14,794 research outputs found

    Weakening of the stratospheric polar vortex by Arctic sea-ice loss

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    Successive cold winters of severely low temperatures in recent years have had critical social and economic impacts on the mid-latitude continents in the Northern Hemisphere. Although these cold winters are thought to be partly driven by dramatic losses of Arctic sea-ice, the mechanism that links sea-ice loss to cold winters remains a subject of debate. Here, by conducting observational analyses and model experiments, we show how Arctic sea-ice loss and cold winters in extra-polar regions are dynamically connected through the polar stratosphere. We find that decreased sea-ice cover during early winter months (November-December), especially over the Barents-Kara seas, enhances the upward propagation of planetary-scale waves with wavenumbers of 1 and 2, subsequently weakening the stratospheric polar vortex in mid-winter (January-February). The weakened polar vortex preferentially induces a negative phase of Arctic Oscillation at the surface, resulting in low temperatures in mid-latitudes.open11167174Ysciescopu

    Knowledge Distillation for Multi-task Learning

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    Multi-task learning (MTL) is to learn one single model that performs multiple tasks for achieving good performance on all tasks and lower cost on computation. Learning such a model requires to jointly optimize losses of a set of tasks with different difficulty levels, magnitudes, and characteristics (e.g. cross-entropy, Euclidean loss), leading to the imbalance problem in multi-task learning. To address the imbalance problem, we propose a knowledge distillation based method in this work. We first learn a task-specific model for each task. We then learn the multi-task model for minimizing task-specific loss and for producing the same feature with task-specific models. As the task-specific network encodes different features, we introduce small task-specific adaptors to project multi-task features to the task-specific features. In this way, the adaptors align the task-specific feature and the multi-task feature, which enables a balanced parameter sharing across tasks. Extensive experimental results demonstrate that our method can optimize a multi-task learning model in a more balanced way and achieve better overall performance.Comment: We propose a knowledge distillation method for addressing the imbalance problem in multi-task learnin

    Magnetars and pulsars: a missing link

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    There is growing evidence that soft gamma-ray repeaters (SGRs) and anomalous X-ray pulsars (AXPs) are isolated neutron stars with superstrong magnetic fields, i.e., magnetars, marking them a distinguished species from the conventional species of spindown-powered isolated neutron stars, i.e., radio pulsars. The current arguments in favor of the magnetar interpretation of SGR/AXP phenomenology will be outlined, and the two energy sources in magnetars, i.e. a magnetic dissipation energy and a spindown energy, will be reviewed. I will then discuss a missing link between magnetars and pulsars, i.e., lack of the observational evidence of the spindown-powered behaviors in known magnetars. Some recent theoretical efforts in studying such behaviors will be reviewed along with some predictions testable in the near future.Comment: Invited talk at the Sixth Pacific Rim Conference on Stellar Astrophysics, a tribute to Helmut A. Abt, July 11-17, 2002, Xi'an. To appear in the proceedings (eds. K. S. Cheng, K. C. Leung & T. P. Li

    Deception in context: coding nonverbal cues, situational variables and risk of detection

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    There are many situations in which deception may arise and understanding the behaviors associated with it are compounded by various contexts in which it may occur. This paper sets out a coding protocol for identifying cues to deception and reports on three studies, in which deception was studied in different contexts. The contexts involved manipulating risks (i.e., probability) of being detected and reconnaissance, both of which are related to terrorist activities. Two of the studies examined the impact of changing the risks of deception detection, whilst the third investigated increased cognitive demand of duplex deception tasks including reconnaissance and deception. In all three studies, cues to deception were analyzed in relation to observable body movements and subjective impressions given by participants. In general, the results indicate a pattern of hand movement reduction by deceivers, and suggest the notion that raising the risk of detection influences deceivers? behaviors. Participants in the higher risk condition displayed increased negative affect (found in deceivers) and tension (found in both deceivers and truth-tellers) than those in lower risk conditions

    Curcumin Enhances Bortezomib Treatment of Myeloma by Inhibiting Heat Shock Protein 90 Expression

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    Purpose: To investigate whether curcumin augments bortezomib-induced apoptosis in myeloma cells (MM1.R line), and to explore the molecular mechanism with regard to heat shock protein 90 (HSP90) expression.Methods: MTT cell viability assay was used to assess growth inhibition of MM1.R cells at different concentrations of curcumin alone and also combined with 0.01 mM bortezomib. Annexin V and propidium iodide (PI) labeling were used to detect apoptosis. Caspase 3, caspase 9, NF-κB, and HSP 90 protein expression were measured by Western blotting.Results: Curcumin alone inhibited MM1.R cell growth and increased apoptosis in a concentration dependent manner. When curcumin was combined with low concentration (0.01 mM) bortezomib, both effects(viability inhibition and apoptosis induction increased (p < 0.05), whereas bortezomib alone had no effect (p > 0.05). Western blotting revealed that for curcumin and combined treatments, expression of the apoptotic markers, caspase 3 and caspase 9, increased while expression of NF-κB and HSP 90 decreased (p < 0.05). Again, low concentration bortezomib alone had no effect, whereas the combined treatment showed the largest effect, thus suggesting that the actions of curcumin and bortezomib are synergistic.Conclusion: Curcumin increased MM1.R cell sensitivity to bortezomib, which may be due to suppression of NF-κB and HSP90 activity.Keywords: Curcumin, Bortezomib, Myeloma cells, Cell growth, Apoptosis, Heat shock protein 9

    Corticosterone mediates electroacupuncture-produced anti-edema in a rat model of inflammation

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    <p>Abstract</p> <p>Background</p> <p>Electroacupuncture (EA) has been reported to produce anti-edema and anti-hyperalgesia effects on inflammatory disease. However, the mechanisms are not clear. The present study investigated the biochemical mechanisms of EA anti-inflammation in a rat model.</p> <p>Methods</p> <p>Three experiments were conducted on male Sprague-Dawley rats (n = 7–8/per group). Inflammation was induced by injecting complete Freund's adjuvant (CFA) subcutaneously into the plantar surface of one hind paw. Experiment 1 measured plasma corticosterone (CORT) levels to see if EA regulates CORT secretion. Experiment 2 studied the effects of the adrenal gland on the therapeutic actions of EA using adrenalectomy (ADX) rats. Experiment 3 determined whether a prototypical glucocorticoid receptor antagonist, RU486, affects EA anti-edema. EA treatment, 10 Hz at 3 mA and 0.1 ms pulse width, was given twice, for 20 min each, once immediately after CFA administration and again 2 h post-CFA. Plasma CORT levels, paw thickness, indicative of the intensity of inflammation, and paw withdrawal latency (PWL) were measured 2 h and 5 h after the CFA injection.</p> <p>Results</p> <p>EA significantly increased plasma corticosterone levels 2 h (5 folds) and 5 h (10 folds) after CFA administration compared to sham EA control, but EA alone in naive rats and CFA alone did not induce significant increases in corticosterone. Adrenalectomy blocked EA-produced anti-edema, but not EA anti-hyperalgesia. RU486 (15 μl, 15 μg/μl), a prototypical glucocorticoid receptor antagonist, also prevented EA anti-edema.</p> <p>Conclusion</p> <p>The data demonstrate that EA activates the adrenals to increase plasma corticosterone levels and suppress edema and suggest that EA effects differ in healthy subjects and in those with pathologies.</p

    What limits supercurrents in high temperature superconductors? A microscopic model of cuprate grain boundaries

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    The interface properties of high-temperature cuprate superconductors have been of interest for many years, and play an essential role in Josephson junctions, superconducting cables, and microwave electronics. In particular, the maximum critical current achievable in high-Tc wires and tapes is well known to be limited by the presence of grain boundaries, regions of mismatch between crystallites with misoriented crystalline axes. In studies of single, artificially fabricated grain boundaries the striking observation has been made that the critical current Jc of a grain boundary junction depends exponentially on the misorientation angle. Until now microscopic understanding of this apparently universal behavior has been lacking. We present here the results of a microscopic evaluation based on a construction of fully 3D YBCO grain boundaries by molecular dynamics. With these structures, we calculate an effective tight-binding Hamiltonian for the d-wave superconductor with a grain boundary. The critical current is then shown to follow an exponential suppression with grain boundary angle. We identify the buildup of charge inhomogeneities as the dominant mechanism for the suppression of the supercurrent.Comment: 28 pages, 12 figure

    Serum microRNA array analysis identifies miR-140-3p, miR-33b-3p and miR-671-3p as potential osteoarthritis biomarkers involved in metabolic processes.

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    Background: MicroRNAs (miRNAs) in circulation have emerged as promising biomarkers. In this study, we aimed to identify a circulating miRNA signature for osteoarthritis (OA) patients and in combination with bioinformatics analysis to evaluate the utility of selected differentially expressed miRNAs in the serum as potential OA biomarkers. Methods: Serum samples were collected from 12 primary OA patients, and 12 healthy individuals were screened using the Agilent Human miRNA Microarray platform interrogating 2549 miRNAs. Receiver Operating Characteristic (ROC) curves were constructed to evaluate the diagnostic performance of the deregulated miRNAs. Expression levels of selected miRNAs were validated by quantitative real-time PCR (qRT-PCR) in all serum and in articular cartilage samples from OA patients (n = 12) and healthy individuals (n = 7). Bioinformatics analysis was used to investigate the involved pathways and target genes for the above miRNAs. Results: We identified 279 differentially expressed miRNAs in the serum of OA patients compared to controls. Two hundred and five miRNAs (73.5%) were upregulated and 74 (26.5%) downregulated. ROC analysis revealed that 77 miRNAs had area under the curve (AUC) > 0.8 and p < 0.05. Bioinformatics analysis in the 77 miRNAs revealed that their target genes were involved in multiple signaling pathways associated with OA, among which FoxO, mTOR, Wnt, pI3K/akt, TGF-β signaling pathways, ECM-receptor interaction, and fatty acid biosynthesis. qRT-PCR validation in seven selected out of the 77 miRNAs revealed 3 significantly downregulated miRNAs (hsa-miR-33b-3p, hsa-miR-671-3p, and hsa-miR-140-3p) in the serum of OA patients, which were in silico predicted to be enriched in pathways involved in metabolic processes. Target-gene analysis of hsa-miR-140-3p, hsa-miR-33b-3p, and hsa-miR-671-3p revealed that InsR and IGFR1 were common targets of all three miRNAs, highlighting their involvement in regulation of metabolic processes that contribute to OA pathology. Hsa-miR-140-3p and hsa-miR-671-3p expression levels were consistently downregulated in articular cartilage of OA patients compared to healthy individuals. Conclusions: A serum miRNA signature was established for the first time using high density resolution miR-arrays in OA patients. We identified a three-miRNA signature, hsa-miR-140-3p, hsa-miR-671-3p, and hsa-miR-33b-3p, in the serum of OA patients, predicted to regulate metabolic processes, which could serve as a potential biomarker for the evaluation of OA risk and progression.Peer reviewedFinal Published versio

    Small Airway Dysfunction in Asthma Is Associated with Perceived Respiratory Symptoms, Non-Type 2 Airway Inflammation, and Poor Responses to Therapy.

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    BACKGROUND: Emerging evidence has indicated that small airway dysfunction (SAD) contributes to the clinical expression of asthma. OBJECTIVES: The aim of the study was to explore the relationships of SAD assessed by forced expiratory flow between 25 and 75% (FEF25-75%), with clinical and inflammatory profile and treatment responsiveness in asthma. METHOD: In study I, dyspnea intensity (Borg scale), chest tightness, wheezing and cough (visual analog scales, VASs), and pre- and post-methacholine challenge testing (MCT) were analyzed in asthma patients with SAD and non-SAD. In study II, asthma subjects with SAD and non-SAD underwent sputum induction, and inflammatory mediators in sputum were detected. Asthma patients with SAD and non-SAD receiving fixed treatments were prospectively followed up for 4 weeks in study III. Spirometry, Asthma Control Questionnaire (ACQ), and Asthma Control Test (ACT) were carried out to define treatment responsiveness. RESULTS: SAD subjects had more elevated ΔVAS for dyspnea (p = 0.027) and chest tightness (p = 0.032) after MCT. Asthma patients with SAD had significantly elevated interferon (IFN)-γ in sputum (p < 0.05), and Spearman partial correlation found FEF25-75% significantly related to IFN-γ and interleukin-8 (both having p < 0.05). Furthermore, multivariable regression analysis indicated SAD was significantly associated with worse treatment responses (decrease in ACQ ≥0.5 and increase in ACT ≥3) (p = 0.022 and p = 0.032). CONCLUSIONS: This study indicates that SAD in asthma predisposes patients to greater dyspnea intensity and chest tightness during bronchoconstriction. SAD patients with asthma are characterized by non-type 2 inflammation that may account for poor responsiveness to therapy
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