1. |
- Liu, Junwei, et al.
(author)
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Polymer synergy for efficient hole transport in solar cells and photodetectors
- 2023
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In: Energy & Environmental Science. - : ROYAL SOC CHEMISTRY. - 1754-5692 .- 1754-5706.
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Journal article (peer-reviewed)abstract
- Hole transport materials (HTMs) have greatly advanced the progress of solution-based electronic devices in the past few years. Nevertheless, most devices employing dopant-free organic HTMs can only deliver inferior performance. In this work, we introduced a novel "polymer synergy" strategy to develop versatile dopant-free polymer HTMs for quantum dot/perovskite solar cells and photodetectors. With this synergy strategy, the optical, electrical and aggregation properties of polymer HTMs can be modulated, resulting in complementary absorption, high hole mobility, favorable energy landscape and moderate aggregation. Moreover, a clear orientational transition was observed for the developed HTMs with a 9-fold increase in the face-on/edge-on ratio, providing a highway-like carrier transport for electronic devices, as revealed by in situ characterization and ultrafast transient absorption. With these benefits, the photovoltaic and photodetection performance of quantum dot devices were boosted from 11.8% to 13.5% and from 2.95 x 10(12) to 3.41 x 10(13) Jones (over a 10-fold increase), respectively. Furthermore, the developed polymer HTMs can also significantly enhance the photovoltaic and photodetection performance of perovskite devices from 15.1% to 22.7% and from 2.7 x 10(12) to 2.17 x 10(13)Jones with the same device structure, indicating their great application potential in the emerging optoelectronics.
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2. |
- Sampson, Joshua N., et al.
(author)
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Analysis of Heritability and Shared Heritability Based on Genome-Wide Association Studies for 13 Cancer Types
- 2015
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In: Journal of the National Cancer Institute. - : Oxford University Press (OUP). - 0027-8874 .- 1460-2105. ; 107:12
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Journal article (peer-reviewed)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, Xiaohua, et al.
(author)
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Tacrolimus Causes Hypertension by Increasing Vascular Contractility via RhoA (Ras Homolog Family Member A)/ROCK (Rho-Associated Protein Kinase) Pathway in Mice
- 2022
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In: Hypertension. - : Ovid Technologies (Wolters Kluwer Health). - 0194-911X .- 1524-4563. ; 79:10, s. 2228-2238
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Journal article (peer-reviewed)abstract
- Background: To provide tacrolimus is first-line treatment after liver and kidney transplantation. However, hypertension and nephrotoxicity are common tacrolimus side effects that limit its use. Although tacrolimus-related hypertension is well known, the underlying mechanisms are not. Here, we test whether tacrolimus-induced hypertension involves the RhoA (Ras homolog family member A)/ROCK (Rho-associated protein kinase) pathway in male C57Bl/6 mice. methods: Intra-arterial blood pressure was measured under anesthesia. The reactivity of renal afferent arterioles and mesenteric arteries were assessed in vitro using microperfusion and wire myography, respectively. Results: Tacrolimus induced a transient rise in systolic arterial pressure that was blocked by the RhoA/ROCK inhibitor Fasudil (12.0 +/- 0.9 versus 3.2 +/- 0.7; P<0.001). Moreover, tacrolimus reduced the glomerular filtration rate, which was also prevented by Fasudil (187 +/- 20 versus 281 +/- 8.5; P<0.001). Interestingly, tacrolimus enhanced the sensitivity of afferent arterioles and mesenteric arteries to Ang II (angiotensin II), likely due to increased intracellular Ca2+ mobilization and sensitization. Fasudil prevented increased Ang II-sensitivity and blocked Ca2+ mobilization and sensitization. Preincubation of mouse aortic vascular smooth muscle cells with tacrolimus activated the RhoA/ROCK/MYPT-1 (myosin phosphatase targeting subunit 1) pathway. Further, tacrolimus increased cytoplasmic reactive oxygen species generation in afferent arterioles (107 +/- 5.9 versus 163 +/- 6.4; P<0.001) and in cultured mouse aortic vascular smooth muscle cells (100 +/- 7.5 versus 160 +/- 23.2; P<0.01). Finally, the reactive oxygen species scavenger Tempol inhibited tacrolimus-induced Ang II hypersensitivity in afferent arterioles and mesenteric arteries. Conclusions: The RhoA/ROCK pathway may play an important role in tacrolimus-induced hypertension by enhancing Ang II-specific vasoconstriction, and reactive oxygen species may participate in this process by activating the RhoA/ROCK pathway.
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4. |
- Wang, Zhaoming, et al.
(author)
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Imputation and subset-based association analysis across different cancer types identifies multiple independent risk loci in the TERT-CLPTM1L region on chromosome 5p15.33
- 2014
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In: Human Molecular Genetics. - : Oxford University Press (OUP). - 0964-6906 .- 1460-2083. ; 23:24, s. 6616-6633
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Journal article (peer-reviewed)abstract
- Genome-wide association studies (GWAS) have mapped risk alleles for at least 10 distinct cancers to a small region of 63 000 bp on chromosome 5p15.33. This region harbors the TERT and CLPTM1L genes; the former encodes the catalytic subunit of telomerase reverse transcriptase and the latter may play a role in apoptosis. To investigate further the genetic architecture of common susceptibility alleles in this region, we conducted an agnostic subset-based meta-analysis (association analysis based on subsets) across six distinct cancers in 34 248 cases and 45 036 controls. Based on sequential conditional analysis, we identified as many as six independent risk loci marked by common single-nucleotide polymorphisms: five in the TERT gene (Region 1: rs7726159, P = 2.10 × 10(-39); Region 3: rs2853677, P = 3.30 × 10(-36) and PConditional = 2.36 × 10(-8); Region 4: rs2736098, P = 3.87 × 10(-12) and PConditional = 5.19 × 10(-6), Region 5: rs13172201, P = 0.041 and PConditional = 2.04 × 10(-6); and Region 6: rs10069690, P = 7.49 × 10(-15) and PConditional = 5.35 × 10(-7)) and one in the neighboring CLPTM1L gene (Region 2: rs451360; P = 1.90 × 10(-18) and PConditional = 7.06 × 10(-16)). Between three and five cancers mapped to each independent locus with both risk-enhancing and protective effects. Allele-specific effects on DNA methylation were seen for a subset of risk loci, indicating that methylation and subsequent effects on gene expression may contribute to the biology of risk variants on 5p15.33. Our results provide strong support for extensive pleiotropy across this region of 5p15.33, to an extent not previously observed in other cancer susceptibility loci.
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5. |
- Yong, Zhihua, et al.
(author)
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Unravelling uniaxial strain effects on electronic correlations, hybridization and bonding in transition metal oxides
- 2019
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In: Acta Materialia. - : Elsevier BV. - 1359-6454. ; 164, s. 618-626
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Journal article (peer-reviewed)abstract
- The interplay among spin, lattice, charge and orbit is of central importance for several rich and fascinating properties of oxides, and is the subject of intense research at present. Here, we present an approach to manipulate this interplay by Sn doping to effectively apply uniaxial strain on the TiO2 lattice. The evolution of this interplay in pseudo-homoepitaxial Ti1-xSnxO2 films is measured using a combination of X-ray absorption near edge spectroscopy at the O K and Ti L3,2-edges. Supported by various theoretical calculations, we find that the multiplet-type electronic correlations, long-range bonding and hybridization in the system can be controlled by independently modifying uniaxial strain, thereby allowing us to establish the correlations among these effects, doping concentration, and strain. This significantly widens the phase space for experimental exploration of predictive models and leads to new possibilities for manipulation over materials’ functional properties. The methodology presented here can be applied in general to study the nature of the multiplet-type electronic correlations and bonding properties in octahedral-coordinated 3dN transition metal oxides.
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