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Sökning: WFRF:(Park Hyun) > Uppsala universitet

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1.
  • Park, Sung-Joon, et al. (författare)
  • Autonomous Interfacial Assembly of Polymer Nanofilms via Surfactant-Regulated Marangoni Instability
  • 2023
  • Ingår i: Nano Letters. - : American Chemical Society (ACS). - 1530-6984 .- 1530-6992. ; 23:11, s. 4822-4829
  • Tidskriftsartikel (refereegranskat)abstract
    • Interfacialpolymerization (IP) provides a versatile platform forfabricating defect-free functional nanofilms for various applications,including molecular separation, energy, electronics, and biomedicalmaterials. Unfortunately, coupled with complex natural instabilityphenomena, the IP mechanism and key parameters underlying the structuralevolution of nanofilms, especially in the presence of surfactantsas an interface regulator, remain puzzling. Here, we interfaciallyassembled polymer nanofilm membranes at the free water-oilinterface in the presence of differently charged surfactants and comprehensivelycharacterized their structure and properties. Combined with computationalsimulations, an in situ visualization of interfacial film formationdiscovered the critical role of Marangoni instability induced by thesurfactants via various mechanisms in structurally regulating thenanofilms. Despite their different instability-triggering mechanisms,the delicate control of the surfactants enabled the fabrication ofdefect-free, ultra-permselective nanofilm membranes. Our study identifiescritical IP parameters that allow us to rationally design nanofilms,coatings, and membranes for target applications.
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2.
  • Sampson, Joshua N., et al. (författare)
  • Analysis of Heritability and Shared Heritability Based on Genome-Wide Association Studies for 13 Cancer Types
  • 2015
  • Ingår i: Journal of the National Cancer Institute. - : Oxford University Press (OUP). - 0027-8874 .- 1460-2105. ; 107:12
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Studies of related individuals have consistently demonstrated notable familial aggregation of cancer. We aim to estimate the heritability and genetic correlation attributable to the additive effects of common single-nucleotide polymorphisms (SNPs) for cancer at 13 anatomical sites. Methods: Between 2007 and 2014, the US National Cancer Institute has generated data from genome-wide association studies (GWAS) for 49 492 cancer case patients and 34 131 control patients. We apply novel mixed model methodology (GCTA) to this GWAS data to estimate the heritability of individual cancers, as well as the proportion of heritability attributable to cigarette smoking in smoking-related cancers, and the genetic correlation between pairs of cancers. Results: GWAS heritability was statistically significant at nearly all sites, with the estimates of array-based heritability, h(l)(2), on the liability threshold (LT) scale ranging from 0.05 to 0.38. Estimating the combined heritability of multiple smoking characteristics, we calculate that at least 24% (95% confidence interval [CI] = 14% to 37%) and 7% (95% CI = 4% to 11%) of the heritability for lung and bladder cancer, respectively, can be attributed to genetic determinants of smoking. Most pairs of cancers studied did not show evidence of strong genetic correlation. We found only four pairs of cancers with marginally statistically significant correlations, specifically kidney and testes (rho = 0.73, SE = 0.28), diffuse large B-cell lymphoma (DLBCL) and pediatric osteosarcoma (rho = 0.53, SE = 0.21), DLBCL and chronic lymphocytic leukemia (CLL) (rho = 0.51, SE = 0.18), and bladder and lung (rho = 0.35, SE = 0.14). Correlation analysis also indicates that the genetic architecture of lung cancer differs between a smoking population of European ancestry and a nonsmoking Asian population, allowing for the possibility that the genetic etiology for the same disease can vary by population and environmental exposures. Conclusion: Our results provide important insights into the genetic architecture of cancers and suggest new avenues for investigation.
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3.
  • Wang, Haidong, et al. (författare)
  • Estimates of global, regional, and national incidence, prevalence, and mortality of HIV, 1980-2015 : the Global Burden of Disease Study 2015.
  • 2016
  • Ingår i: The lancet. HIV. - : Elsevier. - 2352-3018. ; 3:8, s. e361-e387
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Timely assessment of the burden of HIV/AIDS is essential for policy setting and programme evaluation. In this report from the Global Burden of Disease Study 2015 (GBD 2015), we provide national estimates of levels and trends of HIV/AIDS incidence, prevalence, coverage of antiretroviral therapy (ART), and mortality for 195 countries and territories from 1980 to 2015.METHODS: For countries without high-quality vital registration data, we estimated prevalence and incidence with data from antenatal care clinics and population-based seroprevalence surveys, and with assumptions by age and sex on initial CD4 distribution at infection, CD4 progression rates (probability of progression from higher to lower CD4 cell-count category), on and off antiretroviral therapy (ART) mortality, and mortality from all other causes. Our estimation strategy links the GBD 2015 assessment of all-cause mortality and estimation of incidence and prevalence so that for each draw from the uncertainty distribution all assumptions used in each step are internally consistent. We estimated incidence, prevalence, and death with GBD versions of the Estimation and Projection Package (EPP) and Spectrum software originally developed by the Joint United Nations Programme on HIV/AIDS (UNAIDS). We used an open-source version of EPP and recoded Spectrum for speed, and used updated assumptions from systematic reviews of the literature and GBD demographic data. For countries with high-quality vital registration data, we developed the cohort incidence bias adjustment model to estimate HIV incidence and prevalence largely from the number of deaths caused by HIV recorded in cause-of-death statistics. We corrected these statistics for garbage coding and HIV misclassification.FINDINGS: Global HIV incidence reached its peak in 1997, at 3·3 million new infections (95% uncertainty interval [UI] 3·1-3·4 million). Annual incidence has stayed relatively constant at about 2·6 million per year (range 2·5-2·8 million) since 2005, after a period of fast decline between 1997 and 2005. The number of people living with HIV/AIDS has been steadily increasing and reached 38·8 million (95% UI 37·6-40·4 million) in 2015. At the same time, HIV/AIDS mortality has been declining at a steady pace, from a peak of 1·8 million deaths (95% UI 1·7-1·9 million) in 2005, to 1·2 million deaths (1·1-1·3 million) in 2015. We recorded substantial heterogeneity in the levels and trends of HIV/AIDS across countries. Although many countries have experienced decreases in HIV/AIDS mortality and in annual new infections, other countries have had slowdowns or increases in rates of change in annual new infections.INTERPRETATION: Scale-up of ART and prevention of mother-to-child transmission has been one of the great successes of global health in the past two decades. However, in the past decade, progress in reducing new infections has been slow, development assistance for health devoted to HIV has stagnated, and resources for health in low-income countries have grown slowly. Achievement of the new ambitious goals for HIV enshrined in Sustainable Development Goal 3 and the 90-90-90 UNAIDS targets will be challenging, and will need continued efforts from governments and international agencies in the next 15 years to end AIDS by 2030.
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4.
  • Flannick, Jason, et al. (författare)
  • Data Descriptor : Sequence data and association statistics from 12,940 type 2 diabetes cases and controls
  • 2017
  • Ingår i: Scientific Data. - : Springer Science and Business Media LLC. - 2052-4463. ; 4
  • Tidskriftsartikel (refereegranskat)abstract
    • To investigate the genetic basis of type 2 diabetes (T2D) to high resolution, the GoT2D and T2D-GENES consortia catalogued variation from whole-genome sequencing of 2,657 European individuals and exome sequencing of 12,940 individuals of multiple ancestries. Over 27M SNPs, indels, and structural variants were identified, including 99% of low-frequency (minor allele frequency [MAF] 0.1-5%) non-coding variants in the whole-genome sequenced individuals and 99.7% of low-frequency coding variants in the whole-exome sequenced individuals. Each variant was tested for association with T2D in the sequenced individuals, and, to increase power, most were tested in larger numbers of individuals (> 80% of low-frequency coding variants in similar to ~82 K Europeans via the exome chip, and similar to ~90% of low-frequency non-coding variants in similar to ~44 K Europeans via genotype imputation). The variants, genotypes, and association statistics from these analyses provide the largest reference to date of human genetic information relevant to T2D, for use in activities such as T2D-focused genotype imputation, functional characterization of variants or genes, and other novel analyses to detect associations between sequence variation and T2D.
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5.
  • Fuchsberger, Christian, et al. (författare)
  • The genetic architecture of type 2 diabetes
  • 2016
  • Ingår i: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 536:7614, s. 41-47
  • Tidskriftsartikel (refereegranskat)abstract
    • The genetic architecture of common traits, including the number, frequency, and effect sizes of inherited variants that contribute to individual risk, has been long debated. Genome-wide association studies have identified scores of common variants associated with type 2 diabetes, but in aggregate, these explain only a fraction of the heritability of this disease. Here, to test the hypothesis that lower-frequency variants explain much of the remainder, the GoT2D and T2D-GENES consortia performed whole-genome sequencing in 2,657 European individuals with and without diabetes, and exome sequencing in 12,940 individuals from five ancestry groups. To increase statistical power, we expanded the sample size via genotyping and imputation in a further 111,548 subjects. Variants associated with type 2 diabetes after sequencing were overwhelmingly common and most fell within regions previously identified by genome-wide association studies. Comprehensive enumeration of sequence variation is necessary to identify functional alleles that provide important clues to disease pathophysiology, but large-scale sequencing does not support the idea that lower-frequency variants have a major role in predisposition to type 2 diabetes.
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6.
  • Kim, Bokyeong, et al. (författare)
  • Decoupled Address Translation for Heterogeneous Memory Systems
  • 2020
  • Ingår i: PACT '20. - New York, NY, USA : ASSOC COMPUTING MACHINERY. - 9781450380751 ; , s. 155-156
  • Konferensbidrag (refereegranskat)abstract
    • The support for the heterogeneous memory in the conventional virtual memory has an inherent problem. For the efficient translation in the critical translation lookaside buffers (TLBs), the page size has been growing. However, the heterogeneous memory management requires a nimble fine-grained migration mechanism to quickly move necessary memory portions to the precious fast memory. To address the challenges posed by the conflicting goals in the heterogeneous memory support, this paper proposes to decouple the address translation into a two-step process. The decoupling resolves the conflict as the critical core-side TLBs perform the translation to an intermediate address space, and the memory-side translation provides the actual physical location of the memory devices.
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7.
  • Kim, Bokyeong, et al. (författare)
  • Supporting Dynamic Translation Granularity for Hybrid Memory Systems
  • 2022
  • Ingår i: 2022 IEEE 40th International Conference on Computer Design (ICCD). - : Institute of Electrical and Electronics Engineers (IEEE). - 9781665461863 - 9781665461870 ; , s. 25-32
  • Konferensbidrag (refereegranskat)abstract
    • Hybrid memory has become a promising new solution for meeting ever growing memory capacity demands in a cost-effective way. In hybrid memory systems, the fast and high bandwidth memory is used to store performance-critical data, while the slow and low bandwidth memory provides capacity backup. In supporting such hybridization, virtual memory is the key mechanism, which can combine different memory components to a single memory view. For efficient translation for virtual memory, page size has been growing. However, the hybrid memory support requires fine-grained migration to quickly move only necessary memory portions to the precious fast memory. To address the challenges posed by the conflicting goals in the hybrid memory support based on virtual memory, this paper investigates decoupling of address translation into a two-step process. With the two-level translation, the critical core-side TLBs perform the translation to an intermediate address space, and the memory-side translation provides the actual physical location in memory devices. As the second-level translation handling page migration across different memory types, is decoupled from the first-level translation, it allows dynamic adjustment of its mapping granularity to improve the efficiency of translation and data reuse in the fast memory. This paper proposes a hardware architecture which identifies the memory access behavior of an application online and selects the best mapping granularity for the second-level translation.
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8.
  • Kwon, Hyuk Sung, et al. (författare)
  • Early increment of soluble triggering receptor expressed on myeloid cells 2 in plasma might be a predictor of poor outcome after ischemic stroke
  • 2020
  • Ingår i: Journal of clinical neuroscience. - : ELSEVIER SCI LTD. - 0967-5868 .- 1532-2653. ; 73, s. 215-218
  • Tidskriftsartikel (refereegranskat)abstract
    • Soluble triggering receptor expressed on myeloid cells 2 (sTREM2) is derived from cleavage of TREM2, which is expressed on the cell surface of microlgia and other tissue-specific macrophages. In the present study, the changes in the sTREM2 levels after ischemic stroke (IS) and their association with clinical outcomes were evaluated. A total of 43 patients diagnosed with non-cardioembolic IS between June 2011 and May 2014 were consecutively included in this study. Patients treated with intravenous thrombolysis or intra-arterial thrombectomy were excluded. Plasma samples were collected three times (days 1, 7, and 90) after ictus. The sTREM2 level was measured in the samples using the highly sensitive solid-phase proximity ligation assay (SP-PLA). Among the 43 subjects, higher initial NIH stroke scale (NIHSS) score (P = 0.005), early increment of sTREM2 (P < 0.001), and late decrement of sTREM2 (P = 0.002), were more common in patients with poor outcome. Based on multivariate analysis, initial NIHSS score (P = 0.015) and early increment of sTREM2 (P = 0.032) were independently associated with poor outcome. The results from the present study indicate that increment of sTREM2 level at the early phase was a predictor of poor outcome. Serial follow-up of sTREM2 may aid prognosis after stroke.
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9.
  • Park, Ji-Won, et al. (författare)
  • Beetle Immunity
  • 2010
  • Ingår i: Advances in Experimental Medicine and Biology. - Boston, MA : Springer US. - 0065-2598 .- 2214-8019. ; 708, s. 163-180
  • Tidskriftsartikel (refereegranskat)abstract
    • Genetic studies have elegantly characterized the innate immune response in Drosophila melanogaster. However, these studies have a limited ability to reveal the biochemical mechanisms underlying the innate immune response. To investigate the biochemical basis of how insects recognize invading microbes and how these recognition signals activate the innate immune response, it is necessary to use insects, from which larger amounts of hemolymph can be extracted. Using the larvae from two species of beetle, Tenebrio molitor and Holotrichia diomphalia, we elucidated the mechanisms underlying pathogenic microbe recognition. In addition, we studied the mechanism of host defense molecule amplification. In particular, we identified several pattern recognition proteins, serine proteases, serpins and antimicrobial peptides and examined how these molecules affect innate immunity.
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10.
  • Park, So Yeon, et al. (författare)
  • Sustainable lead management in halide perovskite solar cells
  • 2020
  • Ingår i: Nature Sustainability. - : NATURE RESEARCH. - 2398-9629. ; 3:12
  • Tidskriftsartikel (refereegranskat)abstract
    • The most-efficient solar cells use Pb-based halide perovskites; however, their toxicity poses environmental and health risks. Here, the authors report an adsorbent that allows for sustainable Pb management in these devices. Despite the rapid development of perovskite solar cells (PSCs) toward commercialization, the toxic lead (Pb) ions in PSCs pose a potential threat to the environment, health and safety. Managing Pb via recycling represents a promising approach to mitigating its toxicity. However, managing Pb from commonly used organic solvents has been challenging due to the lack of suitable Pb adsorbents. Here, we report a new adsorbent for both separation and recovery of Pb from PSC pollutants. The synthesized iron-incorporated hydroxyapatite possesses a strongly negatively charged surface that improves electrostatic interaction through surface-charge delocalization, thus leading to enhanced Pb adsorption. We demonstrate the feasibility of a complete Pb management process, including the purification of Pb-containing non-aqueous solvents below 15 parts per 10(9), a level compliant with the standards of the US Environmental Protection Agency, as well as recycling of 99.97% of Pb ions by forming lead iodide.
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