cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.3798783.v1
title: GPCRs through the keyhole: the role of protein flexibility in ligand binding to β-adrenoceptors

description: G protein-coupled receptors (GPCRs) are proteins of pharmaceutical importance, with over 30% of all drugs in clinical use targeting them. Increasing numbers of X-ray crystal (XRC) structures of GPCRs offer a wealth of data relating to ligand binding. For the β-adrenoceptors (β-ARs), XRC structures are available for human β<sub>2</sub>- and turkey β<sub>1</sub>-subtypes, in complexes with a range of ligands. While these structures provide insight into the origins of ligand structure-activity relationships (SARs), questions remain. The ligands in all published complexed XRC structures lack extensive substitution, with no obvious way the ligand-binding site can accommodate β<sub>1</sub>-AR-selective antagonists with extended side-chains <i>para</i>- to the common aryloxypropanolamine pharmacophore. Using standard computational docking tools with such ligands generally returns poses that fail to explain known SARs. Application of our Active Site Pressurisation modelling method to β-AR XRC structures and homology models, however, reveals a dynamic area in the ligand-binding pocket that, through minor changes in amino acid side chain orientations, opens a fissure between transmembrane helices H4 and H5, exposing intra-membrane space. This fissure, which we term the “keyhole”, is ideally located to accommodate extended moieties present in many high-affinity β<sub>1</sub>-AR-selective ligands, allowing the rest of the ligand structure to adopt a canonical pose in the orthosteric binding site. We propose the keyhole may be a feature of both β<sub>1</sub>- and β<sub>2</sub>-ARs, but that subtle structural differences exist between the two, contributing to subtype-selectivity. This has consequences for the rational design of future generations of subtype-selective ligands for these therapeutically important targets.
DOI: 10.6084/m9.figshare.3798774
title: Dataset for: Segmented Polynomials for Incidence Rate Estimation from Prevalence data

description: The study considers the problem of estimating incidence of a non remissible infection (or disease) with possibly differential mortality using data from a(several) cross-sectional prevalence survey(s). Fitting segmented polynomial models is proposed to estimate the incidence as a function of age, using the maximum likelihood method. The approach allows automatic search for optimal position of knots and model selection is performed using the Akaike Information Criterion. The method is applied to simulated data and to estimate HIV incidence among men in Zimbabwe using data from both the NIMH Project Accept (HPTN 043) and Zimbabwe Demographic Health Surveys (2005-2006).
DOI: 10.6084/m9.figshare.3798774.v1
title: Dataset for: Segmented Polynomials for Incidence Rate Estimation from Prevalence data

description: The study considers the problem of estimating incidence of a non remissible infection (or disease) with possibly differential mortality using data from a(several) cross-sectional prevalence survey(s). Fitting segmented polynomial models is proposed to estimate the incidence as a function of age, using the maximum likelihood method. The approach allows automatic search for optimal position of knots and model selection is performed using the Akaike Information Criterion. The method is applied to simulated data and to estimate HIV incidence among men in Zimbabwe using data from both the NIMH Project Accept (HPTN 043) and Zimbabwe Demographic Health Surveys (2005-2006).
DOI: 10.6084/m9.figshare.3798651
title: Rhombohedral to Bernal structural transformation in trilayer graphene

description: The poster was presented in Graphene 2016, April 19-22, Genova Italy
DOI: 10.6084/m9.figshare.3798579
title: Data Citations

description: Presentation at the Data-PASS Workshop Clarifying Data Citation and Sharing – Some Practical Information for Journals APSA 2016<br>
DOI: 10.6084/m9.figshare.3798579.v1
title: Data Citations

description: Presentation at the Data-PASS Workshop Clarifying Data Citation and Sharing – Some Practical Information for Journals APSA 2016<br>
DOI: 10.6084/m9.figshare.3798573
title: Considerable pancreatic tumor motion during breath-holding

description: <b>Background:</b> Breath-holding (BH) is often used to reduce abdominal organ motion during radiotherapy. However, for inhale BH, abdominal tumor motion <i>during</i> BH has not yet been investigated. The aim of this study was to quantify tumor motion during inhale BH and tumor position variations between consecutive inhale BHs in pancreatic cancer patients. <b>Material and methods:</b> Twelve patients with intratumoral fiducials were included and asked to perform three consecutive 30-second inhale BHs on each of three measurement days. During BH, lateral fluoroscopic movies were obtained and a two-dimensional (2D) image correlation algorithm was used to track the fiducials and the diaphragm, yielding the tumor and diaphragm motion during each BH. The tumor position variation between consecutive BHs was obtained from the difference in initial tumor position between consecutive BHs on a single measurement day. <b>Results:</b> We observed tumor motion during BH with a mean absolute maximum displacement over all BHs of 4.2 mm (range 1.0–11.0 mm) in inferior-superior (IS) direction and 2.7 mm (range 0.5–8.0 mm) in anterior-posterior (AP) direction. We found only a moderate correlation between tumor and diaphragm motion in the IS direction (Pearson’s correlation coefficient |<i>r</i>|&gt;0.6 in 45 of 76 BHs). The mean tumor position variation between consecutive BHs was 0.2 [standard deviation (SD) 1.7] mm in the inferior direction and 0.5 (SD 0.8) mm in the anterior direction. <b>Conclusion:</b> We observed substantial pancreatic tumor motion during BH as well as considerable position variation between consecutive BHs on a single day. We recommend further quantifying these uncertainties before introducing breath-hold during radiation treatment of pancreatic cancer patients. Also, the diaphragm cannot be used as a surrogate for pancreatic tumor motion.
DOI: 10.6084/m9.figshare.3798573.v1
title: Considerable pancreatic tumor motion during breath-holding

description: <b>Background:</b> Breath-holding (BH) is often used to reduce abdominal organ motion during radiotherapy. However, for inhale BH, abdominal tumor motion <i>during</i> BH has not yet been investigated. The aim of this study was to quantify tumor motion during inhale BH and tumor position variations between consecutive inhale BHs in pancreatic cancer patients. <b>Material and methods:</b> Twelve patients with intratumoral fiducials were included and asked to perform three consecutive 30-second inhale BHs on each of three measurement days. During BH, lateral fluoroscopic movies were obtained and a two-dimensional (2D) image correlation algorithm was used to track the fiducials and the diaphragm, yielding the tumor and diaphragm motion during each BH. The tumor position variation between consecutive BHs was obtained from the difference in initial tumor position between consecutive BHs on a single measurement day. <b>Results:</b> We observed tumor motion during BH with a mean absolute maximum displacement over all BHs of 4.2 mm (range 1.0–11.0 mm) in inferior-superior (IS) direction and 2.7 mm (range 0.5–8.0 mm) in anterior-posterior (AP) direction. We found only a moderate correlation between tumor and diaphragm motion in the IS direction (Pearson’s correlation coefficient |<i>r</i>|&gt;0.6 in 45 of 76 BHs). The mean tumor position variation between consecutive BHs was 0.2 [standard deviation (SD) 1.7] mm in the inferior direction and 0.5 (SD 0.8) mm in the anterior direction. <b>Conclusion:</b> We observed substantial pancreatic tumor motion during BH as well as considerable position variation between consecutive BHs on a single day. We recommend further quantifying these uncertainties before introducing breath-hold during radiation treatment of pancreatic cancer patients. Also, the diaphragm cannot be used as a surrogate for pancreatic tumor motion.
DOI: 10.6084/m9.figshare.3798543
title: Datasets of DNA sequencing (Illumina) of ladybird beetles

description: The library names refer to:<br>46: Hippodamia convergens (TruSeq Nano, HiSeq 2500 Rapid Mode, 2x250 bp, insert size 550 bp, 250 cycle kit, 2% of the flow cell)<br>68: Harmonia axyridis (TruSeq Nano, HiSeq 2500 Rapid Mode, 2x250 bp, insert size 550 bp, 250 cycle kit, 2% of the flow cell)<br>BioA: Cycloneda sanguinea (TruSeq Nano, HiSeq 2500 Rapid Mode, 2x250 bp, insert size 550 bp, 250 cycle kit, 2% of the flow cell)<br>DebPool: several insect species multiplexed (TruSeq Nano, MiSeq, 2x250 bp, insert size 850 bp, 500 cycle kit, 15% flowcell)
DOI: 10.6084/m9.figshare.3798543.v2
title: Datasets of DNA sequencing (Illumina) of ladybird beetles

description: The library names refer to:<br>46: Hippodamia convergens (TruSeq Nano, HiSeq 2500 Rapid Mode, 2x250 bp, insert size 550 bp, 250 cycle kit, 2% of the flow cell)<br>68: Harmonia axyridis (TruSeq Nano, HiSeq 2500 Rapid Mode, 2x250 bp, insert size 550 bp, 250 cycle kit, 2% of the flow cell)<br>BioA: Cycloneda sanguinea (TruSeq Nano, HiSeq 2500 Rapid Mode, 2x250 bp, insert size 550 bp, 250 cycle kit, 2% of the flow cell)<br>DebPool: several insect species multiplexed (TruSeq Nano, MiSeq, 2x250 bp, insert size 850 bp, 500 cycle kit, 15% flowcell)
DOI: 10.6084/m9.figshare.3798543.v1
title: New draft item

description: Datasets of DNA sequencing (Illumina) of ladybird beetles.<br>The library names refer to:<br>46: Hippodamia convergens (TruSeq Nano, HiSeq 2500 Rapid Mode, 2x250 bp, insert size 550 bp, 250 cycle kit, 2% of the flow cell)<br>68: Harmonia axyridis (TruSeq Nano, HiSeq 2500 Rapid Mode, 2x250 bp, insert size 550 bp, 250 cycle kit, 2% of the flow cell)<br>BioA: Cycloneda sanguinea (TruSeq Nano, HiSeq 2500 Rapid Mode, 2x250 bp, insert size 550 bp, 250 cycle kit, 2% of the flow cell)<br>DebPool: several insect species multiplexed (TruSeq Nano, MiSeq, 2x250 bp, insert size 850 bp, 500 cycle kit, 15% flowcell)
DOI: 10.6084/m9.figshare.3798471
title: A signaling cascade including ARID1A, GADD45B and DUSP1 induces apoptosis and affects the cell cycle of germ cell cancers after romidepsin treatment

description: In Western countries, the incidence of testicular germ cell cancers (GCC) is steadily rising over the last decades. Mostly, men between 20 and 40 years of age are affected. In general, patients suffering from GCCs are treated by orchiectomy and radio- or chemotherapy. Due to resistance mechanisms, intolerance to the therapy or denial of chemo- / radiotherapy by the patients, GCCs are still a lethal threat, highlighting the need for alternative treatment strategies.In this study, we revealed that germ cell cancer cell lines are highly sensitive to the histone deacetylase inhibitor romidepsin <em>in vitro</em> and <em>in vivo</em>, highlighting romidepsin as a potential therapeutic option for GCC patients.Romidepsin-mediated inhibition of histone deacetylases led to disturbances of the chromatin landscape. This resulted in locus-specific histone-hyper- or hypoacetylation. We found that hypoacetylation at the <em>ARID1A</em> promotor caused repression of the SWI/SNF-complex member <em>ARID1A</em>. In consequence, this resulted in upregulation of the stress-sensors and apoptosis-regulators <em>GADD45B</em>, <em>DUSP1</em> and <em>CDKN1A</em>. RNAi-driven knock down of <em>ARID1A</em> mimicked in parts the effects of romidepsin, while CRISPR/Cas9-mediated deletion of <em>GADD45B</em> attenuated the romidepsin-provoked induction of apoptosis and cell cycle alterations.We propose a signaling cascade involving <em>ARID1A</em>, <em>GADD45B</em> and <em>DUSP1</em> as mediators of the romidepsin effects in GCC cells.<br>
DOI: 10.6084/m9.figshare.3798471.v1
title: A signaling cascade including ARID1A, GADD45B and DUSP1 induces apoptosis and affects the cell cycle of germ cell cancers after romidepsin treatment

description: In Western countries, the incidence of testicular germ cell cancers (GCC) is steadily rising over the last decades. Mostly, men between 20 and 40 years of age are affected. In general, patients suffering from GCCs are treated by orchiectomy and radio- or chemotherapy. Due to resistance mechanisms, intolerance to the therapy or denial of chemo- / radiotherapy by the patients, GCCs are still a lethal threat, highlighting the need for alternative treatment strategies.In this study, we revealed that germ cell cancer cell lines are highly sensitive to the histone deacetylase inhibitor romidepsin <em>in vitro</em> and <em>in vivo</em>, highlighting romidepsin as a potential therapeutic option for GCC patients.Romidepsin-mediated inhibition of histone deacetylases led to disturbances of the chromatin landscape. This resulted in locus-specific histone-hyper- or hypoacetylation. We found that hypoacetylation at the <em>ARID1A</em> promotor caused repression of the SWI/SNF-complex member <em>ARID1A</em>. In consequence, this resulted in upregulation of the stress-sensors and apoptosis-regulators <em>GADD45B</em>, <em>DUSP1</em> and <em>CDKN1A</em>. RNAi-driven knock down of <em>ARID1A</em> mimicked in parts the effects of romidepsin, while CRISPR/Cas9-mediated deletion of <em>GADD45B</em> attenuated the romidepsin-provoked induction of apoptosis and cell cycle alterations.We propose a signaling cascade involving <em>ARID1A</em>, <em>GADD45B</em> and <em>DUSP1</em> as mediators of the romidepsin effects in GCC cells.<br>
DOI: 10.6084/m9.figshare.3798471.v2
title: A signaling cascade including ARID1A, GADD45B and DUSP1 induces apoptosis and affects the cell cycle of germ cell cancers after romidepsin treatment

description: In Western countries, the incidence of testicular germ cell cancers (GCC) is steadily rising over the last decades. Mostly, men between 20 and 40 years of age are affected. In general, patients suffering from GCCs are treated by orchiectomy and radio- or chemotherapy. Due to resistance mechanisms, intolerance to the therapy or denial of chemo- / radiotherapy by the patients, GCCs are still a lethal threat, highlighting the need for alternative treatment strategies.In this study, we revealed that germ cell cancer cell lines are highly sensitive to the histone deacetylase inhibitor romidepsin <em>in vitro</em> and <em>in vivo</em>, highlighting romidepsin as a potential therapeutic option for GCC patients.Romidepsin-mediated inhibition of histone deacetylases led to disturbances of the chromatin landscape. This resulted in locus-specific histone-hyper- or hypoacetylation. We found that hypoacetylation at the <em>ARID1A</em> promotor caused repression of the SWI/SNF-complex member <em>ARID1A</em>. In consequence, this resulted in upregulation of the stress-sensors and apoptosis-regulators <em>GADD45B</em>, <em>DUSP1</em> and <em>CDKN1A</em>. RNAi-driven knock down of <em>ARID1A</em> mimicked in parts the effects of romidepsin, while CRISPR/Cas9-mediated deletion of <em>GADD45B</em> attenuated the romidepsin-provoked induction of apoptosis and cell cycle alterations.We propose a signaling cascade involving <em>ARID1A</em>, <em>GADD45B</em> and <em>DUSP1</em> as mediators of the romidepsin effects in GCC cells.<br>
DOI: 10.6084/m9.figshare.3798471.v3
title: A signaling cascade including ARID1A, GADD45B and DUSP1 induces apoptosis and affects the cell cycle of germ cell cancers after romidepsin treatment

description: In Western countries, the incidence of testicular germ cell cancers (GCC) is steadily rising over the last decades. Mostly, men between 20 and 40 years of age are affected. In general, patients suffering from GCCs are treated by orchiectomy and radio- or chemotherapy. Due to resistance mechanisms, intolerance to the therapy or denial of chemo- / radiotherapy by the patients, GCCs are still a lethal threat, highlighting the need for alternative treatment strategies.In this study, we revealed that germ cell cancer cell lines are highly sensitive to the histone deacetylase inhibitor romidepsin <em>in vitro</em> and <em>in vivo</em>, highlighting romidepsin as a potential therapeutic option for GCC patients.Romidepsin-mediated inhibition of histone deacetylases led to disturbances of the chromatin landscape. This resulted in locus-specific histone-hyper- or hypoacetylation. We found that hypoacetylation at the <em>ARID1A</em> promotor caused repression of the SWI/SNF-complex member <em>ARID1A</em>. In consequence, this resulted in upregulation of the stress-sensors and apoptosis-regulators <em>GADD45B</em>, <em>DUSP1</em> and <em>CDKN1A</em>. RNAi-driven knock down of <em>ARID1A</em> mimicked in parts the effects of romidepsin, while CRISPR/Cas9-mediated deletion of <em>GADD45B</em> attenuated the romidepsin-provoked induction of apoptosis and cell cycle alterations.We propose a signaling cascade involving <em>ARID1A</em>, <em>GADD45B</em> and <em>DUSP1</em> as mediators of the romidepsin effects in GCC cells.<br>
DOI: 10.6084/m9.figshare.3798471.v4
title: A signaling cascade including ARID1A, GADD45B and DUSP1 induces apoptosis and affects the cell cycle of germ cell cancers after romidepsin treatment

description: In Western countries, the incidence of testicular germ cell cancers (GCC) is steadily rising over the last decades. Mostly, men between 20 and 40 years of age are affected. In general, patients suffering from GCCs are treated by orchiectomy and radio- or chemotherapy. Due to resistance mechanisms, intolerance to the therapy or denial of chemo- / radiotherapy by the patients, GCCs are still a lethal threat, highlighting the need for alternative treatment strategies.In this study, we revealed that germ cell cancer cell lines are highly sensitive to the histone deacetylase inhibitor romidepsin <em>in vitro</em> and <em>in vivo</em>, highlighting romidepsin as a potential therapeutic option for GCC patients.Romidepsin-mediated inhibition of histone deacetylases led to disturbances of the chromatin landscape. This resulted in locus-specific histone-hyper- or hypoacetylation. We found that hypoacetylation at the <em>ARID1A</em> promotor caused repression of the SWI/SNF-complex member <em>ARID1A</em>. In consequence, this resulted in upregulation of the stress-sensors and apoptosis-regulators <em>GADD45B</em>, <em>DUSP1</em> and <em>CDKN1A</em>. RNAi-driven knock down of <em>ARID1A</em> mimicked in parts the effects of romidepsin, while CRISPR/Cas9-mediated deletion of <em>GADD45B</em> attenuated the romidepsin-provoked induction of apoptosis and cell cycle alterations.We propose a signaling cascade involving <em>ARID1A</em>, <em>GADD45B</em> and <em>DUSP1</em> as mediators of the romidepsin effects in GCC cells.<br>
DOI: 10.6084/m9.figshare.3798471.v6
title: A signaling cascade including ARID1A, GADD45B and DUSP1 induces apoptosis and affects the cell cycle of germ cell cancers after romidepsin treatment

description: In Western countries, the incidence of testicular germ cell cancers (GCC) is steadily rising over the last decades. Mostly, men between 20 and 40 years of age are affected. In general, patients suffering from GCCs are treated by orchiectomy and radio- or chemotherapy. Due to resistance mechanisms, intolerance to the therapy or denial of chemo- / radiotherapy by the patients, GCCs are still a lethal threat, highlighting the need for alternative treatment strategies.In this study, we revealed that germ cell cancer cell lines are highly sensitive to the histone deacetylase inhibitor romidepsin <em>in vitro</em> and <em>in vivo</em>, highlighting romidepsin as a potential therapeutic option for GCC patients.Romidepsin-mediated inhibition of histone deacetylases led to disturbances of the chromatin landscape. This resulted in locus-specific histone-hyper- or hypoacetylation. We found that hypoacetylation at the <em>ARID1A</em> promotor caused repression of the SWI/SNF-complex member <em>ARID1A</em>. In consequence, this resulted in upregulation of the stress-sensors and apoptosis-regulators <em>GADD45B</em>, <em>DUSP1</em> and <em>CDKN1A</em>. RNAi-driven knock down of <em>ARID1A</em> mimicked in parts the effects of romidepsin, while CRISPR/Cas9-mediated deletion of <em>GADD45B</em> attenuated the romidepsin-provoked induction of apoptosis and cell cycle alterations.We propose a signaling cascade involving <em>ARID1A</em>, <em>GADD45B</em> and <em>DUSP1</em> as mediators of the romidepsin effects in GCC cells.<br>
DOI: 10.6084/m9.figshare.3798471.v5
title: A signaling cascade including ARID1A, GADD45B and DUSP1 induces apoptosis and affects the cell cycle of germ cell cancers after romidepsin treatment

description: In Western countries, the incidence of testicular germ cell cancers (GCC) is steadily rising over the last decades. Mostly, men between 20 and 40 years of age are affected. In general, patients suffering from GCCs are treated by orchiectomy and radio- or chemotherapy. Due to resistance mechanisms, intolerance to the therapy or denial of chemo- / radiotherapy by the patients, GCCs are still a lethal threat, highlighting the need for alternative treatment strategies.In this study, we revealed that germ cell cancer cell lines are highly sensitive to the histone deacetylase inhibitor romidepsin <em>in vitro</em> and <em>in vivo</em>, highlighting romidepsin as a potential therapeutic option for GCC patients.Romidepsin-mediated inhibition of histone deacetylases led to disturbances of the chromatin landscape. This resulted in locus-specific histone-hyper- or hypoacetylation. We found that hypoacetylation at the <em>ARID1A</em> promotor caused repression of the SWI/SNF-complex member <em>ARID1A</em>. In consequence, this resulted in upregulation of the stress-sensors and apoptosis-regulators <em>GADD45B</em>, <em>DUSP1</em> and <em>CDKN1A</em>. RNAi-driven knock down of <em>ARID1A</em> mimicked in parts the effects of romidepsin, while CRISPR/Cas9-mediated deletion of <em>GADD45B</em> attenuated the romidepsin-provoked induction of apoptosis and cell cycle alterations.We propose a signaling cascade involving <em>ARID1A</em>, <em>GADD45B</em> and <em>DUSP1</em> as mediators of the romidepsin effects in GCC cells.<br>
DOI: 10.6084/m9.figshare.3798465
title: Storify collection of tweets from LIS journal publishing presentation

description: This is a Storify collection of tweets from concurrent session 6, LIS journal publishing for the digital age: A GLAMR dissemination and preservation model, at the ALIA National conference in Adelaide, Australia, 30 August 2016.Conference link: [https://nationalconference.alia.org.au/content/lis-journal-publishing-digital-age]<br>1. PDF [attached to this record] 2. XML [https://storify.com/jayechats/lis-journal-publishing-for-the-digital-age.xml]3. HTML [https://storify.com/jayechats/lis-journal-publishing-for-the-digital-age.html].4. JSON [https://api.storify.com/v1/stories/jayechats/lis-journal-publishing-for-the-digital-age]The live link to the storify: [https://storify.com/jayechats/lis-journal-publishing-for-the-digital-age]The archive link to the storify: [http://web.archive.org/web/*/https://storify.com/jayechats/lis-journal-publishing-for-the-digital-age]<br>
DOI: 10.6084/m9.figshare.3798465.v1
title: Storify collection of tweets from LIS journal publishing presentation

description: This is a Storify collection of tweets from concurrent session 6, LIS journal publishing for the digital age: A GLAMR dissemination and preservation model, at the ALIA National conference in Adelaide, Australia, 30 August 2016.Conference link: [https://nationalconference.alia.org.au/content/lis-journal-publishing-digital-age]<br>1. PDF [attached to this record] 2. XML [https://storify.com/jayechats/lis-journal-publishing-for-the-digital-age.xml]3. HTML [https://storify.com/jayechats/lis-journal-publishing-for-the-digital-age.html].4. JSON [https://api.storify.com/v1/stories/jayechats/lis-journal-publishing-for-the-digital-age]The live link to the storify: [https://storify.com/jayechats/lis-journal-publishing-for-the-digital-age]The archive link to the storify: [http://web.archive.org/web/*/https://storify.com/jayechats/lis-journal-publishing-for-the-digital-age]<br>