Find research datasets worth reusing

opencc-by-4.0Sep 2022View details →

Outcome of severe COVID-19: spotlight on fatigue, fatiguability, multidomain complaints and pattern of cognitive deficits in a case series without prior brain dysfunction and without COVID-19-related stroke and/or cardiac arrest

Outcome of severe COVID-19: spotlight on fatigue, fatiguability, multidomain complaints and pattern of cognitive deficits in a case series without prior brain dysfunction and without COVID-19-related stroke and/or cardiac arrest Valérie Beaud1, Sonia Crottaz-Herbette1, Vincent Dunet2, Jean-François Knebel1, Pierre-Alexandre Bart3, Stephanie Clarke1 1 Service of Neuropsychology and Neurorehabilitation, Lausanne University Hospital and University of Lausanne, 1011 Lausanne, Switzerland 2 Service of Diagnostic and Interventional Radiology, Lausanne University Hospital and University of Lausanne, 1011 Lausanne, Switzerland 3 Service of Internal Medicine, Lausanne University Hospital and University of Lausanne, 1011 Lausanne, Switzerland ABSTRACT Background: Cognitive deficits were often reported during the acute and post-acute stages of severe COVID-19 and were often, but not always, associated with signs of brain damage. Population-wide surveys highlighted the need for investigations into the nature, the severity and the evolution of cognitive, behavioural and psychiatric deficits. Case presentation: We report the outcome at 12 months after severe COVID-19 involving intensive care unit stay and mechanical ventilation in six patients. None of the patients had history of prior brain dysfunction and none sustained stroke and/or cardiac arrest during COVID-19. A pervading mental and physical fatigue was consistently reported as well as numerous multidomain complaints, which affect to some extend everyday life, and for some of the patients a mental fatiguability, a certain degree of neurobehavioural (apathy) and/or psychiatric (anxiety) dysfunction. Standardized neuropsychological tests revealed for 4 of the 6 patients the occurrence relatively isolated of cognitive dysfunction or performance at the lower limit of the norm in some, but not all attentional, executive and/or working memory tests. Somatic scales highlighted the presence of dyspnoea, muscle weakness, olfactory disorder and/or minor sleep problems in some but not all patients. Conclusion: Fatigue, fatiguability, multidomain complaints, which affect to some extend everyday life, cognitive dysfunction or performance at the lower limit of the norm and a certain degree of neurobehavioural and/or psychiatric and/or somatic dysfunction can occur in the aftermath of severe COVID-19 even in the absence of neurological antecedents or of COVID-19-related stroke and/or cardiac arrest.

opencc-by-4.0Dec 2017View details →

Factor XII deletion mitigates cerebral microbleed load but not hemodynamic dysfunction in the arcAβ mice

Cerebrovascular dysfunction and a prothrombotic state have been found in patients with Alzheimer’s disease (AD). The factor XII (FXII)-driven activated contact system has been implicated in the vascular pathology and inflammation in AD patients and AD mouse models. Here we investigated the effect of genetic deletion of FXII on AD-related vascular dysfunction using magnetic resonance imaging (MRI). AD mouse line ArcAβ, arcAβ/FXII-/-, FXII-/- and non-transgenic littermates  of 17 months of age (n = 40) were assessed for 1) cerebral microbleeds (CMB) load using susceptibility weighted imaging (SWI) MRI, 2) cerebral blood flow (CBF) using arterial spin labeling, and 3) vascular reactivity by estimating changes in cerebral blood volume (∆CBV) during hypercapnic stimulus using acetazolamide.

opencc-by-4.0Jul 2018View details →

Development of an imaging toolbox to assess the therapeutic potential and biodistribution of macrophages in a mouse model of multiple organ dysfunction

Data set to accompany manuscript entitled "Development of an imaging toolbox to assess the therapeutic potential and biodistribution of regenerative therapies in a mouse model of multiple organ dysfunction " which can be found on BioRxiv.

opencc-by-4.0Jun 2021View details →

Modality-specific dysfunctional neural processing of social-abstract and non-social-concrete information in schizophrenia

Schizophrenia is characterized by marked communication dysfunctions encompassing potential impairments in the processing of social-abstract and non-social-concrete information, especially in everyday situations where multiple modalities are present in the form of speech and gesture. To date, the neurobiological basis of these deficits remains elusive. In a functional magnetic resonance imaging (fMRI) study, 17 patients with schizophrenia or schizoaffective disorder, and 18 matched controls watched videos of an actor speaking, gesturing (unimodal), and both speaking and gesturing (bimodal) about social or non-social events in a naturalistic way. Participants were asked to judge whether each video contains person-related (social) or object-related (non-social) information. When processing social-abstract content, patients showed reduced activation in the medial prefrontal cortex (mPFC) only in the gesture but not in the speech condition. For non-social-concrete content, remarkably, reduced neural activation for patients in the left postcentral gyrus and the right insula was observed only in the speech condition. Moreover, in the bimodal conditions, patients displayed improved task performance and comparable activation to controls in both social and non-social content. To conclude, patients with schizophrenia displayed modality-specific aberrant neural processing of social and non-social information, which is not present for the bimodal conditions. This finding provides novel insights into dysfunctional multimodal communication in schizophrenia, and may have potential therapeutic implications.

opencc-by-4.0Dec 2022View details →

Cytoscape files - Systems-level analyses of protein-protein interaction network dysfunctions via epichaperomics identify cancer-specific mechanisms of stress adaptation

Cytoscape files of pathway enrichment analyses and PPI mapping associated with manuscript https://www.nature.com/articles/s41467-023-39241-7 Systems-level analyses of protein-protein interaction network dysfunctions via epichaperomics identify cancer-specific mechanisms of stress adaptation Anna Rodina1,11, Chao Xu1,11, Chander S. Digwal1,11, Suhasini Joshi1,11, Anand R. Santhaseela1, Sadik Bay1, Swathi Merugu1, Aftab Alam1, Pengrong Yan1, Chenghua Yang1,12, Tanaya Roychowdhury1, Palak Panchal1, Liza Shrestha1, Yanlong Kang1, Sahil Sharma1, Yogita Patel2, Justina Almadovar1, Adriana Corben3,13, Mary Alpaugh1,14, Shanu Modi4, Monica L. Guzman5, Teng Fei6, Tony Taldone1, Stephen D. Ginsberg7,8, Hediye Erdjument-Bromage9, Thomas A. Neubert9, Katia Manova-Todorova10, Jason C. Young2, Meng-Fu Bryan Tsou10, Tai Wang1,*, Gabriela Chiosis1,4,* Abstract Systems-level assessments of protein-protein interaction (PPI) network dysfunctions are currently out-of-reach because approaches enabling proteome-wide identification, analysis, and modulation of context-specific PPI changes in native (unengineered) cells and tissues are lacking. Herein, we take advantage of first-in-class chemical binders of maladaptive scaffolding structures termed epichaperomes and develop an epichaperome-based ‘omics platform, epichaperomics, to identify PPI alterations in disease. We provide multiple lines of evidence, at both biochemical and functional levels, demonstrating the importance of these probes to identify and study PPI network dysfunctions and provide mechanistically and therapeutically relevant proteome-wide insights. As proof-of-principle, we derive systems-level insight into PPI dysfunctions of cancer cells which enabled the discovery of a context-dependent mechanism by which cancer cells enhance the fitness of mitotic protein networks. Importantly, our systems levels analyses support the use of epichaperome chemical binders as therapeutic strategies aimed at normalizing PPI networks.

dryad36/100

Large leaf hydraulic safety margins limit the risk of drought-induced leaf hydraulic dysfunction in Neotropical rainforest canopy tree species

The sequence of key water potential thresholds from the onset of water stress to mortality, and the timing of stomatal closure with regard to leaf xylem embolism formation are essential to characterizing plant adaptive strategies to drought. This constitutes a critical knowledge gap for tropical rainforest species, which may be less vulnerable to drought than previously thought. We recorded key leaf and stem water potential thresholds, leaf hydraulic safety margins (HSMleaf), leaf stomatal safety margins (SSMleaf) and estimated native embolism levels during a normal-intensity dry season across 18 Neotropical rainforest tree species. We also solved a sequence of key water potential thresholds. Additionally, we provide a cross-biome analysis of SSMleaf encompassing 97 species from four major biomes based on a literature survey. In the studied rainforest species, leaf turgor loss point, used as a surrogate for stomatal closure, typically occurred before the onset of leaf xylem embolism. Most species exhibited positive HSMleaf and SSMleaf, with contrasting values across species and nearly absent embolism levels during the dry season irrespective of the experienced midday leaf water potentials. Our results point out that leaf xylem embolism is not routine for Neotropical rainforest tree species. Based on our proposal of the water potential sequence for tropical rainforest trees, we argue that leaf xylem embolism is a rare event for these species. This was supported by the literature survey, indicating that across biomes, most woody species have rather large SSMleaf and that leaves of tropical rainforest trees are not necessarily more vulnerable than in other biomes. However, we found evidence that some tropical rainforest species may be more vulnerable than others to ongoing climate change. Our data provide an opportunity to parametrize tree-based or land-surface models for tropical rainforests.

opencc-zeroMar 2023View details →

opencc-by-4.0Oct 2023View details →

Endothelial barrier dysfunction in systemic inflammation is mediated by soluble VE-cadherin interfering VE-PTP signalling

Original dataset for publication in iScience

opencc-by-4.0Oct 2023View details →

Data from: Single-cell analysis identifies conserved features of immune dysfunction in simulated microgravity and spaceflight

3-dimensional super-resolution microscopy volumes of human PBMCs recorded on a Zeiss LSM980 Airyscan2 laser scanning confocal microscope. Sample preparation and image capture: Live PBMCs were stained with 60 nM MitoTracker Red-CMX-Ros (ThermoFisher, Waltham, MA) either in 6-well plates or in the microgravity chambers for the last 2 hr of the microgravity simulation. At the end of the microgravity simulation cells were immediately fixed by 1:1 mixing the cell suspensions with 2× concentrated fixative (10% Sucrose (w/v) 120 mM KCl, 1% (w/v) glutaraldehyde, 8% (w/v) PFA pH 7.4) and incubated for 15 minutes at room temperature followed by 15 minutes on ice. Fixed cells were washed and stored in PBS until further staining for up to a week at 4 °C. 1 million fixed cells were resuspended in 1 mL of permeabilization solution (0.1% TritonX-100 in PBS) for 5 minutes. After twice washing in PBS, pellets were resuspended in 0.5 mL 1% BSA PBS containing Phalloidin-iFluor-488 (cat# ab176753, Abcam plc., Cambridge, UK) at the manufacturer’s recommended dilution, and were incubated for 90 minutes with gentle agitation. After washing in PBS, cells were stained with Hoechst 33342 (1 µg/mL in PBS) for 10 minutes. The fixed-stained cells were immobilized at 3 × 105 cells per well density in glass-bottom 96-well microplates (Greiner Bio-One, Monroe, NC), which were pre-coated with polyethyleneimine (1:15,000 (w/v)) for 16 hours in a 37 °C incubator, and washed twice with PBS. Microplates with the cell suspensions were centrifuged in a swing plate rotor centrifuge (Eppendorf 5810 R) at 400 × g and for 10 min and then fixed on the surface by adding an equal volume of 8% (w/v) PFA for 5 min. Finally, the fixative was replaced with 100 µL of antifade reagent (Vector Prolong Gold (ThermoFisher)). Samples were imaged immediately after this procedure on a Zeiss LSM980 Airyscan2 laser scanning confocal microscope (Carl Zeiss Microscopy, White Plains, NY). Single PBMCs were manually selected for recording based on low-resolution preview scans showing only nuclei. All singlet cells were selected in a small neighborhood to avoid biases. In each microscopy session, 24-40 cells were selected for recording in one well for each condition. This was performed in an interleaved manner, capturing 6-8 cells at a time, and then moving to the next well and then repeating this multiple times using the Experiment Designer module for automation. Super-resolution volumes of (358 × 358 × 70 pixels, 0.035 × 0.035 × 0.13 µm/voxel resolution) were recorded in the above-determined positions using Definite Focus autofocusing. A Plan-Apochromat 63 × 1.40 Oil lens, Airyscan2 SR (super-resolution) mode with optimal sampling and frame switching between 3 fluorescence channels to minimize spectral cross-bleed were used. MitoTracker Red, iFluor488, and Hoechs33342 were excited with 561, 488, and 405 nm solid-state lasers, respectively, using the optimal emission filter for each channel. 3D Airyscan2 processing was performed with standard filtering settings. File naming: Four zip files were deposited named as <Donor#id>.zip, where id goes from 1 to 4. Each zip file contains the following Zeiss Microscopy format image files: <Condition>_<Donor#id>_<Stain#batch>_<Cell>.czi <Condition>: <ul> <li>1G – Control culturing in 6-well plates for 25h</li> <li>uG – simulated microgravity culturing for 25h in NASA Rotating Wall Vessels</li> <li>1G+TLR – as above, with TLR 7/8 agonist (1 μM R848)</li> <li>uG+TLR– as above, with TLR 7/8 agonist (1 μM R848)</li> <li>1G+CyD– as above, with cytochalasin D</li> <li>uG+CyD– as above, with cytochalasin D</li> <li>1G+Q – as above, with quercetin 50µM</li> <li>uG+Q – as above, with quercetin 50µM</li> </ul> <Donor#id>: 1-4 indicates biological replicates <Stain#batch>: 1-2 indicates experimental replicates of phalloidin staining and imaging session <Cell>: arbitrary number to distinguish images within the same condition/donor/stain set. See image analysis pipelines used with these data at: https://github.com/gerencserlab/Superresolution-actin-and-mitochondria-analysis

Maximizing trEatment of Neurological Dysfunction Using INtravenous Guanfacine Study

ClinicalTrials.gov study NCT04742673. IPD Sharing: Not stated. Countries: 1. Publications: 1.

closedIPD-NOFeb 2026View details →

Reflex Therapy of Temporomandibular Dysfunctions

ClinicalTrials.gov study NCT07321483. IPD Sharing: NO. Countries: 1. Publications: 2.

controlledIPD-YESFeb 2026View details →

Vascular Dysfunction in Black Individuals: Roles of Nitric Oxide and Endothelin-1

ClinicalTrials.gov study NCT04770155. IPD Sharing: YES. Countries: 1. Publications: 5.

closedIPD-NOFeb 2026View details →

Study and Treatment of Visual Dysfunction and Motor Fatigue in Multiple Sclerosis

ClinicalTrials.gov study NCT02391961. IPD Sharing: NO. Countries: 1. Publications: 1.

Pain, Sexual Dysfunction, and Depression in Hemodialysis Patients

ClinicalTrials.gov study NCT00692419. IPD Sharing: Not stated. Countries: 1. Publications: 11.

A Study for Patients With Erectile Dysfunction to Test Whether Tadalafil Taken Once a Day Can Better Improve Psychological Outcomes.

ClinicalTrials.gov study NCT00734604. IPD Sharing: Not stated. Countries: 9. Publications: 1.

Evaluating Predictors & Interventions in Sphincter of Oddi Dysfunction

ClinicalTrials.gov study NCT00688662. IPD Sharing: Not stated. Countries: 1. Publications: 4.

Perfluorohexylcotane (NOV03) for the Treatment of Signs and Symptoms of Dry Eye Disease Associated With Meibomian Gland Dysfunction (Gobi Study)

ClinicalTrials.gov study NCT04139798. IPD Sharing: Not stated. Countries: 1. Publications: 2.

FFA-Induced Hypertension and Endothelial Dysfunction

ClinicalTrials.gov study NCT00589888. IPD Sharing: Not stated. Countries: 1. Publications: 1.

A Placebo-Controlled Trial of CLBS16 in Subjects With Coronary Microvascular Dysfunction

ClinicalTrials.gov study NCT04614467. IPD Sharing: Not stated. Countries: 1. Publications: 1.

controlledIPD-YESFeb 2026View details →

Green Tea Confections For Managing Postprandial Hyperglycemia-Induced Vascular Endothelial Dysfunction

ClinicalTrials.gov study NCT01857258. IPD Sharing: YES. Countries: 1. Publications: 1.