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Sökning: WFRF:(Xu Jia)

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  • 2019
  • Tidskriftsartikel (refereegranskat)
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4.
  • Klionsky, Daniel J., et al. (författare)
  • Guidelines for the use and interpretation of assays for monitoring autophagy
  • 2012
  • Ingår i: Autophagy. - : Informa UK Limited. - 1554-8635 .- 1554-8627. ; 8:4, s. 445-544
  • Forskningsöversikt (refereegranskat)abstract
    • In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field.
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8.
  • Kristan, Matej, et al. (författare)
  • The first visual object tracking segmentation VOTS2023 challenge results
  • 2023
  • Ingår i: 2023 IEEE/CVF International conference on computer vision workshops (ICCVW). - : Institute of Electrical and Electronics Engineers Inc.. - 9798350307443 - 9798350307450 ; , s. 1788-1810
  • Konferensbidrag (refereegranskat)abstract
    • The Visual Object Tracking Segmentation VOTS2023 challenge is the eleventh annual tracker benchmarking activity of the VOT initiative. This challenge is the first to merge short-term and long-term as well as single-target and multiple-target tracking with segmentation masks as the only target location specification. A new dataset was created; the ground truth has been withheld to prevent overfitting. New performance measures and evaluation protocols have been created along with a new toolkit and an evaluation server. Results of the presented 47 trackers indicate that modern tracking frameworks are well-suited to deal with convergence of short-term and long-term tracking and that multiple and single target tracking can be considered a single problem. A leaderboard, with participating trackers details, the source code, the datasets, and the evaluation kit are publicly available at the challenge website1
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9.
  • Zhou, J. M., et al. (författare)
  • Digoxin is associated with worse outcomes in patients with heart failure with reduced ejection fraction
  • 2020
  • Ingår i: Esc Heart Failure. - : Wiley. - 2055-5822. ; 7:1, s. 139-147
  • Tidskriftsartikel (refereegranskat)abstract
    • Aims The aim of this study was to investigate the impact of digoxin use on the outcomes of patients with heart failure with reduced ejection fraction (HFrEF) and its possible interaction with atrial fibrillation or use of currently guideline-recommended treatments in the real world in China. Methods and results Patients hospitalized with HFrEF from 45 hospitals participating in the China National Heart Failure Registration Study (CN-HF) were enrolled to assess the all-cause mortality, HF mortality, all-cause re-hospitalization, and HF re-hospitalization associated with digoxin use. Eight hundred eighty-two eligible HFrEF patients in the CN-HF registry were included: 372 patients with digoxin and 510 patients without digoxin. Among them, 794 (90.0%) patients were followed up for the endpoint events, with a median follow-up of 28.6 months. Kaplan-Meier survival analysis showed that the all-cause mortality (P < 0.001) and all-cause re-hospitalization (P = 0.020) were significantly higher in digoxin group than non-digoxin group, while HF mortality (P = 0.232) and HF re-hospitalization (P = 0.098) were similar between the two groups. The adjusted Cox proportional-hazards regression analysis demonstrated that digoxin use remained as an independent risk factor for increased all-cause mortality [hazard ratio (HR) 1.76; 95% confidence interval (CI) 1.27-2.44; P = 0.001] and all-cause re-hospitalization (HR 1.27; 95% CI 1.03-1.57; P = 0.029) in HFrEF patients and the predictive value of digoxin for all-cause mortality irrespective of rhythm or in combination with other guideline-recommended therapies. Conclusions Digoxin use is independently associated with increased risk of all-cause mortality and all-cause re-hospitalization in HFrEF patients.
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10.
  • Aad, G., et al. (författare)
  • 2011
  • swepub:Mat__t
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  • Aad, G, et al. (författare)
  • 2015
  • swepub:Mat__t
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  • Aad, G., et al. (författare)
  • 2010
  • swepub:Mat__t
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  • Aad, G., et al. (författare)
  • 2010
  • swepub:Mat__t
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20.
  • Luo, Yifei, et al. (författare)
  • Technology Roadmap for Flexible Sensors
  • 2023
  • Ingår i: ACS Nano. - : American Chemical Society. - 1936-0851 .- 1936-086X. ; 17:6, s. 5211-5295
  • Forskningsöversikt (refereegranskat)abstract
    • Humans rely increasingly on sensors to address grand challenges and to improve quality of life in the era of digitalization and big data. For ubiquitous sensing, flexible sensors are developed to overcome the limitations of conventional rigid counterparts. Despite rapid advancement in bench-side research over the last decade, the market adoption of flexible sensors remains limited. To ease and to expedite their deployment, here, we identify bottlenecks hindering the maturation of flexible sensors and propose promising solutions. We first analyze challenges in achieving satisfactory sensing performance for real-world applications and then summarize issues in compatible sensor-biology interfaces, followed by brief discussions on powering and connecting sensor networks. Issues en route to commercialization and for sustainable growth of the sector are also analyzed, highlighting environmental concerns and emphasizing nontechnical issues such as business, regulatory, and ethical considerations. Additionally, we look at future intelligent flexible sensors. In proposing a comprehensive roadmap, we hope to steer research efforts towards common goals and to guide coordinated development strategies from disparate communities. Through such collaborative efforts, scientific breakthroughs can be made sooner and capitalized for the betterment of humanity.
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21.
  • Xu, Qin, et al. (författare)
  • Loss of TET reprograms Wnt signaling through impaired demethylation to promote lung cancer development
  • 2022
  • Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences (PNAS). - 0027-8424 .- 1091-6490. ; 119:6
  • Tidskriftsartikel (refereegranskat)abstract
    • Oncogenic imbalance of DNA methylation is well recognized in cancer development. The ten-eleven translocation (TET) family of dioxygenases, which facilitates DNA demethylation, is frequently dysregulated in cancers. How such dysregulation contributes to tumorigenesis remains poorly understood, especially in solid tumors which present infrequent mutational incidence of TET genes. Here, we identify loss-of-function mutations of TET in 7.4% of human lung adenocarcinoma (LUAD), which frequently co-occur with oncogenic KRAS mutations, and this co-occurrence is predictive of poor survival in LUAD patients. Using an autochthonous mouse model of KrasG12D-driven LUAD, we show that individual or combinational loss of Tet genes markedly promotes tumor development. In this Kras-mutant and Tet-deficient model, the premalignant lung epithelium undergoes neoplastic reprogramming of DNA methylation and transcription, with a particular impact on Wnt signaling. Among the Wnt-associated components that undergo reprogramming, multiple canonical Wnt antagonizing genes present impaired expression arising from elevated DNA methylation, triggering aberrant activation of Wnt signaling. These impairments can be largely reversed upon the restoration of TET activity. Correspondingly, genetic depletion of beta-catenin, the transcriptional effector of Wnt signaling, substantially reverts the malignant progression of Tet-deficient LUAD. These findings reveal TET enzymes as critical epigenetic barriers against lung tumorigenesis and highlight the therapeutic vulnerability of TET-mutant lung cancer through targetingWnt signaling.
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22.
  • Xu, Zhen, et al. (författare)
  • Computational optimization of fuel supply, syngas composition, and intake conditions for a syngas/diesel RCCI engine
  • 2018
  • Ingår i: Fuel. - : Elsevier BV. - 0016-2361. ; 234, s. 120-134
  • Tidskriftsartikel (refereegranskat)abstract
    • By utilizing the promising alternative fuel of syngas, and the syngas/diesel dual-fuel reactivity controlled compression ignition (RCCI) is a potential combustion strategy for internal combustion engines. However, the optimal operating parameters for syngas/diesel RCCI engines under wide operating conditions have not been investigated. In this study, the operating parameters include fuel supply, syngas composition, and intake conditions of a syngas/diesel RCCI engine were optimized under wide load by integrating the KIVA-3V code and the non-dominated sort genetic algorithm II (NSGA-II). The results indicated that nitrogen oxides (NOx) emissions can be controlled in considerably low levels, and the efficient combustion of the premixed syngas in the squish region can be realized with high premix ratio and early pilot injection of diesel. Equivalent indicated specific fuel consumption (EISFC) and ringing intensity (RI) are the major issues for the optimization at low and mid load, respectively. The double diesel injection strategy with the relatively late main injection timing is an effective way to both improve combustion efficiency at the low load and reduce RI at the mid load. For the double diesel injection, the ratio of pilot injection is controlled in a narrow range to provide sufficient high reactivity fuel in the piston bowl and to avoid the local high-temperature combustion region simultaneously. With the restrictions of EISFC and RI, the optimal H2 fraction in the syngas is 60–80%. Based on the optimal fuel supply and intake conditions, a syngas with 75% H2 and the diluent factor C of 0.8 is capable of realizing the high efficiency, moderate combustion, and low emissions for the RCCI engine at full load range.
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23.
  • 2017
  • swepub:Mat__t
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24.
  • Aad, G., et al. (författare)
  • 2011
  • swepub:Mat__t (refereegranskat)
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25.
  • Aad, G., et al. (författare)
  • 2011
  • Tidskriftsartikel (refereegranskat)
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26.
  • Aad, G., et al. (författare)
  • 2012
  • swepub:Mat__t (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2011
  • swepub:Mat__t (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2013
  • swepub:Mat__t (refereegranskat)
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29.
  • Aad, G., et al. (författare)
  • 2013
  • Tidskriftsartikel (refereegranskat)
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30.
  • Aad, G., et al. (författare)
  • 2013
  • Ingår i: New Journal of Physics. - : IOP Publishing. - 1367-2630. ; 15
  • Tidskriftsartikel (refereegranskat)
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31.
  • Aad, G., et al. (författare)
  • 2012
  • swepub:Mat__t (refereegranskat)
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32.
  • Aad, G., et al. (författare)
  • 2012
  • swepub:Mat__t (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2012
  • swepub:Mat__t (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2012
  • swepub:Mat__t (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2012
  • swepub:Mat__t (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2012
  • swepub:Mat__t (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2012
  • swepub:Mat__t (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2012
  • swepub:Mat__t (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2012
  • swepub:Mat__t (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2015
  • Tidskriftsartikel (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2013
  • Tidskriftsartikel (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2013
  • Tidskriftsartikel (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2012
  • swepub:Mat__t (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2011
  • swepub:Mat__t (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2013
  • Tidskriftsartikel (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2011
  • swepub:Mat__t (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2011
  • swepub:Mat__t (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2011
  • swepub:Mat__t (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2012
  • swepub:Mat__t (refereegranskat)
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  • Aad, G., et al. (författare)
  • 2012
  • Tidskriftsartikel (refereegranskat)
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