| 1. |
- Chen, Ling, et al.
(författare)
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Reliable and efficient RAR-based distributed model training in computing power network
- 2024
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Ingår i: Journal of Optical Communications and Networking. - 1943-0620 .- 1943-0639. ; 16:5, s. 527-540
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Tidskriftsartikel (refereegranskat)abstract
- The computing power network (CPN) is a novel network technology that integrates computing power from the cloud, edge, and terminals using IP/optical cross-layer networks for distributed computing. CPNs can provide an effective solution for distributed model training (DMT). As a bandwidth optimization architecture based on data parallelism, ring all-reduce (RAR) is widely used in DMT. However, any node or link failure on the ring can interrupt or block the requests deployed on the ring. Meanwhile, due to the resource competition of batch RAR-based DMT requests, inappropriate scheduling strategies will also lead to low training efficiency or congestion. As far as we know, there is currently no research that considers the survivability of rings in scheduling strategies for RAR-based DMT. To fill this gap, we propose a scheduling scheme for RAR-based DMT requests in CPNs to optimize the allocation of computing and wavelength resources considering the time dimension while ensuring reliability. In practical scenarios, service providers may focus on different performance metrics. We formulate an integer linear programming (ILP) model and a RAR-based DMT deployment algorithm (RDDA) to solve this problem considering four optimization objectives under the premise of the minimum blocking rate: minimum computing resource consumption, minimum wavelength resource consumption, minimum training time, and maximum reliability. Simulation results demonstrate that our model satisfies the reliability requirements while achieving corresponding optimal performance for DMT requests under four optimization objectives.
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| 2. |
- Arosio, Paolo, et al.
(författare)
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Microfluidic Diffusion Analysis of the Sizes and Interactions of Proteins under Native Solution Conditions.
- 2016
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Ingår i: ACS Nano. - : American Chemical Society (ACS). - 1936-086X .- 1936-0851. ; 10:1, s. 333-341
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Tidskriftsartikel (refereegranskat)abstract
- Characterizing the sizes and interactions of macromolecules under native conditions is a challenging problem in many areas of molecular sciences, which fundamentally arises from the polydisperse nature of biomolecular mixtures. Here, we describe a microfluidic platform for diffusional sizing based on monitoring micron-scale mass transport simultaneously in space and time. We show that the global analysis of such combined space-time data enables the hydrodynamic radii of individual species within mixtures to be determined directly by deconvoluting average signals into the contributions from the individual species. We demonstrate that the ability to perform rapid noninvasive sizing allows this method to be used to characterize interactions between biomolecules under native conditions. We illustrate the potential of the technique by implementing a single-step quantitative immunoassay that operates on a time scale of seconds and detects specific interactions between biomolecules within complex mixtures.
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| 3. |
- Liu, Yuzhong, et al.
(författare)
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Weaving of organic threads into a crystalline covalent organic framework
- 2016
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Ingår i: Science. - : American Association for the Advancement of Science (AAAS). - 0036-8075 .- 1095-9203. ; 351:6271, s. 365-369
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Tidskriftsartikel (refereegranskat)abstract
- A three-dimensional covalent organic framework (COF-505) constructed from helical organic threads, designed to be mutually weaving at regular intervals, has been synthesized by imine condensation reactions of aldehyde functionalized copper(I)-bisphenanthroline tetrafluoroborate, Cu(PDB)2(BF4), and benzidine (BZ). The copper centers are topologically independent of the weaving within the COF structure and serve as templates for bringing the threads into a woven pattern rather than the more commonly observed parallel arrangement. The copper(I) ions can be reversibly removed and added without loss of the COF structure, for which a tenfold increase in elasticity accompanies its demetalation. The threads in COF-505 have many degrees of freedom for enormous deviations to take place between them, throughout the material, without undoing the weaving of the overall structure.
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| 4. |
- Saar, Kadi L., et al.
(författare)
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On-chip label-free protein analysis with downstream electrodes for direct removal of electrolysis products
- 2017
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Ingår i: Lab on a Chip. - : Royal Society of Chemistry (RSC). - 1473-0197 .- 1473-0189. ; 18:1, s. 162-170
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Tidskriftsartikel (refereegranskat)abstract
- The ability to apply highly controlled electric fields within microfluidic devices is valuable as a basis for preparative and analytical processes. A challenge encountered in the context of such approaches in conductive media, including aqueous buffers, is the generation of electrolysis products at the electrode/liquid interface which can lead to contamination, perturb fluid flows and generally interfere with the measurement process. Here, we address this challenge by designing a single layer microfluidic device architecture where the electric potential is applied outside and downstream of the microfluidic device while the field is propagated back to the chip via the use of a co-flowing highly conductive electrolyte solution that forms a stable interface at the separation region of the device. The co-flowing electrolyte ensures that all the generated electrolysis products, including Joule heat and gaseous products, are flowed away from the chip without coming into contact with the analytes while the single layer fabrication process where all the structures are defined lithographically allows producing the devices in a simple yet highly reproducible manner. We demonstrate that by allowing stable and effective application of electric fields in excess of 100 V cm-1, the described platform provides the basis for rapid separation of heterogeneous mixtures of proteins and protein complexes directly in their native buffers as well as for the simultaneous quantification of their charge states. We illustrate this by probing the interactions in a mixture of an amyloid forming protein, amyloid-β, and a molecular chaperone, Brichos, known to inhibit the process of amyloid formation. The availability of a platform for applying stable electric fields and its compatibility with single-layer soft-lithography processes opens up the possibility of separating and analysing a wide range of molecules on chip, including those with similar electrophoretic mobilities.
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| 5. |
- Xie, Bushan, et al.
(författare)
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High-throughput screening identified mitoxantrone to induce death of hepatocellular carcinoma cells with autophagy involvement
- 2020
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Ingår i: Biochemical and Biophysical Research Communications - BBRC. - : ACADEMIC PRESS INC ELSEVIER SCIENCE. - 0006-291X .- 1090-2104. ; 521:1, s. 232-237
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Tidskriftsartikel (refereegranskat)abstract
- The use of highly efficient high-throughput screening (HTS) platform has recently gained more attention as a plausible approach to identify de novo therapeutic application potential of conventional anti-tumor drugs for cancer treatments. In this study, we used hepatocellular carcinoma (HCC) cells as models to identify cytotoxic compounds by HTS. To identify cytotoxic compounds for potential HCC treatments, 3271 compounds from three well established small molecule libraries were screened against HCC cell lines. Thirty-two small molecules were identified from the primary screen to induce cell death. Particularly, mitoxantrone (MTX), which is an established antineoplastic drug, significantly and specifically inhibited the growth and proliferation of HCC cells in vitro. Mechanistic studies of LC3-II, p62 and phosphorylation of p70S6K in HepG2 cells revealed that MTX treatment induced mTOR-dependent autophagy activation, which was further confirmed by the autophagic flux assay using lysosomal inhibitor chloroquine (CQ). In the combined treatment of MTX and CQ where autophagy was inhibited by CQ the elevations of cleaved Caspase-3 and PARP were observed, indicating the enhanced apoptosis in HepG2 cells. Taken together, we hypothesize that MTX-induced autophagy plays an pro-survival role in HCC treatment. Combined treatment with autophagy inhibitor may combat the chemo-resistance of HCC to MTX treatment and therefore deserves future clinical investment.
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| 6. |
- Yang, Chen, et al.
(författare)
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Nuclear IGF1R interact with PCNA to preserve DNA replication after DNA-damage in a variety of human cancers
- 2020
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Ingår i: PLOS ONE. - : Public Library Science. - 1932-6203. ; 15:7
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Tidskriftsartikel (refereegranskat)abstract
- Nuclear IGF1R has been linked to poor outcome in cancer. We recently showed that nuclear IGF1R phosphorylates PCNA and increases DNA damage tolerance. In this paper we aimed to describe this mechanism in cancer tissue as well as in cancer cell lines. In situ proximity ligation assay identified frequent IGF1R and PCNA colocalization in many cancer types. IGF1R/PCNA colocalization was more frequently increased in tumor cells than in adjacent normal, and more prominent in areas with dysplasia and invasion. However, the interaction was often lost in tumors with poor response to neoadjuvant treatment and most metastatic lesions. In two independent cohorts of serous ovarian carcinomas and oropharyngeal squamous cell carcinomas, stronger IGF1R/PCNA colocalization was significantly associated with a higher overall survival. Ex vivo irradiation of ovarian cancer tissue acutely induced IGF1R/PCNA colocalization together with ?H2AX-foci formations. In vitro, RAD18 mediated mono-ubiquitination of PCNA during replication stress was dependent on IGF1R kinase activity. DNA fiber analysis revealed that IGF1R activation could rescue stalled DNA replication forks, but only in cancer cells with baseline IGF1R/PCNA interaction. We believe that the IGF1R/PCNA interaction is a basic cellular mechanism to increase DNA stress tolerance during proliferation, but that this mechanism is lost with tumor progression in conjunction with accumulated DNA damage and aberrant strategies to tolerate genomic instability. To exploit this mechanism in IGF1R targeted therapy, IGF1R inhibitors should be explored in the context of concomitant induction of DNA replication stress as well as in earlier clinical stages than previously tried.
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