cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.35092/yhjc.12536015.v1
title: Data tables and analysis scripts supporting "Kinetics of fast tetramerization of the huntington exon 1 protein probed by concentration-dependent on-resonance R1rho measurements" A. Ceccon, V. Tugarinov and G.M. Clore, J. Phys. Chem. Lett.

description: Experimental data (15N/13Calpha exchange induced shifts and R1rho data at 3 RF field strengths) and MATLAB analysis scripts for the paper entitled "Kinetics of fast tetramerization of the huntington exon 1 protein probed by concentration-dependent on-resonance R1rho measurements" by A. Ceccon, V. Tugarinov and G.M. Clore. J. Phys. Chem. Lett. jz-2020-016369 http://dx.doi.org/10.1021/acs.jpclett.0c01636<br><br>Abstract: An approach for the quantitative description of the kinetics of very fast exchange processes (t<sub>ex</sub> &lt; 50-100 microseconds) associated with transient, reversible protein oligomerization, is presented. We show that on-resonance <sup>15</sup>N-<i>R1rho</i> measurements conducted as a function of protein concentration at several spin-lock radio-frequency field strengths are indispensable for unambiguous determination of the rate constants for interconversion between monomeric and higher order oligomeric species. The approach is experimentally demonstrated on the study of fast, reversible tetramerization of full-length huntingtin exon 1 protein, htt<sup>ex1</sup>, responsible for Huntington’s disease. Incorporation of concentration-dependent <sup>15</sup>N-<i>R</i><sub>2,eff</sub> data, obtained from on-resonance <i>R1rho</i> measurements performed at three spin-lock field strengths, into analysis of the kinetic scheme describing reversible tetramerization of htt<sup>ex1</sup>, allowed us to uniquely determine the rate constants of interconversion between the various species. This approach serves as a valuable complement to the existing array of NMR techniques for studying early, transient oligomerization events in protein aggregation pathways.
DOI: 10.35092/yhjc.12552218
title: Supplemental Table 1 for "Leucine supplementation augments skeletal muscle mitochondrial respiration during recovery following 7 days of physical inactivity in older adults"

description: Mitochondrial respiration measures determined using OroBors high resolution respirometry Protocol 1. Since all OroBoros measurements originate from the same muscle biopsy sample, these are presented as technical replicates (with the exception of State 4<sub>o</sub>). All outcomes have units of (pmol O<sub>2</sub>/sec/mg tissue).<br><br>Supplemental Table supporting: <br>"Leucine supplementation augments skeletal muscle mitochondrial respiration during recovery following 7 days of physical inactivity in older adults"<br><br>Emily J. Arentson-Lantz, Jasmine Mikovic, Nisha Bhattarai, Christopher S. Fry, Severine Lamone, and Doug Paddon-Jones<br><br>In older adults, leucine supplementation attenuates the loss of skeletal muscle mass and function during bed rest. We sought to determine if leucine could also preserve and/or restore mitochondrial function and muscle oxidative capacity during periods of disuse and rehabilitation. Healthy older adults (69.1 ±1.1 years) consumed a structured diet with supplemental leucine (LEU: 0.06 g/ kg body weight/ meal; n=8) or alanine (CON: 0.06 g/ kg body weight/meal; n=8) during 7 days of bed rest and 5 days of inpatient rehabilitation. A 75 g oral glucose tolerance test was performed at baseline (PreBR), after bed rest (PostBR) and rehabilitation (PostRehab) and used to calculate an indicator of insulin sensitivity, metabolic clearance rate. (MCR). Tissue samples from the <i>m. vastus lateralis</i> were collected PreBR, PostBR, and PostRehab to assess mitochondrial respiratory capacity and protein markers of the oxidative phosphorylation and a marker of the antioxidant defense systems. During bed rest, leucine tended to preserve insulin sensitivity (Change in MCR, CON vs. LEU: -3.5 ± 0.82 vs LEU: -0.98 ± 0.88, p=0.054), but had no effect on mitochondrial respiratory capacity (Change in State 3<sub>+succinate</sub> CON vs. LEU -3.3 ± 6.1 vs. 7.3 ± 4.1 pmol O<sub>2</sub>/sec/mg tissue, p=0.19) Following rehabilitation, leucine increased ATP-linked respiration (CON vs. LEU: -8.9 ± 6.2 vs. 18.8 ± 3.7 pmol O<sub>2</sub>/sec/mg tissue, p=0.014). While the expression of mitochondrial respiratory and antioxidant proteins was not impacted, leucine supplementation preserved specific pathways of mitochondrial respiration, insulin sensitivity and a marker of oxidative stress during bed rest and rehabilitation.
DOI: 10.35092/yhjc.12556268
title: Supplemental Table supporting: "Beyond premature ovarian insufficiency: Staging reproductive aging in adolescent and young adult cancer survivors"

description: Table: Window Study participants by eligibility for the current analysis on staging reproductive aging<br>Table supports manuscript titled: Beyond premature ovarian insufficiency: Staging reproductive aging in adolescent and young adult cancer survivors"<br>AbstractContext: While stages of reproductive aging for women in the general population are well described by STRAW+10 criteria, this is largely unknown for female survivors of adolescent and young adult cancers (AYA survivors). Objective: To evaluate application of STRAW+10 criteria in AYA survivors using bleeding patterns with and without endocrine biomarkers, and assess how cancer treatment gonadotoxicity is related to reproductive aging stage. Design: The analytic sample (n=338) included AYA survivors from the Window Study cohort. Menstrual bleeding data and dried blood spots for AMH and FSH measurements (Ansh DBS ELISAs) were utilized for reproductive aging stage assessment. Cancer treatment data were abstracted from medical records.Results: Among participants, mean age 34.0±4.5 and at a mean of 6.9±4.6 years since cancer treatment, the most common cancers were lymphomas (31%), breast (23%), and thyroid (17%). Twenty-nine percent was unclassifiable by STRAW+10 criteria. Most unclassifiable survivors exhibited bleeding patterns consistent with the menopausal transition, but had reproductive stage AMH and/or FSH levels. For classifiable survivors (48% peak reproductive, 30% late reproductive, 12% early transition, 3% late transition, 7% post-menopause), endocrine biomarkers distinguished among peak, early and late stages. Gonadotoxic treatments were associated with more advanced stages in a dose-dependent manner. Conclusions: We demonstrate a novel association between gonadotoxic treatments and advanced stages. Without endocrine biomarkers, bleeding pattern alone can “upstage” AYA survivors. Moreover, a large proportion of AYA survivors exhibited combinations of endocrine biomarkers and bleeding patterns that do not fit STRAW+10 criteria, suggesting the need for modified staging for this population. <br>
DOI: 10.35092/yhjc.12556268.v1
title: Supplemental Table supporting: "Beyond premature ovarian insufficiency: Staging reproductive aging in adolescent and young adult cancer survivors"

description: Table: Window Study participants by eligibility for the current analysis on staging reproductive aging<br>Table supports manuscript titled: Beyond premature ovarian insufficiency: Staging reproductive aging in adolescent and young adult cancer survivors"<br>AbstractContext: While stages of reproductive aging for women in the general population are well described by STRAW+10 criteria, this is largely unknown for female survivors of adolescent and young adult cancers (AYA survivors). Objective: To evaluate application of STRAW+10 criteria in AYA survivors using bleeding patterns with and without endocrine biomarkers, and assess how cancer treatment gonadotoxicity is related to reproductive aging stage. Design: The analytic sample (n=338) included AYA survivors from the Window Study cohort. Menstrual bleeding data and dried blood spots for AMH and FSH measurements (Ansh DBS ELISAs) were utilized for reproductive aging stage assessment. Cancer treatment data were abstracted from medical records.Results: Among participants, mean age 34.0±4.5 and at a mean of 6.9±4.6 years since cancer treatment, the most common cancers were lymphomas (31%), breast (23%), and thyroid (17%). Twenty-nine percent was unclassifiable by STRAW+10 criteria. Most unclassifiable survivors exhibited bleeding patterns consistent with the menopausal transition, but had reproductive stage AMH and/or FSH levels. For classifiable survivors (48% peak reproductive, 30% late reproductive, 12% early transition, 3% late transition, 7% post-menopause), endocrine biomarkers distinguished among peak, early and late stages. Gonadotoxic treatments were associated with more advanced stages in a dose-dependent manner. Conclusions: We demonstrate a novel association between gonadotoxic treatments and advanced stages. Without endocrine biomarkers, bleeding pattern alone can “upstage” AYA survivors. Moreover, a large proportion of AYA survivors exhibited combinations of endocrine biomarkers and bleeding patterns that do not fit STRAW+10 criteria, suggesting the need for modified staging for this population. <br>
DOI: 10.35092/yhjc.12568577
title: Data and code for "Spatial attention enhances network, cellular and subthreshold responses in mouse visual cortex," Speed et al., Nature Communications 2020.

description: This data archive contains all code and data necessary to replicate each main text figure and associated statistical comparisons in the following article: <br>Speed, A., Del Rosario, J., Mikail, N., & Haider, B. (2020). Spatial attention enhances network, cellular and subthreshold responses in mouse visual cortex. Nature communications, 11(1), 505. https://doi.org/10.1038/s41467-020-14355-4<br>The data and code is compatible with Matlab 2016b or later. <br>The data archive is organized as self-contained subfolders corresponding to the results found in each main figure (e.g., folder 'F1' for results of Figure 1). Each subfolder contains the minimally processed data structures and commented code for replication of the published figures. <br><br>Abstract of associated publication: Internal brain states strongly modulate sensory processing during behaviour. Studies of visual processing in primates show that attention to space selectively improves behavioural and neural responses to stimuli at the attended locations. Here we develop a visual spatial task for mice that elicits behavioural improvements consistent with the effects of spatial attention, and simultaneously measure network, cellular, and subthreshold activity in primary visual cortex. During trial-by-trial behavioural improvements, local field potential (LFP) responses to stimuli detected inside the receptive field (RF) strengthen. Moreover, detection inside the RF selectively enhances excitatory and inhibitory neuron responses to task-irrelevant stimuli and suppresses noise correlations and low frequency LFP fluctuations. Whole-cell patch-clamp recordings reveal that detection inside the RF increases synaptic activity that depolarizes membrane potential responses at the behaviorally relevant location. Our study establishes that mice display fundamental signatures of visual spatial attention spanning behavioral, network, cellular, and synaptic levels, providing new insight into rapid cognitive enhancement of sensory signals in visual cortex.
DOI: 10.35092/yhjc.12568577.v1
title: Data and code for "Spatial attention enhances network, cellular and subthreshold responses in mouse visual cortex," Speed et al., Nature Communications 2020.

description: This data archive contains all code and data necessary to replicate each main text figure and associated statistical comparisons in the following article: <br>Speed, A., Del Rosario, J., Mikail, N., & Haider, B. (2020). Spatial attention enhances network, cellular and subthreshold responses in mouse visual cortex. Nature communications, 11(1), 505. https://doi.org/10.1038/s41467-020-14355-4<br>The data and code is compatible with Matlab 2016b or later. <br>The data archive is organized as self-contained subfolders corresponding to the results found in each main figure (e.g., folder 'F1' for results of Figure 1). Each subfolder contains the minimally processed data structures and commented code for replication of the published figures. <br><br>Abstract of associated publication: Internal brain states strongly modulate sensory processing during behaviour. Studies of visual processing in primates show that attention to space selectively improves behavioural and neural responses to stimuli at the attended locations. Here we develop a visual spatial task for mice that elicits behavioural improvements consistent with the effects of spatial attention, and simultaneously measure network, cellular, and subthreshold activity in primary visual cortex. During trial-by-trial behavioural improvements, local field potential (LFP) responses to stimuli detected inside the receptive field (RF) strengthen. Moreover, detection inside the RF selectively enhances excitatory and inhibitory neuron responses to task-irrelevant stimuli and suppresses noise correlations and low frequency LFP fluctuations. Whole-cell patch-clamp recordings reveal that detection inside the RF increases synaptic activity that depolarizes membrane potential responses at the behaviorally relevant location. Our study establishes that mice display fundamental signatures of visual spatial attention spanning behavioral, network, cellular, and synaptic levels, providing new insight into rapid cognitive enhancement of sensory signals in visual cortex.
DOI: 10.35092/yhjc.12576890
title: Coupling of store-operated calcium entry to vasoconstriction is acid-sensing ion channel 1a dependent in pulmonary but not mesenteric arteries

description: The data presented in this entry are associated with manuscript entitled "<b>Coupling of store-operated calcium entry to vasoconstriction is acid-sensing ion channel 1a dependent in pulmonary but not mesenteric arteries</b>" and include:1) <b>Vessel Data:</b> vasoreactivity and simutaneous calcium responses in isolated pulmonary and mesenteric arteries in response to endothelin-1 and store-operated calcium entry2) <b>PLA Data</b>: Duolink proximity ligation assay data for ASIC1-STIM1 and Orai1-STIM1 in pulmonary and mesenteric vascular smooth muscle cells3) <b>S1_Raw_Image</b>: Images of raw gels (PCR) or western blots used in manuscript.
DOI: 10.35092/yhjc.12576890.v1
title: Coupling of store-operated calcium entry to vasoconstriction is acid-sensing ion channel 1a dependent in pulmonary but not mesenteric arteries

description: The data presented in this entry are associated with manuscript entitled "<b>Coupling of store-operated calcium entry to vasoconstriction is acid-sensing ion channel 1a dependent in pulmonary but not mesenteric arteries</b>" and include:1) <b>Vessel Data:</b> vasoreactivity and simutaneous calcium responses in isolated pulmonary and mesenteric arteries in response to endothelin-1 and store-operated calcium entry2) <b>PLA Data</b>: Duolink proximity ligation assay data for ASIC1-STIM1 and Orai1-STIM1 in pulmonary and mesenteric vascular smooth muscle cells3) <b>S1_Raw_Image</b>: Images of raw gels (PCR) or western blots used in manuscript.
DOI: 10.35092/yhjc.12584993
title: Survival curves of wild-type and perforin-2 (mpeg1) deficient mice challenged with Yersinia pseudotuberculosis or an isogenic cif::aadA mutant

description: <b>Figure 8</b>. Survival of C57Bl/6 mice inoculated orogastrically with 10^8 CFU of <i>Yersinia pseudotuberculosis</i> or an isogenic <i>cif::aadA</i> mutant. <br><b>Figure 9</b>. Survival curves for two different lineages of perforin-2 (Mpeg1) +/+, +/−, and −/− mice after orogastric inoculation with 10^6 CFU of <i>Yersinia pseudotuberculosis</i> or an isogenic <i>cif::aadA</i> mutant.<br>The accompanying <b>Dataset/Table</b> contains the data for Figures 8 and 9. This data was originally published in "<i>Enteric Pathogens Deploy Cell Cycle Inhibiting Factors to Block the Bactericidal Activity of Perforin-2</i>," McCormack, Lyapichev,Olsson, Podack, and Munson. Elife. 2015 Sep 29;4:e06505. doi: 10.7554/eLife.06505.PMID: 26418746 PMCID: PMC4626573 DOI: 10.7554/eLife.06505. Published under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original authors and source are credited. <br>Please see the citation for methods and experimental details.<br><br>Abstract of associated publication: Perforin-2 (MPEG1) is an effector of the innate immune system that limits the proliferation and spread of medically relevant Gram-negative, -positive, and acid fast bacteria. We show here that a cullin-RING E3 ubiquitin ligase (CRL) complex containing cullin-1 and βTrCP monoubiquitylates Perforin-2 in response to pathogen associated molecular patterns such as LPS. Ubiquitylation triggers a rapid redistribution of Perforin-2 and is essential for its bactericidal activity. Enteric pathogens such as Yersinia pseudotuberculosis and enteropathogenic Escherichia coli disarm host cells by injecting cell cycle inhibiting factors (Cifs) into mammalian cells to deamidate the ubiquitin-like protein NEDD8. Because CRL activity is dependent upon NEDD8, Cif blocks ubiquitin dependent trafficking of Perforin-2 and thus, its bactericidal activity. Collectively, these studies further underscore the biological significance of Perforin-2 and elucidate critical molecular events that culminate in Perforin-2-dependent killing of both intracellular and extracellular, cell-adherent bacteria.
DOI: 10.35092/yhjc.12584993.v1
title: Survival curves of wild-type and perforin-2 (mpeg1) deficient mice challenged with Yersinia pseudotuberculosis or an isogenic cif::aadA mutant

description: <b>Figure 8</b>. Survival of C57Bl/6 mice inoculated orogastrically with 10^8 CFU of <i>Yersinia pseudotuberculosis</i> or an isogenic <i>cif::aadA</i> mutant. <br><b>Figure 9</b>. Survival curves for two different lineages of perforin-2 (Mpeg1) +/+, +/−, and −/− mice after orogastric inoculation with 10^6 CFU of <i>Yersinia pseudotuberculosis</i> or an isogenic <i>cif::aadA</i> mutant.<br>The accompanying <b>Dataset/Table</b> contains the data for Figures 8 and 9. This data was originally published in "<i>Enteric Pathogens Deploy Cell Cycle Inhibiting Factors to Block the Bactericidal Activity of Perforin-2</i>," McCormack, Lyapichev,Olsson, Podack, and Munson. Elife. 2015 Sep 29;4:e06505. doi: 10.7554/eLife.06505.PMID: 26418746 PMCID: PMC4626573 DOI: 10.7554/eLife.06505. Published under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original authors and source are credited. <br>Please see the citation for methods and experimental details.<br><br>Abstract of associated publication: Perforin-2 (MPEG1) is an effector of the innate immune system that limits the proliferation and spread of medically relevant Gram-negative, -positive, and acid fast bacteria. We show here that a cullin-RING E3 ubiquitin ligase (CRL) complex containing cullin-1 and βTrCP monoubiquitylates Perforin-2 in response to pathogen associated molecular patterns such as LPS. Ubiquitylation triggers a rapid redistribution of Perforin-2 and is essential for its bactericidal activity. Enteric pathogens such as Yersinia pseudotuberculosis and enteropathogenic Escherichia coli disarm host cells by injecting cell cycle inhibiting factors (Cifs) into mammalian cells to deamidate the ubiquitin-like protein NEDD8. Because CRL activity is dependent upon NEDD8, Cif blocks ubiquitin dependent trafficking of Perforin-2 and thus, its bactericidal activity. Collectively, these studies further underscore the biological significance of Perforin-2 and elucidate critical molecular events that culminate in Perforin-2-dependent killing of both intracellular and extracellular, cell-adherent bacteria.
DOI: 10.35092/yhjc.12585431
title: Supplemental Tables supporting "Inhibition of mitochondrial respiration impairs nutrient consumption and metabolite transport in human retinal pigment epithelium"

description: In the present study, we use targeted-metabolomics and metabolite tracing with <sup>13</sup>C glucose to investigate how inhibition of mitochondrial respiration influences the intracellular and extracellular metabolome in primary human RPE cells. Our findings demonstrate that · Inhibition of mitochondrial metabolism causes early and unique changes in medium metabolites;· RPE cells with dysfunctional mitochondria export less glucose, pyruvate, citrate, ketone bodies and other nutrients, but release massive amounts of lactate, hypoxanthine, and other nucleosides;· Changes of medium metabolites consistently reflect intracellular changes.<br><br>Here we provide supplement tables, including the method we used and details in mass spectrometry.<br><br>Supports preprint: Inhibition of mitochondrial respiration impairs nutrient consumption and metabolite transport in human retinal pigment epithelium. Rui Zhang, Abbi L Engel, Yekai Wang, Bo Li, Weiyong Shen, Mark C Gillies, Jennifer Chao, Jianhai Du. bioRxiv 2020.05.11.086827; doi: https://doi.org/10.1101/2020.05.11.086827<br><br>Preprint abstract: Mitochondrial respiration in mammalian cells not only generates ATP to meet their own energy needs but also couples with biosynthetic pathways to produce metabolites that can be exported to support neighboring cells. However, how defects in mitochondrial respiration influence these biosynthetic and exporting pathways remains poorly understood. Mitochondrial dysfunction in retinal pigment epithelium (RPE) cells is an emerging contributor to the death of their neighboring photoreceptors in degenerative retinal diseases including age-related macular degeneration. In this study, we used targeted-metabolomics and 13C tracing to investigate how inhibition of mitochondrial respiration influences the intracellular and extracellular metabolome. We found inhibition of mitochondrial respiration strikingly influenced both the intracellular and extracellular metabolome in primary RPE cells. Intriguingly, the extracellular metabolic changes sensitively reflected the intracellular changes. These changes included substantially enhanced glucose consumption and lactate production, reduced release of pyruvate, citrate and ketone bodies, and massive accumulation of multiple amino acids and nucleosides. In conclusion, these findings reveal a metabolic signature of nutrient consumption and release in mitochondrial dysfunction in RPE cells. Testing medium metabolites provides a sensitive and noninvasive method to assess mitochondrial function in nutrient utilization and transport.