cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.15468/dl.ydykf2
title: Occurrence Download

description: A dataset listing the 57 species recorded in GBIF matching the query:
{
 "and" : [
 "Country is one of (Costa Rica, Panama, El Salvador, Guatemala, Nicaragua, Honduras, Belize)",
 "TaxonKey is Limnichidae"
 ]
}

 The dataset's 57 records were derived from 19 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0003126-251120083545085/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.13140/rg.2.2.33743.96164
title: CS3362 -C Programming and Data Structures Laboratory
DOI: 10.15468/dl.pqymrv
title: Occurrence Download

description: A dataset containing 60 species occurrences available in GBIF matching the query:
{
 "and" : [
 "TaxonKey is one of (Sinobambusa tootsik (Makino) Makino ex Nakai)",
 "BasisOfRecord is one of (Specimen, Human Observation, Observation, Living Specimen, Machine Observation, Literature Occurrence)",
 "HasCoordinate is true",
 "HasGeospatialIssue is false"
 ]
}

 The dataset includes 60 records from 18 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0009440-250515123054153/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.eupjbw
title: Occurrence Download

description: A dataset containing 1750 species occurrences available in GBIF matching the query:
{
 "and" : [
 "Country is China",
 "HasCoordinate is true",
 "HasGeospatialIssue is false",
 "TaxonKey is Idesia polycarpa Maxim."
 ]
}

 The dataset includes 1750 records from 23 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0006606-250525065834625/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.5281/zenodo.8388598
title: Dataset used in the study "Urban microclimate simulations based on GIS data to mitigate thermal hot-spots: Tree design scenarios in an industrial area of Florence"

description: This dataset repository includes input and output spatial data of urban microclimate simulations performed through QGIS and ENVI-met software used in the study "Urban microclimate simulations based on GIS data to mitigate thermal hot-spots: Tree design scenarios in an industrial area of Florence", published in the Building and Environment Journal, https://doi.org/10.1016/j.buildenv.2023.110854.
DOI: 10.5281/zenodo.8388599
title: Dataset used in the study "Urban microclimate simulations based on GIS data to mitigate thermal hot-spots: Tree design scenarios in an industrial area of Florence"

description: This dataset repository includes input and output spatial data of urban microclimate simulations performed through QGIS and ENVI-met software used in the study "Urban microclimate simulations based on GIS data to mitigate thermal hot-spots: Tree design scenarios in an industrial area of Florence", published in the Building and Environment Journal, https://doi.org/10.1016/j.buildenv.2023.110854.
DOI: 10.6084/m9.figshare.28756986
title: Established and emerging roles of protein kinases in regulating primary sensory neurons in injury-and inflammation-associated pain

description: Recent seminal neuroscience research has significantly increased our knowledge on cellular and molecular responses of various cells in the pain pathway to peripheral nerve injuries and inflammatory processes. Transcriptomic and epigenetic analysis of primary sensory neurons (PSNs) in animal models of peripheral injuries revealed new insights into altered gene expression profiles and epigenetic modifications, which, via increasing spinal nociceptive input, lead to the development of pain. Among the various classes of molecules involved in driving differential gene expression, protein kinases, the enzymes that catalyze the phosphorylation of molecules, are emerging to control histone modification and chromatin remodeling needed for the alteration in transcriptional activity. Here, we focused on how protein kinases contribute to transcriptomic changes and pathways of induced reprogramming within PSNs upon peripheral nerve injury and inflammation. We conducted systematic literature search across multiple databases, including PubMed, NIH ClinicalTrials.gov portal and GEOData from 1980 to 2024 and compared protein kinase expression frequencies between publicly available RNA sequencing datasets of PSNs and investigated differences in protein kinase expression levels after peripheral nerve injury. Novel findings support a new concept that protein kinases constitute regulatory hubs of reprogramming of PSNs, which offers novel analgesic approaches.
DOI: 10.6084/m9.figshare.28756986.v1
title: Established and emerging roles of protein kinases in regulating primary sensory neurons in injury-and inflammation-associated pain

description: Recent seminal neuroscience research has significantly increased our knowledge on cellular and molecular responses of various cells in the pain pathway to peripheral nerve injuries and inflammatory processes. Transcriptomic and epigenetic analysis of primary sensory neurons (PSNs) in animal models of peripheral injuries revealed new insights into altered gene expression profiles and epigenetic modifications, which, via increasing spinal nociceptive input, lead to the development of pain. Among the various classes of molecules involved in driving differential gene expression, protein kinases, the enzymes that catalyze the phosphorylation of molecules, are emerging to control histone modification and chromatin remodeling needed for the alteration in transcriptional activity. Here, we focused on how protein kinases contribute to transcriptomic changes and pathways of induced reprogramming within PSNs upon peripheral nerve injury and inflammation. We conducted systematic literature search across multiple databases, including PubMed, NIH ClinicalTrials.gov portal and GEOData from 1980 to 2024 and compared protein kinase expression frequencies between publicly available RNA sequencing datasets of PSNs and investigated differences in protein kinase expression levels after peripheral nerve injury. Novel findings support a new concept that protein kinases constitute regulatory hubs of reprogramming of PSNs, which offers novel analgesic approaches.
DOI: 10.6084/m9.figshare.28590920
title: A chromosome 2 locus influences the onset of radiation-induced lung disease in mice

description: The onset of distress from radiation-induced lung disease differs among patients and among inbred strains of mice exposed to thoracic cavity radiotherapy. For the latter specifically, C3H/HeJ mice present distress due to pneumonitis at approximately 10–14 weeks following thoracic irradiation, while C57BL/6J mice show distress due to pneumonitis with pulmonary fibrosis at 22–30 weeks. Mapping studies completed in offspring derived from these inbred strains revealed a chromosome 2 locus to be linked to onset of distress in irradiated mice. Herein, we bred and phenotyped a panel of chromosome 2 subcongenic mice with 64 Mb of C3H/HeJ alleles on a C57BL/6J background, to investigate the contribution of the chromosome 2 locus to radiation-induced lung disease. Mice received 18 Gy to the thoracic cavity and were monitored for the onset of distress. Lung disease was assessed histologically and with bronchoalveolar lavage. Following whole thorax irradiation, subcongenic mice with C3H/HeJ alleles from 95 to 123 Mb showed significantly earlier onset of respiratory distress (16–22 weeks; <i>p</i> &lt; .02) from pneumonitis and fibrosis compared to C57BL/6J mice. These subcongenic mice did not differ from C57BL/6J mice in pneumonitis (<i>p</i> = .23), mast cell counts (<i>p</i> = .96), or lavage neutrophils (<i>p</i> = .69), evident at distress. <i>In silico</i> analyses reveal 246 protein coding genes mapped within the reduced region, 52 of which differ in pulmonary expression of C3H/HeJ, compared to C57BL/6J, mice after whole thorax irradiation. We have identified a 28 Mb region of chromosome 2 to influence the onset of radiation-induced lung disease in mice.
DOI: 10.6084/m9.figshare.28590920.v1
title: A chromosome 2 locus influences the onset of radiation-induced lung disease in mice

description: The onset of distress from radiation-induced lung disease differs among patients and among inbred strains of mice exposed to thoracic cavity radiotherapy. For the latter specifically, C3H/HeJ mice present distress due to pneumonitis at approximately 10–14 weeks following thoracic irradiation, while C57BL/6J mice show distress due to pneumonitis with pulmonary fibrosis at 22–30 weeks. Mapping studies completed in offspring derived from these inbred strains revealed a chromosome 2 locus to be linked to onset of distress in irradiated mice. Herein, we bred and phenotyped a panel of chromosome 2 subcongenic mice with 64 Mb of C3H/HeJ alleles on a C57BL/6J background, to investigate the contribution of the chromosome 2 locus to radiation-induced lung disease. Mice received 18 Gy to the thoracic cavity and were monitored for the onset of distress. Lung disease was assessed histologically and with bronchoalveolar lavage. Following whole thorax irradiation, subcongenic mice with C3H/HeJ alleles from 95 to 123 Mb showed significantly earlier onset of respiratory distress (16–22 weeks; <i>p</i> &lt; .02) from pneumonitis and fibrosis compared to C57BL/6J mice. These subcongenic mice did not differ from C57BL/6J mice in pneumonitis (<i>p</i> = .23), mast cell counts (<i>p</i> = .96), or lavage neutrophils (<i>p</i> = .69), evident at distress. <i>In silico</i> analyses reveal 246 protein coding genes mapped within the reduced region, 52 of which differ in pulmonary expression of C3H/HeJ, compared to C57BL/6J, mice after whole thorax irradiation. We have identified a 28 Mb region of chromosome 2 to influence the onset of radiation-induced lung disease in mice.
DOI: 10.6084/m9.figshare.28597636
title: The role of polysaccharide POM extracted from <i>Pleurotus ostreatus</i> in curbing and treating the harmful effects on liver and kidney resulting from radiation exposure

description: This research assesses the radioprotective and antioxidant activity of polysaccharide (POM) derived from <i>Pleurotus ostreatus</i> strain on rats suffering from metabolic problems due to irradiation. The crude POM obtained through chemical analysis was found to consist of glucose, galactose, and fructose in 1:1.2:0.1 ratio but was absent of uronic acid, and sulfate. Moreover, it demonstrated radical scavenging activity (45.21-84.21%) at 5 mg/ml concentration. A total of thirty-two male Sprague-Dawley rats were used and split into four groups: control, radiation (whole body RT with 5 Gy gamma rays), POM treatment (28 days at 100 mg/kg body weight), POM + radiation (n = 8 rats/group). Monitoring of body weight was done and on day 28, cardiac blood samples were collected and tested on liver and kidney function indices. ELISA was used to test for inflammatory factors and liver and kidney sections were stained with hematoyxlin-eosin, and other tests for DNA fragmentation were undertaken. The rats that underwent radiation exhibited reduced body weights, metabolic disruption, and decrease in antioxidant enzyme activities. The histological analysis displayed edema of hepatic cells, inflammatory cell infiltration, and vacuolar degeneration. On the other hand, rats in the POM + Radiation group showed less severe pathological changes. POM treated rats had restored their liver and kidney functions, lower TBARS, higher total protein, and improved antioxidant enzyme activities. POM treatment effectively alleviates liver and kidney damage caused by radiation exposure.
DOI: 10.6084/m9.figshare.28597636.v1
title: The role of polysaccharide POM extracted from <i>Pleurotus ostreatus</i> in curbing and treating the harmful effects on liver and kidney resulting from radiation exposure

description: This research assesses the radioprotective and antioxidant activity of polysaccharide (POM) derived from <i>Pleurotus ostreatus</i> strain on rats suffering from metabolic problems due to irradiation. The crude POM obtained through chemical analysis was found to consist of glucose, galactose, and fructose in 1:1.2:0.1 ratio but was absent of uronic acid, and sulfate. Moreover, it demonstrated radical scavenging activity (45.21-84.21%) at 5 mg/ml concentration. A total of thirty-two male Sprague-Dawley rats were used and split into four groups: control, radiation (whole body RT with 5 Gy gamma rays), POM treatment (28 days at 100 mg/kg body weight), POM + radiation (n = 8 rats/group). Monitoring of body weight was done and on day 28, cardiac blood samples were collected and tested on liver and kidney function indices. ELISA was used to test for inflammatory factors and liver and kidney sections were stained with hematoyxlin-eosin, and other tests for DNA fragmentation were undertaken. The rats that underwent radiation exhibited reduced body weights, metabolic disruption, and decrease in antioxidant enzyme activities. The histological analysis displayed edema of hepatic cells, inflammatory cell infiltration, and vacuolar degeneration. On the other hand, rats in the POM + Radiation group showed less severe pathological changes. POM treated rats had restored their liver and kidney functions, lower TBARS, higher total protein, and improved antioxidant enzyme activities. POM treatment effectively alleviates liver and kidney damage caused by radiation exposure.
DOI: 10.6084/m9.figshare.28933483
title: LBDNet inter-laboratory comparison at high doses of ionizing radiation using the dicentric plus caffeine assay

description: To assess the performance of the LBDNet laboratories in estimating dose over 5 Gy of ionizing radiation using the dicentric chromosome plus caffeine assay. Dose-response curve fitting: Peripheral blood was irradiated <i>in vitro</i> between 5 and 25 Gy. Then, the DC plus caffeine assay was carried out. Thirteen laboratories received and analyzed metaphase images. The linear dose-response curve was fitted for each laboratory. Dose estimation was performed analyzing coded metaphase images from three different irradiated samples (7.5, 15, 20 Gy) and using the fitted curve from every laboratory. The dose estimation accuracy was within the expected dose ranges. The 76.9%, 84.6% and 69.2% of the estimated doses fell into the ± 20% of the true radiation dose. The 92.3%, 92.3%, and 61.5% of the 95% of the confidence interval of the estimated doses included the true radiation dose. The trueness was 0.9%, 4.4% and 9.6%. The Coefficients of Variation of the estimated doses were 14.5%, 16.1% and 17.8%. Results from only one laboratory were deemed questionable for dose estimation, based on the <i>Z-score</i> derived from robust methods. The intercomparison study yielded satisfactory results; however, dose estimation accuracy tended to decrease, and variability between laboratory results increased as the dose level rose.
DOI: 10.6084/m9.figshare.28933483.v1
title: LBDNet inter-laboratory comparison at high doses of ionizing radiation using the dicentric plus caffeine assay

description: To assess the performance of the LBDNet laboratories in estimating dose over 5 Gy of ionizing radiation using the dicentric chromosome plus caffeine assay. Dose-response curve fitting: Peripheral blood was irradiated <i>in vitro</i> between 5 and 25 Gy. Then, the DC plus caffeine assay was carried out. Thirteen laboratories received and analyzed metaphase images. The linear dose-response curve was fitted for each laboratory. Dose estimation was performed analyzing coded metaphase images from three different irradiated samples (7.5, 15, 20 Gy) and using the fitted curve from every laboratory. The dose estimation accuracy was within the expected dose ranges. The 76.9%, 84.6% and 69.2% of the estimated doses fell into the ± 20% of the true radiation dose. The 92.3%, 92.3%, and 61.5% of the 95% of the confidence interval of the estimated doses included the true radiation dose. The trueness was 0.9%, 4.4% and 9.6%. The Coefficients of Variation of the estimated doses were 14.5%, 16.1% and 17.8%. Results from only one laboratory were deemed questionable for dose estimation, based on the <i>Z-score</i> derived from robust methods. The intercomparison study yielded satisfactory results; however, dose estimation accuracy tended to decrease, and variability between laboratory results increased as the dose level rose.
DOI: 10.6084/m9.figshare.30952984
title: Proteotoxic stress triggers TFEB- and TFE3-mediated autophagy and lysosomal biogenesis via non-canonical MTORC1 inactivation

description: Proteotoxic stress, arising from conditions that cause misfolded protein accumulation, is closely linked to the pathogenesis of multiple diseases. Macroautophagy/autophagy activation is considered a compensatory mechanism to maintain protein homeostasis, but the underlying regulatory mechanisms remain incompletely understood. Here, we show that proteotoxic stress induced by proteasome inhibition, puromycin treatment, or polyglutamine-expanded HTT (huntingtin) expression promotes nuclear accumulation of TFEB and TFE3, key regulators of lysosomal biogenesis and autophagy. Mechanistically, TFEB activation under proteotoxic stress occurs independently of canonical MTORC1 inactivation mediated by TSC2 or ATF4. Instead, it involves non-canonical inhibition of MTORC1 via RRAG GTPases. Proteotoxic stress disrupts the RRAGC-TFEB interaction, preventing TFEB recruitment to lysosomes and subsequent MTORC1 phosphorylation. An activated RRAGC mutant rescues impaired lysosomal localization and nuclear accumulation of TFEB, while co-overexpression of FLCN and FNIP2, a GAP for RRAGC, partially restores stress-induced TFEB dephosphorylation. In addition, proteasome inhibition activates non-canonical autophagy. Deletion of <i>ATG16L1</i> or <i>ATG5</i>, which known blocks Atg8-family protein lipidation and sequesters the FLCN-FNIP2 complex, partially abolishes proteotoxic stress-induced TFEB dephosphorylation and nuclear accumulation. Together, these findings demonstrate that proteotoxic stress triggers both non-canonical autophagy and TFEB-mediated canonical autophagy, with Atg8-family protein lipidation contributing to TFEB activation. Our results provide novel insights into how proteotoxic stress engages non-canonical MTORC1 inhibition and TFEB activation, thereby enhancing understanding of cellular adaptation to proteotoxic stress. <b>Abbreviations</b>: ALP, autophagy-lysosomal pathway; ATF4, activating transcription factor 4; Baf A1, bafilomycin A<sub>1</sub>; CHX, cycloheximide; BTZ, bortezomib; CFZ, carfilzomib; CQ, chloroquine; CTSB, cathepsin B; CTSD, cathepsin D; DQ-BSA, dequenched-bovine serum albumin; EIF4EBP1/4EBP1, eukaryotic translation initiation factor 4E binding protein 1; ER, endoplasmic reticulum; MAP1LC3B/LC3B, microtubule associated protein 1 light chain 3 beta; MG132, carbobenzoxy-Leu-Leu-leucinal; MTORC1, mechanistic target of rapamycin kinase complex 1; RPS6KB1/p70, ribosomal protein S6 kinase B1; RRAG, Ras related GTP binding; SQSTM1/p62, sequestosome 1; TFE3, transcription factor E3; TFEB, transcription factor EB; TSC2, TSC complex subunit 2; tfLC3, tandem fluorescent LC3; UPS, ubiquitin-proteasome system.
DOI: 10.6084/m9.figshare.30952984.v1
title: Proteotoxic stress triggers TFEB- and TFE3-mediated autophagy and lysosomal biogenesis via non-canonical MTORC1 inactivation

description: Proteotoxic stress, arising from conditions that cause misfolded protein accumulation, is closely linked to the pathogenesis of multiple diseases. Macroautophagy/autophagy activation is considered a compensatory mechanism to maintain protein homeostasis, but the underlying regulatory mechanisms remain incompletely understood. Here, we show that proteotoxic stress induced by proteasome inhibition, puromycin treatment, or polyglutamine-expanded HTT (huntingtin) expression promotes nuclear accumulation of TFEB and TFE3, key regulators of lysosomal biogenesis and autophagy. Mechanistically, TFEB activation under proteotoxic stress occurs independently of canonical MTORC1 inactivation mediated by TSC2 or ATF4. Instead, it involves non-canonical inhibition of MTORC1 via RRAG GTPases. Proteotoxic stress disrupts the RRAGC-TFEB interaction, preventing TFEB recruitment to lysosomes and subsequent MTORC1 phosphorylation. An activated RRAGC mutant rescues impaired lysosomal localization and nuclear accumulation of TFEB, while co-overexpression of FLCN and FNIP2, a GAP for RRAGC, partially restores stress-induced TFEB dephosphorylation. In addition, proteasome inhibition activates non-canonical autophagy. Deletion of <i>ATG16L1</i> or <i>ATG5</i>, which known blocks Atg8-family protein lipidation and sequesters the FLCN-FNIP2 complex, partially abolishes proteotoxic stress-induced TFEB dephosphorylation and nuclear accumulation. Together, these findings demonstrate that proteotoxic stress triggers both non-canonical autophagy and TFEB-mediated canonical autophagy, with Atg8-family protein lipidation contributing to TFEB activation. Our results provide novel insights into how proteotoxic stress engages non-canonical MTORC1 inhibition and TFEB activation, thereby enhancing understanding of cellular adaptation to proteotoxic stress. <b>Abbreviations</b>: ALP, autophagy-lysosomal pathway; ATF4, activating transcription factor 4; Baf A1, bafilomycin A<sub>1</sub>; CHX, cycloheximide; BTZ, bortezomib; CFZ, carfilzomib; CQ, chloroquine; CTSB, cathepsin B; CTSD, cathepsin D; DQ-BSA, dequenched-bovine serum albumin; EIF4EBP1/4EBP1, eukaryotic translation initiation factor 4E binding protein 1; ER, endoplasmic reticulum; MAP1LC3B/LC3B, microtubule associated protein 1 light chain 3 beta; MG132, carbobenzoxy-Leu-Leu-leucinal; MTORC1, mechanistic target of rapamycin kinase complex 1; RPS6KB1/p70, ribosomal protein S6 kinase B1; RRAG, Ras related GTP binding; SQSTM1/p62, sequestosome 1; TFE3, transcription factor E3; TFEB, transcription factor EB; TSC2, TSC complex subunit 2; tfLC3, tandem fluorescent LC3; UPS, ubiquitin-proteasome system.
DOI: 10.15468/dl.pp5mss
title: Occurrence Download

description: A dataset containing 68432 species occurrences available in GBIF matching the query:
{
 "and" : [
 "OccurrenceStatus is Present",
 "TaxonKey is Erigeron bonariensis"
 ]
}

 The dataset includes 68432 records from 1022 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0002334-260120142942310/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.