cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.15468/dl.h4pxng
title: Occurrence Download

description: A dataset containing 3543 species occurrences available in GBIF matching the query:
{
 "and" : [
 {
 "and" : [
 "HasGeospatialIssue is false",
 "HasCoordinate is true",
 "OccurrenceStatus is Present",
 {
 "not" : {
 "BasisOfRecord" : [
 "is one of (Fossil, Living Specimen)"
 ]
 }
 }
 ]
 },
 "SpeciesKey is Agriotes obscurus (Linnaeus, 1758)",
 "Year is greater than or equal to 2004",
 "Year is less than or equal to 2023"
 ]
}

 The dataset includes 3543 records from 172 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0088483-240626123714530/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.gssef7
title: Occurrence Download

description: A dataset containing 465203719 species occurrences available in GBIF matching the query:
{
 "TaxonKey" : [
 "is Tracheophyta"
 ]
}

 The dataset includes 465203719 records from 14632 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0088437-240626123714530/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.5123872
title: Supplementary Material for: Pancreatic Carcinoma Cell Lines Reflect Frequency and Variability of Cancer Stem Cell Markers in Clinical Tissue

description: <b><i>Background:</i></b> Pancreatic cancer is one of the most deadly malignancies with insufficient therapeutic options and poor outcome. Cancer stem cells (CSCs) are thought to be responsible for progression and therapy resistance. We investigated the potential of pancreatic cell lines for CSC research by analyzing to what extent they contain CSC populations and how representative these are compared to clinical tissue.<b><i> Methods:</i></b> Six pancreatic cancer cell lines were analyzed by flow cytometry for CD326, CD133, CD44, CD24, CXCR4 and ABCG2. Subsequently, 70 primary pancreatic tissues were evaluated for CD326, CD133 and CD44 by immunohistochemistry. <b><i>Results:</i></b> All the cell lines but one showed a stable expression pattern throughout biological replicates. Marker expression in clinical tissue of CD44 distinguished normal patients from pancreatic carcinoma patients with a sensitivity of 50% at 80% specificity and metastasized from nonmetastasized carcinomas with 69% sensitivity at 100% specificity. <b><i>Conclusions:</i></b> Our results indicate a link between elevated CD44 expression, malignancy and metastasis of pancreatic tissue. Furthermore, individual pancreatic cell lines show a substantial amount of cells with CSC properties which is comparable with interpatient variability detected in primary tissue. These pancreatic cancer cell lines could thus serve for urgently needed pharmacological CSC in vitro research.
DOI: 10.6084/m9.figshare.5123887.v1
title: Supplementary Material for: Modelling Genetic Susceptibility to Multiple Sclerosis with Family Data

description: A genetic contribution to susceptibility is well established in multiple sclerosis (MS) and 57 associated genetic loci have been identified. We have undertaken a meta-analysis of familial risk studies with the aims of providing definitive figures for risks to relatives, performing a segregation analysis and estimating the proportion of the overall genetic risk that currently identified genes represent. We have used standard methods of meta-analysis combined with novel approaches to age adjustment to provide directly comparable estimates of lifetime risk. The overall recurrence risk for monozygotic twins was 18.2% and for siblings 2.7%. The recurrence risk for dizygotic twins was significantly higher than for siblings. The overall estimate of sibling relative risk (λ<sub>S</sub>) was 16.8. Risks for older relatives (parents, siblings, aunts, uncles and cousins) show a latitudinal gradient, in line with population risk. No latitudinal gradient for λ<sub>S</sub> was seen. Segregation analysis supports a multiplicative model of one locus of moderate effect with many loci of small effect. The estimated contribution of the 57 known MS loci is 18–24% of λ<sub>S</sub>. This meta-analysis supports the notion of MS being in part the result of multiple genetic susceptibility factors and environmental factors.
DOI: 10.6084/m9.figshare.5123866
title: Supplementary Material for: The Robustness of Generalized Estimating Equations for Association Tests in Extended Family Data

description: Variance components analysis (VCA), the traditional method for handling correlations within families in genetic association studies, is computationally intensive for genome-wide analyses, and the computational burden of VCA increases with family size and the number of genetic markers. Alternative approaches that do not require the computation of familial correlations are preferable, provided that they do not inflate type I error or decrease power. We performed a simulation study to evaluate practical alternatives to VCA that use regression with generalized estimating equations (GEE) in extended family data. We compared the properties of linear regression with GEE applied to an entire extended family structure (GEE-EXT) and GEE applied to nuclear family structures split from these extended families (GEE-SPL) to variance components likelihood-based methods (FastAssoc). GEE-EXT was evaluated with and without robust variance estimators to estimate the standard errors. We observed similar average type I error rates from GEE-EXT and FastAssoc compared to GEE-SPL. Type I error rates for the GEE-EXT method with a robust variance estimator were marginally higher than the nominal rate when the minor allele frequency (MAF) was &lt;0.1, but were close to the nominal rate when the MAF was ≥0.2. All methods gave consistent effect estimates and had similar power. In summary, the GEE framework with the robust variance estimator, the computationally fastest and least data management-intensive approach, appears to work well in extended families and thus provides a reasonable alternative to full variance components approaches for extended pedigrees in a genome-wide association study setting.
DOI: 10.6084/m9.figshare.5123869
title: Supplementary Material for: Ara h 2 and Ara h 6 Have Similar Allergenic Activity and Are Substantially Redundant

description: <b><i>Background:</i></b> The moderately homologous (approx. 60%) proteins Ara h 2 and Ara h 6 are the most potent peanut allergens. This study was designed to define the relative individual contributions of Ara h 2 and Ara h 6 to the overall allergenic activity of a crude peanut extract (CPE). <b><i>Methods:</i></b> Ara h 2 and Ara h 6 were removed from CPE by gel filtration chromatography. Ara h 2.01, Ara h 2.02 and Ara h 6 were further purified (&gt;99%). The potency of each allergen and the ability of these allergens to reconstitute the allergenic activity of CPE depleted of Ara h 2 and Ara h 6 was measured with RBL SX-38 cells sensitized with IgE from sensitized peanut allergic patients. <b><i>Results:</i></b> The potency of the native proteins were significantly different (p &lt; 0.0001) although not dramatically so, with a rank order of Ara h 2.01 &gt; Ara h 2.02 &gt; Ara h 6. The addition of either purified Ara h 2 or Ara h 6 independently at their original concentration to CPE depleted of both Ara h 2 and Ara h 6 restored 80–100% of the original CPE allergenic activity. Addition of both Ara h 2 and Ara h 6 consistently completely restored the allergenic activity of CPE. <b><i>Conclusions:</i></b> These studies indicate that either Ara h 2 or Ara h 6 independently can account for most of the allergenic activity in a CPE and demonstrate important redundancy in the allergenic activity of these related molecules.
DOI: 10.6084/m9.figshare.5123875.v1
title: Supplementary Material for: Meta-Analysis Shows Strong Positive Association of the TNF-α Gene with Tumor Stage in Bladder Cancer

description: There is no consensus on the association between the <i>tumor necrosis factor-</i>α<i> (TNF-</i>α<i>)</i> gene promoter –308 A/G single nucleotide polymorphisms and bladder cancer risk. To obtain a more precise estimation of this correlation, we conducted a meta-analysis. The PubMed, MEDLINE, Cochrane Library and China National Knowledge Infrastructure (CNKI) databases were searched for relevant published studies. Seven case-control studies with a total of 1,311 cases and 1,436 controls were identified and analyzed. A notable correlation was observed between the <i>TNF-</i>α genotype and bladder cancer grade (<i>AA+GA </i>vs. <i>GG;</i> odds ratio 1.96, 95% confidence interval 1.37–2.80, p = 0.0002). In summary, this meta-analysis demonstrates that the <i>TNF-</i>α –308 <i>AA+GA</i> genotype may be a marker to the tumor-invasive stage of bladder cancer.
DOI: 10.6084/m9.figshare.5123857
title: Supplementary Material for: ‘a’-Position-Mutated and G4-Mutated Hemagglutinin-Neuraminidase Proteins of Newcastle Disease Virus Impair Fusion and Hemagglutinin-Neuraminidase-Fusion Interaction by Different Mechanisms

description: <b><i>Objectives:</i></b> To determine the effects of heptad repeat regions (HRs) and N-linked carbohydrate sites of the Newcastle disease virus hemagglutinin-neuraminidase (HN) protein on fusion of HN and fusion (F) proteins and HN-F interaction. <b><i>Methods:</i></b> We mutated six ‘a’ residues in the HRs and four asparagines in N-linked carbohydrate sites to alanine in the HN protein. A vaccinia-T7 RNA polymerase expression system was used to express HN cDNAs in BHK-21 cells to determine the HN functions. Deglycosylation was treated with PGNase F digestion. The formation of HN-F protein complexes was determined by the coimmunoprecipitation assay. <b><i>Results:</i></b> Each HR-mutated protein interfered with fusion and the HN-F interaction. The G4-mutated protein not only impaired fusion and HN-F interaction but also decreased activities in cell fusion promotion, hemadsorption and neuraminidase. <b><i>Conclusions:</i></b> It is assumed that two different mechanisms for mutations in these two regions are responsible for the decreased fusion promotion activity and the reduced ability of interaction with F protein. Mutations in the HRs impair fusion and HN-F interaction by altering the transmission of a signal from the globular domain to the F-specific region in the stalk, but the G4 mutation modulates fusion and HN-F interaction by the misfolding of some important structures.
DOI: 10.6084/m9.figshare.5123860
title: Supplementary Material for: Bacterial Stimulation of the TLR-MyD88 Pathway Modulates the Homeostatic Expression of Ileal Paneth Cell α-Defensins

description: Paneth cell α-defensins are antimicrobial peptides involved in the control of the intestinal microbiota and immunological homeostasis. In mice, they are encoded by multiple, highly homologous genes <i>(Defa)</i>. The transcriptional activity of ileal <i>Defa</i> genes was studied in response to pharmacological and genetic perturbations of the intestinal environment of C57BL/6 mice. <i>Defa</i> gene transcription was sensitive to oral antibiotic administration suggesting that commensal microbes regulate <i>Defa</i> expression. Ileal microbiota analysis showed that decreased transcription of <i>Defa</i> genes correlated with depletion of <i>Lactobacillus</i>. <i>Defa</i> expression was partially restored in vivo by lactobacillus administration to antibiotic-treated mice. <i>Defa</i> transcripts were less abundant in ex vivo, microbiota-free intestinal explants but recovered after explant exposure to UV-killed bacteria, Toll-like receptor (TLR)-2 or TLR4 agonists. Genetic deficiency of several TLRs or MyD88 led to dramatic drops in <i>Defa</i> transcription in vivo. These results show that Paneth cell <i>Defa</i> genes are regulated by commensal bacteria through TLR-MyD88 signaling and provide a further understanding of the dysregulation of intestinal homeostasis that occurs as a result of imbalances in the populations of commensal bacteria.
DOI: 10.6084/m9.figshare.5123863
title: Supplementary Material for: A de novo sSMC(22) Characterized by High-Resolution Arrays in a Girl with Cat-Eye Syndrome without Coloboma

description: Cat-eye syndrome (CES) results from trisomy or tetrasomy of proximal 22q originated by a small supernumerary marker chromosome (sSMC). Two critical regions for the major clinical features of CES (CESCRs) have been suggested; however, CES clinical presentation often does not correlate with the sSMC genetic content. We report here a CES girl without coloboma and carrier of a de novo type I sSMC(22) as determined by G- and C-banding, NOR staining and microarrays. This sSMC included 6 distal genes outside the original CESCR and led to a tetrasomy for 22q11.1–22q11.21. The patient’s final karyotype was 47,XX,+psu dic(22)(q11.21).arr 22q11.1q11.21(15,250,000–17,035,860)×4 dn. The amplified region outside of CESCR included some genes that may be related to neurologic, heart and renal abnormalities. Conversely, even though the amplification included the <i>CECR2</i> gene, a major candidate for eye features, there was no coloboma in the patient. The genetic delineation of the present sSMC further strengthens that the CES clinical presentation does not fit completely with the duplicated genetic content and that CES is actually a genomic disorder. Furthermore, since we observed no mosaicism, we believe that other mechanisms might be behind the variability of CES phenotypes as well, mainly those related with functional interactions among amplified genes.
DOI: 10.6084/m9.figshare.5123860.v1
title: Supplementary Material for: Bacterial Stimulation of the TLR-MyD88 Pathway Modulates the Homeostatic Expression of Ileal Paneth Cell α-Defensins

description: Paneth cell α-defensins are antimicrobial peptides involved in the control of the intestinal microbiota and immunological homeostasis. In mice, they are encoded by multiple, highly homologous genes <i>(Defa)</i>. The transcriptional activity of ileal <i>Defa</i> genes was studied in response to pharmacological and genetic perturbations of the intestinal environment of C57BL/6 mice. <i>Defa</i> gene transcription was sensitive to oral antibiotic administration suggesting that commensal microbes regulate <i>Defa</i> expression. Ileal microbiota analysis showed that decreased transcription of <i>Defa</i> genes correlated with depletion of <i>Lactobacillus</i>. <i>Defa</i> expression was partially restored in vivo by lactobacillus administration to antibiotic-treated mice. <i>Defa</i> transcripts were less abundant in ex vivo, microbiota-free intestinal explants but recovered after explant exposure to UV-killed bacteria, Toll-like receptor (TLR)-2 or TLR4 agonists. Genetic deficiency of several TLRs or MyD88 led to dramatic drops in <i>Defa</i> transcription in vivo. These results show that Paneth cell <i>Defa</i> genes are regulated by commensal bacteria through TLR-MyD88 signaling and provide a further understanding of the dysregulation of intestinal homeostasis that occurs as a result of imbalances in the populations of commensal bacteria.
DOI: 10.6084/m9.figshare.5123866.v1
title: Supplementary Material for: The Robustness of Generalized Estimating Equations for Association Tests in Extended Family Data

description: Variance components analysis (VCA), the traditional method for handling correlations within families in genetic association studies, is computationally intensive for genome-wide analyses, and the computational burden of VCA increases with family size and the number of genetic markers. Alternative approaches that do not require the computation of familial correlations are preferable, provided that they do not inflate type I error or decrease power. We performed a simulation study to evaluate practical alternatives to VCA that use regression with generalized estimating equations (GEE) in extended family data. We compared the properties of linear regression with GEE applied to an entire extended family structure (GEE-EXT) and GEE applied to nuclear family structures split from these extended families (GEE-SPL) to variance components likelihood-based methods (FastAssoc). GEE-EXT was evaluated with and without robust variance estimators to estimate the standard errors. We observed similar average type I error rates from GEE-EXT and FastAssoc compared to GEE-SPL. Type I error rates for the GEE-EXT method with a robust variance estimator were marginally higher than the nominal rate when the minor allele frequency (MAF) was &lt;0.1, but were close to the nominal rate when the MAF was ≥0.2. All methods gave consistent effect estimates and had similar power. In summary, the GEE framework with the robust variance estimator, the computationally fastest and least data management-intensive approach, appears to work well in extended families and thus provides a reasonable alternative to full variance components approaches for extended pedigrees in a genome-wide association study setting.
DOI: 10.6084/m9.figshare.5123857.v1
title: Supplementary Material for: ‘a’-Position-Mutated and G4-Mutated Hemagglutinin-Neuraminidase Proteins of Newcastle Disease Virus Impair Fusion and Hemagglutinin-Neuraminidase-Fusion Interaction by Different Mechanisms

description: <b><i>Objectives:</i></b> To determine the effects of heptad repeat regions (HRs) and N-linked carbohydrate sites of the Newcastle disease virus hemagglutinin-neuraminidase (HN) protein on fusion of HN and fusion (F) proteins and HN-F interaction. <b><i>Methods:</i></b> We mutated six ‘a’ residues in the HRs and four asparagines in N-linked carbohydrate sites to alanine in the HN protein. A vaccinia-T7 RNA polymerase expression system was used to express HN cDNAs in BHK-21 cells to determine the HN functions. Deglycosylation was treated with PGNase F digestion. The formation of HN-F protein complexes was determined by the coimmunoprecipitation assay. <b><i>Results:</i></b> Each HR-mutated protein interfered with fusion and the HN-F interaction. The G4-mutated protein not only impaired fusion and HN-F interaction but also decreased activities in cell fusion promotion, hemadsorption and neuraminidase. <b><i>Conclusions:</i></b> It is assumed that two different mechanisms for mutations in these two regions are responsible for the decreased fusion promotion activity and the reduced ability of interaction with F protein. Mutations in the HRs impair fusion and HN-F interaction by altering the transmission of a signal from the globular domain to the F-specific region in the stalk, but the G4 mutation modulates fusion and HN-F interaction by the misfolding of some important structures.
DOI: 10.6084/m9.figshare.5123863.v1
title: Supplementary Material for: A de novo sSMC(22) Characterized by High-Resolution Arrays in a Girl with Cat-Eye Syndrome without Coloboma

description: Cat-eye syndrome (CES) results from trisomy or tetrasomy of proximal 22q originated by a small supernumerary marker chromosome (sSMC). Two critical regions for the major clinical features of CES (CESCRs) have been suggested; however, CES clinical presentation often does not correlate with the sSMC genetic content. We report here a CES girl without coloboma and carrier of a de novo type I sSMC(22) as determined by G- and C-banding, NOR staining and microarrays. This sSMC included 6 distal genes outside the original CESCR and led to a tetrasomy for 22q11.1–22q11.21. The patient’s final karyotype was 47,XX,+psu dic(22)(q11.21).arr 22q11.1q11.21(15,250,000–17,035,860)×4 dn. The amplified region outside of CESCR included some genes that may be related to neurologic, heart and renal abnormalities. Conversely, even though the amplification included the <i>CECR2</i> gene, a major candidate for eye features, there was no coloboma in the patient. The genetic delineation of the present sSMC further strengthens that the CES clinical presentation does not fit completely with the duplicated genetic content and that CES is actually a genomic disorder. Furthermore, since we observed no mosaicism, we believe that other mechanisms might be behind the variability of CES phenotypes as well, mainly those related with functional interactions among amplified genes.
DOI: 10.6084/m9.figshare.5123848
title: Supplementary Material for: Photodynamic Properties of Vital Dyes for Vitreoretinal Surgery

description: The purpose of this study was to evaluate photodynamic properties of indocyanine green (ICG), brilliant blue G (BBG) and trypan blue (TB) as currently used vital dyes for chromovitrectomy. Under consideration of intraoperative illumination intensities and dye concentrations, a simulative in vitro investigation was set up. Therefore, standardized dilutions of original ICG, BBG and TB vials were irradiated at a wavelength of 366 nm with an intensity of 14 µW/cm<sup>2</sup> between 0 and 48 h. After this, all samples were measured spectroscopically in a 220- to 750-nm bandwidth. Analyzing the vital dyes over the time course, an exponential photolysis was observed for ICG, whereas BBG and TB presented photostable properties. Regarding ICG, 5% of the concentration was degraded to toxic metabolites every 20 min. For this reason, our study provides evidence that intraocular dye concentrations and modern endoillumination systems alone cannot fully prevent ICG photodegradation.
DOI: 10.6084/m9.figshare.5123851
title: Yeasts associated with hymenoptera

description: Fasta file with yeast sequences and accompanying metadata file with strain information.Note: Strains Wasp_YB16 is a synonym for YB16 and Bumblebee_BB202 is a synonym for BB202. <br>version 0.0, date 05.21.2018
DOI: 10.6084/m9.figshare.5123854
title: Supplementary Material for: Genomic Sequence and Analysis of EhV-99B1, a New Coccolithovirus from the Norwegian Fjords

description: Coccolithoviruses are giant dsDNA viruses that infect <i>Emiliania huxleyi</i>, the most ubiquitous marine microalga. Here, we present the genome of the latest coccolithovirus strain to be sequenced, EhV-99B1, and compare it with two other coccolithovirus genomes (EhV-86 and EhV-163). EhV-99B1 shares a pairwise nucleotide identity of 98% with EhV-163 (the two strains were isolated from the same Norwegian fjord but in different years), and just 96.5% with EhV-86 (isolated in the same spring as EhV-99B1 but in the English Channel). We confirmed and extended the list of relevant genomic differences between these EhVs from the Norwegian fjord and EhVs from the English Channel, namely the removal/insertions of: a phosphate permease, an endonuclease, a transposase, and two specific tRNAs. As a whole, this study provided new clues and insights into the diversity and mechanisms driving the evolution of these large oceanic viruses, in particular those processes involving selfish genetic elements.