145 research outputs found

    Infer and Adapt: Bipedal Locomotion Reward Learning from Demonstrations via Inverse Reinforcement Learning

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    Enabling bipedal walking robots to learn how to maneuver over highly uneven, dynamically changing terrains is challenging due to the complexity of robot dynamics and interacted environments. Recent advancements in learning from demonstrations have shown promising results for robot learning in complex environments. While imitation learning of expert policies has been well-explored, the study of learning expert reward functions is largely under-explored in legged locomotion. This paper brings state-of-the-art Inverse Reinforcement Learning (IRL) techniques to solving bipedal locomotion problems over complex terrains. We propose algorithms for learning expert reward functions, and we subsequently analyze the learned functions. Through nonlinear function approximation, we uncover meaningful insights into the expert's locomotion strategies. Furthermore, we empirically demonstrate that training a bipedal locomotion policy with the inferred reward functions enhances its walking performance on unseen terrains, highlighting the adaptability offered by reward learning

    Sustainable development in natural resources industry: is geopolitical risk a catalyst for corporate excess cash holdings?

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    With the outbreak of the Russia-Ukraine conflict, combined with the COVID-19 epidemic and the Federal Reserve’s interest rate hike, geopolitical risks have increased sharply, which has brought great pressure on the sustainable development of natural resources industry. This study aims to discuss the impact of geopolitical risk (GPR) on corporate excess cash holdings in China’s natural resources industry. The findings suggest that GRP can encourage enterprises in the natural resources industry to hold more excess cash. The findings still hold with a suite of robustness tests. The study also evidences that the above effect is more significant for state-owned enterprises, enterprises in the mining industry, and large-scale enterprises. Finally, further results show that with the increase of GPR, enterprises with strong risk-taking capacity tend to hold more excess cash, while enterprises registered in higher market-oriented regions are inclined to retain less excess cash. These findings can conduce to a deep understanding of the influence of GPR on corporate excess cash holdings and serve as a reference for policy-makers to adjust policies

    Platelet Distribution Width Levels Can Be a Predictor in the Diagnosis of Persistent Organ Failure in Acute Pancreatitis

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    Purpose. The change of serum platelet indices such as platelet distribution width (PDW) has been reported in a series of inflammatory reaction and clinical diseases. However, the relationship between PDW and the incidence of persistent organ failure (POF) in acute pancreatitis (AP) has not been elucidated so far. Materials and Methods. A total of 135 patients with AP admitted within 72 hours from symptom onset of AP at our center between December 2014 and January 2016 were included in this retrospective study. Demographic parameters on admission, organ failure assessment, laboratory data, and in-hospital mortality were compared between patients with and without POF. Multivariable logistic regression analyses were utilized to evaluate the predictive value of serum PDW for POF. Results. 30 patients were diagnosed with POF. Compared to patients without POF, patients with POF showed a significantly higher value of serum PDW on admission (14.88 ± 2.24 versus 17.60 ± 1.96%, P<0.001). After multivariable analysis, high PDW level remained a risk factor for POF (odds ratio 39.42, 95% CI: 8.64–179.77; P<0.001). A PDW value of 16.45% predicted POF with an area under the curve (AUC) of 0.870, a sensitivity with 0.867, and a specificity with 0.771, respectively. Conclusions. Our results indicate that serum PDW on admission could be a predictive factor in AP with POF and may serve as a potential prognostic factor

    FBXO38 regulates ocular melanoma proliferation through the PI3K-Akt signaling pathway

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    Objective·To investigate the effect of F-box only protein 38 (FBXO38) on the ocular melanoma proliferation and the potential regulatory pathway.Methods·Human skin cutaneous melanoma A375 and human uveal melanoma OMM2.3 cell lines with FBXO38 knockdown and overexpression were constructed by FBXO38 short hairpin RNA (shRNA) and FBXO38 overexpression plasmids respectively. Knockdown and overexpression efficiency of FBXO38 at transcription and protein levels were verified by using quantitative real-time PCR (qRT-PCR) and Western blotting. The effects of FBXO38 on melanoma cell proliferation were detected through clonal formation assay, BrdU immunofluorescence staining and CCK8 cell proliferation assay. By using The Cancer Genome Atlas (TCGA) database, differentially expressed genes were analyzed in the high and low expression groups of FBXO38. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment was performed to reveal the signaling pathways associated with FBXO38. CCK8 cell proliferation assay was used to detect the inhibition rates of the signaling pathway inhibitors on cells with different FBXO38 expression levels. qRT-PCR and Western blotting were used to detect whether the signaling pathway was activated after knocking down FBXO38.Results·qRT-PCR and Western blotting verified that mRNA and protein expression levels of FBXO38 in FBXO38 knockdown A375 and OMM2.3 cell lines decreased compared with the control group, while the expression levels of FBXO38 in the overexpression cell lines increased compared with wild type group (P<0.05). Clonal formation assay, BrdU immunofluorescence staining and CCK8 cell proliferation assay showed that FBXO38 knockdown significantly enhanced the proliferation of A375 and OMM2.3 cells (P<0.05), while overexpression of FBXO38 inhibited melanoma cell proliferation (P<0.05). Enrichment analysis showed that in skin cutaneous melanoma and uveal melanoma, FBXO38 expression influenced the phosphoinositide 3-kinase/protein kinase B (PI3K-Akt) pathway activation. Compared with those in the control group, the inhibition rates of PI3K inhibitor LY294002 and mTOR1 inhibitor Everolimus in the FBXO38 knockdown group significantly improved (P<0.05), while their inhibition rates of the overexpression group significantly decreased compared with those of control cells (P<0.05). Western blotting results showed that after knocking down FBXO38, expression levels of PTEN, P21 and P53 proteins decreased, while expression level of MDM2 protein increased. The qRT-PCR results showed a significant decrease in P53 transcription level (P<0.05) and a significant increase in MDM2 transcription level in FBXO38 knockdown cells (P<0.05).Conclusion·FBXO38 plays a role in regulating the proliferation of ocular melanoma, and this regulatory effect is related to the PI3K-Akt signaling pathway

    CogNLG: Cognitive Graph for KG-to-text Generation

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    Knowledge graph (KG) has been fully considered in natural language generation (NLG) tasks. A KG can help models generate controllable text and achieve better performance. However, most existing related approaches still lack explainability and scalability in large-scale knowledge reasoning. In this work, we propose a novel CogNLG framework for KG-to-text generation tasks. Our CogNLG is implemented based on the dual-process theory in cognitive science. It consists of two systems: one system acts as the analytic system for knowledge extraction, and another is the perceptual system for text generation by using existing knowledge. During text generation, CogNLG provides a visible and explainable reasoning path. Our framework shows excellent performance on all datasets and achieves a BLEU score of 36.7, which increases by 6.7 compared to the best competitor

    Effects of acidification on nitrification and associated nitrous oxide emission in estuarine and coastal waters

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    In the context of an increasing atmospheric carbon dioxide (CO2) level, acidification of estuarine and coastal waters is greatly exacerbated by land-derived nutrient inputs, coastal upwelling, and complex biogeochemical processes. A deeper understanding of how nitrifiers respond to intensifying acidification is thus crucial to predict the response of estuarine and coastal ecosystems and their contribution to global climate change. Here, we show that acidification can significantly decrease nitrification rate but stimulate generation of byproduct nitrous oxide (N2O) in estuarine and coastal waters. By varying CO2 concentration and pH independently, an expected beneficial effect of elevated CO2 on activity of nitrifiers (“CO2-fertilization” effect) is excluded under acidification. Metatranscriptome data further demonstrate that nitrifiers could significantly up-regulate gene expressions associated with intracellular pH homeostasis to cope with acidification stress. This study highlights the molecular underpinnings of acidification effects on nitrification and associated greenhouse gas N2O emission, and helps predict the response and evolution of estuarine and coastal ecosystems under climate change and human activities.publishedVersio

    The Effect of the Antimicrobial Peptide Plectasin on the Growth Performance, Intestinal Health, and Immune Function of Yellow-Feathered Chickens

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    The goal of the study was to test the effects of an antibiotic substitute, plectasin, on the growth performance, immune function, intestinal morphology and structure, intestinal microflora, ileal mucosal layer construction and tight junctions, ileal immune-related cytokines, and blood biochemical indices of yellow-feathered chickens. A total of 1,500 one-day-old yellow-feathered chicks were randomly divided into four dietary treatment groups with five replicates in each group and 75 yellow-feathered chicks in each replication, as follows: basal diet (group A); basal diet supplemented with 10 mg enramycin/kg of diet (group B), basal diet supplemented with 100 mg plectasin/kg of diet (group C), and basal diet supplemented with 200 mg plectasin/kg of diet (group D). It was found that the dietary antimicrobial peptide plectasin could improve the ADG and had better F/G for the overall period of 1–63 days. Dietary plectasin can enhance H9N2 avian influenza virus (AIV) and Newcastle disease virus (NDV) antibody levels of yellow-feathered chickens at 21, and 35 days of age. Dietary plectasin can enhance the intestine structure, inhibit Escherichia coli and proinflammatory cytokines in the ileum, and ameliorate the blood biochemical indices of yellow-feathered chickens at 21 days of age. This study indicates that the antimicrobial peptide plectasin has beneficial effects on the growth performance, intestinal health and immune function of yellow-feathered chickens

    The cardiomyocyte disrupts pyrimidine biosynthesis in non-myocytes to regulate heart repair

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    Various populations of cells are recruited to the heart after cardiac injury, but little is known about whether cardiomyocytes directly regulate heart repair. Using a murine model of ischemic cardiac injury, we demonstrate that cardiomyocytes play a pivotal role in heart repair by regulating nucleotide metabolism and fates of nonmyocytes. Cardiac injury induced the expression of the ectonucleotidase ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1), which hydrolyzes extracellular ATP to form AMP. In response to AMP, cardiomyocytes released adenine and specific ribonucleosides that disrupted pyrimidine biosynthesis at the orotidine monophosphate (OMP) synthesis step and induced genotoxic stress and p53-mediated cell death of cycling nonmyocytes. As nonmyocytes are critical for heart repair, we showed that rescue of pyrimidine biosynthesis by administration of uridine or by genetic targeting of the ENPP1/AMP pathway enhanced repair after cardiac injury. We identified ENPP1 inhibitors using small molecule screening and showed that systemic administration of an ENPP1 inhibitor after heart injury rescued pyrimidine biosynthesis in nonmyocyte cells and augmented cardiac repair and postinfarct heart function. These observations demonstrate that the cardiac muscle cell regulates pyrimidine metabolism in nonmuscle cells by releasing adenine and specific nucleosides after heart injury and provide insight into how intercellular regulation of pyrimidine biosynthesis can be targeted and monitored for augmenting tissue repair
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