Find research datasets worth reusing
Search datasets from major research repositories and use ShareScore to quickly assess how well each record supports discovery, access, and reuse.
282
datasets available to search
ShareScore release 0.9.0
Dataset results
282 results for “Data Deficient”
TEM Data on Strontium-deficient SrxCoO2–CoO2 nanotubes
<p>Raw data ((scanning) transmission electron microscopy images, diffraction patterns and EDX/EELS spectra) obtained for work on Strontium-deficient SrxCoO2–CoO2 nanotubes as a high ampacity and high conductivity material published in Materials Horizons</p>
Data from: Collaborative Research: Influence of phosphorus deficiency on enigmatic biological methane production in oxic freshwater lakes
<p>Data from: Collaborative Research: Influence of phosphorus deficiency on enigmatic biological methane production in oxic freshwater lakes</p> <p>NSF Projects 1951002 (PI: Matthew J. Church), 1950963 (PI: John E. Dore)</p>
Open data repository, Boehm-Sturm et al., Phenotyping placental oxygenation in Lgals1 deficient mice using 19F MRI
<p>Open data repository of journal article "Phenotyping placental oxygenation in Lgals1 deficient mice using <sup>19</sup>F MRI"</p>
Data from: Offspring behavioral outcomes following maternal allergic asthma in the IL-4-deficient mouse
<p>Background: Maternal allergies and asthma during pregnancy have been associated with increased risk of ASD and ADHD to the child. Previous rodent studies have demonstrated that inducing a T helper-2 (Th2)-mediated allergic response during pregnancy leads to an offspring behavioral phenotype characterized by decreased social interaction and increased stereotypies. Interleukin-4 is a key signal in the Th2 immune cascade, but its role in fetal brain development and subsequent impacts of maternal allergic asthma (MAA) on offspring behavioral deficits have yet to be determined.</p> <p>Objective: In this study, we investigated whether the absence of IL-4 signaling would mitigate MAA-induced behavioral changes.</p> <p>Methods: C57BL/6J and Interleukin-4 knockout (IL-4 KO) mice were sensitized to ovalbumin and exposed to repeated allergic asthma aerosol inductions throughout pregnancy. Offspring were assessed on Juvenile Reciprocal Social Interaction, Elevated Plus Maze, Open Field Exploration, Novel Object Recognition, Forced Swim, Marble-burying, and Grooming tasks.</p> <p>Results: MAA during pregnancy resulted in decreased social interactions in male C57 offspring and impaired memory performance in both male and female C57 mice. These deficits were not observed in IL-4 KO mice exposed to MAA. However, we observed genotype effects in IL-4 KO mice including altered motor performance and anxiety-associated responses.</p> <p>Conclusion: MAA-induced social and cognitive behavioral alterations are IL-4 dependent. IL-4KO offspring display genotype-specific differences suggesting IL-4 signaling is important for typical developmental processes.</p>
16S rRNA Sequencing Data of Fecal Microbiota in an Italian Cohort of Patients with CDKL5 Deficiency Disorder
<h3>Summary of the study </h3> <p>CDKL5 deficiency disorder (CDD) is a neurodevelopmental condition characterized by global developmental delay, early-onset seizures, intellectual disability, visual and motor impairments, distinct from Rett Syndrome (RTT) due to the absence of a clear regression period. Gastrointestinal (GI) disturbances and signs of subclinical immune dysregulation are common in CDD patients, yet the underlying causes are unknown. Recent studies hint at a possible link between neurological disorders and gut microbiota, an unexplored area in CDD. In this groundbreaking study, we examined fecal microbiota in CDD patients and their healthy relatives, revealing differences in bacterial diversity and composition. We further investigated microbiota changes based on various factors, including the severity of GI issues, seizure frequency, sleep disorders, food intake type, neuro-behavioral features (assessed through the RTT Behaviour Questionnaire – RSBQ), and ambulation capacity. </p> <p>Our findings suggest a potential connection between CDD, microbiota, and symptom severity. This study represents the first exploration of the gut-microbiota-brain axis in CDD patients, contributing to the growing body of research on the role of gut microbiota in neurodevelopmental disorders. It opens doors to potential interventions targeting intestinal microbes to enhance the well-being of individuals with CDD.</p> <h3>Mehods</h3> <p>The Dataset represent the raw data (.fastq) obtained from the sequencing of the fecal samples from 17 Italian Patients with CDD, and 17 Healthy Relatives (i.e. siblings or mother), collected at a single time-point.</p> <p>Samples from Patients affected by CDD are called CDD, samples from Healthy Relatives are called HC-CDD (i.e. healthy controls of patients affected by CDD). For details about the sample names see the “Explanation Table”.</p> <p>Bacterial DNA was extracted from fecal samples using the QIAmp Powerfexal DNA Kit (Qiagen, Germany) following the manufacturer's protocol. The 16S rRNA sequencing and analysis was performed by a service offered by Zymo Research (Germany).</p> <p><em>Targeted Library Preparation</em>: The DNA samples were prepared for targeted sequencing with the Quick-16S™ NGS Library Prep Kit (Zymo Research). The primer sets used were Quick-16S™ Primer Set V3-V4 (Zymo Research). The sequencing library was prepared using an innovative library preparation process in which PCR reactions were performed in real-time PCR machines to control cycles and therefore limit PCR chimera formation. The final PCR products were quantified with qPCR fluorescence readings and pooled together based on equal molarity. The final pooled library was cleaned up with the Select-a-Size DNA Clean & Concentrator™, then quantified with TapeStation® (Agilent Technologies, Santa Clara, CA) and Qubit® (Thermo Fisher Scientific, Waltham, WA). </p> <p><em>Sequencing:</em> The final library was sequenced on Illumina® MiSeq™ with a v3 reagent kit (600 cycles). </p>
Ultrasound Vevo 2100 data on ascending and abdominal aneurysms in ApoE-deficient mice - baseline and early stage
<p>This dataset contains raw data of ultrasound measurements taken of the ascending and abdominal aorta of Ang II-infused mice. Data were taken at baseline (prior to pump implantation) and at an early stage of disease development. Data can be openend with the Vevo 2100 analysis software provided by Fujifilm.</p> <p> </p> <p> </p>
SLC35A2 deficiency reduces protein levels of core 1 β-1,3-galactosyltransferase 1 (C1GalT1) and its chaperone Cosmc and affects their subcellular localization - yet unpublished supplementary data
<p>The upload contains raw data files used for the article "SLC35A2 deficiency reduces protein levels of core 1 β-1,3-galactosyltransferase 1 (C1GalT1) and its chaperone Cosmc and affects their subcellular localization".</p> <p><strong>Article abstract</strong></p> <p>Nucleotide sugar transporters (NSTs) are multitransmembrane proteins, localized in the Golgi apparatus and/or endoplasmic reticulum, which provide glycosylation enzymes with their substrates. It has been demonstrated that NSTs may form complexes with functionally related glycosyltransferases, especially in the N-glycosylation pathway. However, potential interactions of NSTs with enzymes mediating the biosynthesis of mucin-type O-glycans have not been addressed to date. Here we report that UDP-galactose transporter (UGT; SLC35A2) associates with core 1 β-1,3-galactosyltransferase 1 (C1GalT1; T-synthase). This provides the first example of an interaction between an enzyme that acts exclusively in the O-glycosylation pathway and an NST. We also found that SLC35A2 associated with the C1GalT1-specific chaperone Cosmc, and that the endogenous Cosmc was localized in both the endoplasmic reticulum and Golgi apparatus of wild-type HEK293T cells. Furthermore, in SLC35A2-deficient cells protein levels of C1GalT1 and Cosmc were decreased and their Golgi localization was less pronounced. Finally, we identified SLC35A2 as a novel molecular target for the antifungal agent itraconazole. Based on our findings we propose that NSTs may contribute to the stabilization of their interaction partners and help them to achieve target localization in the cell, most likely by facilitating their assembly into larger functional units. </p> <p>The Word document (Data description.docx) contains a description of each file.</p>
Non-systematic surveys reveal increases in areas occupied by endangered and data-deficient Nubian bustard
<p>This repository contains the R scripts and data to reproduce the analysis of the manuscript <a href="https://doi.org/10.1016/j.gecco.2023.e02682">https://doi.org/10.1016/j.gecco.2023.e02682</a></p>
Data from: Offspring behavioral outcomes following maternal allergic asthma in the IL-4-deficient mouse
Open the record for dataset details and reuse information.
Data from: Genome-wide Screens Implicate Loss of Cullin Ring Ligase 3 in Persistent Proliferation and Genome Instability in TP53-Deficient Cells
<p>CSV files of whole-Genome Knockout Screens for Proliferation and Tumorigenic Growth. The data is retrieved from:</p> <p>Title: "Genome-wide Screens Implicate Loss of Cullin Ring Ligase 3 in Persistent Proliferation and Genome Instability in TP53-Deficient Cells"</p> <p>DOI: https://doi.org/10.1016/j.celrep.2020.03.029</p> <p>The excel sheet with data shown in figure 1B is converted to CSV files.</p>
Data from: Safety of single low-dose primaquine in glucose-6-phosphate dehydrogenase deficient falciparum-infected African males: two open-label, randomized, safety trials
Background: Primaquine (PQ) actively clears mature Plasmodium falciparum gametocytes but in glucose-6-phosphate dehydrogenase deficient (G6PDd) individuals can cause hemolysis. We assessed the safety of low-dose PQ in combination with artemether-lumefantrine (AL) or dihydroartemisinin-piperaquine (DP) in G6PDd African males with asymptomatic P. falciparum malaria. Methods and findings: In Burkina Faso, G6PDd adult males were randomized to treatment with AL alone (n = 10) or with PQ at 0.25 (n = 20) or 0.40 mg/kg (n = 20) dosage; G6PD-normal males received AL plus 0.25 (n = 10) or 0.40 mg/kg (n = 10) PQ. In The Gambia, G6PDd adult males and boys received DP alone (n = 10) or with 0.25 mg/kg PQ (n = 20); G6PD-normal males received DP plus 0.25 (n = 10) or 0.40 mg/kg (n = 10) PQ. The primary study endpoint was change in hemoglobin concentration during the 28-day follow-up. Cytochrome P-450 isoenzyme 2D6 (CYP2D6) metabolizer status, gametocyte carriage, haptoglobin, lactate dehydrogenase levels and reticulocyte counts were also determined. In Burkina Faso, the mean maximum absolute change in hemoglobin was -2.13 g/dL (95% confidence interval [CI], -2.78, -1.49) in G6PDd individuals randomized to 0.25 PQ mg/kg and -2.29 g/dL (95% CI, -2.79, -1.79) in those receiving 0.40 PQ mg/kg. In The Gambia, the mean maximum absolute change in hemoglobin concentration was -1.83 g/dL (95% CI, -2.19, -1.47) in G6PDd individuals receiving 0.25 PQ mg/kg. After adjustment for baseline concentrations, hemoglobin reductions in G6PDd individuals in Burkina Faso were more pronounced compared to those in G6PD-normal individuals receiving the same PQ doses (P = 0.062 and P = 0.022, respectively). Hemoglobin levels normalized during follow-up. Abnormal haptoglobin and lactate dehydrogenase levels provided additional evidence of mild transient hemolysis post-PQ. Conclusions: Single low-dose PQ in combination with AL and DP was associated with mild and transient reductions in hemoglobin. None of the study participants developed moderate or severe anemia; there were no severe adverse events. This indicates that single low-dose PQ is safe in G6PDd African males when used with artemisinin-based combination therapy.
Data for PNASnexus article Aldehyde dehydrogenase 3A1 deficiency leads to mitochondrial dysfunction and impacts salivary gland stem cell phenotype
<p>Adult salivary stem/progenitor cells (SSPC) have an intrinsic property to self-renew in order to maintain tissue architecture and homeostasis. Adult salivary glands have been documented to harbor SSPC, which have been shown to play a vital role in the regeneration of the glandular structures post radiation damage. We have previously demonstrated that activation of aldehyde dehydrogenase 3A1 (ALDH3A1) after radiation reduced aldehyde accumulation in SSPC, leading to less apoptosis and improved salivary function. We subsequently found that sustained pharmacological ALDH3A1 activation is critical to enhance regeneration of murine submandibular gland after radiation damage. Further investigation shows that ALDH3A1 function is crucial for SSPC self-renewal and survival even in the absence of radiation stress. Salivary glands from <em>Aldh3a1</em>-null mice have fewer acinar structures than wildtype mice. ALDH3A1 deletion or pharmacological inhibition in SSPC leads to a decrease in mitochondrial DNA copy number, lower expression of mitochondrial specific genes and proteins, structural abnormalities, lower membrane potential, and reduced cellular respiration. Loss or inhibition of ALDH3A1 also elevates ROS levels and accumulation of ALDH3A1 substrate 4-hydroxynonenal (4-HNE, a lipid peroxidation product), leading to decreased survival of murine SSPC that can be rescued by treatment with 4-HNE specific carbonyl scavengers. Our data indicate that ALDH3A1 activity protects mitochondrial function and is important for the regeneration activity of SSPC. This knowledge will help to guide our translational strategy of applying ALDH3A1 activators in the clinic to prevent radiation-related hyposalivation in head and neck cancer patients.</p>
Data for Human milk lactoferrin variation in relation to maternal inflammation and iron deficiency in northern Kenya
<p>This file contains the data utilized for a journal manuscript, "Human milk lactoferrin variation in relation to maternal inflammation and iron deficiency in northern Kenya" by Fujita, Wander, Paredes Ruvalcaba, and Odo, currently under review for publication. Data are found under the Data tab, and the variable coding information under the Code tab.</p> <p>Please contact Fujita (masakof@msu.edu) for questions regarding the data.</p> <p>In using the data, please cite the DOI for this file and the above-mentioned article. Also, please acknowledge the following parties for grant support:</p> <p> National Science Foundation (BCS-0622358, BCS-1638167);</p> <p> Wenner-Gren Foundation (Gr. 7460, Gr. 9278);</p> <p> African Futures Research Leadership Program of the Alliances for African Partnership, Michigan State University; and</p> <p> Provost Undergraduate Research Initiative Grant, Michigan State University </p> <p>The data originates in the 2006 fieldwork among the Ariaal people in northern Kenya under approvals by the institutional review boards of the University of Washington and Kenya Medical Research Institute. The lactoferrin concentration in milk was determined more recently using de-identified milk specimens, and as such required no further approvals.</p> <p> </p>
data set related to article A Nervous System-Specific Model of Creatine Transporter Deficiency Recapitulates the Cognitive Endophenotype of the Disease: a Longitudinal Study
<p>This record contains raw data related to article A Nervous System-Specific Model of Creatine Transporter Deficiency Recapitulates the Cognitive Endophenotype of the Disease: a Longitudinal Study</p>
Data and R code used in Baudson et al (2019) Developmental plasticity of Brachypodium distachyon in response to P deficiency: modulation by inoculation with phosphate-solubilizing bacteria
<p>This repository contains the raw data and R code used for the following paper: Baudson et al (2019) Developmental plasticity of <em>Brachypodium distachyon</em> in response to P deficiency: modulation by inoculation with phosphate-solubilizing bacteria</p>
Ndufs4 knockout mice with isolated complex I deficiency engage a futile adaptive brain response - supplementary data
<p>This study aims to provide insight into the Leigh Syndrome pathomechanism at the sub-brain level. To this end, a comparative proteome analysis was performed on various brain regions of 6 wildtype (WT) and 6 whole body (WB) Ndufs4-/- (WB-KO) mice over two experiments. Samples were collected at six weeks after birth (i.e. ~ one week prior to WB-KO death). For the first experiment samples were collected from a brain slice (BrSl), which contained (parts of) the CC, HC, hypothalamus, thalamus, caudate putamen, and olfactory areas. For the second experiment the analysed brain regions consisted of cerebellum (CB), cerebral cortex (CC), hippocampus (HC), inferior colliculust (IC), and superior colliculus (SC).</p>
Supplementary Data for 'Altered body iron distribution and microcytosis in mice deficient in iron regulatory protein 2 (IRP2).'
<p>Supplementary data for Galy, B., Ferring, D., Minana, B., Bell, O., Janser, H.G., Muckenthaler, M., Schümann, K. and Hentze, M.W., 2005. Altered body iron distribution and microcytosis in mice deficient in iron regulatory protein 2 (IRP2). <em>Blood</em>, <em>106</em>(7), pp.2580-2589.</p>
Data from: Safety of single low-dose primaquine in glucose-6-phosphate dehydrogenase deficient falciparum-infected African males: two open-label, randomized, safety trials
Open the record for dataset details and reuse information.
Data for PNASnexus article Aldehyde dehydrogenase 3A1 deficiency leads to mitochondrial dysfunction and impacts salivary gland stem cell phenotype
Open the record for dataset details and reuse information.
Data from: Medium-chain fatty acid receptor GPR84 deficiency leads to metabolic homeostasis dysfunction in mice fed high-fat diet
Open the record for dataset details and reuse information.
ScienceDex guides
Understand access before you commit
These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.