cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.25345/c5ch2v
title: MassIVE MSV000083954 - Proteomic analysis reveals that topoisomerase 2A is associated with defective sperm head morphology
title: Male infertility is widespread and estimated to affect 1 in 20 men. Whilst in some cases the aetiology of the condition is well understood, for at least 50% of men, the underlying cause is yet to be classified. The majority of infertile men produce enough spermatozoa, however it is a combination of poor sperm motility, associated with a modified cell morphology that contribute to infertility. One of the major limitations of using morphology to inform male fertility status is that the evaluation is highly subjective, due to the fact that it has to be done by microscopic examination. As such, biomarkers of male infertility are needed to help establish a more consistent diagnosis. In the present study, we compared nuclear extracts from both high- and low-quality spermatozoa by LC-MS/MS based proteomic analysis. Our data shows that nuclear retention of proteins is a common facet amongst low quality male reproductive cells. In particular, we demonstrate that the presence of Topoisomerase 2A in sperm heads, is highly correlated to poor head morphology. Topoisomerase A is therefore a potential new biomarker for confirming male infertility in clinical practice.
DOI: 10.25407/jacbts.8253752
title: Figure 3: Cross-Linking of GPVI-Fc With Anti–Human-Fc IgG or Anti–Human-Fc Fab2 Increases Its Inhibition of Platelet Aggregation Stimulated by Collagen or Plaque Under Flow

description: Buffer (control), GPVI-Fc, or GPVI-Fc (50 μg/ml; 333 nM) premixed with equimolar anti–human-Fc IgG or anti–human-Fc Fab2 antibodies for crosslinking was added to blood containing DiOC6 for platelet visualization and perfused over plaque homogenate at a shear rate of 600/s. <b>(A)</b> Representative micrographs display platelet coverage of plaque at 2, 5, and 9 min after start of blood flow. <b>(B)</b> Effect of buffer, GPVI-Fc, GPVI-Fc*IgG-XL, or GPVI-Fc*Fab2-XL on the kinetics of platelet deposition from flowing blood onto plaque and collagen. Measurements are each second. Mean <b>(solid line)</b> ± SD <b>(shaded area)</b>; n = 4 to 6. Comparison at 2, 5, and 9 min by using repeated measures analysis of variance or if inappropriate by repeated measures analysis of variance on ranks (only 2 min). Significance of secondary pair-wise comparisons by Tukey correction is indicated by bars. ∗p &lt; 0.05. <b>(C)</b> Kinetics of not cross-linked and cross-linked GPVI-Fc binding to collagen. (Videos 3 and 4 present additional details.) GPVI-Fc pre-incubated with PE-labeled anti–human-Fc Fab2 (20:1 mol/mol) (GPVI-Fc*Fab2) or with an equimolar mixture of PE-labeled and unlabeled anti–human-Fc Fab2 (1:10) for cross-linking (GPVI-Fc*Fab2-XL), was added to blood (333 nM GPVI-Fc final concentration) containing abciximab and perfused over collagen at a shear rate of 600/s. Binding of PE-labeled GPVI-Fc (cross-linked or not cross-linked) to collagen was quantified every second by fluorescence microscopy using a 10× objective. <b>Top:</b> Time course of GPVI-Fc*Fab2 and GPVI-Fc*Fab2-XL binding to collagen (area coverage). Mean <b>(solid line)</b> ± SD <b>(shaded area)</b>; n = 4. <b>Bottom:</b> Fluorescence intensity surface plots of GPVI-Fc*Fab2 and GPVI-Fc*Fab2-XL bound to collagen at 3 min after start of blood flow. Color gradients indicate increase of fluorescence intensity. Abbreviations as in Figures 1 and 2.
DOI: 10.25407/jacbts.8253752.v1
title: Figure 3: Cross-Linking of GPVI-Fc With Anti–Human-Fc IgG or Anti–Human-Fc Fab2 Increases Its Inhibition of Platelet Aggregation Stimulated by Collagen or Plaque Under Flow

description: Buffer (control), GPVI-Fc, or GPVI-Fc (50 μg/ml; 333 nM) premixed with equimolar anti–human-Fc IgG or anti–human-Fc Fab2 antibodies for crosslinking was added to blood containing DiOC6 for platelet visualization and perfused over plaque homogenate at a shear rate of 600/s. <b>(A)</b> Representative micrographs display platelet coverage of plaque at 2, 5, and 9 min after start of blood flow. <b>(B)</b> Effect of buffer, GPVI-Fc, GPVI-Fc*IgG-XL, or GPVI-Fc*Fab2-XL on the kinetics of platelet deposition from flowing blood onto plaque and collagen. Measurements are each second. Mean <b>(solid line)</b> ± SD <b>(shaded area)</b>; n = 4 to 6. Comparison at 2, 5, and 9 min by using repeated measures analysis of variance or if inappropriate by repeated measures analysis of variance on ranks (only 2 min). Significance of secondary pair-wise comparisons by Tukey correction is indicated by bars. ∗p &lt; 0.05. <b>(C)</b> Kinetics of not cross-linked and cross-linked GPVI-Fc binding to collagen. (Videos 3 and 4 present additional details.) GPVI-Fc pre-incubated with PE-labeled anti–human-Fc Fab2 (20:1 mol/mol) (GPVI-Fc*Fab2) or with an equimolar mixture of PE-labeled and unlabeled anti–human-Fc Fab2 (1:10) for cross-linking (GPVI-Fc*Fab2-XL), was added to blood (333 nM GPVI-Fc final concentration) containing abciximab and perfused over collagen at a shear rate of 600/s. Binding of PE-labeled GPVI-Fc (cross-linked or not cross-linked) to collagen was quantified every second by fluorescence microscopy using a 10× objective. <b>Top:</b> Time course of GPVI-Fc*Fab2 and GPVI-Fc*Fab2-XL binding to collagen (area coverage). Mean <b>(solid line)</b> ± SD <b>(shaded area)</b>; n = 4. <b>Bottom:</b> Fluorescence intensity surface plots of GPVI-Fc*Fab2 and GPVI-Fc*Fab2-XL bound to collagen at 3 min after start of blood flow. Color gradients indicate increase of fluorescence intensity. Abbreviations as in Figures 1 and 2.
DOI: 10.25407/jacbts.8254814
title: Figure 3: Ca

description: <b>(A)</b> Increases in intracellular calcium levels ([Ca<sup>2+</sup>]i) due to external Ca<sup>2+</sup> entry were demonstrated by augmentation of Fluo-4 signals in stretched AE cells <b>(right panels)</b> but not in control cells <b>(left panels)</b>. Fluorescence recordings were initiated after acute cyclic stretch holding at maximum distension while confocal imaging. <b>(B)</b> Quantitative time curves of Ca<sup>2+</sup> entry into AE cells in control cells (n = 37), and in cells stretched at 5% (n = 58) and 10% (n = 72) intensity. Bar graph shows mean increase in [Ca<sup>2+</sup>]i at different stretch intensities. <b>(C)</b> Representative time curves of Ca<sup>2+</sup> entry after 10% stretch in control (n = 45) and stretched AE cells pre-treated with inhibitors of mechanosensitive (GsMTx-4; n = 55), store-operated (2-aminoethoxydiphenyl borate [2-APB]; n = 60) and voltage-gated (nifedipine; n = 55) Ca<sup>2+</sup> channels. Bar graphs for mean data are shown. <b>(D)</b> Addition of TRPC-6-specific pore-blocking (TRPC-6 Ab) attenuated Ca<sup>2+</sup> influx in 10% stretched cells (control: n = 40; 10% stretch: n = 36; 10% stretch + TRPC-6 Ab: n = 38). For <b>(B to D)</b>, internal stores were pre-emptied with thapsigargin to rule out contributions from internal endoplasmic reticulum Ca<sup>2+</sup> release to F/F0. Data are shown as mean ± SEM. *p ❖p &lt; 0.001 versus 10% stretch. See Supplemental Video 1. Abbreviations as in Figures 1 and 2.
DOI: 10.25407/jacbts.8254814.v1
title: Figure 3: Ca

description: <b>(A)</b> Increases in intracellular calcium levels ([Ca<sup>2+</sup>]i) due to external Ca<sup>2+</sup> entry were demonstrated by augmentation of Fluo-4 signals in stretched AE cells <b>(right panels)</b> but not in control cells <b>(left panels)</b>. Fluorescence recordings were initiated after acute cyclic stretch holding at maximum distension while confocal imaging. <b>(B)</b> Quantitative time curves of Ca<sup>2+</sup> entry into AE cells in control cells (n = 37), and in cells stretched at 5% (n = 58) and 10% (n = 72) intensity. Bar graph shows mean increase in [Ca<sup>2+</sup>]i at different stretch intensities. <b>(C)</b> Representative time curves of Ca<sup>2+</sup> entry after 10% stretch in control (n = 45) and stretched AE cells pre-treated with inhibitors of mechanosensitive (GsMTx-4; n = 55), store-operated (2-aminoethoxydiphenyl borate [2-APB]; n = 60) and voltage-gated (nifedipine; n = 55) Ca<sup>2+</sup> channels. Bar graphs for mean data are shown. <b>(D)</b> Addition of TRPC-6-specific pore-blocking (TRPC-6 Ab) attenuated Ca<sup>2+</sup> influx in 10% stretched cells (control: n = 40; 10% stretch: n = 36; 10% stretch + TRPC-6 Ab: n = 38). For <b>(B to D)</b>, internal stores were pre-emptied with thapsigargin to rule out contributions from internal endoplasmic reticulum Ca<sup>2+</sup> release to F/F0. Data are shown as mean ± SEM. *p ❖p &lt; 0.001 versus 10% stretch. See Supplemental Video 1. Abbreviations as in Figures 1 and 2.
DOI: 10.25407/jacbts.8254820
title: Figure 4: Effects of Chronic (24 h) Cyclic Stretch on [Ca

description: <b>(A)</b> Control <b>(top panel)</b> and stretched <b>(bottom panel)</b> AE cells were stained with Fluo-4 following administration of hyperforin to activate TRPC-6. In control cells, strong and continuous Ca<sup>2+</sup> influx through the evenly distributed TRPC-6 channels at the cell surface is indicated <b>(white arrows, top panel inset)</b>. In chronically stretched cells, Ca<sup>2+</sup> influx at the cell membrane is restricted to small, localized areas that form a <b>green punctate pattern (white arrows, bottom panel inset)</b>. <b>(B)</b> Bar graph showing the effects of chronic stretch, hyperforin, and 1-oleoyl-2-acetyl-sn-glycerol (OAG), a mechanosensitive channel activator, on the [Ca<sup>2+</sup>]i (respective cell numbers = 26, 30, 32, 25, 33, 40, in the order shown in graph). Ca<sup>2+</sup> uptake by TRPC-6 and mechanosensitive Ca<sup>2+</sup> channels, in general, is lower in the 24-h stretched AE cells compared with the non-stretched (control) cells. <b>(C)</b> Representative TRPC-6 immunoblot of biotin-labeled/streptavidin-immunoprecipitated cell membrane fraction (M) and total cell lysate (T) from 0-, 1-, and 24-h stretched AE cells, showing depleted levels of TRPC-6 in the cell membrane fraction of the 24-h stretched cells. Bar graph shows quantification of TRPC-6 levels from 3 separate experiments. β-tubulin immunolabeling was used as loading control. See Supplemental Figure 7C for full Western blots. All values are mean ± SEM. *p &lt; 0.001 versus control cells. See Supplemental Videos 2, 3, and 4. Abbreviations as in Figures 1, 2, and 3.
DOI: 10.25407/jacbts.8254820.v1
title: Figure 4: Effects of Chronic (24 h) Cyclic Stretch on [Ca

description: <b>(A)</b> Control <b>(top panel)</b> and stretched <b>(bottom panel)</b> AE cells were stained with Fluo-4 following administration of hyperforin to activate TRPC-6. In control cells, strong and continuous Ca<sup>2+</sup> influx through the evenly distributed TRPC-6 channels at the cell surface is indicated <b>(white arrows, top panel inset)</b>. In chronically stretched cells, Ca<sup>2+</sup> influx at the cell membrane is restricted to small, localized areas that form a <b>green punctate pattern (white arrows, bottom panel inset)</b>. <b>(B)</b> Bar graph showing the effects of chronic stretch, hyperforin, and 1-oleoyl-2-acetyl-sn-glycerol (OAG), a mechanosensitive channel activator, on the [Ca<sup>2+</sup>]i (respective cell numbers = 26, 30, 32, 25, 33, 40, in the order shown in graph). Ca<sup>2+</sup> uptake by TRPC-6 and mechanosensitive Ca<sup>2+</sup> channels, in general, is lower in the 24-h stretched AE cells compared with the non-stretched (control) cells. <b>(C)</b> Representative TRPC-6 immunoblot of biotin-labeled/streptavidin-immunoprecipitated cell membrane fraction (M) and total cell lysate (T) from 0-, 1-, and 24-h stretched AE cells, showing depleted levels of TRPC-6 in the cell membrane fraction of the 24-h stretched cells. Bar graph shows quantification of TRPC-6 levels from 3 separate experiments. β-tubulin immunolabeling was used as loading control. See Supplemental Figure 7C for full Western blots. All values are mean ± SEM. *p &lt; 0.001 versus control cells. See Supplemental Videos 2, 3, and 4. Abbreviations as in Figures 1, 2, and 3.
DOI: 10.25407/jacbts.8254823
title: Figure 5: Ca

description: <b>(A)</b> Representative Ca<sup>2+</sup> transient traces from cardiomyocytes (CMs) bathed in Tyrode’s solution (control cells) or pre-conditioned with media collected from AE cells with or without stretch and addition of TRPC-6 pore-blocking Ab. <b>(B)</b> Bar graphs showing Ca<sup>2+</sup> transient amplitude and frequency in CMs pre-conditioned with media from AE cells with or without stretch and addition of TRPC-6 pore-blocking Ab. All values are mean ± SEM. *p &lt; 0.025 versus control cells; <sup>❖</sup>p &lt; 0.001 versus nonstretched cells (without Ab). See Supplemental Videos 5, 6, and 7. iPS = induced pluripotent stem; other abbreviations as in Figures 1 and 2.
DOI: 10.25407/jacbts.8254823.v1
title: Figure 5: Ca

description: <b>(A)</b> Representative Ca<sup>2+</sup> transient traces from cardiomyocytes (CMs) bathed in Tyrode’s solution (control cells) or pre-conditioned with media collected from AE cells with or without stretch and addition of TRPC-6 pore-blocking Ab. <b>(B)</b> Bar graphs showing Ca<sup>2+</sup> transient amplitude and frequency in CMs pre-conditioned with media from AE cells with or without stretch and addition of TRPC-6 pore-blocking Ab. All values are mean ± SEM. *p &lt; 0.025 versus control cells; <sup>❖</sup>p &lt; 0.001 versus nonstretched cells (without Ab). See Supplemental Videos 5, 6, and 7. iPS = induced pluripotent stem; other abbreviations as in Figures 1 and 2.
DOI: 10.25407/jacbts.8254847
title: Figure 1: Hydrogel Delivery Device Creates a Temporary Compartment for Biomaterial Gel Delivery Within the Pericardial Space

description: Schematic representation of lateral <b>(A)</b> and frontal view <b>(B)</b> of the device placed over the cardiac epicardium within the pericardial space. The device forms a lateral wall for the gel compartment, whereas the pericardium and epicardium act as a natural roof and floor, respectively <b>(A and B)</b>. Once in position, the device is secured in place by gentle suction ports <b>(C, white arrows)</b> to the epicardium as floor, and the pericardium as ceiling. Gel components are delivered through separate lumens and combined only after exiting the device <b>(B and C, asterisk)</b> through ports arrayed around fence <b>(C, black arrows)</b>. Electrical sensors <b>(C, arrowhead)</b> allow precise placement over areas of electrical abnormalities, such as infarcts. See Supplemental Video 1.
DOI: 10.25407/jacbts.8254847.v1
title: Figure 1: Hydrogel Delivery Device Creates a Temporary Compartment for Biomaterial Gel Delivery Within the Pericardial Space

description: Schematic representation of lateral <b>(A)</b> and frontal view <b>(B)</b> of the device placed over the cardiac epicardium within the pericardial space. The device forms a lateral wall for the gel compartment, whereas the pericardium and epicardium act as a natural roof and floor, respectively <b>(A and B)</b>. Once in position, the device is secured in place by gentle suction ports <b>(C, white arrows)</b> to the epicardium as floor, and the pericardium as ceiling. Gel components are delivered through separate lumens and combined only after exiting the device <b>(B and C, asterisk)</b> through ports arrayed around fence <b>(C, black arrows)</b>. Electrical sensors <b>(C, arrowhead)</b> allow precise placement over areas of electrical abnormalities, such as infarcts. See Supplemental Video 1.
DOI: 10.14457/cu.the.2013.1383
title: EFFECTS OF BACKGROUND COLOUR ON VISUAL FATIGUE FROM READING ON TABLET

description: This study aimed to investigate the effect of visual fatigue from reading on a tablet when the background luminance and colour were changed. Six levels of background luminance were tested. They were the level with the same luminance as paper (68 cd/m2), three levels with 15%, 30% and 70% increased, and two levels with 15% and 30% decreased from the paper luminance under the same lighting condition. Six background colours with the same luminance as paper were tested: white, red, green, blue, yellow and purple. Subjects read pseudo-text containing 10 lines per page. There were two types of pseudo-text: Thai and English; each had 3 pages. The time subjects spent finding the target letters that were randomly inserted in the pseudo-text was recorded. After the reading tasks, subjects rated the degrees of visual fatigue symptoms that possibly occurred during the tasks. They also answered the general questionnaire about the familiarity of using a tablet and colour preference. Fifty university students with 18 – 35 years of age took part in the experiments. The results showed that the main factor that affected visual fatigue was luminance. Reading media did not affect visual fatigue when the luminance was equal. The level of luminance that tended to cause visual fatigue was +70% from the paper luminance. Colour did not affect visual fatigue. Nevertheless, there was a tendency that red background was the most suitable for reading.
DOI: 10.25407/jacbts.8254889
title: Figure 2: Human Platelet Accrual on Plasma VWF

description: <b>(A)</b> Main chain schematic of the human von Willebrand factor (VWF)-A1 domain depicting residues that differ from its murine counterpart. <b>Colored spheres</b> denote the following: <b>black</b> are residues with buried side chains, <b>green</b> have partially buried side chains, <b>red</b> have exposed side chains on the front and upper surfaces, and <b>gold</b> have exposed side chains on the lower and back surfaces. <b>Circled in blue</b> is residue 1326, which plays a key role in permitting interactions with the GPIbα on human and mouse platelets (29). Accumulation of platelets on <b>(B)</b> surface-immobilized human plasma VWF or <b>(C)</b> murine plasma VWF<sup>HA1</sup> is shown. Citrated whole blood from neonatal patients or healthy adults was perfused over the reactive substrate for 3 min (wall shear rate of 1,600 s<sup>−1</sup>) before assessing the number of interacting platelets. <b>(D)</b> Percentage of translocating platelets that became firmly adherent in response to infusion of buffer containing adenosine diphosphate (20 μM). The human GPIbα function blocking monoclonal antibody (mAb) 6D1 (10 μg/ml) or the αIIbβ3 inhibitor abciximab (10 μg/ml) was added to blood 10 min before use. See Supplemental Video 1. Data represent the mean ± SEM (n = 10 individuals per age group). ***p &lt; 0.001 for antibody treatment versus no treatment according to Mann-Whitney <i>U</i> test. CHD = congenital heart disease.
DOI: 10.25407/jacbts.8254889.v1
title: Figure 2: Human Platelet Accrual on Plasma VWF

description: <b>(A)</b> Main chain schematic of the human von Willebrand factor (VWF)-A1 domain depicting residues that differ from its murine counterpart. <b>Colored spheres</b> denote the following: <b>black</b> are residues with buried side chains, <b>green</b> have partially buried side chains, <b>red</b> have exposed side chains on the front and upper surfaces, and <b>gold</b> have exposed side chains on the lower and back surfaces. <b>Circled in blue</b> is residue 1326, which plays a key role in permitting interactions with the GPIbα on human and mouse platelets (29). Accumulation of platelets on <b>(B)</b> surface-immobilized human plasma VWF or <b>(C)</b> murine plasma VWF<sup>HA1</sup> is shown. Citrated whole blood from neonatal patients or healthy adults was perfused over the reactive substrate for 3 min (wall shear rate of 1,600 s<sup>−1</sup>) before assessing the number of interacting platelets. <b>(D)</b> Percentage of translocating platelets that became firmly adherent in response to infusion of buffer containing adenosine diphosphate (20 μM). The human GPIbα function blocking monoclonal antibody (mAb) 6D1 (10 μg/ml) or the αIIbβ3 inhibitor abciximab (10 μg/ml) was added to blood 10 min before use. See Supplemental Video 1. Data represent the mean ± SEM (n = 10 individuals per age group). ***p &lt; 0.001 for antibody treatment versus no treatment according to Mann-Whitney <i>U</i> test. CHD = congenital heart disease.
DOI: 10.25407/jacbts.8254892
title: Figure 3: Cangrelor Reduces Human Platelet Thrombus Formation in Avatar Mice

description: <b>(A to D)</b> Time course of fluorescent platelets accumulating on laser-injured arterioles contained with the cremaster muscle of von Willebrand factor<sup>HA1</sup> mice. Cangrelor (30-μg/kg bolus; 4-μg/kg/min infusion) or abciximab (0.25-μg/kg bolus; 0.125-μg/kg/min infusion) were administered intravenously after establishing baseline thrombus formation in the absence of drug. n = 15 (age 0 to 28 days); n = 10 (age 1 to 10 years); n = 8 (age 11 to 18 years); n = 15 for adults. <b>(E)</b> Maximal thrombus size pre- and post-administration of cangrelor in the same animal. Each symbol represents the area of a thrombus in 1 arteriole of an avatar mouse. <b>(F)</b> Percent change in thrombus size in response to cangrelor treatment based on data shown in <b>E</b>. See Supplemental Video 2. Data represent mean ± SEM. ***p &lt; 0.001 for drug versus no treatment according to the Mann-Whitney <i>U</i> test.
DOI: 10.25407/jacbts.8254892.v1
title: Figure 3: Cangrelor Reduces Human Platelet Thrombus Formation in Avatar Mice

description: <b>(A to D)</b> Time course of fluorescent platelets accumulating on laser-injured arterioles contained with the cremaster muscle of von Willebrand factor<sup>HA1</sup> mice. Cangrelor (30-μg/kg bolus; 4-μg/kg/min infusion) or abciximab (0.25-μg/kg bolus; 0.125-μg/kg/min infusion) were administered intravenously after establishing baseline thrombus formation in the absence of drug. n = 15 (age 0 to 28 days); n = 10 (age 1 to 10 years); n = 8 (age 11 to 18 years); n = 15 for adults. <b>(E)</b> Maximal thrombus size pre- and post-administration of cangrelor in the same animal. Each symbol represents the area of a thrombus in 1 arteriole of an avatar mouse. <b>(F)</b> Percent change in thrombus size in response to cangrelor treatment based on data shown in <b>E</b>. See Supplemental Video 2. Data represent mean ± SEM. ***p &lt; 0.001 for drug versus no treatment according to the Mann-Whitney <i>U</i> test.
DOI: 10.4119/unibi/2934439
title: Online Appendix III: German transcripts and English translations

description: This is part of the Online Appendix of the book Talking Collective Action. It provides the original German transcripts of all the English translations of transcripts in the book. The excerpts are thus cross-referenced with the English excerpts in the book. The excerpts are from transcripts of meetings that are based on audio-recordings. They were recorded, anonymized, transcribed, and translated by the author. More information about the activists and activities mentioned in the excerpts can be found in Talking Collective Action, including transcript conven­tions.
DOI: 10.4119/unibi/2934449
title: Online Appendix II: Additional data and analyses
DOI: 10.17632/wk3z3gzrzy.2
title: Data for: Performance Analysis of a Hybrid Ground Source Heat Pump System Integrated with Liquid Dry Cooler

description: The uploaded file is a zipped file containing major raw data collected as a result of running simulation models.
DOI: 10.21227/692c-1562
title: Frequency Spectrum Waterfall Image

description: Frequency spectrum waterfall image dataset