cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.4038447
title: GameBus Pilot Studies (6): Internal Consistency Reliability - Chronbach's Alpha

description: Internal consistency reliability estimates (Cronbach’s coefficient alpha) for the eight SF-36v2 scales for pre- and post-test of both pilot locations.Most health dimension scales exceed the recommended 0.70, while others score excellent with close to or over 0.90.<br>** However, we do have to mention that two scales - BP and SF - exist of two items in SF36v2 that measure said constructs and do not provide a proper alpha value for the post-tests of Trial A and Trial B respectively . For these, a negative alpha is determined. Although theoretically, this should not be possible, we are sure that all (if needed) items are re-coded in SPSS & the 'QualityMetric Health Outcomes Scoring Software 4.5’ software package and no other issues exist, before actually calculating the alpha values. This has also been confirmed by the SF-36 Guide Book, section 2.3: p.11 (Zee & Sanderman, 2012). **<br>Zee, K. I. Van Der, & Sanderman, R. (2012). Het meten van de algemene gezondheidstoestand met de RAND-36. Een handleiding. Groningen.
DOI: 10.7910/dvn/v1rjpf/a29f26
title: blc20170920_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4038441
title: Data for Ryan and Gauthier 2016

description: data set for "Gender Differences in Recognition of Toy Faces Suggest a Contribution of Experience", Ryan & Gauthier, 2016, Vision Research <br>
DOI: 10.7910/dvn/v1rjpf/ehl4f7
title: blc20170728_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4038438
title: Nanomechanical properties of MscL <b>α</b> helices: A steered molecular dynamics study

description: Gating of mechanosensitive (MS) channels is driven by a hierarchical cascade of movements and deformations of transmembrane helices in response to bilayer tension. Determining the intrinsic mechanical properties of the individual transmembrane helices is therefore central to understanding the intricacies of the gating mechanism of MS channels. We used a constant-force steered molecular dynamics (SMD) approach to perform unidirectional pulling tests on all the helices of MscL in <i>M. tuberculosis</i> and <i>E. coli</i> homologs. Using this method, we could overcome the issues encountered with the commonly used constant-velocity SMD simulations, such as low mechanical stability of the helix during stretching and high dependency of the elastic properties on the pulling rate. We estimated Young's moduli of the α-helices of MscL to vary between 0.2 and 12.5 GPa with TM2 helix being the stiffest. We also studied the effect of water on the properties of the pore-lining TM1 helix. In the absence of water, this helix exhibited a much stiffer response. By monitoring the number of hydrogen bonds, it appears that water acts like a ‘lubricant’ (softener) during TM1 helix elongation. These data shed light on another physical aspect underlying hydrophobic gating of MS channels, in particular MscL.
DOI: 10.6084/m9.figshare.4038447.v3
title: GameBus Pilot Studies (6): Internal Consistency Reliability - Chronbach's Alpha

description: Internal consistency reliability estimates (Cronbach’s coefficient alpha) for the eight SF-36v2 scales for pre- and post-test of both pilot locations.Most health dimension scales exceed the recommended 0.70, while others score excellent with close to or over 0.90.<br>** However, we do have to mention that two scales - BP and SF - exist of two items in SF36v2 that measure said constructs and do not provide a proper alpha value for the post-tests of Trial A and Trial B respectively . For these, a negative alpha is determined. Although theoretically, this should not be possible, we are sure that all (if needed) items are re-coded in SPSS & the 'QualityMetric Health Outcomes Scoring Software 4.5’ software package and no other issues exist, before actually calculating the alpha values. This has also been confirmed by the SF-36 Guide Book, section 2.3: p.11 (Zee & Sanderman, 2012). **<br>Zee, K. I. Van Der, & Sanderman, R. (2012). Het meten van de algemene gezondheidstoestand met de RAND-36. Een handleiding. Groningen.
DOI: 10.7910/dvn/v1rjpf/atsljv
title: blc20170401_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4038438.v2
title: Nanomechanical properties of MscL <b>α</b> helices: A steered molecular dynamics study

description: Gating of mechanosensitive (MS) channels is driven by a hierarchical cascade of movements and deformations of transmembrane helices in response to bilayer tension. Determining the intrinsic mechanical properties of the individual transmembrane helices is therefore central to understanding the intricacies of the gating mechanism of MS channels. We used a constant-force steered molecular dynamics (SMD) approach to perform unidirectional pulling tests on all the helices of MscL in <i>M. tuberculosis</i> and <i>E. coli</i> homologs. Using this method, we could overcome the issues encountered with the commonly used constant-velocity SMD simulations, such as low mechanical stability of the helix during stretching and high dependency of the elastic properties on the pulling rate. We estimated Young's moduli of the α-helices of MscL to vary between 0.2 and 12.5 GPa with TM2 helix being the stiffest. We also studied the effect of water on the properties of the pore-lining TM1 helix. In the absence of water, this helix exhibited a much stiffer response. By monitoring the number of hydrogen bonds, it appears that water acts like a ‘lubricant’ (softener) during TM1 helix elongation. These data shed light on another physical aspect underlying hydrophobic gating of MS channels, in particular MscL.
DOI: 10.6084/m9.figshare.4038438.v1
title: Nanomechanical properties of MscL alpha helices: A steered molecular dynamics study

description: Gating of mechanosentive (MS) channels is driven by a hierarchical cascade of movements and deformations of transmembrane helices in response to bilayer tension. Determining the intrinsic mechanical properties of the individual transmembrane helices is therefore central to understanding the intricacies of the gating mechanism of MS channels. We used a constant-force steered molecular dynamics (SMD) approach to perform unidirectional pulling tests on all the helices of MscL in <i>M. tuberculosis</i> and <i>E. coli</i> homologs. Using this method, we could overcome the issues encountered with the commonly used constant-velocity SMD simulations, such as low mechanical stability of the helix during stretching and high dependency of the elastic properties on the pulling rate. We estimated Young's moduli of the α-helices of MscL to vary between 0.2 and 12.5 GPa with TM2 helix being the stiffest. We also studied the effect of water on the properties of the pore-lining TM1 helix. In the absence of water, this helix exhibited a much stiffer response. By monitoring the number of hydrogen bonds, it appears that water acts like a ‘lubricant’ (softener) during TM1 helix elongation. These data shed light on another physical aspect underlying hydrophobic gating of MS channels, in particular MscL.
DOI: 10.6084/m9.figshare.4038447.v2
title: GameBus Pilot Studies (5): Internal Consistency Reliability - Chronbach's Alpha

description: Internal consistency reliability estimates (Cronbach’s coefficient alpha) for the eight SF-36v2 scales for pre- and post-test of both pilot locations.Most health dimension scales exceed the recommended 0.70, while others score excellent with close to or over 0.90.<br>** However, we do have to mention that two scales - BP and SF - exist of two items in SF36v2 that measure said constructs and do not provide a proper alpha value for the post-tests of Trial A and Trial B respectively . For these, a negative alpha is determined. Although theoretically, this should not be possible, we are sure that all (if needed) items are re-coded in SPSS & the 'QualityMetric Health Outcomes Scoring Software 4.5’ software package and no other issues exist, before actually calculating the alpha values. This has also been confirmed by the SF-36 Guide Book, section 2.3: p.11 (Zee & Sanderman, 2012). **<br>Zee, K. I. Van Der, & Sanderman, R. (2012). Het meten van de algemene gezondheidstoestand met de RAND-36. Een handleiding. Groningen.
DOI: 10.7910/dvn/v1rjpf/i00d9z
title: blc20170824_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4038432
title: Mouse V1 grating plaid correlations

description: Figure 5c from Muir et al. Accepted at Plos Comp Biol.
DOI: 10.7910/dvn/v1rjpf/khssdw
title: blc20170329_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4038432.v1
title: Mouse V1 grating plaid correlations

description: Figure 5c from Muir et al. Accepted at Plos Comp Biol.
DOI: 10.7910/dvn/v1rjpf/ntg5wl
title: blc20171007_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4038423
title: Dysfunctional mitochondrial fission impairs cell reprogramming

description: We have recently shown that mitochondrial fission is induced early in reprogramming in a Drp1-dependent manner; however, the identity of the factors controlling Drp1 recruitment to mitochondria was unexplored. To investigate this, we used a panel of RNAi targeting factors involved in the regulation of mitochondrial dynamics and we observed that MiD51, Gdap1 and, to a lesser extent, Mff were found to play key roles in this process. Cells derived from Gdap1-null mice were used to further explore the role of this factor in cell reprogramming. Microarray data revealed a prominent down-regulation of cell cycle pathways in Gdap1-null cells early in reprogramming and cell cycle profiling uncovered a G2/M growth arrest in Gdap1-null cells undergoing reprogramming. High-Content analysis showed that this growth arrest was DNA damage-independent. We propose that lack of efficient mitochondrial fission impairs cell reprogramming by interfering with cell cycle progression in a DNA damage-independent manner.
DOI: 10.7910/dvn/v1rjpf/lu5l4h
title: blc20170806_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4038423.v1
title: Dysfunctional mitochondrial fission impairs cell reprogramming

description: We have recently shown that mitochondrial fission is induced early in reprogramming in a Drp1-dependent manner; however, the identity of the factors controlling Drp1 recruitment to mitochondria was unexplored. To investigate this, we used a panel of RNAi targeting factors involved in the regulation of mitochondrial dynamics and we observed that MiD51, Gdap1 and, to a lesser extent, Mff were found to play key roles in this process. Cells derived from Gdap1-null mice were used to further explore the role of this factor in cell reprogramming. Microarray data revealed a prominent down-regulation of cell cycle pathways in Gdap1-null cells early in reprogramming and cell cycle profiling uncovered a G2/M growth arrest in Gdap1-null cells undergoing reprogramming. High-Content analysis showed that this growth arrest was DNA damage-independent. We propose that lack of efficient mitochondrial fission impairs cell reprogramming by interfering with cell cycle progression in a DNA damage-independent manner.
DOI: 10.6084/m9.figshare.4038429.v2
title: Histone chaperone ASF1B promotes human <b>β</b>-cell proliferation via recruitment of histone H3.3

description: Anti-silencing function 1 (ASF1) is a histone H3-H4 chaperone involved in DNA replication and repair, and transcriptional regulation. Here, we identify ASF1B, the mammalian paralog to ASF1, as a proliferation-inducing histone chaperone in human β-cells. Overexpression of ASF1B led to distinct transcriptional signatures consistent with increased cellular proliferation and reduced cellular death. Using multiple methods of monitoring proliferation and mitotic progression, we show that overexpression of ASF1B is sufficient to induce human β-cell proliferation. Co-expression of histone H3.3 further augmented β-cell proliferation, whereas suppression of endogenous H3.3 attenuated the stimulatory effect of ASF1B. Using the histone binding-deficient mutant of ASF1B (V94R), we show that histone binding to ASF1B is required for the induction of β-cell proliferation. In contrast to H3.3, overexpression of histone H3 variants H3.1 and H3.2 did not have an impact on ASF1B-mediated induction of proliferation. Our findings reveal a novel role of ASF1B in human β-cell replication and show that ASF1B and histone H3.3A synergistically stimulate human β-cell proliferation.
DOI: 10.6084/m9.figshare.4038414
title: Expression and prognostic significance of the autoimmune regulator gene in breast cancer cells

description: The autoimmune regulator gene (AIRE) plays a fundamental role in tolerance by promoting the expression of tissue-specific antigens in medullary thymic epithelial cells (mTECs). Recently, AIRE expression was detected also in human keratinocytes and in tumors originating in stratified epithelia. Here, we tested whether AIRE is expressed in cancer cells. We analyzed AIRE expression in cancer cases from The Cancer Genome Atlas (TCGA) RNA-seq dataset and we found association with better outcome. AIRE protein expression was verified by immunohistochemistry in a cohort of 39 human breast cancer specimens and its prognostic relevance was confirmed in microarray-based gene expression data set NKI-295 and KM-Plotter. Both in the RNA-seq and gene expression datasets analyzed, AIRE expression was an independent strong prognostic factor for relapse-free survival (RFS), particularly in estrogen receptor-positive tumors. Enrichment of translation-related pathways was observed in AIRE-expressing tumors by Ingenuity Pathway Analysis and a significant increase of cells in G1 phase and activation of caspase cascades was induced by AIRE transfection in breast cancer luminal cell lines, suggesting that AIRE-induced over-translation of proteins lead to cycle arrest and apoptosis. These data are the first to identify AIRE expression in breast cancer and an association with prognosis.
DOI: 10.6084/m9.figshare.4038429.v1
title: Histone Chaperone ASF1B Promotes Human β-cell proliferation via Recruitment of Histone H3.3

description: Anti-silencing function 1 (ASF1) is a histone H3-H4 chaperone involved in DNA replication and repair, and transcriptional regulation. Here, we identify ASF1B, the mammalian paralog to ASF1, as a proliferation-inducing histone chaperone in human β-cells. Overexpression of ASF1B led to distinct transcriptional signatures consistent with increased cellular proliferation and reduced cellular death. Using multiple methods of monitoring proliferation and mitotic progression, we show that overexpression of ASF1B is sufficient to induce human β-cell proliferation. Co-expression of histone H3.3 further augmented β-cell proliferation, whereas suppression of endogenous H3.3 attenuated the stimulatory effect of ASF1B. Using the histone binding-deficient mutant of ASF1B (V94R), we show that histone binding to ASF1B is required for the induction of β-cell proliferation. In contrast to H3.3, overexpression of histone H3 variants H3.1 and H3.2 did not have an impact on ASF1B-mediated induction of proliferation. Our findings reveal a novel role of ASF1B in human β-cell replication and show that ASF1B and histone H3.3A synergistically stimulate human β-cell proliferation.
DOI: 10.7910/dvn/v1rjpf/gu3tbq
title: blc20171105_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4038405
title: GameBus Pilot Studies (5): Individual Normative values of the SF-36v2 dimension scores

description: Individual normative values of the SF-36v2 survey are presented for the pre- and post-measurement of both GameBus trial locations.Several individual participants showed overall statistically significant improvement in the physical and/or mental health (MSC) scale score.
DOI: 10.7910/dvn/v1rjpf/ij1sur
title: blc20170102_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4038405.v1
title: GameBus Pilot Studies: Individual Normative values of the SF-36v2 dimension scores

description: Individual normative values of the SF-36v2 survey are presented for the pre- and post-measurement of both GameBus trial locations.Several individual participants showed overall statistically significant improvement in the physical and/or mental health (MSC) scale score.
DOI: 10.6084/m9.figshare.4038414.v1
title: Expression And Prognostic Significance Of The Autoimmune Regulator Gene In Breast Cancer Cells

description: The autoimmune regulator gene (AIRE) plays a fundamental role in tolerance by promoting the expression of tissue-specific antigens in medullary thymic epithelial cells (mTECs). Recently, AIRE expression was detected also in human keratinocytes and in tumors originating in stratified epithelia. Here, we tested whether AIRE is expressed in cancer cells. We analyzed AIRE expression in cancer cases from The Cancer Genome Atlas (TCGA) RNA-seq dataset and we found association with better outcome. AIRE protein expression was verified by immunohistochemistry in a cohort of 39 human breast cancer specimens and its prognostic relevance was confirmed in microarray-based gene expression dataset NKI-295 and KM-Plotter. Both in the RNA-seq and gene expression datasets analyzed, AIRE expression was an independent strong prognostic factor for relapse-free survival (RFS), particularly in estrogen receptor-positive tumors. Enrichment of translation-related pathways was observed in AIRE-expressing tumors by Ingenuity Pathway Analysis and a significant increase of cells in G1 phase and activation of caspase cascades was induced by AIRE transfection in breast cancer luminal cell lines, suggesting that AIRE-induced over-translation of proteins lead to cycle arrest and apoptosis. These data are the first to identify AIRE expression in breast cancer and an association with prognosis.
DOI: 10.7910/dvn/v1rjpf/g6d09q
title: blc20170826_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4038405.v3
title: GameBus Pilot Studies (5): Individual Normative values of the SF-36v2 dimension scores

description: Individual normative values of the SF-36v2 survey are presented for the pre- and post-measurement of both GameBus trial locations.Several individual participants showed overall statistically significant improvement in the physical and/or mental health (MSC) scale score.
DOI: 10.7910/dvn/v1rjpf/rpqhuj
title: blc20171029_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4038405.v2
title: GameBus Pilot Studies (4): Individual Normative values of the SF-36v2 dimension scores

description: Individual normative values of the SF-36v2 survey are presented for the pre- and post-measurement of both GameBus trial locations.Several individual participants showed overall statistically significant improvement in the physical and/or mental health (MSC) scale score.
DOI: 10.7910/dvn/v1rjpf/e1woli
title: blc20170616_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4038366
title: Golgi proteins in circulating human platelets are distributed across non-stacked, scattered structures

description: Platelets are small, anucleate cell fragments that are central to hemostasis, thrombosis, and inflammation. They are derived from megakaryocytes from which they inherit their organelles. As platelets can synthesize proteins and contain many of the enzymes of the secretory pathway, one might expect all mature human platelets to contain a stacked Golgi apparatus, the central organelle of the secretory pathway. By thin section electron microscopy, stacked membranes resembling the stacked Golgi compartment in megakaryocytes and other nucleated cells can be detected in both proplatelets and platelets. However, the incidence of such structures is low and whether each and every platelet contains such a structure remains an open question. By single-label, immunofluorescence staining, Golgi glycosyltransferases are found within each platelet and map to scattered structures. Whether these structures are positive for marker proteins from multiple Golgi subcompartments remains unknown. Here, we have applied state-of-the-art techniques to probe the organization state of the Golgi apparatus in resting human platelets. By the whole cell volume technique of serial-block-face scanning electron microscopy (SBF-SEM), we failed to observe stacked, Golgi-like structures in any of the 65 platelets scored. When antibodies directed against Golgi proteins were tested against HeLa cells, labeling was restricted to an elongated juxtanuclear ribbon characteristic of a stacked Golgi apparatus. By multi-label immunofluorescence microscopy, we found that each and every resting human platelet was positive for cis, trans, and trans Golgi network (TGN) proteins. However, in each case, the proteins were found in small puncta scattered about the platelet. At the resolution of deconvolved, widefield fluorescence microscopy, these proteins had limited tendency to map adjacent to one another. When the results of 3D structured illumination microscopy (3D SIM), a super resolution technique, were scored quantitatively, the Golgi marker proteins failed to map together indicating at the protein level considerable degeneration of the platelet Golgi apparatus relative to the layered stack as seen in the megakaryocyte. In conclusion, we suggest that these results have important implications for organelle structure/function relationships in the mature platelet and the extent to which Golgi apparatus organization is maintained in platelets. Our results suggest that Golgi proteins in circulating platelets are present within a series of scattered, separated structures. As separate elements, selective sets of Golgi enzymes or sugar nucleotides could be secreted during platelet activation. The establishment of the functional importance, if any, of these scattered structures in sequential protein modification in circulating platelets will require further research.
DOI: 10.7910/dvn/v1rjpf/xof0ru
title: blc20170223_03.txt.gz

description: :unav