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K-anonymous Signaling Scheme
[article]
2013
arXiv
pre-print
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We incorporate signaling scheme into Ad Auction setting, to achieve better welfare and revenue while protect users' privacy. We propose a new K-anonymous signaling scheme setting, prove the hardness of the corresponding welfare/revenue maximization problem, and finally propose the algorithms to approximate the optimal revenue or welfare.
arXiv:1311.6638v2
fatcat:tm5ph43tv5fmrpfap3ftxidr7e
Scrypt Is Maximally Memory-Hard
[chapter]
2017
Lecture Notes in Computer Science
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Memory-hard functions (MHFs) are hash algorithms whose evaluation cost is dominated by memory cost. As memory, unlike computation, costs about the same across different platforms, MHFs cannot be evaluated at significantly lower cost on dedicated hardware like ASICs. MHFs have found widespread applications including password hashing, key derivation, and proofs-of-work. This paper focuses on scrypt, a simple candidate MHF designed by Percival, and described in RFC 7914. It has been used within a
doi:10.1007/978-3-319-56617-7_2
fatcat:hgoqht4am5hv7gzssya5icaxta
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... umber of cryptocurrencies (e.g., Litecoin and Dogecoin) and has been an inspiration for Argon2d, one of the winners of the recent password-hashing competition. Despite its popularity, no rigorous lower bounds on its memory complexity are known. We prove that scrypt is optimally memory hard, i.e., its cumulative memory complexity (cmc) in the parallel random oracle model is Ω(n 2 w), where w and n are the output length and number of invocations of the underlying hash function, respectively. High cmc is a strong security target for MHFs introduced by Alwen and Serbinenko (STOC '15) which implies high memory cost even for adversaries who can amortise the cost over many evaluations and evaluate the underlying hash functions many times in parallel. Our proof is the first showing optimal memory hardness for any MHF. Our result improves both quantitatively and qualitatively upon the recent work by Alwen et al. (EUROCRYPT '16) who proved a weaker lower bound of Ω(n 2 w/ log 2 n) for a restricted class of adversaries.
Oblivious Parallel RAM: Improved Efficiency and Generic Constructions
[chapter]
2015
Lecture Notes in Computer Science
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Binyi Chen was partially supported by NSF grants CNS-1423566 and CNS-1514526, and a gift from the Gareatis Foundation. Huijia Lin was partially supported by NSF grants CNS-1528178 and CNS-1514526. ...
doi:10.1007/978-3-662-49099-0_8
fatcat:5xasyzvp5rhdnjwnaqgagrlj6i
Thermotunable Terahertz Negative-Index Metamaterials with Dielectric Spheres Embedded in Semiconductor Host
2018
Advances in Condensed Matter Physics
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A possibility to realize thermotunable isotropic negative-index metamaterials up to terahertz regime is theoretically investigated. The proposed composite metamaterials consist of dielectric spheres embedded randomly in a semiconductor host medium. As the variation in the intrinsic carrier density in InSb due to a variation in temperature thus changes the plasma frequency, we show theoretically the provided composite metamaterials whose index of refraction is thermally tunable and potentially
doi:10.1155/2018/2794161
fatcat:wvl6jwjohrhvrgzteaxg4dtdbm
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... ss propagation loss. Furthermore, the effects of the radius of the dielectric sphere on the modulation frequency and bandwidth are discussed. Finally, we find that the design parameters for the composites can be scaled for application in the higher frequency regions.
Mapping Deep Neural Networks on SpiNNaker2
2020
Proceedings of the Neuro-inspired Computational Elements Workshop
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SpiNNaker is an efficient many-core architecture for the real-time simulation of spiking neural networks. To also speed up deep neural networks (DNNs), the 2nd generation SpiNNaker2 will contain dedicated DNN accelerators in each processing element. When realizing large CNNs on SpiNNaker2, layers have to be split, mapped and scheduled onto 144 processing elements. We describe the underlying mapping procedure with optimized data reuse to achieve inference of VGG-16 and ResNet-50 models in tens
doi:10.1145/3381755.3381778
dblp:conf/nice/KelberWVPLSM20
fatcat:pj56lmralnaddhcxx66l4f3hjm
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... milliseconds. KEYWORDS Neural algorithms and machine learning, SpiNNaker2, deep neural networks, neuromorphic hardware
Osthole improves therapy for osteoporosis through increasing autophagy of mesenchymal stem cells
2019
Experimental animals
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Osteoporosis is a common skeletal disorder resulting in elevated fracture risk. Improvement of osteogenic differentiation is thought to be the top priority in osteoporosis treatment projects. Significant characteristics of bone marrow mesenchymal stem cells (BMMSCs), especially attractive ability to differentiate into osteoblasts, have made them alternatives for osteoporosis treatment. However, therapeutic effect with BMMSCs remains to be improved. Here, osthole, a bioactive simple coumarin
doi:10.1538/expanim.18-0178
pmid:31155553
pmcid:PMC6842796
fatcat:74clns4dtjh2ximydqtc66uahe
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... vative extracted from many medicinal plants, was introduced to pre-stimulate BMMSCs and then applied in osteoporosis therapy. The results showed that osthole-treated-BMMSCs (OBMMSCs) brought a better outcome than BMMSCs alone in estrogen deficiency-induced osteoporosis model. And elevated autophagy level was suggested to be the underlying mechanism of the ability of osthole to promote osteoblast differentiation, which is indicated by the upregulation of protein and mRNA expression level of autophagy-associated genes, Beclin1 and LC3. We concluded from these experiments that OBMMSCs are more effective than BMMSCs in osteoporosis treatment maybe through upregulation level of autophagy level induced by osthole.
BAF-Detector: An Efficient CNN-Based Detector for Photovoltaic Cell Defect Detection
[article]
2021
arXiv
pre-print
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2020 pre-print arXiv:2012.10631v1 fatcat:5ixlvmcepfdtjaxtci4l6nbwwu
Chen is with the School of Artificial Intelligence and Data Science, Hebei University of Technology, Tianjin 300130, China (e-mail: haiyong.chen@hebut.edu.cn). ...
Chen et al. [25] proposed a weakly supervised CNN model with attention mechanism to accomplish surface defect classification and segmentation in solar cell image. Du et al. ...
arXiv:2012.10631v2
fatcat:in6wxtaptzb53fyeze6wvdzdpy
Outcomes and Experiences of Child-Bearing Women with Nasopharyngeal Carcinoma
2020
Cancer Management and Research
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Nasopharyngeal carcinoma (NPC) is more common among women in Southeast Asia. An important issue is whether it is safe for them to bear children after treatment and when it is safe to do so. We conducted this study to explore the relation between fertility and prognosis in child-bearing women with NPC. Child-bearing women were defined as young women between the ages of 18 and 30. A total of 127 eligible child-bearing NPC patients were identified from December 2003 to December 2014. The patients
doi:10.2147/cmar.s265371
pmid:32943937
pmcid:PMC7481289
fatcat:5ubqvzfulnd7pchiiefrg6nyge
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... ere divided into two groups, depending on whether or not they had post-therapeutic births. The Kaplan-Meier method was used for survival analyses. The Log rank test was used to compare two survival curves and the independent significances of different prognostic factors were assessed by Cox proportional hazards regression analysis. The 5-year overall survival (OS) and disease-free survival (DFS) in the Childbirth group were significantly higher than those in the Non-Childbirth group (100% vs 88.8%, P = 0.026 and 100% vs 77.5%, P = 0.007, respectively). In the Childbirth group, no difference was found in the 5-year DFS between different birth interval times, from 1 to 5 years after treatment. The clinical stage was identified as the risk factor of OS (HR = 101.725, 95% CI: 2.160-4790.910, P = 0.019), and consequent childbirth after treatment was associated with favorable DFS (HR = 0.148, 95% CI: 0.034-0.643, P = 0.011). Post-therapeutic birth did not increase the mortality risk of child-bearing women with NPC. There was no significant correlation between the subsequent birth time window after treatment and the prognosis.
KMT2A promotes melanoma cell growth by targeting hTERT signaling pathway
2017
Cell Death and Disease
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Melanoma is an aggressive cutaneous malignancy, illuminating the exact mechanisms and finding novel therapeutic targets are urgently needed. In this study, we identified KMT2A as a potential target, which promoted the growth of human melanoma cells. KMT2A knockdown significantly inhibited cell viability and cell migration and induced apoptosis, whereas KMT2A overexpression effectively promoted cell proliferation in various melanoma cell lines. Further study showed that KMT2A regulated melanoma
doi:10.1038/cddis.2017.285
pmid:28726783
pmcid:PMC5550845
fatcat:mjfd6dzzwvhfxkota5k3lzkchm
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... ell growth by targeting the hTERT-dependent signal pathway. Knockdown of KMT2A markedly inhibited the promoter activity and expression of hTERT, and hTERT overexpression rescued the viability inhibition caused by KMT2A knockdown. Moreover, KMT2A knockdown suppressed tumorsphere formation and the expression of cancer stem cell markers, which was also reversed by hTERT overexpression. In addition, the results from a xenograft mouse model confirmed that KMT2A promoted melanoma growth via hTERT signaling. Finally, analyses of clinical samples demonstrated that the expression of KMT2A and hTERT were positively correlated in melanoma tumor tissues, and KMT2A high expression predicted poor prognosis in melanoma patients. Collectively, our results indicate that KMT2A promotes melanoma growth by activating the hTERT signaling, suggesting that the KMT2A/hTERT signaling pathway may be a potential therapeutic target for melanoma.
On the Complexity of Scrypt and Proofs of Space in the Parallel Random Oracle Model
[chapter]
2016
Lecture Notes in Computer Science
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Binyi Chen was partially supported by NSF grants CNS-1423566 and CNS-1514526, and a gift from the Gareatis Foundation. ...
doi:10.1007/978-3-662-49896-5_13
fatcat:vi4jj37t4negbmthhobqm3m4jm
Downregulation of NMI promotes tumor growth and predicts poor prognosis in human lung adenocarcinomas
2017
Molecular Cancer
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N-myc (and STAT) interactor (NMI) plays vital roles in tumor growth, progression, and metastasis. In this study, we identified NMI as a potential tumor suppressor in lung cancer and explored its molecular mechanism involved in lung cancer progression. Methods: Human lung cancer cell lines and a mouse xenograft model was used to study the effect of NMI on tumor growth. The expression of NMI, COX-2 and relevant signaling proteins were examined by Western blot. Tissue microarray
doi:10.1186/s12943-017-0705-9
pmid:29025423
pmcid:PMC5639741
fatcat:k7zusxhh5fgnhej7djdtpulple
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... analysis was performed to assess the correlation between NMI and COX-2 expression in lung cancer patients. Results: NMI was highly expressed in normal lung cells and tissues, but lowly expressed in lung cancer cells and tissues. Overexpression of NMI induced apoptosis, suppressed lung cancer cell growth and migration, which were mediated by up-regulation of the cleaved caspase-3/9 and down-regulation of phosphorylated PI3K/AKT, MMP2/MMP9, β-cadherin, and COX-2/PGE2. In contrast, knockdown of NMI promoted lung cancer cell colony formation and migration, which were correlated with the increased expression of phosphorylated PI3K/AKT, MMP2/MMP9, β-cadherin and COX-2/PGE2. Further study showed that NMI suppressed COX-2 expression through inhibition of the p50/p65 NF-κB acetylation mediated by p300. The xenograft lung cancer mouse models also confirmed the NMI-mediated suppression of tumor growth by inhibiting COX-2 signaling. Moreover, tissue microarray immunohistochemical analysis of lung adenocarcinomas also demonstrated a negative correlation between NMI and COX-2 expression. Kaplan-Meier analysis indicated that the patients with high level of NMI had a significantly better prognosis. Conclusions: Our study showed that NMI suppressed tumor growth by inhibiting PI3K/AKT, MMP2/MMP9, COX-2/PGE2 signaling pathways and p300-mediated NF-κB acetylation, and predicted a favorable prognosis in human lung adenocarcinomas, suggesting that NMI was a potential tumor suppressor in lung cancer.
FAM83D associates with high tumor recurrence after liver transplantation involving expansion of CD44+ carcinoma stem cells
2016
OncoTarget
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To investigate the potential oncogene promoting recurrence of hepatocellular carcinoma (HCC) following liver transplantation (LT), throughput RNA sequencing was performed in a subgroup of HCC patients. The up-regulated FAM83D in HCC tissues was found and further verified in 150 patients by real-time PCR and immunohistochemistry. FAM83D overexpression significantly correlated with high HCC recurrence rate following LT and poor HCC characteristics such as high AFP, poor differentiation. Of cancer
doi:10.18632/oncotarget.12715
pmid:27769048
pmcid:PMC5363599
fatcat:snjdqivnnvhxjnweolo45r6zua
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... stem cells (CSCs) markers, CD44 expression was effectively suppressed when FAM83D was knocked down by siRNA. Meanwhile, the siRNA transfected cells suppressed formation of sphere and ability of self-renew. In a xenograft tumorigenesis model, FAM83D knockdown apparently inhibited tumor growth and metastasis. Microarray assays revealed that FAM83D promotes CD44 expression via activating the MAPK, TGF-β and Hippo signaling pathways. Furthermore, CD44 knockdown presented reverse effect on above signaling pathways, which suggested that FAM83D was a key activator of loop between CD44 and above signaling pathways. In conclusion, FAM83D promotes HCC recurrence by promoting CD44 expression and CD44 + CSCs malignancy. FAM83D provides a novel therapeutic approach against HCC recurrence after LT.
MYCN‑amplified neuroblastoma cell‑derived exosomal miR‑17‑5p promotes proliferation and migration of non‑MYCN amplified cells
2021
Molecular Medicine Reports
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Neuroblastoma (NB) is considered a highly prevalent extracranial solid tumor in young children, and the upregulation of N‑myc proto‑oncogene (MYCN) is closely associated with the late stages of NB and poor prognostic outcomes. The current study was designed to evaluate the effects of exosomal microRNA (miRNA/miR)‑17‑5p from MYCN‑amplified NB cells on the proliferative and migratory potential of non‑MYCN amplified NB cells. miR‑17‑5p was found to activate the PI3K/Akt signaling cascade by
doi:10.3892/mmr.2021.11884
pmid:33537818
pmcid:PMC7893779
fatcat:3y2rcf3wv5hi3dpwczhdfeqaui
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... ng PTEN, and the overexpression of miR‑17‑5p was found to promote cellular migration and proliferation in vitro. Further experimentation revealed that the elevated expression of miR‑17‑5p in SK‑N‑BE(2) cell‑derived exosomes significantly promoted the proliferative and migratory capacities of SH‑SY5Y cells by inhibiting PTEN. Collectively, these findings demonstrated that miR‑17‑5p derived from MYCN‑amplified NB cell exosomes promoted the migration and proliferation of non‑MYCN amplified cells, highlighting an exosome‑associated malignant role for miR‑17‑5p.
MicroRNA-452 promotes stem-like cells of hepatocellular carcinoma by inhibiting Sox7 involving Wnt/β-catenin signaling pathway
2016
OncoTarget
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The decrease of microRNA-452 (miR-452) in gliomas promoted stem-like features and tumorigenesis. However, the role of miR-452, especially in regulating cancer stem cells (CSCs) in hepatocellular carcinoma (HCC) remains ambiguous. We enriched stemlike HCC cells by serial passages of hepatospheres with chemotherapeutic agents. Stem-like characteristics including the capabilities of chemo-resistance, stemnessrelated gene expression profiling, self-renewal, tumorigenicity and metastasis formation
doi:10.18632/oncotarget.8584
pmid:27058905
pmcid:PMC5053705
fatcat:dt4m6nfixza5favu7ekfp5krka
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... re detected. MiR-452 was markedly increased in the chemo-resistant hepatospheres and human HCC tissues. and the overexpression of miR-452 in HCC patients predicted poor overall survival. MiR-452 significantly promoted stem-like characteristics in vitro and in vivo. Further, Sox7 was identified as the direct target of miR-452, which could physically bind with β-catenin and TCF4 in the nucleus and then inhibit the activity of Wnt/β-catenin signaling pathway. Finally, the combined chemotherapy of doxorubicin and all-trans retinoic acid (ATRA) showed dramatically efficiency in suppressing HCC metastasis. These data suggested that miR-452 promoted stem-like traits of HCC, which might be a potential therapeutic target for HCC. The combination of doxorubicin and ATRA might be a promising therapy in HCC management.
RBFOX3 Promotes Tumor Growth and Progression via hTERT Signaling and Predicts a Poor Prognosis in Hepatocellular Carcinoma
2017
Theranostics
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Activation of the telomere maintenance mechanism is a key hallmark of cancer. Human telomerase reverse transcriptase (hTERT) is the catalytic subunit of telomerase, which is highly expressed in more than 80% of tumors, including hepatocellular carcinoma (HCC). However, the exact mechanisms by which hTERT is up-regulated in HCCs and promotes tumor growth and progression is not fully understood. The aim of this study was to discover the novel molecular targets that modulate hTERT signaling and
doi:10.7150/thno.19506
pmid:28839469
pmcid:PMC5566111
fatcat:ts4gf72lg5bqjd333hko5v4kf4
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... growth. In this study, we pulled down and identified RBFOX3 (RNA binding protein fox-1 homolog 3) as a novel hTERT promoter-binding protein in HCC cells using biotin-streptavidin-agarose pull-down and proteomics approach, and validated it as a regulatory factor for hTERT signaling and tumor growth in HCCs. Knockdown of RBFOX3 suppressed the promoter activity and expression of hTERT and consequently inhibited the growth and progression of HCC cells in vitro and in vivo. The suppression of HCC growth mediated by RBFOX3 knockdown could be rescued by hTERT overexpression. Conversely, exogenous overexpression of RBFOX3 activated the promoter activity and expression of hTERT and promoted the growth and progression of HCC cells. Moreover, we found that RBFOX3 interacted with AP-2β to regulate the expression of hTERT. Furthermore, we demonstrated that RBFOX3 expression was higher in the tumor tissues of HCC patients compared to the corresponding paracancer tissues, and was positively correlated with hTERT expression. Kaplan-Meier analysis showed that the HCC patients with high levels of RBFOX3 and hTERT had poor prognosis. Collectively, our data indicate that RBFOX3 promotes HCC growth and progression and predicts a poor prognosis by activating the hTERT signaling, and suggest that the RBFOX3/hTERT pathway may be a potential therapeutic target for HCC patients.
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