cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.3535/z68-j79-ekf
title: Animalia

description: Digital Specimen for the physical specimen hosted at Naturalis Biodiversity Center.
DOI: 10.3535/03d-asc-hdf
title: Animalia

description: Digital Specimen for the physical specimen hosted at Naturalis Biodiversity Center.
DOI: 10.3535/633-gzs-3hq
title: Animalia

description: Digital Specimen for the physical specimen hosted at Naturalis Biodiversity Center.
DOI: 10.15468/dl.z4qwup
title: Occurrence Download

description: A dataset containing 0 species occurrences available in GBIF matching the query:
{
 "TaxonKey" : [
 "is Campylorhynchus humilis P.L.Sclater, 1857"
 ]
}

 The dataset includes 0 records from 7 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0377117-210914110416597/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.ngwkyp
title: Occurrence Download

description: A dataset containing 27298474 species occurrences available in GBIF matching the query:
{
 "and" : [
 "BasisOfRecord is Specimen",
 "TaxonKey is Tracheophyta",
 "RecordNumber is not null",
 "RecordedBy is not null",
 "EventDate is not null"
 ]
}

 The dataset includes 27298474 records from 480 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0007179-200221144449610/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.ksayv3
title: Occurrence Download

description: A dataset containing 3501715 species occurrences available in GBIF matching the query:
{
 "TaxonKey" : [
 "is Fulica atra Linnaeus, 1758"
 ]
}

 The dataset includes 3501715 records from 1347 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0377099-210914110416597/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.6084/m9.figshare.31361761
title: Multifunctional plasmonic gold nanoisland films for enhanced cell theranostics through photothermal therapy and surface-enhanced Raman scattering detection

description: Plasmonic gold nanomaterials have numerous applications in biomedical therapy and sensing. In this work, plasmonic gold nanoisland films (AuNIFs) were demonstrated to have significant applications in photothermal therapy and surface-enhanced Raman scattering (SERS) detection. A seed-mediated growth method was used to fabricate AuNIFs on glass substrates. Material Characterizations confirmed the successful preparation of AuNIFs. Surface plasmon resonance produced a broad UV-Vis absorption spectrum (400–1000 nm). Under 808-nm near-infrared (NIR) laser irradiation (1.5 mW/cm<sup>2</sup>), AuNIFs reached 65°C, generating sufficient heat to kill Vero epithelial cells. The cell death rate of Vero cells under laser irradiation was estimated to be 1.38 times higher than that in the absence of laser irradiation. The AuNIFs exhibited stable photothermal performance under cyclic laser exposure for 10 min and outperformed conventional photothermal therapy in eradicating Vero cells. Compared to bare glass slides, AuNIFs promoted more-confluent Vero cell growth. Additionally, the AuNIF platform enhanced the Raman signal of Vero cells according to a SERS analysis. Fluorescence imaging confirmed laser-induced cell death, as indicated by green fluorescence. By integrating photothermal therapy and SERS detection, AuNIFs demonstrated strong potential as multifunctional substrates for cell theranostics.
DOI: 10.6084/m9.figshare.31361761.v1
title: Multifunctional plasmonic gold nanoisland films for enhanced cell theranostics through photothermal therapy and surface-enhanced Raman scattering detection

description: Plasmonic gold nanomaterials have numerous applications in biomedical therapy and sensing. In this work, plasmonic gold nanoisland films (AuNIFs) were demonstrated to have significant applications in photothermal therapy and surface-enhanced Raman scattering (SERS) detection. A seed-mediated growth method was used to fabricate AuNIFs on glass substrates. Material Characterizations confirmed the successful preparation of AuNIFs. Surface plasmon resonance produced a broad UV-Vis absorption spectrum (400–1000 nm). Under 808-nm near-infrared (NIR) laser irradiation (1.5 mW/cm<sup>2</sup>), AuNIFs reached 65°C, generating sufficient heat to kill Vero epithelial cells. The cell death rate of Vero cells under laser irradiation was estimated to be 1.38 times higher than that in the absence of laser irradiation. The AuNIFs exhibited stable photothermal performance under cyclic laser exposure for 10 min and outperformed conventional photothermal therapy in eradicating Vero cells. Compared to bare glass slides, AuNIFs promoted more-confluent Vero cell growth. Additionally, the AuNIF platform enhanced the Raman signal of Vero cells according to a SERS analysis. Fluorescence imaging confirmed laser-induced cell death, as indicated by green fluorescence. By integrating photothermal therapy and SERS detection, AuNIFs demonstrated strong potential as multifunctional substrates for cell theranostics.
DOI: 10.48526/rgu-wt-3255747
title: Talking about prisons

description: The Talking about Prisons project, funded by the British Academy, was completed between January 2024 and November 2025. The study investigated the social practices that inform visitor engagement with difficult heritage in prison museums drawing upon Peterhead Prison Museum as a case study. An Ethnomethodological Conversation Analysis (EMCA) approach was adopted for data collection and analysis, using small Go Pro cameras to film visitor interaction across five exhibits at the museum. Exhibits were selected as they presented an opportunity to examine engagement with different types of difficult heritage at the museum. This included analysis of visitor talk, gesture, facial expression and interaction with space, objects and people. An adapted version of the Jefferson transcription system was used for EMCA analysis. An opt-out approach was used for data collection with visitors informed at the start of their tour via staff and an information leaflet, with the option to inform research staff ahead of exhibit entry if they did not wish to be filmed and the opportunity to contact the research team to withdraw data post-visit. A systematic approach to data management after collection ensured that all minors and vulnerable adults were removed from data analysis. Data provided in this data set is a subset of the wider data set used to inform published outputs and focus on the Cat O' Nine Tails and Murder Cell exhibits.
DOI: 10.15468/dl.32bhra
title: Occurrence Download

description: A dataset containing 10 species occurrences available in GBIF matching the query:
{
 "and" : [
 "Country is Denmark",
 "HasCoordinate is true",
 "HasGeospatialIssue is false",
 "OccurrenceStatus is Present",
 "PublishingOrg is 1a4e6112-b3af-402e-b29f-c2ade2167f72",
 "TaxonKey is Muscardinus avellanarius",
 "Year 2024-2026"
 ]
}

 The dataset includes 10 records from 2 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0027020-260208012135463/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.6084/m9.figshare.30856424
title: Avarol protects HT22 neuronal cells from BV2 microglia cell-derived neuroinflammation in lipopolysaccharide-induction model

description: Pathological neuroinflammation is a critical factor that disrupts neuronal activity and, when sustained, ultimately contributes to neuronal death. Among the primary mediators of neuroinflammation, microglia play a central role in modulating brain immunity. However, their overactivation is closely associated with neuronal damage and structural remodeling of brain tissue, leading to the onset and progression of various neurodegenerative diseases. We investigated the neuroprotective effects of avarol, a marine-derived sesquiterpenoid, focusing on its ability to inhibit lipopolysaccharide (LPS)-induced overactivation of BV2 microglial cells and its subsequent impact on neuronal activity in HT-22 hippocampal neuronal cells. Pretreatment with avarol significantly attenuated the LPS-induced release of pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), as well as oxidative stress markers such as reactive oxygen species (ROS) and nitric oxide (NO). These inhibitory effects were further substantiated by a dose-dependent reduction in nuclear translocation of nuclear factor-kappa B (NF-κB), a key transcription factor involved in the inflammatory signaling cascade. Regarding the interaction between microglia and neurons, both conditioned medium and co-culture systems demonstrated that avarol significantly attenuated alterations in neuronal plasticity-related molecules—such as nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF)—induced by activated microglia. Overall, these findings suggest that avarol exerts neuroprotective effects through the modulation of microglia-mediated neuroinflammation. Importantly, avarol’s capacity to traverse the blood-brain barrier highlights its potential as an effective pharmacological agent in mitigating neuroinflammation-associated neurological disorders.
DOI: 10.6084/m9.figshare.30856424.v1
title: Avarol protects HT22 neuronal cells from BV2 microglia cell-derived neuroinflammation in lipopolysaccharide-induction model

description: Pathological neuroinflammation is a critical factor that disrupts neuronal activity and, when sustained, ultimately contributes to neuronal death. Among the primary mediators of neuroinflammation, microglia play a central role in modulating brain immunity. However, their overactivation is closely associated with neuronal damage and structural remodeling of brain tissue, leading to the onset and progression of various neurodegenerative diseases. We investigated the neuroprotective effects of avarol, a marine-derived sesquiterpenoid, focusing on its ability to inhibit lipopolysaccharide (LPS)-induced overactivation of BV2 microglial cells and its subsequent impact on neuronal activity in HT-22 hippocampal neuronal cells. Pretreatment with avarol significantly attenuated the LPS-induced release of pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), as well as oxidative stress markers such as reactive oxygen species (ROS) and nitric oxide (NO). These inhibitory effects were further substantiated by a dose-dependent reduction in nuclear translocation of nuclear factor-kappa B (NF-κB), a key transcription factor involved in the inflammatory signaling cascade. Regarding the interaction between microglia and neurons, both conditioned medium and co-culture systems demonstrated that avarol significantly attenuated alterations in neuronal plasticity-related molecules—such as nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF)—induced by activated microglia. Overall, these findings suggest that avarol exerts neuroprotective effects through the modulation of microglia-mediated neuroinflammation. Importantly, avarol’s capacity to traverse the blood-brain barrier highlights its potential as an effective pharmacological agent in mitigating neuroinflammation-associated neurological disorders.
DOI: 10.6084/m9.figshare.30931680
title: Multi-omics profiling uncovers candidate genes for the treatment of graves’ disease

description: This Summary-data-based Mendelian randomization (SMR) study investigates the genetic basis of Graves’ disease (GD) using a multi-omics approach to elucidate biological mechanisms and identify therapeutic candidates. SMR and Bayesian colocalization analyzed GD associations with methylation (mQTL), expression (eQTL), and protein quantitative trait loci (pQTL) using FinnGen as the discovery cohort. Top SNPs underwent methylation-gene expression and gene expression-protein interaction analyses. Key findings were validated against an independent GWAS dataset. Functional enrichment characterized pathways for eQTL-SMR-derived loci. The Drug Signatures Database (DsigDB) predicted potential drugs. Significant multi-omics associations were found. mQTL analysis linked GD to 1,772 methylation sites (294 genes); eQTL identified 157 genes. pQTL signals appeared in two cohorts (4 genes deCODE; 16 genes UKB-PPP). AGER and AIF1 were consistent across omics. AIF1 showed strong GD associations (mQTL OR 1.09; eQTL OR 1.44; deCODE-pQTL OR 3.17; UKB-PPP-pQTL OR 3.46). Integrated analysis revealed a positive correlation between AGER DNA methylation and expression, but negative for AIF1, with colocalization support (PPH3 + PPH4 &gt; 0.8). SMR showed inverse pQTL associations for AGER and positive for AIF1, also colocalized. Independent GWAS validation confirmed GD associations with AGER and AIF1 at pQTL. Enrichment indicated immune/inflammatory pathways. Drug predictions included agents for AGER (Oleanolic Acid, Rutin, Estriol, GW9662) and AIF1 (Quinoline). This study provides novel insights into GD pathogenesis, highlighting AGER and AIF1 as therapeutically relevant genes. Findings offer valuable insights for GD treatment strategies and potential drug development streamlining, warranting further experimental validation.
DOI: 10.6084/m9.figshare.30931680.v1
title: Multi-omics profiling uncovers candidate genes for the treatment of graves’ disease

description: This Summary-data-based Mendelian randomization (SMR) study investigates the genetic basis of Graves’ disease (GD) using a multi-omics approach to elucidate biological mechanisms and identify therapeutic candidates. SMR and Bayesian colocalization analyzed GD associations with methylation (mQTL), expression (eQTL), and protein quantitative trait loci (pQTL) using FinnGen as the discovery cohort. Top SNPs underwent methylation-gene expression and gene expression-protein interaction analyses. Key findings were validated against an independent GWAS dataset. Functional enrichment characterized pathways for eQTL-SMR-derived loci. The Drug Signatures Database (DsigDB) predicted potential drugs. Significant multi-omics associations were found. mQTL analysis linked GD to 1,772 methylation sites (294 genes); eQTL identified 157 genes. pQTL signals appeared in two cohorts (4 genes deCODE; 16 genes UKB-PPP). AGER and AIF1 were consistent across omics. AIF1 showed strong GD associations (mQTL OR 1.09; eQTL OR 1.44; deCODE-pQTL OR 3.17; UKB-PPP-pQTL OR 3.46). Integrated analysis revealed a positive correlation between AGER DNA methylation and expression, but negative for AIF1, with colocalization support (PPH3 + PPH4 &gt; 0.8). SMR showed inverse pQTL associations for AGER and positive for AIF1, also colocalized. Independent GWAS validation confirmed GD associations with AGER and AIF1 at pQTL. Enrichment indicated immune/inflammatory pathways. Drug predictions included agents for AGER (Oleanolic Acid, Rutin, Estriol, GW9662) and AIF1 (Quinoline). This study provides novel insights into GD pathogenesis, highlighting AGER and AIF1 as therapeutically relevant genes. Findings offer valuable insights for GD treatment strategies and potential drug development streamlining, warranting further experimental validation.
DOI: 10.6084/m9.figshare.30963745
title: Intranasal triptolide in mice: a strategy to reduce neuroinflammation and boost cognitive function

description: This study developed triptolide-loaded liposomes (TPL) for intranasal delivery to mitigate systemic toxicity of free triptolide (TP) while enhancing therapeutic efficacy in neuroinflammatory and Alzheimer’s disease (AD) models. Biodistribution of luciferin liposomes was compared across oral, intravenous, and nasal routes using <i>in vivo</i> imaging. TPL was prepared <i>via</i> thin-film hydration with optimized phospholipid/cholesterol ratios. Safety profiles of intranasal TPL and TP were evaluated in wild-type mice. Efficacy was assessed in LPS-induced neuroinflammation and APP/PS1 AD models through behavioral tests, histopathology, and molecular analyses. Nasal administration demonstrated superior brain accumulation of luciferin liposomes compared to oral and intravenous routes. Optimized TPL exhibited spherical morphology with appropriate particle size, high drug encapsulation efficiency, and sustained release characteristics. Intranasal TPL showed reduced systemic toxicity relative to free TP. In disease models, TPL significantly improved behavioral and cognitive performance in both LPS-treated and APP/PS1 mice. Histopathological analysis revealed attenuated neuronal damage, reduced Aβ plaque deposition, and suppressed glial activation (IBA-1 and GFAP expression). Molecular studies demonstrated downregulation of pro-inflammatory cytokines (TNF-α, IL-1β, COX-2, IL-6) and apoptosis markers (Bax, Caspase-3), accompanied by increased expression of survival-related proteins (p-Akt, Bcl-2). The nasal TPL delivery system effectively enhances brain targeting of TP while reducing systemic exposure. Its multimodal mechanisms—including anti-inflammatory effects, amyloid pathology modulation, and apoptosis regulation—support therapeutic potential for neurodegenerative disorders.
DOI: 10.6084/m9.figshare.30963745.v1
title: Intranasal triptolide in mice: a strategy to reduce neuroinflammation and boost cognitive function

description: This study developed triptolide-loaded liposomes (TPL) for intranasal delivery to mitigate systemic toxicity of free triptolide (TP) while enhancing therapeutic efficacy in neuroinflammatory and Alzheimer’s disease (AD) models. Biodistribution of luciferin liposomes was compared across oral, intravenous, and nasal routes using <i>in vivo</i> imaging. TPL was prepared <i>via</i> thin-film hydration with optimized phospholipid/cholesterol ratios. Safety profiles of intranasal TPL and TP were evaluated in wild-type mice. Efficacy was assessed in LPS-induced neuroinflammation and APP/PS1 AD models through behavioral tests, histopathology, and molecular analyses. Nasal administration demonstrated superior brain accumulation of luciferin liposomes compared to oral and intravenous routes. Optimized TPL exhibited spherical morphology with appropriate particle size, high drug encapsulation efficiency, and sustained release characteristics. Intranasal TPL showed reduced systemic toxicity relative to free TP. In disease models, TPL significantly improved behavioral and cognitive performance in both LPS-treated and APP/PS1 mice. Histopathological analysis revealed attenuated neuronal damage, reduced Aβ plaque deposition, and suppressed glial activation (IBA-1 and GFAP expression). Molecular studies demonstrated downregulation of pro-inflammatory cytokines (TNF-α, IL-1β, COX-2, IL-6) and apoptosis markers (Bax, Caspase-3), accompanied by increased expression of survival-related proteins (p-Akt, Bcl-2). The nasal TPL delivery system effectively enhances brain targeting of TP while reducing systemic exposure. Its multimodal mechanisms—including anti-inflammatory effects, amyloid pathology modulation, and apoptosis regulation—support therapeutic potential for neurodegenerative disorders.
DOI: 10.6084/m9.figshare.31025898
title: Micheliolide alleviates myocardial ischemia/reperfusion injury in rats via KEAP1/NRF2-mediated suppression of oxidative stress and inflammation

description: After acute myocardial infarction (AMI), reperfusion therapy can help restore blood flow and nutritional support to the ischemic myocardium, thereby limiting ongoing myocardial injury. However, its effectiveness is increasingly challenged by myocardial ischemia-reperfusion (I/R) injury. In this regard, micheliolide (MCL) has been reported to exert beneficial effects in cardiovascular disease. Herein, we aimed to determine the mechanism underlying the cardioprotective effects of MCL in a rat I/R model. Rats were randomly divided into a control group, an I/R group, and an I/R + MCL group. After a two-week intervention, their serum and heart tissues were collected. Myocardial histopathology was assessed using Hematoxylin-Eosin (HE) staining, and cardiomyocyte apoptosis was evaluated by TUNEL staining. Levels of CK-MB, cTnI, BNP, TNF-α, IL-1β, and IL-6 in serum and cardiac tissue were measured using the enzyme-linked immunosorbent assay (ELISA). Commercial kits were used to measure cardiac MDA, SOD, GSH-Px, and ROS. Western blotting was performed to detect KEAP1, NRF2, and apoptosis-related proteins in the rats’ cardiac tissues. MCL treatment reduced KEAP1 expression and increased NRF2 expression in myocardial tissue, decreased cardiomyocyte apoptosis, improved cardiac function, alleviated myocardial tissue damage, and lowered inflammatory and oxidative stress levels in I/R rats. MCL regulates the KEAP1/NRF2 signaling pathway to reduce oxidative stress and inflammation, producing a cardioprotective effect in rats with acute myocardial infarction undergoing ischemia-reperfusion injury.
DOI: 10.6084/m9.figshare.31025898.v1
title: Micheliolide alleviates myocardial ischemia/reperfusion injury in rats via KEAP1/NRF2-mediated suppression of oxidative stress and inflammation

description: After acute myocardial infarction (AMI), reperfusion therapy can help restore blood flow and nutritional support to the ischemic myocardium, thereby limiting ongoing myocardial injury. However, its effectiveness is increasingly challenged by myocardial ischemia-reperfusion (I/R) injury. In this regard, micheliolide (MCL) has been reported to exert beneficial effects in cardiovascular disease. Herein, we aimed to determine the mechanism underlying the cardioprotective effects of MCL in a rat I/R model. Rats were randomly divided into a control group, an I/R group, and an I/R + MCL group. After a two-week intervention, their serum and heart tissues were collected. Myocardial histopathology was assessed using Hematoxylin-Eosin (HE) staining, and cardiomyocyte apoptosis was evaluated by TUNEL staining. Levels of CK-MB, cTnI, BNP, TNF-α, IL-1β, and IL-6 in serum and cardiac tissue were measured using the enzyme-linked immunosorbent assay (ELISA). Commercial kits were used to measure cardiac MDA, SOD, GSH-Px, and ROS. Western blotting was performed to detect KEAP1, NRF2, and apoptosis-related proteins in the rats’ cardiac tissues. MCL treatment reduced KEAP1 expression and increased NRF2 expression in myocardial tissue, decreased cardiomyocyte apoptosis, improved cardiac function, alleviated myocardial tissue damage, and lowered inflammatory and oxidative stress levels in I/R rats. MCL regulates the KEAP1/NRF2 signaling pathway to reduce oxidative stress and inflammation, producing a cardioprotective effect in rats with acute myocardial infarction undergoing ischemia-reperfusion injury.
DOI: 10.7807/immo:red:hk:suf:v6.2
title: RWI Real Estate Data - Hauskauf - suf
title: RWI Real Estate Data - Houses for Sale - suf

description: ImmobilienScout24 ist die größte Immobilien-Internetplattform in Deutschland. Auf der Website werden sowohl Immobilien zur privaten als auch zur gewerblichen Nutzung angeboten. Die Daten umfassen jedoch nur Wohnimmobilien. Der Datensatz umfasst die meisten auf der Plattform erhobenen Merkmale wie z.B. Preis, Größe und Ausstattung der Wohneinheit, aber auch generierte Informationen wie die Dauer der Inseratverfügbarkeit.
description: ImmobilienScout24 is the largest real estate internet platform in Germany. Properties for private as well as commercial use are offered on the website. However, the data only cover residential properties. The dataset covers most characteristics collected on the platform like price, size and characteristics of the housing unit but also automatically generated items like the duration of the advertisement spell.
description: RWI-GEO-RED
description: RWI-GEO-RED
description: Computer-based observation
description: alle Häuser zum Verkauf auf der Webseite ImmobilienScout24
description: all houses for sale at ImmobilienScout24
description: full sample