112 research outputs found

    Robust Knowledge Adaptation for Federated Unsupervised Person ReID

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    Person Re-identification (ReID) has been extensively studied in recent years due to the increasing demand in the public security sector. However, collecting and modelling with sensitive personal data raises privacy concerns. Therefore, federated learning has been studied for Person ReID, which aims to share minimal sensitive data between different parties (clients). However, the statistical heterogeneity between client domains under a federated setting remains as a challenge, which limits the process of knowledge aggregation across clients and often leads to inferior identification accuracy. Additionally, existing federated learning-based person ReID methods generally rely on laborious and time-consuming data annotations, which has the scalability issues to deploy them for real-world Person ReID. Therefore, this thesis aims to address the unsupervised person ReID problem under a federated learning scheme. Specifically, two methods are devised: 1.In Chapter 3, we introduce a federated unsupervised cluster-contrastive (FedUCC) learning method for Person ReID. FedUCC introduces a three-stage modelling strategy following a coarse-to-fine manner. In detail, generic knowledge, specialized knowledge and patch knowledge are discovered using a deep neural network. This enables mutual knowledge sharing among clients while retaining local domain-specific knowledge based on the categories of the network components and their parameter settings. 2.In Chapter 4, we propose a novel deep transformer-based architecture - context and camera invariant transformer, namely CCIT, in pursuit of homogeneous image representations by ignoring the irrelevant context and camera bias

    Simulation study of a high‐performance brain PET system with dodecahedral geometry

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    Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/145295/1/mp12996_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/145295/2/mp12996.pd

    Genetic characterization and linkage disequilibrium mapping of resistance to gray leaf spot in maize (Zea mays L.)

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    AbstractGray leaf spot (GLS), caused by Cercospora zeae-maydis, is an important foliar disease of maize (Zea mays L.) worldwide, resistance to which is controlled by multiple quantitative trait loci (QTL). To gain insights into the genetic architecture underlying the resistance to this disease, an association mapping population consisting of 161 inbred lines was evaluated for resistance to GLS in a plant pathology nursery at Shenyang in 2010 and 2011. Subsequently, a genome-wide association study, using 41,101 single-nucleotide polymorphisms (SNPs), identified 51 SNPs significantly (P<0.001) associated with GLS resistance, which could be converted into 31 QTL. In addition, three candidate genes related to plant defense were identified, including nucleotide-binding-site/leucine-rich repeat, receptor-like kinase genes similar to those involved in basal defense. Two genic SNPs, PZE-103142893 and PZE-109119001, associated with GLS resistance in chromosome bins 3.07 and 9.07, can be used for marker-assisted selection (MAS) of GLS resistance. These results provide an important resource for developing molecular markers closely linked with the target trait, enhancing breeding efficiency

    Bubble in the Whale: Identifying the Optical Counterparts and Extended Nebula for the Ultraluminous X-ray Sources in NGC 4631

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    We present a deep optical imaging campaign on the starburst galaxy NGC 4631 with CFHT/MegaCam. By supplementing the HST/ACS and Chandra/ACIS archival data, we search for the optical counterpart candidates of the five brightest X-ray sources in this galaxy, four of which are identified as ultraluminous X-ray sources (ULXs). The stellar environments of the X-ray sources are analyzed using the extinction-corrected color-magnitude diagrams and the isochrone models. We discover a highly asymmetric bubble nebula around X4 which exhibits different morphology in the Hα\alpha and [O III] images. The [O III]/Hα\alpha ratio map shows that the Hα\alpha-bright bubble may be formed mainly via the shock ionization by the one-sided jet/outflow, while the more compact [O III] structure is photoionized by the ULX. We constrain the bubble expansion velocity and interstellar medium density with the MAPPINGS V code, and hence estimate the mechanical power injected to the bubble as Pw5×1040P_w \sim 5\times10^{40} erg s1^{-1} and the corresponding bubble age of 7×105\sim7\times 10^{5} yr. Relativistic jets are needed to provide such level of mechanical power with a mass-loss rate of 107 M yr1\sim10^{-7}\ M_{\odot}\ \rm yr^{-1}. Besides the accretion, the black hole spin is likely an additional energy source for the super-Eddington jet power.Comment: 17 pages, 10 figures, accepted by Ap

    Cytoplasmic p21 is a potential predictor for cisplatin sensitivity in ovarian cancer

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    <p>Abstract</p> <p>Background</p> <p>P21<sup>(WAF1/Cip1) </sup>binds to cyclin-dependent kinase complexes and inhibits their activities. It was originally described as an inhibitor of cancer cell proliferation. However, many recent studies have shown that p21 promotes tumor progression when accumulated in the cell cytoplasm. So far, little is known about the correlation between cytoplasmic p21 and drug resistance. This study was aimed to investigate the role of p21 in the cisplatin resistance of ovarian cancer.</p> <p>Methods</p> <p>RT-PCR, western blot and immunofluorescence were used to detect p21 expression and location in cisplatin-resistant ovarian cancer cell line C13* and its parental line OV2008. Regulation of cytoplasmic p21 was performed through transfection of p21 siRNA, Akt2 shRNA and Akt2 constitutively active vector in the two cell lines; their effects on cisplatin-induced apoptosis were evaluated by flow cytometry. Tumor tissue sections of clinical samples were analyzed by immunohistochemistry.</p> <p>Results</p> <p>p21 predominantly localizes to the cytoplasm in C13* compared to OV2008. Persistent exposure to low dose cisplatin in OV2008 leads to p21 translocation from nuclear to cytoplasm, while it had not impact on p21 localization in C13*. Knockdown of cytoplasmic p21 by p21 siRNA transfection in C13* notably increased cisplatin-induced apoptosis through activation of caspase 3. Inhibition of p21 translocation into the cytoplasm by transfection of Akt2 shRNA into C13* cells significantly increased cisplatin-induced apoptosis, while induction of p21 translocation into the cytoplasm by transfection of constitutively active Akt2 in OV2008 enhanced the resistance to cisplatin. Immunohistochemical analysis of clinical ovarian tumor tissues demonstrated that cytoplasmic p21 was negatively correlated with the response to cisplatin based treatment.</p> <p>Conclusions</p> <p>Cytoplasmic p21 is a novel biomarker of cisplatin resistance and it may represent a potential therapeutic target for ovarian tumors that are refractory to conventional treatment.</p

    Effect of pH on the Interaction of Gold Nanoparticles with DNA and Application in the Detection of Human p53 Gene Mutation

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    Science and Technology Innovation Project of Fujian Province for Young Scientific Researchers, China [2006F3128]; Open Fund of State Key Laboratory for Physical Chemistry of Solid Surfaces, Xiamen University [200602]Gold nanoparticles (GNPs) are widely used to detect DNA. We studied the effect of pH on the assembly/disassembly of single-stranded DNA functionalized GNPs. Based on the different binding affinities of DNA to GNPs, we present a simple and fast way that uses HCl to drive the assembly of GNPs for detection of DNA sequences with single nucleotide differences. The assembly is reversible and can be switched by changing the solution pH. No covalent modification of DNA or GNP surface is needed. Oligonucleotide derived from human p53 gene with one-base substitution can be distinguished by a color change of the GNPs solution or a significant difference of the maximum absorption wavelength (lambda(max)), compared with wildtype sequences. This method enables detection of 10 picomole quantities of target DNA
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