description: MDH Coupled Assay to test for aspartate aminotransferase activity.
DOI: 10.6084/m9.figshare.1456296.v1
title: MDH Coupled Assay

description: MDH Coupled Assay to test for aspartate aminotransferase activity.
DOI: 10.6084/m9.figshare.1457787.v1
title: Reanimating the Signature from the Ashes: On Who There Is

description: The chapter "Reanimating the Signature from the Ashes: On Who There Is" from the dissertation entitled "Creation, Resistance, and Refacement: Postfuturist Storytelling, Cultural Flows, and the Remix." The paper "Mothership : (M)otherness and Authorship in <em>Tainted Love</em> by Stewart Home" presented at the conference<em> Motherhood and Creative Practice: Maternal Structures in Creative</em> <em>Work</em> held on 1-2 June 2015 at London South Bank University is based on this chapter.
DOI: 10.6084/m9.figshare.1456299.v3
title: Structural Investigation of a Putative Phosphoserine Aminotransferase from C.hutchinsonii

description: Figures
DOI: 10.6084/m9.figshare.1457787.v3
title: Reanimating the Signature from the Ashes: On Who There Is

description: The chapter "Reanimating the Signature from the Ashes: On Who There Is" from the dissertation entitled "Creation, Resistance, and Refacement: Postfuturist Storytelling, Cultural Flows, and the Remix." The paper "Mothership : (M)otherness and Authorship in <em>Tainted Love</em> by Stewart Home" presented at the conference<em> Motherhood and Creative Practice: Maternal Structures in Creative</em> <em>Work</em> held on 1-2 June 2015 at London South Bank University is based on this chapter.
DOI: 10.6084/m9.figshare.1456295
title: Reynolds Creek, Idaho: Passive and active bedload tracer data

description: Data from active and passive tracers deployed in Reynolds Creek from spring 2011 and spring 2012. Active tracer data: Grain size distributions, detected motion periods, probabilities of transport with respect to time and discharge, cumulative displacements, average step lengths and rest times. Passive tracer data: Grain size distributions, cumulative displacements and comparison against model prediction.
DOI: 10.6084/m9.figshare.1456313.v1
title: us-ALEX smFRET data

description: An example smFRET us-ALEX measurement in Photon-HDF5 format.
DOI: 10.6084/m9.figshare.1456362.v1
title: Example smFRET data files in Photon-HDF5 format

description: A few smFRET example data files in Photon-HDF5 format. <br>This work was partially supported by NIH Grant R01-GM95904.
DOI: 10.6084/m9.figshare.1457787.v2
title: Reanimating the Signature from the Ashes: On Who There Is

description: The chapter "Reanimating the Signature from the Ashes: On Who There Is" from the dissertation entitled "Creation, Resistance, and Refacement: Postfuturist Storytelling, Cultural Flows, and the Remix." The paper "Mothership : (M)otherness and Authorship in <em>Tainted Love</em> by Stewart Home" presented at the conference<em> Motherhood and Creative Practice: Maternal Structures in Creative</em> <em>Work</em> held on 1-2 June 2015 at London South Bank University is based on this chapter.