cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.1184/r1/8201834.v2
title: Data and Analysis Code for Kantzos 2019: Design of Interpretable CNN. . .

description: This dataset is from the paper: "Design of an Interpretable Convolutional Neural Network for Stress Concentration Prediction in Rough Surfaces" by Kantzos et. al. (2019)<br>Paper Abstract: We present the application of a Convolutional Neural Network (CNN) to relate stress concentrations to surface roughness. Stress concentrations at the low points of rough surfaces are one of the primary causes of fatigue crack initiation but there is no generally accepted way to analyze rough surfaces to predict crack initiation. Synthetically generated rough surfaces, instantiated in a mechanical model allow for the simulation of stress concentrations, creating a database of surface images and corresponding mechanical data. In this work, the CNN is designed and trained to interpret a height map of a surface and, from that data, to predict the stress concentrations created by the surface. Using a simple architecture, the CNN achieved R2 = 0.75 in prediction for test images, i.e., those not used in training. This CNN can be adapted for experimental surfaces thus creating a new and straightforward tool for prediction of crack initiation. Considerable work was taken to minimize the complexity of the CNN architecture and to make it interpretable via viewports.<br><br>Herein are 4 files that can be downloaded to analyze the data, reproduce figures from the paper, and train new CNNs. The files are compressed directories. <br><br>
DOI: 10.1184/r1/8201834.v1
title: Data and Analysis Code for Kantzos 2019: Design of Interpretable CNN. . .

description: This dataset is from the paper: "Design of an Interpretable Convolutional Neural Network for Stress Concentration Prediction in Rough Surfaces" by Kantzos et. al. (2019)<br>Paper Abstract: We present the application of a Convolutional Neural Network (CNN) to relate stress concentrations to surface roughness. Stress concentrations at the low points of rough surfaces are one of the primary causes of fatigue crack initiation but there is no generally accepted way to analyze rough surfaces to predict crack initiation. Synthetically generated rough surfaces, instantiated in a mechanical model allow for the simulation of stress concentrations, creating a database of surface images and corresponding mechanical data. In this work, the CNN is designed and trained to interpret a height map of a surface and, from that data, to predict the stress concentrations created by the surface. Using a simple architecture, the CNN achieved R2 = 0.75 in prediction for test images, i.e., those not used in training. This CNN can be adapted for experimental surfaces thus creating a new and straightforward tool for prediction of crack initiation. Considerable work was taken to minimize the complexity of the CNN architecture and to make it interpretable via viewports.<br><br>Herein are 4 files that can be downloaded to analyze the data, reproduce figures from the paper, and train new CNNs. The files are compressed directories. <br><br>
DOI: 10.6084/m9.figshare.8201603
title: Circuit for Cardinal Direction 2

description: Full circuit for Cardinal direction 2
DOI: 10.6084/m9.figshare.8201603.v1
title: Circuit for Cardinal Direction 2

description: Full circuit for Cardinal direction 2
DOI: 10.6084/m9.figshare.8201600
title: Circuit for Cardinal Direction 1

description: Full circuit for Cardinal direction 1
DOI: 10.6084/m9.figshare.8201597
title: Response of Mi9-Mi4-C3-L5-L1 to sinusoidal stimuli

description: Response to sinusoidal stimulus 10 velocities (0.1Hz - 20Hz) in geometric progression. 10 seconds of data at 0.01 msec time step size. Columns are 2+2+2+2+3+1 (Per neuron in title and last column=input)
DOI: 10.6084/m9.figshare.8201597.v1
title: Response of Mi9-Mi4-C3-L5-L1 to sinusoidal stimuli

description: Response to sinusoidal stimulus 10 velocities (0.1Hz - 20Hz) in geometric progression. 10 seconds of data at 0.01 msec time step size. Columns are 2+2+2+2+3+1 (Per neuron in title and last column=input)
DOI: 10.6084/m9.figshare.8201600.v1
title: Circuit for Cardinal Direction 1

description: Full circuit for Cardinal direction 1
DOI: 10.6084/m9.figshare.8201567
title: Response of Mi9-Mi4-C3-L5-L1 to bar stimuli

description: Response to bar stimulus 10 velocities (12deg/s - 200deg/s) in geometric progression. 10 seconds of data at 0.01 msec time step size. Columns are 2+2+2+2+3+1 (Per neuron in title and last column=input)
DOI: 10.6084/m9.figshare.8201567.v1
title: Response of Mi9-Mi4-C3-L5-L1 to bar stimuli

description: Response to bar stimulus 10 velocities (12deg/s - 200deg/s) in geometric progression. 10 seconds of data at 0.01 msec time step size. Columns are 2+2+2+2+3+1 (Per neuron in title and last column=input)
DOI: 10.6084/m9.figshare.8201561
title: Response of T4 Cardinal Direction 2 to sinusoidal stimuli

description: Response to sinusoidal stimulus 8 directions X 10 velocities (0.1Hz - 20Hz) in geometric progression. 10 seconds of data at 0.01 msec time step size. For cardinal direction 2 circuit
DOI: 10.6084/m9.figshare.8201558
title: Response of T4 Cardinal Direction 1 to sinusoidal stimuli

description: Response to sinusoidal stimulus 8 directions X 10 velocities (0.1Hz - 20Hz) in geometric progression. 10 seconds of data at 0.01 msec time step size. For cardinal direction 1 circuit
DOI: 10.6084/m9.figshare.8201558.v1
title: Response of T4 Cardinal Direction 1 to sinusoidal stimuli

description: Response to sinusoidal stimulus 8 directions X 10 velocities (0.1Hz - 20Hz) in geometric progression. 10 seconds of data at 0.01 msec time step size. For cardinal direction 1 circuit
DOI: 10.6084/m9.figshare.8201561.v1
title: Response of T4 Cardinal Direction 2 to sinusoidal stimuli

description: Response to sinusoidal stimulus 8 directions X 10 velocities (0.1Hz - 20Hz) in geometric progression. 10 seconds of data at 0.01 msec time step size. For cardinal direction 2 circuit
DOI: 10.6084/m9.figshare.8201549
title: Response of T4 Cardinal Direction 2 to bar stimuli

description: Response to bar stimulus 8 directions X 10 velocities (12deg/s - 200deg/s) in geometric progression. 3 seconds of data at 0.01 msec time step size. For cardinal direction 2 circuit
DOI: 10.6084/m9.figshare.8201549.v1
title: Response of T4 Cardinal Direction 2 to bar stimuli

description: Response to bar stimulus 8 directions X 10 velocities (12deg/s - 200deg/s) in geometric progression. 3 seconds of data at 0.01 msec time step size. For cardinal direction 2 circuit
DOI: 10.6084/m9.figshare.8201492
title: Response of T4 Cardinal Direction 1 to bar stimuli

description: Response to bar stimulus 8 directions X 10 velocities (12deg/s - 200deg/s) in geometric progression. 3 seconds of data at 0.01 msec time step size. For cardinal direction 1 circuit
DOI: 10.6084/m9.figshare.8201492.v1
title: Response of T4 Cardinal Direction 1 to bar stimuli

description: Response to bar stimulus 8 directions X 10 velocities (12deg/s - 200deg/s) in geometric progression. 3 seconds of data at 0.01 msec time step size. For cardinal direction 1 circuit
DOI: 10.6084/m9.figshare.8201483
title: 14-grams number

description: 14-grams
DOI: 10.6084/m9.figshare.8201480
title: 14-grams

description: 14-grams
DOI: 10.6084/m9.figshare.8201483.v1
title: 14-grams number

description: 14-grams
DOI: 10.6084/m9.figshare.8201480.v1
title: 14-grams

description: 14-grams
DOI: 10.6084/m9.figshare.8201474
title: Supplemental Tables

description: Supplemental Tables for Tokyo Skytree airborne bacterial study (Uetake et al. 2019).<br>
DOI: 10.6084/m9.figshare.8201459
title: 13-grams number

description: 13-grams
DOI: 10.6084/m9.figshare.8201459.v1
title: 13-grams number

description: 13-grams
DOI: 10.6084/m9.figshare.8201453
title: 13-grams

description: 13-grams
DOI: 10.6084/m9.figshare.8201453.v1
title: 13-grams

description: 13-grams
DOI: 10.6084/m9.figshare.8199416
title: Annotation of Calanus finmarchicus transcriptome (NCBI Bioproject: PRJNA231164)

description: Annotation of Calanus finmarchicus transcriptome (Bioproject PRJNA231164; GBFB00000000.1). Annotated using Trinotate (version 3.0).
DOI: 10.6084/m9.figshare.8199374
title: Brain cooling marginally increases acute upper thermal tolerance in Atlantic cod

description: Physiological mechanisms determining thermal limits in fishes are debated but remain elusive. It has been hypothesised that motor function loss, observed as loss of equilibrium during acute warming, is due to direct thermal effects on brain neuronal function. To test this, we mounted cooling plates on the heads of Atlantic cod (<i>Gadus morhua</i>) and quantified whether local brain cooling increased whole-organism acute upper thermal tolerance. Brain cooling reduced brain temperature by 2-6°C below ambient water and increased thermal tolerance by 0.5 and 0.6°C on average relative to instrumented and uninstrumented controls, respectively, suggesting that direct thermal effects on brain neurons may contribute to setting upper thermal limits in fish. However, the improvement in thermal tolerance with brain cooling was small relative to the difference in brain temperature, demonstrating that other mechanisms (e.g., failure of spinal and peripheral neurons, or muscle) may also contribute to controlling acute thermal tolerance.
DOI: 10.6084/m9.figshare.8199416.v2
title: Annotation of Calanus finmarchicus transcriptome (NCBI Bioproject: PRJNA231164)

description: Annotation of Calanus finmarchicus transcriptome (Bioproject PRJNA231164; GBFB00000000.1). Annotated using Trinotate (version 3.0).
DOI: 10.6084/m9.figshare.8199359
title: 12-grams number

description: 12-grams
DOI: 10.6084/m9.figshare.8199359.v1
title: 12-grams number

description: 12-grams
DOI: 10.6084/m9.figshare.8199356
title: 12-grams

description: 12-grams
DOI: 10.6084/m9.figshare.8199374.v2
title: Brain cooling marginally increases acute upper thermal tolerance in Atlantic cod

description: Physiological mechanisms determining thermal limits in fishes are debated but remain elusive. It has been hypothesised that motor function loss, observed as loss of equilibrium during acute warming, is due to direct thermal effects on brain neuronal function. To test this, we mounted cooling plates on the heads of Atlantic cod (<i>Gadus morhua</i>) and quantified whether local brain cooling increased whole-organism acute upper thermal tolerance. Brain cooling reduced brain temperature by 2-6°C below ambient water and increased thermal tolerance by 0.5 and 0.6°C on average relative to instrumented and uninstrumented controls, respectively, suggesting that direct thermal effects on brain neurons may contribute to setting upper thermal limits in fish. However, the improvement in thermal tolerance with brain cooling was small relative to the difference in brain temperature, demonstrating that other mechanisms (e.g., failure of spinal and peripheral neurons, or muscle) may also contribute to controlling acute thermal tolerance.
DOI: 10.6084/m9.figshare.8199356.v1
title: 12-grams

description: 12-grams
DOI: 10.6084/m9.figshare.8199374.v1
title: Brain cooling marginally increases acute thermal tolerance in Atlantic cod

description: The physiological mechanisms determining thermal limits in fishes are debated but remain elusive. It has been hypothesised that loss of motor function observed as a loss of equilibrium during an acute thermal challenge is due to direct thermal effects on brain neuronal function. To test this hypothesis, we mounted cooling plates on the head of Atlantic cod (<i>Gadus morhua</i>) and quantified whether local cooling of the brain increased whole-organism upper thermal tolerance (CT<sub>max</sub>). Brain cooling reduced brain temperature by 2–6°C and increased CT<sub>max</sub> by 0.5–0.7°C relative to instrumented and uninstrumented controls, suggesting that direct thermal effects on brain neurons might contribute to setting upper thermal limits in fish. However, the improvement in CT<sub>max</sub> with brain cooling was small relative to the difference in brain temperature, demonstrating that other mechanisms (e.g. failure of spinal and peripheral neurons, or muscle) may also contribute to controlling acute thermal tolerance in fishes.
DOI: 10.6084/m9.figshare.8199350
title: 11-grams number

description: 11-grams
DOI: 10.6084/m9.figshare.8199347
title: 11-grams

description: 11-grams
DOI: 10.6084/m9.figshare.8199347.v1
title: 11-grams

description: 11-grams
DOI: 10.6084/m9.figshare.8199350.v1
title: 11-grams number

description: 11-grams
DOI: 10.6084/m9.figshare.8199329
title: 10-grams number

description: 10-grams
DOI: 10.6084/m9.figshare.8199326
title: 10-grams

description: 10-grams
DOI: 10.6084/m9.figshare.8199329.v1
title: 10-grams number

description: 10-grams
DOI: 10.6084/m9.figshare.8199326.v1
title: 10-grams

description: 10-grams
DOI: 10.6084/m9.figshare.8199290
title: Application of Bayesian networks in determining nanoparticle-induced cellular outcomes using transcriptomics

description: Inroads have been made in our understanding of the risks posed to human health and the environment by nanoparticles (NPs) but this area requires continuous research and monitoring. Machine learning techniques have been applied to nanotoxicology with very encouraging results. This study deals with bridging physicochemical properties of NPs, experimental exposure conditions and <i>in vitro</i> characteristics with biological effects of NPs on a molecular cellular level from transcriptomics studies. The bridging is done by developing and implementing Bayesian Networks (BNs) with or without data preprocessing. The BN structures are derived either automatically or methodologically and compared. Early stage nanotoxicity measurements represent a challenge, not least when attempting to predict adverse outcomes and modeling is critical to understanding the biological effects of exposure to NPs. The preprocessed data-driven BN showed improved performance over automatically structured BN and the BN with unprocessed datasets. The prestructured BN captures inter relationships between NP properties, exposure condition and <i>in vitro</i> characteristics and links those with cellular effects based on statistic correlation findings. Information gain analysis showed that exposure dose, NP and cell line variables were the most influential attributes in predicting the biological effects. The BN methodology proposed in this study successfully predicts a number of toxicologically relevant cellular disrupted biological processes such as cell cycle and proliferation pathways, cell adhesion and extracellular matrix responses, DNA damage and repair mechanisms etc., with a success rate &gt;80%. The model validation from independent data shows a robust and promising methodology for incorporating transcriptomics outcomes in a hazard and, by extension, risk assessment modeling framework by predicting affected cellular functions from experimental conditions.
DOI: 10.6084/m9.figshare.8199284
title: Pulmonary toxicity of inhaled nano-sized cerium oxide aerosols in Sprague–Dawley rats

description: Cerium oxide nanoparticles (CeO<sub>2</sub>NPs), used in some diesel fuel additives to improve fuel combustion efficiency and exhaust filter operation, have been detected in ambient air and concerns have been raised about their potential human health impact. The majority of CeO<sub>2</sub>NP inhalation studies undertaken to date have used aerosol particles of larger sizes than the evidence suggests are emitted from vehicles using such fuel additives. Hence, the objective of this study was to investigate the effects of inhaled CeO<sub>2</sub>NP aerosols of a more environmentally relevant size, utilizing a combination of methods, including untargeted multi-omics to enable the broadest possible survey of molecular responses and synchrotron X-ray spectroscopy to investigate cerium speciation. Male Sprague–Dawley rats were exposed by nose-only inhalation to aerosolized CeO<sub>2</sub>NPs (mass concentration 1.8<b> </b>mg/m<sup>3</sup>, aerosol count median diameter 40<b> </b>nm) for 3<b> </b>h/d for 4 d/week, for 1 or 2 weeks and sacrificed at 3 and 7<b> </b>d post-exposure. Markers of inflammation changed significantly in a dose- and time-dependent manner, which, combined with results from lung histopathology and gene expression analyses suggest an inflammatory response greater than that seen in studies using micron-sized ceria aerosols. Lipidomics of lung tissue revealed changes to minor lipid species, implying specific rather than general cellular effects. Cerium speciation analysis indicated a change in Ce<sup>3+</sup>/Ce<sup>4+</sup> ratio within lung tissue. Collectively, these results in conjunction with earlier studies emphasize the importance of aerosol particle size on toxicity determination. Furthermore, the limited effect resolution within 7<b> </b>d suggested the possibility of longer-term effects.
DOI: 10.6084/m9.figshare.8199284.v1
title: Pulmonary toxicity of inhaled nano-sized cerium oxide aerosols in Sprague–Dawley rats

description: Cerium oxide nanoparticles (CeO<sub>2</sub>NPs), used in some diesel fuel additives to improve fuel combustion efficiency and exhaust filter operation, have been detected in ambient air and concerns have been raised about their potential human health impact. The majority of CeO<sub>2</sub>NP inhalation studies undertaken to date have used aerosol particles of larger sizes than the evidence suggests are emitted from vehicles using such fuel additives. Hence, the objective of this study was to investigate the effects of inhaled CeO<sub>2</sub>NP aerosols of a more environmentally relevant size, utilizing a combination of methods, including untargeted multi-omics to enable the broadest possible survey of molecular responses and synchrotron X-ray spectroscopy to investigate cerium speciation. Male Sprague–Dawley rats were exposed by nose-only inhalation to aerosolized CeO<sub>2</sub>NPs (mass concentration 1.8<b> </b>mg/m<sup>3</sup>, aerosol count median diameter 40<b> </b>nm) for 3<b> </b>h/d for 4 d/week, for 1 or 2 weeks and sacrificed at 3 and 7<b> </b>d post-exposure. Markers of inflammation changed significantly in a dose- and time-dependent manner, which, combined with results from lung histopathology and gene expression analyses suggest an inflammatory response greater than that seen in studies using micron-sized ceria aerosols. Lipidomics of lung tissue revealed changes to minor lipid species, implying specific rather than general cellular effects. Cerium speciation analysis indicated a change in Ce<sup>3+</sup>/Ce<sup>4+</sup> ratio within lung tissue. Collectively, these results in conjunction with earlier studies emphasize the importance of aerosol particle size on toxicity determination. Furthermore, the limited effect resolution within 7<b> </b>d suggested the possibility of longer-term effects.
DOI: 10.6084/m9.figshare.8199290.v1
title: Application of Bayesian networks in determining nanoparticle-induced cellular outcomes using transcriptomics

description: Inroads have been made in our understanding of the risks posed to human health and the environment by nanoparticles (NPs) but this area requires continuous research and monitoring. Machine learning techniques have been applied to nanotoxicology with very encouraging results. This study deals with bridging physicochemical properties of NPs, experimental exposure conditions and <i>in vitro</i> characteristics with biological effects of NPs on a molecular cellular level from transcriptomics studies. The bridging is done by developing and implementing Bayesian Networks (BNs) with or without data preprocessing. The BN structures are derived either automatically or methodologically and compared. Early stage nanotoxicity measurements represent a challenge, not least when attempting to predict adverse outcomes and modeling is critical to understanding the biological effects of exposure to NPs. The preprocessed data-driven BN showed improved performance over automatically structured BN and the BN with unprocessed datasets. The prestructured BN captures inter relationships between NP properties, exposure condition and <i>in vitro</i> characteristics and links those with cellular effects based on statistic correlation findings. Information gain analysis showed that exposure dose, NP and cell line variables were the most influential attributes in predicting the biological effects. The BN methodology proposed in this study successfully predicts a number of toxicologically relevant cellular disrupted biological processes such as cell cycle and proliferation pathways, cell adhesion and extracellular matrix responses, DNA damage and repair mechanisms etc., with a success rate &gt;80%. The model validation from independent data shows a robust and promising methodology for incorporating transcriptomics outcomes in a hazard and, by extension, risk assessment modeling framework by predicting affected cellular functions from experimental conditions.
DOI: 10.6084/m9.figshare.8199257
title: 9-grams

description: 9-grams
DOI: 10.6084/m9.figshare.8199266
title: 9-grams number

description: 9-grams
DOI: 10.6084/m9.figshare.8199257.v1
title: 9-grams

description: 9-grams
DOI: 10.6084/m9.figshare.8199266.v1
title: 9-grams number

description: 9-grams
DOI: 10.6084/m9.figshare.8199182
title: 8-grams number

description: 8-grams
DOI: 10.6084/m9.figshare.8199182.v1
title: 8-grams number

description: 8-grams
DOI: 10.25373/ctsnet.8199215
title: Severe Right Atrial and Ventricular Compression From a Massive Morgagni Hernia and Paralyzed Right Hemidiaphragm

description: A 57-year-old woman, with a history of pericardiectomy 20 years before, reported progressive dyspnea and orthopnea. A chest computed tomography scan showed a large anterior diaphragmatic (Morgagni) hernia containing a loop of transverse colon and omentum producing mass effect on the right atrium and ventricle. Significant right ventricular outflow obstruction and a small loculated pericardial effusion were confirmed on cardiac magnetic resonance imaging. A sniff test suggested minimal to no motion of the right hemidiaphragm.<br>Reduction of the herniated transverse colon and omentum was performed via laparotomy, followed by reconstruction of the diaphragmatic defect with Gore-Tex mesh along with drainage of the complex pericardial effusion. This led to resolution of her orthopnea. Due to ongoing exertional dyspnea and continued decline in pulmonary function, she underwent a right hemidiaphragm plication 4 months later. This led to significant improvement in her exercise capacity. At 6-year follow-up, the patient was symptom free with no radiographic recurrence.<br>
DOI: 10.6084/m9.figshare.8199179
title: 8-grams

description: 8-grams
DOI: 10.6084/m9.figshare.8199179.v1
title: 8-grams

description: 8-grams
DOI: 10.25373/ctsnet.8199215.v1
title: Severe Right Atrial and Ventricular Compression From a Massive Morgagni Hernia and Paralyzed Right Hemidiaphragm

description: A 57-year-old woman, with a history of pericardiectomy 20 years before, reported progressive dyspnea and orthopnea. A chest computed tomography scan showed a large anterior diaphragmatic (Morgagni) hernia containing a loop of transverse colon and omentum producing mass effect on the right atrium and ventricle. Significant right ventricular outflow obstruction and a small loculated pericardial effusion were confirmed on cardiac magnetic resonance imaging. A sniff test suggested minimal to no motion of the right hemidiaphragm.<br>Reduction of the herniated transverse colon and omentum was performed via laparotomy, followed by reconstruction of the diaphragmatic defect with Gore-Tex mesh along with drainage of the complex pericardial effusion. This led to resolution of her orthopnea. Due to ongoing exertional dyspnea and continued decline in pulmonary function, she underwent a right hemidiaphragm plication 4 months later. This led to significant improvement in her exercise capacity. At 6-year follow-up, the patient was symptom free with no radiographic recurrence.<br>