cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.15468/dl.78vevs
title: Occurrence Download

description: A dataset containing 71133 species occurrences available in GBIF matching the query:
{
 "TaxonKey" : [
 "is Verbascum lychnitis"
 ]
}

 The dataset includes 71133 records from 923 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0055898-250827131500795/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.hvdk6s
title: Occurrence Download

description: A dataset containing 2872 species occurrences available in GBIF matching the query:
{
 "TaxonKey" : [
 "is Inga oerstediana"
 ]
}

 The dataset includes 2872 records from 161 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0055983-250827131500795/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.ajkysw
title: Occurrence Download

description: A dataset containing 5589 species occurrences available in GBIF matching the query:
{
 "TaxonKey" : [
 "is Cyperus microiria"
 ]
}

 The dataset includes 5589 records from 174 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0055985-250827131500795/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.60952/jer9-5y95
title: Zmiany w miąższu płuc myszy zarażonych 600 i 800 larwami Trichinella spiralis (3)

description: Materiał zdjęciowy uzyskany w ramach badań, których celem było: zbadanie ultrastruktury transformującej komórki mięśniowej na skutek oddziaływania larw Trichinella spiralis na przestrzeni prawie całego okresu życia żywiciela (myszy szczepu BALB/c); opis relacji morfologicznej między komórką pielęgniarką a larwą włośnia krętego w różnym czasie od zarażenia organizmu żywicielskiego; przedstawienie zmian na poziomie rozdzielczości mikroskopu elektronowego, jakie zachodzą w narządach miąższowych, przez które migrują larwy Trichinella spiralis. Do badań użyto 90 immunokompetentnych myszy płci męskiej szczepu BALB/c w wieku 6 - 8 tygodni. Myszy zarażano doustnie różnymi ilościami larw włośnia krętego, a następnie w różnych okresach życia żywiciela pobierano wycinki tkankowe z wątroby, płuc, serca, przepony i mięśnia czterogłowego uda. Materiał tkankowy utrwalono w
roztworze będącym mieszaniną 2 % paraformaldehydu i 2,5% glutaraldehydu w 0,1 M buforze kakodylowym o pH 7,4. Zatopiony materiał biologiczny w żywicach cięto na skrawki
o grubości 5 μm i 50 nm, oglądano w mikroskopie świetlnym i mikroskopie elektronowym JEM 1200 EX, a następnie wykonano mikrografie elektronowe na płytkach TM – 6. Materiał zdjęciowy dotyczy zmian w miąższu płuc myszy zarażonych 600 i 800 larwami Trichinella spiralis.
Na zdjęciu pęcherzyki płucne myszy wykazujące cechy niedodmy wypełnione płynem przesiękowym. W centralnie położonym pęcherzyku płucnym znajduje się makrofag(Ma), który swoimi wypustkami plazmatycznymi ściśle przylega do komórek nabłonkowych. W jego wnętrzu znajdują się zróżnicowane w budowie fagolizosomy. Wszystkie pęcherzyki wykazują cechy niedodmy. Powiększenie 6 000 x.
DOI: 10.17026/dans-xuq-phca
title: Getuigen Verhalen, Herinneringen aan mijn Amsterdamse zusje/broertje, interview 05

description: &lt;p&gt;De familie Baten had vijf jongens en drie meisjes en woonde buitenaf in het dorp Oirlo. Ze namen Sonja Heimann op in hun gezin die ze altijd aanspraken met Tonie. De kinderen Baten wisten dat het om een Joods kind ging. Godswil is de reden dat zijn ouders dit Joodse meisje onderdak hebben gegeven, zegt zoon Joos. Omdat ze ver van de dorpskern woonden ging het meisje niet naar school. Ze deed alles met de andere kinderen mee. Ruim een jaar is Sonja Heimann ondergedoken geweest bij de familie. Het meisje is tijdens de razzia van 6 juli 1944 per vrachtwagen afgevoerd, samen met meerdere kinderen en vaders van Oirlose gezinnen waar Joodse kinderen onderdak kregen. Het meisje is omgekomen op 6 september 1944 in Auschwitz. Zijn ouders hebben nooit geld gekregen voor hun hulp, ook nooit gevraagd. De familie Baten heeft na de oorlog geen contact gehad met de familie van Heimann. Bovendien werd er thuis na de oorlog nooit meer gesproken over die periode.&lt;/p&gt;
description: Date Submitted: 2010-03-23
DOI: 10.17026/dans-xtr-47qk
title: Borghlocatie Zuidhorn proefsleuven Archeologisch proefsleuvenonderzoek Borghlocatie aan de Hanckemalaan en Boslaan te Zuidhorn, gemeente Westerkwartier (GR)

description: &lt;p&gt;Aanleiding tot het onderzoek zijn de nieuwbouwplannen van opdrachtgever binnen het plangebied. Uit het proefsleuvenonderzoek blijkt dat er binnen het onderzoeksgebied sporen van verkavelingen van vóór de aanleg van de es aanwezig zijn. Deze sporen bestaan uit greppels en sloten. Daarnaast is een aantal kuilen en paalkuilen gevonden onder het esdek. Slechts één spoor, sloot S37, is jonger dan het esdek. Deze sloot is door het esdek heen gegraven en dateert op basis van het erin aangetroffen vondstmateriaal uit de 16e/17e eeuw (circa 1500-1700). Dit geeft tevens aan dat het esdek in de late middeleeuwen moet zijn ontstaan (terminus ante quem). Het rijke vondstmateriaal dat in deze sloot is gevonden geeft aan dat sloot S37 bij de ten oosten ervan gelegen Hanckemaborg moet hebben gelegen. De precieze ouderdom van de onder het esdek liggende sloten, greppels en (paal)kuilen is niet goed duidelijk. In de sporen is materiaal aanwezig dat dateert uit de Romeinse tijd en de vroege en late middeleeuwen. Gezien de oriëntatie van de sloten in de werkputten, die gelijk is aan de oriëntatie van de verkaveling die nog aan het begin van de 19e eeuw zichtbaar is, zullen de sloten dateren uit de late middeleeuwen, (vlak) voor het gebied als bouwland of es in gebruik werd genomen. De greppels en de (paal)kuilen kunnen wel een oudere datering hebben, Romeins of vroegmiddeleeuws. De greppels lijken relatief kleine percelen te omgrenzen.&lt;/p&gt;
DOI: 10.15468/dl.5rram3
title: Occurrence Download

description: A dataset containing 1044 species occurrences available in GBIF matching the query:
{
 "and" : [
 "TaxonKey is one of (Rupicapra rupicapra [GBIF Backbone Taxonomy])",
 "Country is one of (Switzerland, Italy)",
 "Geometry POLYGON((6.75 45.75,7.15 45.75,7.15 46.10,6.75 46.10,6.75 45.75))",
 "HasCoordinate is true",
 "OccurrenceStatus is one of (Present)"
 ]
}

 The dataset includes 1044 records from 5 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0055987-250827131500795/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.29987857
title: RNF220 enhances USP22 to promote cell growth, metastasis and stemness in hepatocellular carcinoma by activating the Akt pathway

description: Hepatocellular carcinoma (HCC) is characterized by high metastatic potential and poor prognosis. Ring finger protein 220 (RNF220) has been implicated in tumorigenesis across various cancers; however, its role and associated regulatory mechanisms in HCC remain unclear. In this study, analysis of The Cancer Genome Atlas (TCGA) database revealed that RNF220 expression was significantly elevated in liver hepatocellular carcinoma (LIHC) tissues and was associated with poor prognosis. Further experiments confirmed the upregulation of RNF220 mRNA and protein in HCC tissues. Functional assays demonstrated that RNF220 overexpression promoted cell proliferation, migration and stemness, whereas RNF220 knockdown suppressed these processes in HCC cells. Mechanistically, RNF220 enhanced ubiquitin-specific protease 22 (USP22) expression, leading to activation of the protein kinase B (Akt) pathway. Furthermore, the knockdown of RNF220 inhibited HCC progression, an effect that could be reversed by SC79 (an Akt activator), an Akt activator. In vivo experiments further confirmed that RNF220 aggravated tumor growth and metastasis. In summary, these findings indicate that RNF220 promotes HCC progression by regulating USP22 and activating the Akt pathway, suggesting that RNF220 may serve as a potential biomarker and therapeutic target for HCC.
DOI: 10.6084/m9.figshare.30000795.v1
title: Molecular crossroads: identifying MAPK proteins bridging SMAD and dopamine pathways in breast cancer

description: The transforming growth factor-beta (TGF-β)/SMAD signaling pathway, mitogen-activated protein kinase (MAPK) signaling cascade, and dopamine receptor activity are all implicated in tumor progression. This study investigates molecular interactions among these pathways, identifying MAPK proteins that bridge SMAD and dopamine signaling in the context of breast cancer pathogenesis. A cohort of 405 breast cancer patients was categorized into molecular subtypes: luminal A (<i>n</i> = 130), luminal B HER2-negative (<i>n</i> = 100), luminal B HER2-positive (<i>n</i> = 96), non-luminal HER2-positive (<i>n</i> = 36), and triple-negative breast cancer (TNBC; <i>n</i> = 43). Transcriptomic profiling using microarrays and bioinformatics-based network analysis revealed differentially expressed genes across subtypes. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to validate 11 key transcripts, and protein expression was quantified by enzyme-linked immunosorbent assay (ELISA). MicroRNA (miRNA) regulatory interactions were analyzed to assess post-transcriptional modulation. Among 167 differentially expressed genes, 14 were consistently altered across all subtypes. These included cell division cycle 42 (<i>CDC42</i>), KRAS proto-oncogene, GTPase (<i>KRAS</i>), and transforming growth factor beta 1 (<i>TGFB1</i>), which were upregulated, as well as fibroblast growth factor 2 (<i>FGF2</i>), fibroblast growth factor 7 (<i>FGF7</i>), and insulin-like growth factor 1 <i>(IGF1</i>), which were downregulated. miRNA analysis revealed miR-221, miR-222, and miR-16-5p as regulators of these pathways. ELISA confirmed reduced KIT, IGF1, and FGF family proteins in tumor tissues, with KRAS significantly upregulated. Protein interaction analysis highlighted key hubs linking MAPK, SMAD, and dopamine signaling. This study elucidates crucial molecular intersections between MAPK, SMAD, and dopamine pathways, identifying potential biomarkers and therapeutic targets for breast cancer.
DOI: 10.6084/m9.figshare.29858766
title: METTL3-mediated circ_0003998 serves as oncogene in non-small cell lung cancer through regulating miR-330-5p/CXCL3 axis

description: Circular RNA (circRNA) is involved in the occurrence of many cancers. Nonetheless, the mechanism of circ_0003998 in non-small cell lung cancer (NSCLC) needs to be studied in depth. Real-time quantitative PCR (RT-qPCR) was carried out to check the expression of circ_0003998, microRNA-330-5p (miR-330-5p), chemokine (C-X-C motif) ligand 3 (CXCL3) and methyltransferase-3 (METTL3) in NSCLC tissues and cells. CXCL3, Vimentin and E-cadherin protein levels were measured by western blot. The functions of circ_0003998 in NSCLC cell proliferation, apoptosis, angiogenesis, migration and invasion were tested by clone formation assay, flow cytometry, tube formation assay, wound healing assay, and transwell assay in vitro. The dual-luciferase reporter assay was made to verify the relationship between miR-330-5p and circ_0003998 or CXCL3. Finally, animal experiment was made to further research the function of circ_0003998 on tumor formation in vivo. The interaction between circ_0003998 and METTL3 was analyzed by RNA Immunoprecipitation (RIP) assay, methylated RNA Immunoprecipitation (MeRIP) assay and dual-luciferase reporter assay. In NSCLC tissue and cells, circ_0003998 was markedly overexpressed. Circ_0003998 suppression inhibited NSCLC cell growth, angiogenesis, migration and invasion. Circ_0003998 sponged miR-330-5p, and miR-330-5p inhibitor could reverse the suppression effect of circ_0003998 knockdown on NSCLC cell behaviors. CXCL3 was a downstream target gene of miR-330-5p, and CXCL3 overexpression also reversed the suppressive effect of miR-330-5p on NSCLC cell behaviors. Interference of circ_0003998 reduced NSCLC tumorigenesis by regulating miR-330-5p/CXCL3 axis. Also, METTL3 promoted the expression of circ_0003998 by m6A modification. METTL3-modified circ_0003998 promoted NSCLC cell malignancy through miR-330-5p/CXCL3 axis, suggesting that circ_0003998 might be a new treatment strategy for NSCLC. Circ_0003998 was elevated in NSCLC tissue and cells.Circ_0003998 knockdown significantly repressed NSCLC cell malignancy.Circ_0003998 directly acted on miR-330-5p.miR-330-5p downregulated CXCL3 expression.METTL3 promoted m6A methylation of circ_0003998. Circ_0003998 was elevated in NSCLC tissue and cells. Circ_0003998 knockdown significantly repressed NSCLC cell malignancy. Circ_0003998 directly acted on miR-330-5p. miR-330-5p downregulated CXCL3 expression. METTL3 promoted m6A methylation of circ_0003998.
DOI: 10.6084/m9.figshare.29858766.v1
title: METTL3-mediated circ_0003998 serves as oncogene in non-small cell lung cancer through regulating miR-330-5p/CXCL3 axis

description: Circular RNA (circRNA) is involved in the occurrence of many cancers. Nonetheless, the mechanism of circ_0003998 in non-small cell lung cancer (NSCLC) needs to be studied in depth. Real-time quantitative PCR (RT-qPCR) was carried out to check the expression of circ_0003998, microRNA-330-5p (miR-330-5p), chemokine (C-X-C motif) ligand 3 (CXCL3) and methyltransferase-3 (METTL3) in NSCLC tissues and cells. CXCL3, Vimentin and E-cadherin protein levels were measured by western blot. The functions of circ_0003998 in NSCLC cell proliferation, apoptosis, angiogenesis, migration and invasion were tested by clone formation assay, flow cytometry, tube formation assay, wound healing assay, and transwell assay in vitro. The dual-luciferase reporter assay was made to verify the relationship between miR-330-5p and circ_0003998 or CXCL3. Finally, animal experiment was made to further research the function of circ_0003998 on tumor formation in vivo. The interaction between circ_0003998 and METTL3 was analyzed by RNA Immunoprecipitation (RIP) assay, methylated RNA Immunoprecipitation (MeRIP) assay and dual-luciferase reporter assay. In NSCLC tissue and cells, circ_0003998 was markedly overexpressed. Circ_0003998 suppression inhibited NSCLC cell growth, angiogenesis, migration and invasion. Circ_0003998 sponged miR-330-5p, and miR-330-5p inhibitor could reverse the suppression effect of circ_0003998 knockdown on NSCLC cell behaviors. CXCL3 was a downstream target gene of miR-330-5p, and CXCL3 overexpression also reversed the suppressive effect of miR-330-5p on NSCLC cell behaviors. Interference of circ_0003998 reduced NSCLC tumorigenesis by regulating miR-330-5p/CXCL3 axis. Also, METTL3 promoted the expression of circ_0003998 by m6A modification. METTL3-modified circ_0003998 promoted NSCLC cell malignancy through miR-330-5p/CXCL3 axis, suggesting that circ_0003998 might be a new treatment strategy for NSCLC. Circ_0003998 was elevated in NSCLC tissue and cells.Circ_0003998 knockdown significantly repressed NSCLC cell malignancy.Circ_0003998 directly acted on miR-330-5p.miR-330-5p downregulated CXCL3 expression.METTL3 promoted m6A methylation of circ_0003998. Circ_0003998 was elevated in NSCLC tissue and cells. Circ_0003998 knockdown significantly repressed NSCLC cell malignancy. Circ_0003998 directly acted on miR-330-5p. miR-330-5p downregulated CXCL3 expression. METTL3 promoted m6A methylation of circ_0003998.
DOI: 10.6084/m9.figshare.29891431.v1
title: NSUN2-mediated m5C modification of PGK1 mRNA promotes cell growth, invasion, stemness and glycolysis in gastric cancer

description: To explore functions and mechanisms in gastric cancer (GC) progression. The mRNA and protein levels of NSUN2 and phosphoglycerate kinase 1 (PGK1) were determined by qRT-PCR and western blot. Cell proliferation, apoptosis, invasion and stemness were examined using CCK8 assay, EdU assay, flow cytometry, transwell assay and sphere formation assay. Cell glycolysis was evaluated by detecting glucose consumption, lactate production and ATP/ADP ratio. The interaction between PGK1 and NSUN2 or YBX1 was evaluated using MeRIP assay or RIP assay. Actinomycin D treatment assay was used to detect the effect of NSUN2 or YBX1 knockdown on PGK1 mRNA stability. The protein levels of p-PI3K/PI3K and p-AKT/AKT were tested by western blot. Animal study was performed to confirm the effect of NSUN2/PGK1 axis on GC tumorigenesis. NSUN2 was confirmed to be upregulated in GC tissues and cells. NSUN2 silencing could repress GC cell growth, invasion, stemness and glycolysis. NSUN2 enhanced PGK1 mRNA stability through promoting its m5C modification, and this modification could be recognized by YBX1. Besides, PGK1 overexpression reversed the inhibitory effect of NSUN2 knockdown on GC cell growth, invasion, stemness and glycolysis. In addition, NSUN2/PGK1 axis increased the activity of PI3K/AKT pathway. Animal study revealed that interference of NSUN2 reduced GC tumorigenesis via inactivating the PGK1/PI3K/AKT pathway. NSUN2/PGK1 axis might play a vital role in GC development. NSUN2 knockdown represses GC cell growth, invasion, stemness and glycolysis;NSUN2 promotes PGK1 expression by m5C modification, which can be recognized by YBX1;NSUN2/PGK1 axis activates PI3K/AKT pathway to promote GC cell progression and tumorigenesis. NSUN2 knockdown represses GC cell growth, invasion, stemness and glycolysis; NSUN2 promotes PGK1 expression by m5C modification, which can be recognized by YBX1; NSUN2/PGK1 axis activates PI3K/AKT pathway to promote GC cell progression and tumorigenesis.
DOI: 10.6084/m9.figshare.29891431
title: NSUN2-mediated m5C modification of PGK1 mRNA promotes cell growth, invasion, stemness and glycolysis in gastric cancer

description: To explore functions and mechanisms in gastric cancer (GC) progression. The mRNA and protein levels of NSUN2 and phosphoglycerate kinase 1 (PGK1) were determined by qRT-PCR and western blot. Cell proliferation, apoptosis, invasion and stemness were examined using CCK8 assay, EdU assay, flow cytometry, transwell assay and sphere formation assay. Cell glycolysis was evaluated by detecting glucose consumption, lactate production and ATP/ADP ratio. The interaction between PGK1 and NSUN2 or YBX1 was evaluated using MeRIP assay or RIP assay. Actinomycin D treatment assay was used to detect the effect of NSUN2 or YBX1 knockdown on PGK1 mRNA stability. The protein levels of p-PI3K/PI3K and p-AKT/AKT were tested by western blot. Animal study was performed to confirm the effect of NSUN2/PGK1 axis on GC tumorigenesis. NSUN2 was confirmed to be upregulated in GC tissues and cells. NSUN2 silencing could repress GC cell growth, invasion, stemness and glycolysis. NSUN2 enhanced PGK1 mRNA stability through promoting its m5C modification, and this modification could be recognized by YBX1. Besides, PGK1 overexpression reversed the inhibitory effect of NSUN2 knockdown on GC cell growth, invasion, stemness and glycolysis. In addition, NSUN2/PGK1 axis increased the activity of PI3K/AKT pathway. Animal study revealed that interference of NSUN2 reduced GC tumorigenesis via inactivating the PGK1/PI3K/AKT pathway. NSUN2/PGK1 axis might play a vital role in GC development. NSUN2 knockdown represses GC cell growth, invasion, stemness and glycolysis;NSUN2 promotes PGK1 expression by m5C modification, which can be recognized by YBX1;NSUN2/PGK1 axis activates PI3K/AKT pathway to promote GC cell progression and tumorigenesis. NSUN2 knockdown represses GC cell growth, invasion, stemness and glycolysis; NSUN2 promotes PGK1 expression by m5C modification, which can be recognized by YBX1; NSUN2/PGK1 axis activates PI3K/AKT pathway to promote GC cell progression and tumorigenesis.
DOI: 10.6084/m9.figshare.29987857.v1
title: RNF220 enhances USP22 to promote cell growth, metastasis and stemness in hepatocellular carcinoma by activating the Akt pathway

description: Hepatocellular carcinoma (HCC) is characterized by high metastatic potential and poor prognosis. Ring finger protein 220 (RNF220) has been implicated in tumorigenesis across various cancers; however, its role and associated regulatory mechanisms in HCC remain unclear. In this study, analysis of The Cancer Genome Atlas (TCGA) database revealed that RNF220 expression was significantly elevated in liver hepatocellular carcinoma (LIHC) tissues and was associated with poor prognosis. Further experiments confirmed the upregulation of RNF220 mRNA and protein in HCC tissues. Functional assays demonstrated that RNF220 overexpression promoted cell proliferation, migration and stemness, whereas RNF220 knockdown suppressed these processes in HCC cells. Mechanistically, RNF220 enhanced ubiquitin-specific protease 22 (USP22) expression, leading to activation of the protein kinase B (Akt) pathway. Furthermore, the knockdown of RNF220 inhibited HCC progression, an effect that could be reversed by SC79 (an Akt activator), an Akt activator. In vivo experiments further confirmed that RNF220 aggravated tumor growth and metastasis. In summary, these findings indicate that RNF220 promotes HCC progression by regulating USP22 and activating the Akt pathway, suggesting that RNF220 may serve as a potential biomarker and therapeutic target for HCC.
DOI: 10.6084/m9.figshare.30000795
title: Molecular crossroads: identifying MAPK proteins bridging SMAD and dopamine pathways in breast cancer

description: The transforming growth factor-beta (TGF-β)/SMAD signaling pathway, mitogen-activated protein kinase (MAPK) signaling cascade, and dopamine receptor activity are all implicated in tumor progression. This study investigates molecular interactions among these pathways, identifying MAPK proteins that bridge SMAD and dopamine signaling in the context of breast cancer pathogenesis. A cohort of 405 breast cancer patients was categorized into molecular subtypes: luminal A (<i>n</i> = 130), luminal B HER2-negative (<i>n</i> = 100), luminal B HER2-positive (<i>n</i> = 96), non-luminal HER2-positive (<i>n</i> = 36), and triple-negative breast cancer (TNBC; <i>n</i> = 43). Transcriptomic profiling using microarrays and bioinformatics-based network analysis revealed differentially expressed genes across subtypes. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to validate 11 key transcripts, and protein expression was quantified by enzyme-linked immunosorbent assay (ELISA). MicroRNA (miRNA) regulatory interactions were analyzed to assess post-transcriptional modulation. Among 167 differentially expressed genes, 14 were consistently altered across all subtypes. These included cell division cycle 42 (<i>CDC42</i>), KRAS proto-oncogene, GTPase (<i>KRAS</i>), and transforming growth factor beta 1 (<i>TGFB1</i>), which were upregulated, as well as fibroblast growth factor 2 (<i>FGF2</i>), fibroblast growth factor 7 (<i>FGF7</i>), and insulin-like growth factor 1 <i>(IGF1</i>), which were downregulated. miRNA analysis revealed miR-221, miR-222, and miR-16-5p as regulators of these pathways. ELISA confirmed reduced KIT, IGF1, and FGF family proteins in tumor tissues, with KRAS significantly upregulated. Protein interaction analysis highlighted key hubs linking MAPK, SMAD, and dopamine signaling. This study elucidates crucial molecular intersections between MAPK, SMAD, and dopamine pathways, identifying potential biomarkers and therapeutic targets for breast cancer.
DOI: 10.15468/dl.5xr78v
title: Occurrence Download

description: A dataset containing 1606 species occurrences available in GBIF matching the query:
{
 "TaxonKey" : [
 "is Bridelia stipularis"
 ]
}

 The dataset includes 1606 records from 56 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0055986-250827131500795/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.