cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.3996099.v1
title: Habitat_suitability_models.zip

description: Habitat suitability models for the 20 species used in the connectivity modelling. The models are at a resolution of 10km and projected in Mollweide. The cell values are expressed as percentage of 300m suitable cells (original resolution of the habitat suitability models in Rondinini et al. 2011).
DOI: 10.7910/dvn/v1rjpf/148aqo
title: snk20160208_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.3996102.v1
title: Supplementary Material for: A DNA Hypermethylation Profile Independently Predicts Biochemical Recurrence Following Radical Prostatectomy

description: <b><i>Purpose:</i></b> Detection of DNA hypermethylation is emerging as a novel molecular biomarker for different malignancies. We intend to define whether a hypermethylation profile of patients with prostate cancer (PCa) predicts biochemical recurrence (BCR) after radical prostatectomy (RP). <b><i>Material and Methods:</i></b> Genome-wide methylation analysis was performed using the GoldenGate Methylation Cancer Panel-I (Illumina, Inc.) on 10 normal prostate tissues and 58 tumor samples from patients treated by RP followed for prostate-specific antigen (PSA) failure (&gt;0.4 ng/ml) and disease progression. Patients were classified on the basis of D'Amico criteria according to clinical staging, PSA at diagnosis and Gleason score after pathologist review. Hypermethylation status of 1505 CpGs present in the promoter region of 807 genes was studied. Hierarchical clustering analysis was performed and relationships with outcome were investigated using log-rank analysis and Cox regression model. <b><i>Results:</i></b> We found 28 genes significantly hypermethylated in &gt;20% of the tumors analyzed. Four clusters of patients were characterized by their DNA methylation profile, one at higher risk to develop BCR (p = 0.005). Multivariate analysis revealed patients in this cluster (HR 2.56), and high-risk patients (HR 4.34) according to D'Amico classification were independent predictors of BCR after prostatectomy. From the selected genes <i>MT1A</i>, <i>ALOX12</i>, <i>GSTM2</i>, <i>APC</i>, <i>MYCL2</i> and <i>RARB</i> hypermethylation predicted BCR and <i>GSTM2 </i>(HR 3.78) and <i>MYCL2 </i>hypermethylation (HR 2.71) did so independently. <b><i>Conclusion:</i></b> Epigenetic silencing of <i>GSTM2</i> and <i>MYCL2</i> comprise novel molecular markers to predict BCR after surgery for medium- and high-risk localized PCa undergoing surgical treatment and hypermethylation of these genes could be incorporated to the clinical and pathological factors defining the patient at higher risk of PSA failure after prostatectomy. The limitation of the study is that no independent validation cohort is analysed.
DOI: 10.6084/m9.figshare.3996096
title: Supplementary Material for: Loss of Chromosome 18 in Neuroendocrine Tumors of the Small Intestine: The Enigma Remains

description: <b><i>Background/Aims:</i></b> Neuroendocrine tumors of the small intestine (SI-NETs) exhibit an increasing incidence and high mortality rate. Until now, no fundamental molecular event has been linked to the tumorigenesis and progression of these tumors. Only the loss of chromosome 18 (Chr18) has been shown in up to two thirds of SI-NETs, whereby the significance of this alteration is still not understood. We therefore performed the first comprehensive study to identify Chr18-related events at the genetic, epigenetic and gene/protein expression levels. <b><i>Methods:</i></b> We did expression analysis of all seven putative Chr18-related tumor suppressors by quantitative real-time PCR (qRT-PCR), Western blot and immunohistochemistry. Next-generation exome sequencing and SNP array analysis were performed with five SI-NETs with (partial) loss of Chr18. Finally, we analyzed all microRNAs (miRNAs) located on Chr18 by qRT-PCR, comparing Chr18+/- and Chr18+/+ SI-NETs. <b><i>Results:</i></b> Only DCC (deleted in colorectal cancer) revealed loss of/greatly reduced expression in 6/21 cases (29%). No relevant loss of SMAD2, SMAD4, elongin A3 and CABLES was detected. PMAIP1 and maspin were absent at the protein level. Next-generation sequencing did not reveal relevant recurrent somatic mutations on Chr18 either in an exploratory cohort of five SI-NETs, or in a validation cohort (n = 30). SNP array analysis showed no additional losses. The quantitative analysis of all 27 Chr18-related miRNAs revealed no difference in expression between Chr18+/- and Chr18+/+ SI-NETs. <b><i>Conclusion:</i></b> DCC seems to be the only Chr18-related tumor suppressor affected by the monoallelic loss of Chr18 resulting in a loss of DCC protein expression in one third of SI-NETs. No additional genetic or epigenetic alterations were present on Chr18.
DOI: 10.7910/dvn/v1rjpf/xtckzm
title: snk20150309_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.3996096.v1
title: Supplementary Material for: Loss of Chromosome 18 in Neuroendocrine Tumors of the Small Intestine: The Enigma Remains

description: <b><i>Background/Aims:</i></b> Neuroendocrine tumors of the small intestine (SI-NETs) exhibit an increasing incidence and high mortality rate. Until now, no fundamental molecular event has been linked to the tumorigenesis and progression of these tumors. Only the loss of chromosome 18 (Chr18) has been shown in up to two thirds of SI-NETs, whereby the significance of this alteration is still not understood. We therefore performed the first comprehensive study to identify Chr18-related events at the genetic, epigenetic and gene/protein expression levels. <b><i>Methods:</i></b> We did expression analysis of all seven putative Chr18-related tumor suppressors by quantitative real-time PCR (qRT-PCR), Western blot and immunohistochemistry. Next-generation exome sequencing and SNP array analysis were performed with five SI-NETs with (partial) loss of Chr18. Finally, we analyzed all microRNAs (miRNAs) located on Chr18 by qRT-PCR, comparing Chr18+/- and Chr18+/+ SI-NETs. <b><i>Results:</i></b> Only DCC (deleted in colorectal cancer) revealed loss of/greatly reduced expression in 6/21 cases (29%). No relevant loss of SMAD2, SMAD4, elongin A3 and CABLES was detected. PMAIP1 and maspin were absent at the protein level. Next-generation sequencing did not reveal relevant recurrent somatic mutations on Chr18 either in an exploratory cohort of five SI-NETs, or in a validation cohort (n = 30). SNP array analysis showed no additional losses. The quantitative analysis of all 27 Chr18-related miRNAs revealed no difference in expression between Chr18+/- and Chr18+/+ SI-NETs. <b><i>Conclusion:</i></b> DCC seems to be the only Chr18-related tumor suppressor affected by the monoallelic loss of Chr18 resulting in a loss of DCC protein expression in one third of SI-NETs. No additional genetic or epigenetic alterations were present on Chr18.
DOI: 10.6084/m9.figshare.3996084
title: Uganda 2013 AICM HFS and HPS data

description: The data here come from two surveys: a Health Facilities Survey (HFS) and a Health Professionals Survey (HPS). Both sets of data were collected in Uganda in 2013 as part of a study to measure the incidence of abortion in this country. The Abortion Incidence Complications Methodology (AICM), developed the by Guttmacher Institute, can be applied to this data to estimate the incidence of abortion.
DOI: 10.7910/dvn/v1rjpf/atrzpt
title: snk20150613_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.3996072
title: Supplementary Material for: Inhibition of mTOR's Catalytic Site by PKI-587 Is a Promising Therapeutic Option for Gastroenteropancreatic Neuroendocrine Tumor Disease

description: <b><i>Background:</i></b> The characteristic clinical heterogeneity and mostly slow-growing behavior of gastroenteropancreatic neuroendocrine neoplasms (GEP-NENs) cause problems in finding appropriate treatments. Thus, the current therapy options are not satisfactory. PKI-587 is a highly potent, novel dual inhibitor of PI3K and mTORC1/C2. <b><i>Aim:</i></b> We assessed the effects of PKI-587 in different GEP-NEN tumor models, including the poorly differentiated cell line LCC-18, and compared them with those of the established mTORC1 inhibitor everolimus. <b><i>Methods:</i></b> We treated BON, QGP-1, KRJ-I, and LCC-18 cell lines with increasing concentrations of the inhibitor PKI-587, and compared the results with those of everolimus and DMSO. We assessed the impact of the treatments on viability (WST-1 assay), on apoptotic processes (caspase 3/7 assay, JC-1), and on cell cycle regulation (flow cytometry). We determined alterations in signaling mediators by phosphor-specific Western blot analysis and conducted multiplexed gene expression analysis (nCounter® technology). <b><i>Results:</i></b> In all cell lines, PKI-587 dose-dependently inhibited proliferation, whereas everolimus was less effective. Treatment with PKI-587 led to cell cycle arrest and induction of apoptosis and successfully suppressed activity of the direct mTORC1 target 4E-BP1, a crucial factor for tumor genesis only partially inhibited by everolimus. Gene expression analyses revealed relevant changes of RAS, MAPK, STAT, and PI3K pathway genes after treatment. Treatment-dependent and cell line-characteristic effects on AKT/Rb/E2F signaling regarding cell cycle control and apoptosis are extensively discussed in this paper. <b><i>Conclusion:</i></b> PI3K/mTOR dual targeting is a promising new therapeutic approach in neuroendocrine tumor disease that should be evaluated in further clinical trials.
DOI: 10.6084/m9.figshare.3996078
title: Supplementary Material for: High Levels of Soluble Endoglin Induce a Proinflammatory and Oxidative-Stress Phenotype Associated with Preserved NO-Dependent Vasodilatation in Aortas from Mice Fed a High-Fat Diet

description: <b><i>Aims:</i></b> A soluble form of endoglin (sEng) was proposed to participate in the induction of endothelial dysfunction in small blood vessels. Here, we tested the hypothesis that high levels of sEng combined with a high-fat diet induce endothelial dysfunction in an atherosclerosis-prone aorta. <b><i>Methods and Results:</i></b> Six-month-old female and male transgenic mice overexpressing human sEng (<i>Sol-Eng</i><sup><i>+</i></sup>) with low (<i>Sol-Eng</i><sup><i>+</i></sup><i>low</i>) or high (<i>Sol-Eng</i><sup><i>+</i></sup><i>high</i>) levels of plasma sEng were fed a high-fat rodent diet containing 1.25% cholesterol and 40% fat for 3 months. The plasma cholesterol and mouse sEng levels did not differ in the <i>Sol-Eng</i><sup><i>+</i></sup><i>high</i> and <i>Sol-Eng</i><sup><i>+</i></sup><i>low</i> mice. The expression of proinflammatory (P-selectin, ICAM-1, pNFκB and COX-2) and oxidative-stress-related markers (HO-1, NOX-1 and NOX-2) in the aortas of <i>Sol-Eng</i><sup><i>+</i></sup><i>high</i> female mice was significantly higher than in <i>Sol-Eng</i><sup><i>+</i></sup><i>low </i>female mice. Endothelium-dependent vasodilatation induced by acetylcholine was preserved better in the <i>Sol-Eng</i><sup><i>+ </i></sup><i>high</i> female mice than in the <i>Sol-Eng</i><sup><i>+</i></sup><i>low </i>female mice. <b><i>Conclusion:</i></b> These results suggest that high concentrations of sEng in plasma in combination with a high-fat diet induce the simultaneous activation of proinflammatory, pro-oxidative and vasoprotective mechanisms in mice aorta and the balance of these biological processes determines whether the final endothelial phenotype is adaptive or maladaptive.
DOI: 10.7910/dvn/v1rjpf/d1neip
title: snk20161107_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.3996078.v1
title: Supplementary Material for: High Levels of Soluble Endoglin Induce a Proinflammatory and Oxidative-Stress Phenotype Associated with Preserved NO-Dependent Vasodilatation in Aortas from Mice Fed a High-Fat Diet

description: <b><i>Aims:</i></b> A soluble form of endoglin (sEng) was proposed to participate in the induction of endothelial dysfunction in small blood vessels. Here, we tested the hypothesis that high levels of sEng combined with a high-fat diet induce endothelial dysfunction in an atherosclerosis-prone aorta. <b><i>Methods and Results:</i></b> Six-month-old female and male transgenic mice overexpressing human sEng (<i>Sol-Eng</i><sup><i>+</i></sup>) with low (<i>Sol-Eng</i><sup><i>+</i></sup><i>low</i>) or high (<i>Sol-Eng</i><sup><i>+</i></sup><i>high</i>) levels of plasma sEng were fed a high-fat rodent diet containing 1.25% cholesterol and 40% fat for 3 months. The plasma cholesterol and mouse sEng levels did not differ in the <i>Sol-Eng</i><sup><i>+</i></sup><i>high</i> and <i>Sol-Eng</i><sup><i>+</i></sup><i>low</i> mice. The expression of proinflammatory (P-selectin, ICAM-1, pNFκB and COX-2) and oxidative-stress-related markers (HO-1, NOX-1 and NOX-2) in the aortas of <i>Sol-Eng</i><sup><i>+</i></sup><i>high</i> female mice was significantly higher than in <i>Sol-Eng</i><sup><i>+</i></sup><i>low </i>female mice. Endothelium-dependent vasodilatation induced by acetylcholine was preserved better in the <i>Sol-Eng</i><sup><i>+ </i></sup><i>high</i> female mice than in the <i>Sol-Eng</i><sup><i>+</i></sup><i>low </i>female mice. <b><i>Conclusion:</i></b> These results suggest that high concentrations of sEng in plasma in combination with a high-fat diet induce the simultaneous activation of proinflammatory, pro-oxidative and vasoprotective mechanisms in mice aorta and the balance of these biological processes determines whether the final endothelial phenotype is adaptive or maladaptive.
DOI: 10.7910/dvn/v1rjpf/tnczjm
title: snk20150927_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.3996006
title: Supplementary Material for: The POU/Oct Transcription Factor Pdm1/nub Is Necessary for a Beneficial Gut Microbiota and Normal Lifespan of Drosophila

description: Maintenance of a stable gut microbial community relies on a delicate balance between immune defense and immune tolerance. We have used <i>Drosophila</i> to study how the microbial gut flora is affected by changes in host genetic factors and immunity. Flies with a constitutively active gut immune system, due to a mutation in the POU transcriptional regulator <i>Pdm1/nubbin (nub)</i> gene, had higher loads of bacteria and a more diverse taxonomic composition than controls. In addition, the microbial composition shifted considerably during the short lifespan of the <i>nub</i><sup><i>1</i></sup> mutants. This shift was characterized by a loss of relatively few OTUs (operational taxonomic units) and a remarkable increase in a large number of <i>Acetobacter </i>spp<i>.</i> and <i>Leuconostoc</i> spp. Treating <i>nub</i><sup><i>1</i></sup> mutant flies with antibiotics prolonged their lifetime survival by more than 100%. Immune gene expression was also persistently high in the presence of antibiotics, indicating that the early death was not a direct consequence of an overactive immune defense but rather an indirect consequence of the microbial load and composition. Thus, changes in host genotype and an inability to regulate the normal growth and composition of the gut microbiota leads to a shift in the microbial community, dysbiosis and early death.<br>
DOI: 10.6084/m9.figshare.3995757
title: Supplementary Material for: How Much Do We Know about Maintaining Treatment Response after Successful Acne Therapy? Systematic Review on the Efficacy and Safety of Acne Maintenance Therapy

description: After cessation of successful initial acne therapy, patients often experience flares. Consecutive maintenance treatment after successful induction therapy is promoted by guidelines; however, little is known about the efficacy/safety of different maintenance regimens. A systematic review on acne maintenance treatments was conducted. We identified 5 randomized controlled trials [RCTs; adapalene vs. vehicle or vs. no treatment (3 RCTs), adapalene/benzoyl peroxide (BPO) vs. vehicle, combination/monotherapy of minocycline (systemic)/tazarotene/placebo] and 3 non-RCTs on systemic isotretinoin, adapalene/BPO and azelaic acid. The results of adapalene versus vehicle/no treatment varied depending on the reported outcome. The ‘number of patients maintaining at least 50% improvement' counting inflammatory lesions/non-inflammatory lesions with adapalene was superior to vehicle (risk ratio, RR 1.24, 95% confidence interval, CI 1.08-1.43/RR 1.34, 95% CI 1.18-1.59). However, no significant differences were found in 2 of 3 RCTs for maintaining ‘clear/almost clear' or ‘mild acne' or on the global grading score. For the combination regimens of minocycline/tazarotene/placebo, no significant differences were found. Adapalene/BPO was superior to vehicle counting inflammatory lesions/non-inflammatory lesions (RR 1.61, 95% CI 1.31-1.99; RR 1.80, 95% CI 1.44-2.26). Due to the scarcity of studies, few conclusions can be drawn. More homogeneous outcome measures and specific maintenance study designs may lead to more robust findings.
DOI: 10.7910/dvn/v1rjpf/ummdrf
title: snk20150907_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.3995601
title: Supplementary Material for: Escherichia colimazEF Toxin-Antitoxin System as a Tool to Target Cell Ablation in Plants

description: <b><i>Background/Aims:</i></b> The <i>Escherichia coli</i> MazF is an endoribonuclease that cleaves mRNA at ACA sequences, thereby triggering inhibition of protein synthesis. The aim of this study is to evaluate the efficiency of the <i>mazEF</i> toxin-antitoxin system in plants to develop biotechnological tools for targeted cell ablation. <b><i>Methods:</i></b> A double transformation strategy, combining expression of the <i>mazE</i> antitoxin gene under the control of the <i>CaMV 35S</i> promoter, reported to drive expression in all plant cells except within the tapetum, together with the expression of the <i>mazF </i>gene under the control of the <i>TA29</i> tapetum-specific promoter in transgenic tobacco, was applied. <b><i>Results:</i></b> No transgenic <i>TA29-mazF</i> line could be regenerated, suggesting that the <i>TA29</i> promoter is not strictly tapetum specific and that MazF is toxic for plant cells. The regenerated<i> 35S-mazE</i>/<i>TA29-mazF</i> double-transformed lines gave a unique phenotype where the tapetal cell layer was necrosed resulting in the absence of pollen. <b><i>Conclusion:</i></b> These results show that the <i>E. coli</i><i>mazEF</i> system can be used to induce death of specific plant cell types and can provide a new tool to plant cell ablation.
DOI: 10.7910/dvn/v1rjpf/nn0cwh
title: snk20150103_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.3995319
title: Supplementary Material for: The Effect of an Emollient Containing Urea, Ceramide NP, and Lactate on Skin Barrier Structure and Function in Older People with Dry Skin

description: Xerosis affects up to 75% of older people and develops as a result of a skin barrier defect. Emollients are widely used to treat xerosis; however, there is limited understanding of the differences between them and their effects on the skin barrier in older people. This study aimed to compare the effect of a commercially available emollient containing 5% urea, ceramide NP and lactate (test emollient) to an alternative emollient without these additives (control emollient) on the properties of the skin barrier in older people. Two cohorts of 21 volunteers aged &gt;60 years with dry skin were recruited. The first applied the test emollient to one forearm and no treatment to the other for 28 days. The second compared the test emollient to the control emollient observing the same parameters. Effects on the skin barrier were determined by measuring skin barrier function, hydration, skin surface pH and by analysing Fourier transform infrared spectra before and after treatment. A third cohort of 6 young adults was recruited to investigate the effect of a single treatment with the test emollient on the molecular structure of the skin barrier at greater depths by employing the tape-stripping technique. The test emollient hydrated the skin to a significantly greater extent and for a longer period of time compared to the control emollient, an effect associated with a significant elevation of carboxylate groups (a marker of natural moisturizing factor content) within the stratum corneum. Furthermore, the test emollient imparted additional benefits to the structure and function of the skin barrier not exhibited by the control emollient. In conclusion, the test emollient addressed the pathological features of xerotic aged skin, supporting its use as first-line therapy for xerotic skin conditions in this population.
DOI: 10.6084/m9.figshare.3995319.v1
title: Supplementary Material for: The Effect of an Emollient Containing Urea, Ceramide NP, and Lactate on Skin Barrier Structure and Function in Older People with Dry Skin

description: Xerosis affects up to 75% of older people and develops as a result of a skin barrier defect. Emollients are widely used to treat xerosis; however, there is limited understanding of the differences between them and their effects on the skin barrier in older people. This study aimed to compare the effect of a commercially available emollient containing 5% urea, ceramide NP and lactate (test emollient) to an alternative emollient without these additives (control emollient) on the properties of the skin barrier in older people. Two cohorts of 21 volunteers aged &gt;60 years with dry skin were recruited. The first applied the test emollient to one forearm and no treatment to the other for 28 days. The second compared the test emollient to the control emollient observing the same parameters. Effects on the skin barrier were determined by measuring skin barrier function, hydration, skin surface pH and by analysing Fourier transform infrared spectra before and after treatment. A third cohort of 6 young adults was recruited to investigate the effect of a single treatment with the test emollient on the molecular structure of the skin barrier at greater depths by employing the tape-stripping technique. The test emollient hydrated the skin to a significantly greater extent and for a longer period of time compared to the control emollient, an effect associated with a significant elevation of carboxylate groups (a marker of natural moisturizing factor content) within the stratum corneum. Furthermore, the test emollient imparted additional benefits to the structure and function of the skin barrier not exhibited by the control emollient. In conclusion, the test emollient addressed the pathological features of xerotic aged skin, supporting its use as first-line therapy for xerotic skin conditions in this population.
DOI: 10.7910/dvn/v1rjpf/aibe2o
title: snk20160316_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/eu9bix
title: snk20160930_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/payxxq
title: snk20150421_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/rguumq
title: snk20160713_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/rxbjvt
title: snk20150923_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/lqfnvn
title: snk20161013_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/byg1sd
title: snk20150518_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/imtypt
title: snk20160213_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/uxwv1c
title: snk20150925_03.txt.gz

description: :unav