1,177 research outputs found

    How much information is lost when sampling driving behavior data? Indicators to quantify the extent of information loss

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    Purpose – Individuals’ driving behavior data are becoming available widely through Global Positioning System devices and on-board diagnostic systems. The incoming data can be sampled at rates ranging from one Hertz (or even lower) to hundreds of Hertz. Failing to capture substantial changes in vehicle movements over time by “undersampling” can cause loss of information and misinterpretations of the data, but “oversampling” can waste storage and processing resources. The purpose of this study is to empirically explore how micro-driving decisions to maintain speed, accelerate or decelerate, can be best captured, without substantial loss of information. Design/methodology/approach – This study creates a set of indicators to quantify the magnitude of information loss (MIL). Each indicator is calculated as a percentage to index the extent of information loss (EIL) in different situations. An overall information loss index named EIL is created to combine the MIL indicators. Data from a driving simulator study collected at 20 Hertz are analyzed (N = 718,481 data points from 35,924 s of driving tests). The study quantifies the relationship between information loss indicators and sampling rates. Findings – The results show that marginally more information is lost as data are sampled down from 20 to 0.5 Hz, but the relationship is not linear. With four indicators of MILs, the overall EIL is 3.85 per cent for 1-Hz sampling rate driving behavior data. If sampling rates are higher than 2 Hz, all MILs are under 5 per cent for importation loss. Originality/value – This study contributes by developing a framework for quantifying the relationship between sampling rates, and information loss and depending on the objective of their study, researchers can choose the appropriate sampling rate necessary to get the right amount of accuracy

    Mitochondria-Targeted Antioxidant Prevents Cardiac Dysfunction Induced by Tafazzin Gene Knockdown in Cardiac Myocytes

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    Tafazzin, a mitochondrial acyltransferase, plays an important role in cardiolipin side chain remodeling. Previous studies have shown that dysfunction of tafazzin reduces cardiolipin content, impairs mitochondrial function, and causes dilated cardiomyopathy in Barth syndrome. Reactive oxygen species (ROS) have been implicated in the development of cardiomyopathy and are also the obligated byproducts of mitochondria. We hypothesized that tafazzin knockdown increases ROS production from mitochondria, and a mitochondria-targeted antioxidant prevents tafazzin knockdown induced mitochondrial and cardiac dysfunction. We employed cardiac myocytes transduced with an adenovirus containing tafazzin shRNA as a model to investigate the effects of the mitochondrial antioxidant, mito-Tempo. Knocking down tafazzin decreased steady state levels of cardiolipin and increased mitochondrial ROS. Treatment of cardiac myocytes with mito-Tempo normalized tafazzin knockdown enhanced mitochondrial ROS production and cellular ATP decline. Mito-Tempo also significantly abrogated tafazzin knockdown induced cardiac hypertrophy, contractile dysfunction, and cell death. We conclude that mitochondria-targeted antioxidant prevents cardiac dysfunction induced by tafazzin gene knockdown in cardiac myocytes and suggest mito-Tempo as a potential therapeutic for Barth syndrome and other dilated cardiomyopathies resulting from mitochondrial oxidative stress

    Life fingerprints of nuclear reactions in the body of animals

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    Nuclear reactions are a very important natural phenomenon in the universe. On the earth, cosmic rays constantly cause nuclear reactions. High energy beams created by medical devices also induce nuclear reactions in the human body. The biological role of these nuclear reactions is unknown. Here we show that the in vivo biological systems are exquisite and sophisticated by nature in influence on nuclear reactions and in resistance to radical damage in the body of live animals. In this study, photonuclear reactions in the body of live or dead animals were induced with 50-MeV irradiation. Tissue nuclear reactions were detected by positron emission tomography (PET) imaging of the induced beta+ activity. We found the unique tissue "fingerprints" of beta+ (the tremendous difference in beta+ activities and tissue distribution patterns among the individuals) are imprinted in all live animals. Within any individual, the tissue "fingerprints" of 15O and 11C are also very different. When the animal dies, the tissue "fingerprints" are lost. The biochemical, rather than physical, mechanisms could play a critical role in the phenomenon of tissue "fingerprints". Radiolytic radical attack caused millions-fold increases in 15O and 11C activities via different biochemical mechanisms, i.e. radical-mediated hydroxylation and peroxidation respectively, and more importantly the bio-molecular functions (such as the chemical reactivity and the solvent accessibility to radicals). In practice biologically for example, radical attack can therefore be imaged in vivo in live animals and humans using PET for life science research, disease prevention, and personalized radiation therapy based on an individual's bio-molecular response to ionizing radiation

    Anthriscifolcine A, a C18-diterpenoid alkaloid

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    The title compound, C26H39NO7, which was isolated from Delphinium anthriscifolium var. majus, has a lycoctonine carbon skeleton containing four six-membered rings (A, B, D and E) and three five-membered rings (C, F and G). Rings A, B and E adopt chair conformation, while ring D adopts a boat conformation. Rings C and F adopt envelope conformations

    [μ-10,21-Dimethyl-3,6,14,17-tetra­aza­tricyclo­[17.3.1.18,12]tetra­cosa-1(23),8(24),9,11,19,21-hexa­ene-23,24-diolato-κ8 N 3,N 6,O 23,O 24:N 14,N 17,O 23,O 24]bis­[(nitrato-κ2 O,O′)nickel(II)]

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    In the title centrosymmetric dinuclear nickel complex, [Ni2(C22H30N4O2)(NO3)2], each of the two NiII atoms has a distorted octa­hedral geometry, defined by two N atoms and two O atoms from the macrocyclic ligand and two O atoms from a chelating nitrate anion. The two Ni atoms are bridged by two phenolate O atoms, forming a four-membered Ni2O2 ring

    Chemical composition and anti-cholesterol activity of tea (Camellia sinensis) flowers from albino cultivars

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    Albino tea cultivars are mutant tea plants with altered metabolisms. Current studies focus on the leaves while little is known about the flowers. To evaluate tea flowers from different albino cultivars, the chemical composition and anti-cholesterol activity of tea flowers from three albino cultivars (i.e., Baiye No.1, Huangjinya, and Yujinxiang) were compared. According to the results, tea flowers from Yujinxiang had more amino acids but less polyphenols than tea flowers from the other two albino cultivars. A reduced content of procyanidins and a high chakasaponins/floratheasaponins ratio were characteristics of tea flowers from Yujinxiang. In vitro anti-cholesterol activity assays revealed that tea flowers from Yujinxiang exhibited stronger activity in decreasing the micellar cholesterol solubility, but not in cholesterol esterase inhibition and bile salt binding. It was noteworthy that there were no specific differences on the chemical composition and anti-cholesterol activity between tea flowers from albino cultivars and from Jiukeng (a non-albino cultivar). These results increase our knowledges on tea flowers from different albino cultivars and help food manufacturers in the cultivar selection of tea flowers for use

    (5,6:19,20-Dibenzo-1,4,11,14-tetra­oxa-8,17-diaza­cyclo­eicosane-κ4 N 8,O 11,O 14,N 17)dinitrato-κ4 O,O′-cadmium(II)

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    In the title compound, [Cd(NO3)2(C22H30N2O4)], the CdII atom is eight-coordinated by two amine N atoms and two O atoms from the 5,6:19,20-dibenzo-1,4,11,14-tetra­oxa-8,17-diaza­cyclo­eicosane ligand and four O atoms from two nitrate groups. The coordination geometry about Cd is antiprismatic. One nitro O atom is disordered equally over two positions

    PMMTalk: Speech-Driven 3D Facial Animation from Complementary Pseudo Multi-modal Features

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    Speech-driven 3D facial animation has improved a lot recently while most related works only utilize acoustic modality and neglect the influence of visual and textual cues, leading to unsatisfactory results in terms of precision and coherence. We argue that visual and textual cues are not trivial information. Therefore, we present a novel framework, namely PMMTalk, using complementary Pseudo Multi-Modal features for improving the accuracy of facial animation. The framework entails three modules: PMMTalk encoder, cross-modal alignment module, and PMMTalk decoder. Specifically, the PMMTalk encoder employs the off-the-shelf talking head generation architecture and speech recognition technology to extract visual and textual information from speech, respectively. Subsequently, the cross-modal alignment module aligns the audio-image-text features at temporal and semantic levels. Then PMMTalk decoder is employed to predict lip-syncing facial blendshape coefficients. Contrary to prior methods, PMMTalk only requires an additional random reference face image but yields more accurate results. Additionally, it is artist-friendly as it seamlessly integrates into standard animation production workflows by introducing facial blendshape coefficients. Finally, given the scarcity of 3D talking face datasets, we introduce a large-scale 3D Chinese Audio-Visual Facial Animation (3D-CAVFA) dataset. Extensive experiments and user studies show that our approach outperforms the state of the art. We recommend watching the supplementary video
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