| 1. |
- Kanduri, A., et al.
(författare)
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A perspective on dark silicon
- 2017
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Ingår i: The Dark Side of Silicon. - Cham : Springer. - 9783319315966 - 9783319315942 ; , s. 3-20
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Bokkapitel (refereegranskat)abstract
- The possibilities to increase single-core performance have ended due to limited instruction-level parallelism and a high penalty when increasing frequency. This prompted designers to move toward multi-core paradigms [1], largely supported by transistor scaling [2]. Scaling down transistor gate length makes it possible to switch them faster at a lower power, as they have a low capacitance. In this context, an important consideration is power density-the power dissipated per unit area. Dennard’s scaling establishes that reducing physical parameters of transistors allows operating them at lower voltage and thus at lower power, because power consumption is proportional to the square of the applied voltage, keeping power density constant [3]. Dennard’s estimation of scaling effects and constant power density is shown in Table 1.1. Theoretically, scaling down further should result in more computational capacity per unit area. However, scaling is reaching its physical limits to an extent that voltage cannot be scaled down as much as transistor gate length leading to failure of Dennardian trend. This along with a rise in leakage current results in increased power density, rather than a constant power density. Higher power density implies more heat generated in a unit area and hence higher chip temperatures which have to be dissipated through cooling solutions, as increase in temperature beyond a certain level results in unreliable functionality, faster aging, and even permanent failure of the chip. To ensure a safe operation, it is essential for the chip to perform within a fixed power budget [4]. In order to avoid too high power dissipation, a certain part of the chip needs to remain inactive; the inactive part is termed dark silicon [5]. Hence, we have to operate working cores in a multi-core system at less than their full capacity, limiting the performance, resource utilization, and efficiency of the system.
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| 2. |
- Kanduri, A., et al.
(författare)
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Dark silicon patterning : Efficient power utilization through run-time mapping
- 2017
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Ingår i: The Dark Side of Silicon. - Cham : Springer. - 9783319315966 - 9783319315942 ; , s. 237-258
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Bokkapitel (refereegranskat)abstract
- An efficient run-time application mapping approach can considerably enhance resource utilization and mitigate the dark silicon phenomenon. In this chapter, we present a dark silicon aware run-time application mapping approach that patterns active cores alongside the inactive cores in order to evenly distribute power density across the chip. This approach leverages dark silicon to balance the temperature of active cores to provide higher power budget and better resource utilization, within a safe peak operating temperature. In contrast to exhaustive search based mapping techniques, the proposed agile heuristic approach has a negligible run-time overhead. This patterning strategy yields a surplus power budget of up to 17?% along with an improved throughput of up to 21?% in comparison with other state-of-the-art run-time mapping strategies, while the surplus budget is as high as 40?% compared to worst case scenarios.
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| 3. |
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| 4. |
- Haghbayan, M. -H, et al.
(författare)
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MapPro : Proactive runtime mapping for dynamic workloads by quantifying ripple effect of applications on networks-on-chip
- 2015
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Ingår i: Proceedings - 2015 9th IEEE/ACM International Symposium on Networks-on-Chip, NOCS 2015. - New York, NY, USA : Association for Computing Machinery (ACM). - 9781450333962
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Konferensbidrag (refereegranskat)abstract
- Increasing dynamic workloads running on NoC-based many-core systems necessitates efficient runtime mapping strategies. With an unpredictable nature of application profiles, selecting a rational region to map an incoming application is an NP-hard problem in view of minimizing congestion and maximizing performance. In this paper, we propose a proactive region selection strategy which prioritizes nodes that offer lower congestion and dispersion. Our proposed strategy, MapPro, quantitatively represents the propagated impact of spatial availability and dispersion on the network with every new mapped application. This allows us to identify a suitable region to accommodate an incoming application that results in minimal congestion and dispersion. We cluster the network into squares of different radii to suit applications of different sizes and proactively select a suitable square for a new application, eliminating the overhead caused with typical reactive mapping approaches. We evaluated our proposed strategy over different traffic patterns and observed gains of up to 41% in energy efficiency, 28% in congestion and 21% dispersion when compared to the state-of-the-art region selection methods. Copyright 2015 ACM.
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| 5. |
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| 6. |
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| 7. |
- Mondal, B, et al.
(författare)
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Integrative functional genomic analysis identifies epigenetically regulated fibromodulin as an essential gene for glioma cell migration.
- 2017
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Ingår i: Oncogene. - : Springer Science and Business Media LLC. - 0950-9232 .- 1476-5594. ; 36, s. 71-83
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Tidskriftsartikel (refereegranskat)abstract
- An integrative functional genomics study of multiple forms of data are vital for discovering molecular drivers of cancer development and progression. Here, we present an integrated genomic strategy utilizing DNA methylation and transcriptome profile data to discover epigenetically regulated genes implicated in cancer development and invasive progression. More specifically, this analysis identified fibromodulin (FMOD) as a glioblastoma (GBM) upregulated gene because of the loss of promoter methylation. Secreted FMOD promotes glioma cell migration through its ability to induce filamentous actin stress fiber formation. Treatment with cytochalasin D, an actin polymerization inhibitor, significantly reduced the FMOD-induced glioma cell migration. Small interfering RNA and small molecule inhibitor-based studies identified that FMOD-induced glioma cell migration is dependent on integrin-FAK-Src-Rho-ROCK signaling pathway. FMOD lacking C-terminus LRR11 domain (ΔFMOD), which does not bind collagen type I, failed to induce integrin and promote glioma cell migration. Further, FMOD-induced integrin activation and migration was abrogated by a 9-mer wild-type peptide from the FMOD C-terminus. However, the same peptide with mutation in two residues essential for FMOD interaction with collagen type I failed to compete with FMOD, thus signifying the importance of collagen type I-FMOD interaction in integrin activation. Chromatin immunoprecipitation-PCR experiments revealed that transforming growth factor beta-1 (TGF-β1) regulates FMOD expression through epigenetic remodeling of FMOD promoter that involved demethylation and gain of active histone marks with a simultaneous loss of DNMT3A and EZH2 occupancy, but enrichment of Sma- and Mad-related protein-2 (SMAD2) and CBP. FMOD silencing inhibited the TGF-β1-mediated glioma cell migration significantly. In univariate and multivariate Cox regression analysis, both FMOD promoter methylation and transcript levels predicted prognosis in GBM. Thus, this study identified several epigenetically regulated alterations responsible for cancer development and progression. Specifically, we found that secreted FMOD as an important regulator of glioma cell migration downstream of TGF-β1 pathway and forms a potential basis for therapeutic intervention in GBM.
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| 8. |
- Zhou, A. X., et al.
(författare)
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The long noncoding RNA TUNAR modulates Wnt signaling and regulates human β-cell proliferation
- 2021
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Ingår i: American journal of physiology. Endocrinology and metabolism. - : American Physiological Society. - 1522-1555 .- 0193-1849. ; 320:4
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Tidskriftsartikel (refereegranskat)abstract
- Many long noncoding RNAs (lncRNAs) are enriched in pancreatic islets and several lncRNAs are linked to type 2 diabetes (T2D). Although they have emerged as potential players in β-cell biology and T2D, little is known about their functions and mechanisms in human β-cells. We identified an islet-enriched lncRNA, TUNAR (TCL1 upstream neural differentiation-associated RNA), which was upregulated in β-cells of patients with T2D and promoted human β-cell proliferation via fine-tuning of the Wnt pathway. TUNAR was upregulated following Wnt agonism by a glycogen synthase kinase-3 (GSK3) inhibitor in human β-cells. Reciprocally, TUNAR repressed a Wnt antagonist Dickkopf-related protein 3 (DKK3) and stimulated Wnt pathway signaling. DKK3 was aberrantly expressed in β-cells of patients with T2D and displayed a synchronized regulatory pattern with TUNAR at the single cell level. Mechanistically, DKK3 expression was suppressed by the repressive histone modifier enhancer of zeste homolog 2 (EZH2). TUNAR interacted with EZH2 in β-cells and facilitated EZH2-mediated suppression of DKK3. These findings reveal a novel cell-specific epigenetic mechanism via islet-enriched lncRNA that fine-tunes the Wnt pathway and subsequently human β-cell proliferation.NEW & NOTEWORTHY The discovery that long noncoding RNA TUNAR regulates β-cell proliferation may be important in designing new treatments for diabetes.
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| 9. |
- Kanduri, A., et al.
(författare)
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Predictable Application Mapping for Manycore Real-Time and Cyber-Physical Systems
- 2015
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Ingår i: Proceedings - IEEE 9th International Symposium on Embedded Multicore/Manycore SoCs, MCSoC 2015. - 9781479986699 ; , s. 135-142
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Konferensbidrag (refereegranskat)abstract
- Cyber Physical Systems (CPS) are typically implemented on multicore platforms to handle computational pressure and performance requirements. Complex data flows in those applications cause contention among networked processors, resulting in unpredictable performance. In this work, we explore the impact of application mapping on network contention and predictability. A mapping algorithm focusing on minimizing the number of shared paths while not worsening the total path count is proposed. This algorithm is verified against other recent works over synthetic and realistic traffic patterns. The proposed algorithm considerably improved predictability with 0% shared paths and reasonable latency constraints compared to the other recently proposed algorithms.
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| 10. |
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| 11. |
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| 12. |
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| 13. |
- Mattick, J. S., et al.
(författare)
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Long non-coding RNAs: definitions, functions, challenges and recommendations
- 2023
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Ingår i: Nature Reviews Molecular Cell Biology. - : Springer Science and Business Media LLC. - 1471-0072 .- 1471-0080. ; 24:6, s. 430-447
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Tidskriftsartikel (refereegranskat)abstract
- Genes specifying long non-coding RNAs (lncRNAs) occupy a large fraction of the genomes of complex organisms. The term 'lncRNAs' encompasses RNA polymerase I (Pol I), Pol II and Pol III transcribed RNAs, and RNAs from processed introns. The various functions of lncRNAs and their many isoforms and interleaved relationships with other genes make lncRNA classification and annotation difficult. Most lncRNAs evolve more rapidly than protein-coding sequences, are cell type specific and regulate many aspects of cell differentiation and development and other physiological processes. Many lncRNAs associate with chromatin-modifying complexes, are transcribed from enhancers and nucleate phase separation of nuclear condensates and domains, indicating an intimate link between lncRNA expression and the spatial control of gene expression during development. lncRNAs also have important roles in the cytoplasm and beyond, including in the regulation of translation, metabolism and signalling. lncRNAs often have a modular structure and are rich in repeats, which are increasingly being shown to be relevant to their function. In this Consensus Statement, we address the definition and nomenclature of lncRNAs and their conservation, expression, phenotypic visibility, structure and functions. We also discuss research challenges and provide recommendations to advance the understanding of the roles of lncRNAs in development, cell biology and disease.
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| 14. |
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| 15. |
- Wiel, Clotilde, 1987, et al.
(författare)
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BACH1 Stabilization by Antioxidants Stimulates Lung Cancer Metastasis
- 2019
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Ingår i: Cell. - : Elsevier BV. - 0092-8674 .- 1097-4172. ; 178:2, s. 330-345
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Tidskriftsartikel (refereegranskat)abstract
- For tumors to progress efficiently, cancer cells must overcome barriers of oxidative stress. Although dietary antioxidant supplementation or activation of endogenous antioxidants by NRF2 reduces oxidative stress and promotes early lung tumor progression, little is known about its effect on lung cancer metastasis. Here, we show that long-term supplementation with the antioxidants N-acetylcysteine and vitamin E promotes KRAS-driven lung cancer metastasis. The antioxidants stimulate metastasis by reducing levels of free heme and stabilizing the transcription factor BACH1. BACH1 activates transcription of Hexokinase 2 and Gapdh and increases glucose uptake, glycolysis rates, and lactate secretion, thereby stimulating glycolysis-dependent metastasis of mouse and human lung cancer cells. Targeting BACH1 normalized glycolysis and prevented antioxidant-induced metastasis, while increasing endogenous BACH1 expression stimulated glycolysis and promoted metastasis, also in the absence of antioxidants. We conclude that BACH1 stimulates glycolysis-dependent lung cancer metastasis and that BACH1 is activated under conditions of reduced oxidative stress.
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