cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.11762862
title: Candidate genes involved in the defunctionalization and refunctionalization of the urinary bladder induced by bladder anuria and reperfusionem

description: <b>Supplementary Table S1: </b>Demographic data of the 44 patients who received dialysis prior to kidney transplantation.<b>Supplementary Table S2: </b>Primer sets used for the quantitative RT-PCR.<br><b>Supplementary Table S3: </b>List of top and bottom KEGG pathways that were significantly up-regulated and down-regulated from the control to the defunctionalized group and from the defunctionalized to the refunctionalized group in the rabbit DNA microarray analysis stratified with Z-scores of the parametric analysis of gene-set enrichment higher than three.<br><b>Supplementary Table S4:</b> Comparison of the changes in the relative gene expression level of collagens among the rabbit bladder DNA microarray, rabbit bladder RT-PCR, and human bladder RT-PCR of the control and defunctionalized groups and the defunctionalized and refunctionalized groups.
DOI: 10.6084/m9.figshare.11762862.v1
title: Candidate genes involved in the defunctionalization and refunctionalization of the urinary bladder induced by bladder anuria and reperfusionem

description: <b>Supplementary Table S1: </b>Demographic data of the 44 patients who received dialysis prior to kidney transplantation.<b>Supplementary Table S2: </b>Primer sets used for the quantitative RT-PCR.<br><b>Supplementary Table S3: </b>List of top and bottom KEGG pathways that were significantly up-regulated and down-regulated from the control to the defunctionalized group and from the defunctionalized to the refunctionalized group in the rabbit DNA microarray analysis stratified with Z-scores of the parametric analysis of gene-set enrichment higher than three.<br><b>Supplementary Table S4:</b> Comparison of the changes in the relative gene expression level of collagens among the rabbit bladder DNA microarray, rabbit bladder RT-PCR, and human bladder RT-PCR of the control and defunctionalized groups and the defunctionalized and refunctionalized groups.
DOI: 10.6084/m9.figshare.11762655
title: Intracellular recordings showing difference in activity between gamma and alpha rhythms in L4 principal cells

description: Glass microelectrode (sharp) intracellular recordings of V1L4 pyramids (L4 pyr in filename) or stellate cells (stellate in filename) during population gamma rhythms and alpha rhythms. Most recordings are passive (i.e. at rmp once impaled) and from somata. Dendritic recordings are labelled as such in the filename.
DOI: 10.6084/m9.figshare.11762640
title: Raw image examples of biocytin-filled cells and local Kv10.2 antibody signal

description: Examples of neurons in V1L4 filled with biocytin (red) on a filed of Kv10.2 antibody signal. Cell 1 is a bursting pyramid, cell 2 a regular spiking stellate. Images are Zeiss files viewable and manipulable with free Zen software.
DOI: 10.6084/m9.figshare.11762565
title: Local field potential recordings showing V1L4 gamma and alpha in vitro

description: Glass microelectrode LFP recordings from V1L4 in coronal slices showing kainate-induced gamma rhythms and subsequent alpha rhythms on reduced AMPAR-mediated synaptic excitation. Files are axograph format readable with Axograph (read-only version is freely avaible online).
DOI: 10.6084/m9.figshare.11762508
title: 32 channel Field array recording of V1 alpha rhythm in vitro

description: In vitro alpha rhythm model data. 32 channel Tucker Davis electrode system converted to Matlab. Includes raw data with bandwith sufficient to extract unit/MUA activity and local field potential.
DOI: 10.6084/m9.figshare.11762541
title: DLBC.somatic.mutations.txt

description: Somatic mutations of 48 lymphoma cases
DOI: 10.6084/m9.figshare.11762541.v1
title: DLBC.somatic.mutations.txt

description: Somatic mutations of 48 lymphoma cases
DOI: 10.6084/m9.figshare.11762415
title: Survival_ananlysis_driver_genes.txt

description: Survival analysis for driver genes in 48 lymphoma cases
DOI: 10.6084/m9.figshare.11762415.v1
title: Survival_ananlysis_driver_genes.txt

description: Survival analysis for driver genes in 48 lymphoma cases
DOI: 10.6084/m9.figshare.11762400
title: Survival_ananlysis_CNVs.txt

description: CNVs data for survival analysis
DOI: 10.6084/m9.figshare.11762379
title: WGCNA.normalized.read.counts.driver.genes.txt

description: WGCNA expression data of 48 lymphoma cases
DOI: 10.6084/m9.figshare.11762379.v1
title: WGCNA.normalized.read.counts.driver.genes.txt

description: WGCNA expression data of 48 lymphoma cases
DOI: 10.6084/m9.figshare.11762400.v2
title: Survival_ananlysis_CNVs.txt

description: CNVs data for survival analysis
DOI: 10.6084/m9.figshare.11762400.v1
title: Survival_ananlysis_CNVs.txt

description: CNVs data for survival analysis
DOI: 10.6084/m9.figshare.11762349
title: WGCNA clinical features

description: Clinical features of 48 lymphoma cases for WGCNA analysis
DOI: 10.6084/m9.figshare.11762349.v1
title: WGCNA clinical features

description: Clinical features of 48 lymphoma cases for WGCNA analysis
DOI: 10.6084/m9.figshare.11762349.v2
title: WGCNA clinical features

description: Clinical features of 48 lymphoma cases for WGCNA analysis
DOI: 10.6084/m9.figshare.11762232
title: Sulawesi plots soil metals

description: Soil samples were collected from each of the 10 x 10 m subplots within each plot and pooled to form a single sample per plot. Total C measurement used the Walkley and Black method, total N the Kjeldahl method and total soil Al, Ca, Co, Cr, Cu, Fe, K, Mg, Mn, Ni, P and Zn was quantified via digestion of 0.5 g soil in 5 ml HNO<sub>3</sub> and 1 ml HClO<sub>4</sub> at 100 to 200 ° C by ramping over a 7 hour period then diluted to 25 ml with deionised water and analysis on an Agilent Technologies 4100 microwave plasma atomic emission spectrometer (Co, Cr and Ni) or an Agilent Technologies 200 Series atomic absorption spectrometer (all other elements). <br>
DOI: 10.6084/m9.figshare.11762232.v1
title: Sulawesi plots soil metals

description: Soil samples were collected from each of the 10 x 10 m subplots within each plot and pooled to form a single sample per plot. Total C measurement used the Walkley and Black method, total N the Kjeldahl method and total soil Al, Ca, Co, Cr, Cu, Fe, K, Mg, Mn, Ni, P and Zn was quantified via digestion of 0.5 g soil in 5 ml HNO<sub>3</sub> and 1 ml HClO<sub>4</sub> at 100 to 200 ° C by ramping over a 7 hour period then diluted to 25 ml with deionised water and analysis on an Agilent Technologies 4100 microwave plasma atomic emission spectrometer (Co, Cr and Ni) or an Agilent Technologies 200 Series atomic absorption spectrometer (all other elements). <br>
DOI: 10.6084/m9.figshare.11762223
title: Neuronal microRNAs modulate TREK two-pore domain K<sup>+</sup> channel expression and current density

description: The TREK family of leak potassium channels has been found to play critical roles in nociception, sensitivity to general anaesthetics, neuroprotection, and memory. The three members of the family, TREK1, TREK2 and TRAAK establish the resting potential and modify the duration, frequency and amplitude of action potentials. Despite their apparent importance, the repertoire of regulatory interactions utilized by cells to control their expression is poorly understood. Herein, the contribution of miRNAs in the regulation of their post-transcriptional gene expression has been examined. Using different assays, miR-124 and to a lesser extent miR-128 and miR-183 were found to reduce TREK1 and TREK2 levels through specific binding to their 3ʹUTRs. In contrast, miR-9 which was predicted to bind to TRAAK 3ʹUTR, did not alter its expression. Expression of miR-124, miR-128 and miR-183 was found to mirror that of <i>Trek1</i> and <i>Trek2</i> mRNAs during brain development. Moreover, application of proinflammatory mediators in dorsal root ganglion (DRG) neurons revealed an inverse correlation between miR-124 and <i>Trek1</i> and <i>Trek2</i> mRNA expression. Voltage clamp recordings of TREK2-mediated currents showed that miR-124 reduced the sensitivity of TREK2-expressing cells to non-aversive warmth stimulation. Overall, these findings reveal a significant regulatory mechanism by which TREK1 and TREK2 expression and hence activity are controlled in neurons and uncover new druggable targets for analgesia and neuroprotection. <b>Abbreviations:</b> microRNA: miRNA; UTR: untranslated region; K<sub>2p</sub> channels: two-pore domain K<sup>+</sup>channels; DRG: dorsal root ganglion; CNS: central nervous system; FBS: fetal bovine serum; TuD: Tough Decoy; TREK: tandem P-domain weak inward rectifying K<sup>+</sup> (TWIK)-related K<sup>+</sup> channel 1; TRAAK: TWIK-related arachidonic acid K<sup>+</sup>.
DOI: 10.6084/m9.figshare.11762217
title: DLBC.somatic.mutations.txt

description: Somatic mutations in 48 lymphoma cases
DOI: 10.6084/m9.figshare.11762223.v2
title: Neuronal microRNAs modulate TREK two-pore domain K<sup>+</sup> channel expression and current density

description: The TREK family of leak potassium channels has been found to play critical roles in nociception, sensitivity to general anaesthetics, neuroprotection, and memory. The three members of the family, TREK1, TREK2 and TRAAK establish the resting potential and modify the duration, frequency and amplitude of action potentials. Despite their apparent importance, the repertoire of regulatory interactions utilized by cells to control their expression is poorly understood. Herein, the contribution of miRNAs in the regulation of their post-transcriptional gene expression has been examined. Using different assays, miR-124 and to a lesser extent miR-128 and miR-183 were found to reduce TREK1 and TREK2 levels through specific binding to their 3ʹUTRs. In contrast, miR-9 which was predicted to bind to TRAAK 3ʹUTR, did not alter its expression. Expression of miR-124, miR-128 and miR-183 was found to mirror that of <i>Trek1</i> and <i>Trek2</i> mRNAs during brain development. Moreover, application of proinflammatory mediators in dorsal root ganglion (DRG) neurons revealed an inverse correlation between miR-124 and <i>Trek1</i> and <i>Trek2</i> mRNA expression. Voltage clamp recordings of TREK2-mediated currents showed that miR-124 reduced the sensitivity of TREK2-expressing cells to non-aversive warmth stimulation. Overall, these findings reveal a significant regulatory mechanism by which TREK1 and TREK2 expression and hence activity are controlled in neurons and uncover new druggable targets for analgesia and neuroprotection. <b>Abbreviations:</b> microRNA: miRNA; UTR: untranslated region; K<sub>2p</sub> channels: two-pore domain K<sup>+</sup>channels; DRG: dorsal root ganglion; CNS: central nervous system; FBS: fetal bovine serum; TuD: Tough Decoy; TREK: tandem P-domain weak inward rectifying K<sup>+</sup> (TWIK)-related K<sup>+</sup> channel 1; TRAAK: TWIK-related arachidonic acid K<sup>+</sup>.
DOI: 10.6084/m9.figshare.11762223.v1
title: Neuronal microRNAs modulate TREK two-pore domain K<sup>+</sup> channel expression and current density

description: The TREK family of leak potassium channels has been found to play critical roles in nociception, sensitivity to general anaesthetics, neuroprotection, and memory. The three members of the family, TREK1, TREK2 and TRAAK establish the resting potential and modify the duration, frequency and amplitude of action potentials. Despite their apparent importance, the repertoire of regulatory interactions utilized by cells to control their expression is poorly understood. Herein, the contribution of miRNAs in the regulation of their post-transcriptional gene expression has been examined. Using different assays, miR-124 and to a lesser extent miR-128 and miR-183 were found to reduce TREK1 and TREK2 levels through specific binding to their 3ʹUTRs. In contrast, miR-9 which was predicted to bind to TRAAK 3ʹUTR, did not alter its expression. Expression of miR-124, miR-128 and miR-183 was found to mirror that of <i>Trek1</i> and <i>Trek2</i> mRNAs during brain development. Moreover, application of proinflammatory mediators in dorsal root ganglion (DRG) neurons revealed an inverse correlation between miR-124 and <i>Trek1</i> and <i>Trek2</i> mRNA expression. Voltage clamp recordings of TREK2-mediated currents showed that miR-124 reduced the sensitivity of TREK2-expressing cells to non-aversive warmth stimulation. Overall, these findings reveal a significant regulatory mechanism by which TREK1 and TREK2 expression and hence activity are controlled in neurons and uncover new druggable targets for analgesia and neuroprotection.
DOI: 10.6084/m9.figshare.11762217.v1
title: DLBC.somatic.mutations.txt

description: Somatic mutations in 48 lymphoma cases
DOI: 10.6084/m9.figshare.11762193
title: Supplementary Material for: Prevalence, Mortality, and Cause of Death in Charcot-Marie-Tooth Disease in Korea: A Nationwide, Population-Based Study

description: <b><i>Background:</i></b> Charcot-Marie-Tooth disease (CMT) is a group of clinically and genetically heterogeneous disorders that primarily affect the peripheral nervous system. Epidemiological studies of CMT have not yet been performed in Korea. <b><i>Objectives:</i></b> This study was performed to estimate the prevalence of CMT in Korea and the socioeconomic status, mortality, and causes of death of Korean patients with CMT. <b><i>Methods:</i></b> Data on patients with CMT were obtained from the rare intractable disease registry and the National Health Insurance Service for the years 2005–2018. <b><i>Results:</i></b> During the study period, 2,885 CMT patients were enrolled. The prevalence per 100,000 persons in 2018 was 5.2 (6.1 for men and 4.4 for women), peaking at ages 15–39 years, with almost twice as many men (<i>n</i> = 714) as women (<i>n</i> = 402) in this age group. Of the CMT patients, 226 (7.8%) were receiving medical aid, a public assistance program targeting poor individuals, at the time of diagnosis and 253 (8.8%) at last follow-up or death. From 2005 to 2017, 170 patients died, including 118 men and 52 women. The standardized mortality ratio (SMR) was 1.57 (95% CI 1.34–1.83) for all patients and did not differ in men and women. Age-specific SMR was highest in patients aged under 9 years, gradually declining thereafter. Neurologic disease as a cause of death was significantly more frequent in CMT patients than in the general population. <b><i>Conclusions:</i></b> This was the first nationwide epidemiologic study of CMT patients in Korea. This study confirmed the characteristics associated with the prevalence of and mortality from CMT by age and is the first to report the socioeconomic status and causes of death of CMT patients.
DOI: 10.6084/m9.figshare.11762193.v1
title: Supplementary Material for: Prevalence, Mortality, and Cause of Death in Charcot-Marie-Tooth Disease in Korea: A Nationwide, Population-Based Study

description: <b><i>Background:</i></b> Charcot-Marie-Tooth disease (CMT) is a group of clinically and genetically heterogeneous disorders that primarily affect the peripheral nervous system. Epidemiological studies of CMT have not yet been performed in Korea. <b><i>Objectives:</i></b> This study was performed to estimate the prevalence of CMT in Korea and the socioeconomic status, mortality, and causes of death of Korean patients with CMT. <b><i>Methods:</i></b> Data on patients with CMT were obtained from the rare intractable disease registry and the National Health Insurance Service for the years 2005–2018. <b><i>Results:</i></b> During the study period, 2,885 CMT patients were enrolled. The prevalence per 100,000 persons in 2018 was 5.2 (6.1 for men and 4.4 for women), peaking at ages 15–39 years, with almost twice as many men (<i>n</i> = 714) as women (<i>n</i> = 402) in this age group. Of the CMT patients, 226 (7.8%) were receiving medical aid, a public assistance program targeting poor individuals, at the time of diagnosis and 253 (8.8%) at last follow-up or death. From 2005 to 2017, 170 patients died, including 118 men and 52 women. The standardized mortality ratio (SMR) was 1.57 (95% CI 1.34–1.83) for all patients and did not differ in men and women. Age-specific SMR was highest in patients aged under 9 years, gradually declining thereafter. Neurologic disease as a cause of death was significantly more frequent in CMT patients than in the general population. <b><i>Conclusions:</i></b> This was the first nationwide epidemiologic study of CMT patients in Korea. This study confirmed the characteristics associated with the prevalence of and mortality from CMT by age and is the first to report the socioeconomic status and causes of death of CMT patients.
DOI: 10.6084/m9.figshare.11762151
title: Sulawesi primary plot coordinates

description: Forest plot coordinates in Sulawesi
DOI: 10.6084/m9.figshare.11762151.v1
title: Sulawesi primary plot coordinates

description: Forest plot coordinates in Sulawesi
DOI: 10.6084/m9.figshare.11761839
title: Supplementary Material for: Reliability of Home Nocturnal Oximetry in the Diagnosis of Overlap Syndrome in COPD

description: <b><i>Background:</i></b> Chronic obstructive pulmonary disease (COPD) and sleep apnea are common conditions and often coexist. The proper diagnosis of sleep apnea may affect the management and outcome of patients with COPD. <b><i>Objective:</i></b> To determine the accuracy of home nocturnal oximetry to distinguish between nocturnal oxygen desaturation related to COPD alone or to sleep apnea in patients with moderate-to-severe COPD who have significant nocturnal hypoxemia with cyclical changes in saturation. <b><i>Methods:</i></b> This study involved a comparison of home nocturnal oximetry and laboratory-based polysomnography (PSG) in patients with moderate-to-severe COPD considered for inclusion in a trial of nocturnal oxygen therapy. All of the patients had significant nocturnal oxygen desaturation (defined as ≥30% of the recording time with a transcutaneous arterial oxygen saturation &lt;90%) with cyclical changes in saturation suggestive of sleep apnea. <b><i>Results:</i></b> PSG was obtained in 90 patients; 45 patients (mean age = 68 years, SD = 8; 71% men; mean forced expiratory volume in 1 s [FEV<sub>1</sub>] = 50.6% predicted value, SD = 18.6%; data from 41 patients) fulfilled the criteria for sleep apnea (mean apnea-hypopnea index = 32.6 events/h, SD = 19.9) and 45 patients (mean age = 69 years, SD = 8; 87% men; mean FEV<sub>1</sub> predicted value 44.6%, SD = 15%) did not (mean apnea-hypopnea index = 5.5 events/h, SD = 3.8). None of the patients’ characteristics (including demographic, anthropometric, and physiologic measures) predicted the diagnosis of sleep apnea according to PSG results. <b><i>Conclusion:</i></b> The diagnosis of sleep apnea in patients with moderate to severe COPD cannot rely on nocturnal oximetry alone, even when typical cyclical changes in saturation are seen on oximetry tracing. When suspecting an overlap syndrome, a full-night, in-laboratory PSG should be obtained.
DOI: 10.6084/m9.figshare.11761056
title: Incorporation of <i>in vitro</i> metabolism data and physiologically based pharmacokinetic modeling in a risk assessment for chloroprene

description: <b>Objective:</b> To develop a physiologically based pharmacokinetic (PBPK) model for chloroprene in the mouse, rat and human, relying only on <i>in vitro</i> data to estimate tissue metabolism rates and partitioning, and to apply the model to calculate an inhalation unit risk (IUR) for chloroprene. <b>Materials and methods:</b> Female B6C3F1 mice were the most sensitive species/gender for lung tumors in the 2-year bioassay conducted with chloroprene. The PBPK model included tissue metabolism rate constants for chloroprene estimated from results of <i>in vitro</i> gas uptake studies using liver and lung microsomes. To assess the validity of the PBPK model, a 6-hr, nose-only chloroprene inhalation study was conducted with female B6C3F1 mice in which both chloroprene blood concentrations and ventilation rates were measured. The PBPK model was then used to predict dose measures – amounts of chloroprene metabolized in lungs per unit time – in mice and humans. <b>Results:</b> The mouse PBPK model accurately predicted <i>in vivo</i> pharmacokinetic data from the 6-hr, nose-only chloroprene inhalation study. The PBPK model was used to conduct a cancer risk assessment based on metabolism of chloroprene to reactive epoxides in the lung, the target tissue in mice. The IUR was over100-fold lower than the IUR from the EPA Integrated Risk Information System (IRIS), which was based on inhaled chloroprene concentration. The different result from the PBPK model risk assessment arises from use of the more relevant tissue dose metric, amount metabolized, rather than inhaled concentration <b>Discussion and conclusions:</b> The revised chloroprene PBPK model is based on the best available science, including new test animal <i>in vivo</i> validation, updated literature review and a Markov-Chain Monte Carlo analysis to assess parameter uncertainty. Relying on both mouse and human metabolism data also provides an important advancement in the use of quantitative <i>in vitro</i> to <i>in vivo</i> extrapolation (QIVIVE). Inclusion of the best available science is especially important when deriving a toxicity value based on species extrapolation for the potential carcinogenicity of a reactive metabolite.
DOI: 10.6084/m9.figshare.11761056.v1
title: Incorporation of <i>in vitro</i> metabolism data and physiologically based pharmacokinetic modeling in a risk assessment for chloroprene

description: <b>Objective:</b> To develop a physiologically based pharmacokinetic (PBPK) model for chloroprene in the mouse, rat and human, relying only on <i>in vitro</i> data to estimate tissue metabolism rates and partitioning, and to apply the model to calculate an inhalation unit risk (IUR) for chloroprene. <b>Materials and methods:</b> Female B6C3F1 mice were the most sensitive species/gender for lung tumors in the 2-year bioassay conducted with chloroprene. The PBPK model included tissue metabolism rate constants for chloroprene estimated from results of <i>in vitro</i> gas uptake studies using liver and lung microsomes. To assess the validity of the PBPK model, a 6-hr, nose-only chloroprene inhalation study was conducted with female B6C3F1 mice in which both chloroprene blood concentrations and ventilation rates were measured. The PBPK model was then used to predict dose measures – amounts of chloroprene metabolized in lungs per unit time – in mice and humans. <b>Results:</b> The mouse PBPK model accurately predicted <i>in vivo</i> pharmacokinetic data from the 6-hr, nose-only chloroprene inhalation study. The PBPK model was used to conduct a cancer risk assessment based on metabolism of chloroprene to reactive epoxides in the lung, the target tissue in mice. The IUR was over100-fold lower than the IUR from the EPA Integrated Risk Information System (IRIS), which was based on inhaled chloroprene concentration. The different result from the PBPK model risk assessment arises from use of the more relevant tissue dose metric, amount metabolized, rather than inhaled concentration <b>Discussion and conclusions:</b> The revised chloroprene PBPK model is based on the best available science, including new test animal <i>in vivo</i> validation, updated literature review and a Markov-Chain Monte Carlo analysis to assess parameter uncertainty. Relying on both mouse and human metabolism data also provides an important advancement in the use of quantitative <i>in vitro</i> to <i>in vivo</i> extrapolation (QIVIVE). Inclusion of the best available science is especially important when deriving a toxicity value based on species extrapolation for the potential carcinogenicity of a reactive metabolite.