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1,890 results for “Defects”
IO Islamic 127. Burhân-i-Maâthir, A Defective copy of 'Alî bin 'Azîz-allâh Ṭabâṭabâ's History of the Bahmanîs and Niżâmshâhîs of Gulbargah, Bîdar, and Aḥmadnagar
<p>IO Islamic 127. Burhân-i-Maâthir, A Defective copy of ‘Alî bin ‘Azîz-allâh Ṭabâṭabâ’s History of the Bahmanîs and Niżâmshâhîs of Gulbargah, Bîdar, and Aḥmadnagar</p>
High Throughput Pipeline for Segmentation and Defect Identification
<p>HRTEM micrographs of gold and cadmium selenide nanoparticles and corresponding semantic segmentation maps for neural network training.</p>
Replication package with data used in the study: "The effect of code smells on the relationship between design patterns and defects. An empirical study"
<p>This is a replication package with data used in a study by T. Alkhaeir and B. Walter "The effect of code smells on the relationship between design patterns and defects. An empirical study"</p> <p>This dataset contains the following folders:</p> <ul> <li> <p>"Analyzed systems" folder:</p> <ul> <li> <p>For each subject system (Ant-1.7, JEdit-4.2, Lucene-2.4, Camel-1.6, Log4j-1.2, Xalan-2.7, Poi-3.0, Ivy-2.0, Xerces-2.0, Velocity-1.6), we identify the following datasets: SDP, nSDP, SnDP, and nSnDP. Each dataset is represented by a separate csv file.</p> </li> <li> <p>Those csv files include raw data about every class in every release. Each file includes columns which represent:</p> <ul> <li> <p>System: The analyzed system</p> </li> <li> <p>className: A fully qualified class name</p> </li> <li> <p>Pattern: if the class is part of any pattern the cell contains the name of the pattern, and “null” otherwise</p> </li> <li> <p>Smell: if the class is part of affected by any smell the cell contains the name of the smell, and “null” otherwise</p> </li> <li> <p>Bugs: Number of defects reported inside the class (extracted from the PROMISE dataset)</p> </li> </ul> </li> </ul> </li> <li> <p>A "detailed analysis" folder:</p> <ul> <li> <p>For each pattern, we report all the classes which participate in it in all the analyzed systems. The csv files inside this folder follow the same structure as the other csv files reported above</p> </li> </ul> </li> </ul> <p><br> </p>
A dicamba resistance endowing IAA16 mutation leads to significant vegetative growth defects and impaired competitiveness in kochia (Bassia scoparia)
<p class="CxSpFirst"><span>Precise quantification of the fitness cost of synthetic auxins resistance has been impeded by lack of knowledge for the genetic basis of resistance in weeds. Recent elucidation of a resistance endowing IAA16 mutation (G73N) in a key weed species kochia (<i>Bassia scoparia</i>), allows detailed characterization of the contribution of resistance alleles to weed fitness, both in the presence and absence of herbicides.<b> </b>Different G73N genotypes from a segregating resistant parental line (9425) were characterized for cross resistance to dicamba, 2,4-D and fluroxypyr, and changes on stem/leaf morphology and plant architecture. Plant competitiveness and dominance of the fitness effects was quantified through measuring biomass and seed production of three F<sub>2</sub> lines in two runs of glasshouse replacement series studies. G73N confers robust resistance to dicamba but only moderate to weak resistance to 2,4-D and fluroxypyr. G73N mutant plants displayed significant vegetative growth defects: 1) being 30-50% shorter with a more tumbling style plant architecture; 2) had thicker and more ovate (versus lanceolate and linear) leaf blades with lower photosynthesis efficiency, and 40-60% smaller stems with less developed vascular bundle systems. F<sub>2 </sub>mutant plants had impaired plant competitiveness, which produced up to 90% less biomass and seeds in the replacement series study. The pleiotropic effects of G73N was mostly semi-dominant (0.5) and fluctuated with the environments and traits measured. G73N is associated with significant vegetative growth defects and reduced competitiveness in synthetic auxin resistant kochia. Management practices should target resistant kochia's high vulnerability to competition to effectively contain the spread of resistance.</span></p>
Bonding of gold nanoclusters on graphene with and without point defects
<p>Theoretical data set for the Nanomaterials paper "Bonding of gold nanoclusters on graphene with and without point defects".</p> <p>Data structure and formats are described in the README.docx file.</p>
Raw diffraction data from Acta Cryst. 2020, D76, 1057-1065 (Wuhan Asiatic toad influenza virus neuraminidase with lattice-translocation defects)
<p>The ectodomain (residues 79–466) of the neuraminidase from the Wuhan Asiatic toad influenza virus (GenBank accession No. MG600049.1) was crystallized. X-ray diffraction data were collected on beamline BL17U1 at Shanghai Synchrotron Radiation Facility (SSRF) using a Dectris EIGER 16M detector. A total of 100 frames were recorded with an oscillation angle of 1.0 deg. Sharp–diffuse diffraction patterns and native Patterson peaks manifest the pathological imperfection: lattice-translocation defects.</p> <p> </p>
Overexpression of an ALS-associated FUS mutation in C. elegans disrupts NMJ morphology and leads to defective neuromuscular transmission
The amyotrophic lateral sclerosis (ALS) neurodegenerative disorder has been associated with multiple genetic lesions, including mutations in the gene for FUS (Fused in Sarcoma), a nuclear-localized RNA/DNA-binding protein. Neuronal expression of the pathological form of FUS proteins in C. elegans results in mislocalization and aggregation of FUS in the cytoplasm, and leads to impairment of motility. However, the mechanisms by which the mutant FUS disrupts neuronal health and function remain unclear. Here we investigated the impact of ALS-associated FUS on motor neuron health using correlative light and electron microscopy, electron tomography, and electrophysiology. We show that ectopic expression of wild-type or ALS-associated human FUS impairs synaptic vesicle docking at neuromuscular junctions. ALS-associated FUS led to the emergence of a population of large, electron-dense, and filament-filled endosomes. Electrophysiological recording revealed reduced transmission from motor neurons to muscles. Together, these results suggest a pathological effect of ALS-causing FUS at synaptic structure and function organization.
Data from: The strategy of psychopathy: primary psychopathic traits predict defection on low-value relationships
Recent evidence suggests that psychopathy is a trait continuum. This has unappreciated implications for understanding the selective advantage of psychopathic traits. Whereas clinical psychopathy is typically construed as a strategy of unconditional defection, subclinical psychopathy may promote strategic conditional defection, broadening the adaptive niche of psychopathy within human societies. To test this, we focus on a ubiquitous real-life source of conditional behaviour: the expected relational value of social partners, both in terms of their quality and the likely quantity of future interactions with them. We allow for conversational interaction among participants prior to their playing an unannounced, one-shot prisoner's dilemma game, which fosters naturalistic interpersonal evaluation and conditional behavior, while controlling punishment and reputation effects. Individuals scoring higher on Factor 1 (callous affect, interpersonal manipulation) of the Levenson Self-Report Psychopathy Scale show two forms of conditional defection: one after being interrupted more frequently during the conversation, the other after failing to discover cues to future meetings with an interlocutor. Both interaction effects support the hypothesis that primary subclinical psychopathy potentiates defection on those with low expected relational value. These data clarify the function and form of psychopathic traits, while highlighting adaptive variation in human social strategies.
Data from: Regular bottlenecks and restrictions to somatic fusion prevent the accumulation of mitochondrial defects in Neurospora
The replication and segregation of the multi-copy mitochondrial DNA (mtDNA) are not under strict control of the nuclear DNA. Within-cell selection may thus favour variants with an intracellular selective advantage but a detrimental effect on cell fitness. High relatedness among the mtDNA variants of an individual is predicted to disfavour such deleterious selfish genetic elements, but experimental evidence for this hypothesis is scarce. We studied the effect of mtDNA relatedness on the opportunities for suppressive mtDNA variants in the fungus Neurospora carrying the mitochondrial mutator plasmid pKALILO (pKAL). During growth, this plasmid integrates into the mitochondrial genome, generating suppressive mtDNA variants. These mtDNA variants gradually replace the wild-type mtDNA, ultimately culminating in growth arrest and death. We show that regular sequestration of mtDNA variation is required for effective selection against suppressive mtDNA variants. First, bottlenecks in the number of mtDNA copies from which a 'Kalilo' culture started significantly increased the maximum lifespan and variation in life span among cultures. Second, restrictions to somatic fusion among fungal individuals, either by using anastomosis-deficient mutants or by generating allotype diversity, prevented the accumulation of suppressive mtDNA variants. We discuss the implications of these results for the somatic accumulation of mitochondrial defects during ageing.
Data from: Identification of genetic defects in 33 probands with Stargardt disease by WES-based bioinformatics gene panel analysis
Stargardt disease (STGD) is the most common hereditary macular degeneration in juveniles, with loss of central vision occurring in the first or second decade of life. The aim of this study is to identify the genetic defects in 33 probands with Stargardt disease. Clinical data and genomic DNA were collected from 33 probands from unrelated families with STGD. Variants in coding genes were initially screened by whole exome sequencing. Candidate variants were selected from all known genes associated with hereditary retinal dystrophy and then confirmed by Sanger sequencing. Putative pathogenic variants were further validated in available family members and controls. Potential pathogenic mutations were identified in 19 of the 33 probands (57.6%). These mutations were all present in ABCA4, but not in the other four STGD-associated genes or in genes responsible for other retinal dystrophies. Of the 19 probands, ABCA4 mutations were homozygous in one proband and compound heterozygous in 18 probands, involving 28 variants (13 novel and 15 known). Analysis of normal controls and available family members in 12 of the 19 families further support the pathogenicity of these variants. Clinical manifestation of all probands met the diagnostic criteria of STGD. This study provides an overview of a genetic basis for STGD in Chinese patients. Mutations in ABCA4 are the most common cause of STGD in this cohort. Genetic defects in approximately 42.4% of STGD patients await identification in future studies.
Data from: Hyperandrogenism and insulin resistance induce gravid uterine defects in association with mitochondrial dysfunction and aberrant ROS production
Women with polycystic ovary syndrome (PCOS) are at increased risk of miscarriage, which often accompanies the hyperandrogenism and insulin resistance seen in these patients. However, neither the combinatorial interaction between these two PCOS-related etiological factors nor the mechanisms of their actions in the uterus during pregnancy are well understood. We hypothesised that hyperandrogensim and insulin resistance exert a causative role in miscarriage by inducing defects in uterine function that are accompanied by mitochondrial-mediated oxidative stress, inflammation and perturbed gene expression. Here we tested this hypothesis by studying the metabolic, endocrine and uterine abnormalities in pregnant rats after exposure to daily injection of 5α-dihydrotestosterone (DHT, 1.66 mg/kg body weight/day) and/or insulin (6.0 IU/day) from gestational day 7.5 to 13.5. We showed that while DHT-exposed and insulin-exposed pregnant rats presented impaired insulin sensitivity, DHT+insulin-exposed pregnant rats exhibited hyperandrogenism and peripheral insulin resistance, which mirrors pregnant PCOS patients. Compared to controls, hyperandrogenism and insulin resistance in the dam was associated with alterations in uterine morphology and aberrant expression of genes responsible for decidualization (Prl8a2, Fxyd2, and Mt1g), placentation (Fcgr3 and Tpbpa), angiogenesis (Flt1, Angpt1, Angpt2, Ho1, Ccl2, Ccl5, Cxcl9, and Cxcl10) and insulin signaling (Akt, Gsk3 and Gluts). Moreover, we observed changes in uterine mitochondrial function and homeostasis (i.e. mitochondrial DNA copy number and the expression of genes responsible for mitochondrial fusion, fission, biogenesis, and mitophagy) and suppression of both oxidative and antioxidative defenses (i.e. reactive oxygen species, Nrf2 signaling, and interactive networks of antioxidative stress responses) in response to the hyperandrogenism and insulin resistance. These findings demonstrate that hyperandrogenism and insulin resistance induce mitochondria-mediated damage and a resulting imbalance between oxidative and antioxidative stress responses in the gravid uterus.
CONGENITAL HEART DEFECTS
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Replication kit for: Problems with SZZ and Features: An empirical study of the state of practice of defect prediction data collection
<p>This is the replication package for our article "Problems with SZZ and Features: An empirical study of the state of practice of defect prediction data collection". </p> <p>All relevant information is available in the replication-notebook, which is available as executable Jupyter Notebook and as HTML page.</p> <p>The archive release-level-data.tar.gz contains the defect prediction data labeled with IND-JLMIV+R for the 398 releases and is shared for re-use by other researcher for defect prediction experiments. </p> <p>The archive DO_NOT_USE_release-leve-data.tar.gz contains the contains the defect prediction data labeled with 6M-SZZ and should not be re-used. </p> <p>The raw data with the MongoDB required to run the Jupyter Notebook is contained in the SmartSHARK Database release 1.0 (https://smartshark.github.io/dbreleases/ / https://doi.org/10.5281/zenodo.4071448).</p> <p>All materials are licensed under the Apache 2.0 License (see LICENSE file). </p>
Integer topological defects organize stresses driving tissue morphogenesis
<p>Raw data files</p>
Computer Vision-Based Algorithm for Precise Defect Detection and Classification in Photovoltaic Modules
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Evaluation of potential effects and genetic parameters in conformational limb defects in Pura Raza Española horses
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Multi-classifier for RC bridge defects
<p>Classifying concrete defects during a bridge inspection remains a subjective and laborious task. The risk of getting a false result is approximately 50% if different inspectors assess the same concrete defect. This is significant in the light of an over-ageing bridge stock, decreasing infrastructure maintenance budgets and catastrophic bridge collapses as happened in 2018 in Genoa, Italy. To support an automated inspection and an objective bridge defect classification, we propose a three-staged concrete defect classifier that can multi-classify potentially unhealthy bridge areas into their specific defect type in conformity with existing bridge inspection guidelines. Three separate deep neural pre-trained networks are fine-tuned based on multi-source dataset consisting of self-collected image samples plus several Departments of Transportation inspection databases. We show that this approach can reliably classify multiple defect types with an average mean score of 85%. Our presented multi-classifier is a contribution towards developing a mostly or fully inspection schema for a more cost effective and more objective bridge inspection.</p>
Datasets for Software Defect Number Prediction
<p>27 Datasets with ARFF format for Software Defect Number Prediction</p>
Mechanochemically-derived Fe atoms on defective boron nitride for stable propylene production
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Supplementary Data for "Li+ Diffusion in Crystalline Lithium Silicides: Influence of Intrinsic Point Defects"
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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.