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Sökning: WFRF:(Hao Ke)

  • Resultat 121-130 av 154
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121.
  • Ablikim, M., et al. (författare)
  • Study of J/psi and psi(3686) -> Sigma(1385)(0)(Sigma)over-bar(1385)(0) and Xi(0)(Xi)over-bar(0) : Study of J/ψ and ψ(3686) → (1385)0( ¯ 1385)0 and 0¯ 0
  • 2017
  • Ingår i: Physics Letters B. - : ELSEVIER SCIENCE BV. - 0370-2693 .- 1873-2445. ; 770, s. 217-225
  • Tidskriftsartikel (refereegranskat)abstract
    • We study the decays of J/psi and psi(3686) to the final states Sigma(1385)(0)(Sigma) over bar (1385)(0) and Xi(0)(Xi) over bar (0) based on a single baryon tag method using data samples of (1310.6 +/- 7.0) x 10(6) J/psi and (447.9 +/- 2.9) x 10(6) psi(3686) events collected with the BESIII detector at the BEPCII collider. The decays to Sigma(1385)(0)(Sigma) over bar (1385)(0) are observed for the first time. The measured branching fractions of J/psi and psi(3686) to Xi(0)(Xi) over bar (0) are in good agreement with, and much more precise than, the previously published results. The angular parameters for these decays are also measured for the first time. The measured angular decay parameter for J/psi -> Sigma(1385)(0)(Sigma) over bar (1385)(0), alpha = -0.64 +/- 0.03 +/- 0.10, is found to be negative, different to the other decay processes in this measurement. In addition, the "12% rule" and isospin symmetry in the decays of J/psi and psi(3686) to Xi(Xi) over bar and Sigma(1385)(Sigma) over bar (1385) are tested.
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122.
  • Beaumont, Robin N, et al. (författare)
  • Genome-wide association study of placental weight identifies distinct and shared genetic influences between placental and fetal growth.
  • 2023
  • Ingår i: Nature genetics. - 1546-1718 .- 1061-4036. ; 55:11, s. 1807-19
  • Tidskriftsartikel (refereegranskat)abstract
    • A well-functioning placenta is essential for fetal and maternal health throughout pregnancy. Using placental weight as a proxy for placental growth, we report genome-wide association analyses in the fetal (n=65,405), maternal (n=61,228) and paternal (n=52,392) genomes, yielding 40 independent association signals. Twenty-six signals are classified as fetal, four maternal and three fetal and maternal. A maternal parent-of-origin effect is seen near KCNQ1. Genetic correlation and colocalization analyses reveal overlap with birth weight genetics, but 12 loci are classified as predominantly or only affecting placental weight, with connections to placental development and morphology, and transport of antibodies and amino acids. Mendelian randomization analyses indicate that fetal genetically mediated higher placental weight is causally associated with preeclampsia risk and shorter gestational duration. Moreover, these analyses support the role of fetal insulin in regulating placental weight, providing a key link between fetal and placental growth.
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123.
  • Cai, Yunhao, et al. (författare)
  • Effect of the Energy Offset on the Charge Dynamics in Nonfullerene Organic Solar Cells
  • 2020
  • Ingår i: ACS Applied Materials and Interfaces. - : AMER CHEMICAL SOC. - 1944-8244 .- 1944-8252. ; 12:39, s. 43984-43991
  • Tidskriftsartikel (refereegranskat)abstract
    • The energy offset, considered as the driving force for charge transfer between organic molecules, has significant effects on both charge separation and charge recombination in organic solar cells. Herein, we designed material systems with gradually shifting energy offsets, including both positive and negative values. Time-resolved spectroscopy was used to monitor the charge dynamics within the bulk heterojunction. It is striking to find that there is still charge transfer and charge generation when the energy offset reached -0.10 eV (ultraviolet photoelectron spectroscopy data). This work not only indicates the feasibility of the free carrier generation and the following charge separation under the condition of a negative offset but also elucidates the relationship between the charge transfer and the energy offset in the case of polymer chlorination.
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124.
  • Dimas, Antigone S, et al. (författare)
  • Impact of type 2 diabetes susceptibility variants on quantitative glycemic traits reveals mechanistic heterogeneity.
  • 2014
  • Ingår i: Diabetes. - : American Diabetes Association. - 1939-327X .- 0012-1797. ; 63:6, s. 2158-2171
  • Tidskriftsartikel (refereegranskat)abstract
    • Patients with established type 2 diabetes display both beta-cell dysfunction and insulin resistance. To define fundamental processes leading to the diabetic state, we examined the relationship between type 2 diabetes risk variants at 37 established susceptibility loci and indices of proinsulin processing, insulin secretion and insulin sensitivity. We included data from up to 58,614 non-diabetic subjects with basal measures, and 17,327 with dynamic measures. We employed additive genetic models with adjustment for sex, age and BMI, followed by fixed-effects inverse variance meta-analyses. Cluster analyses grouped risk loci into five major categories based on their relationship to these continuous glycemic phenotypes. The first cluster (PPARG, KLF14, IRS1, GCKR) was characterized by primary effects on insulin sensitivity. The second (MTNR1B, GCK) featured risk alleles associated with reduced insulin secretion and fasting hyperglycemia. ARAP1 constituted a third cluster characterized by defects in insulin processing. A fourth cluster (including TCF7L2, SLC30A8, HHEX/IDE, CDKAL1, CDKN2A/2B) was defined by loci influencing insulin processing and secretion without detectable change in fasting glucose. The final group contained twenty risk loci with no clear-cut associations to continuous glycemic traits. By assembling extensive data on continuous glycemic traits, we have exposed the diverse mechanisms whereby type 2 diabetes risk variants impact disease predisposition.
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125.
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126.
  • Franzen, Oscar, et al. (författare)
  • Global analysis of A-to-I RNA editing reveals association with common disease variants
  • 2018
  • Ingår i: PeerJ. - : PeerJ. - 2167-8359. ; 6
  • Tidskriftsartikel (refereegranskat)abstract
    • RNA editing modifies transcripts and may alter their regulation or function. In humans, the most common modification is adenosine to inosine (A-to-I). We examined the global characteristics of RNA editing in 4,301 human tissue samples. More than 1.6 million A-to-I edits were identified in 62% of all protein-coding transcripts. mRNA recoding was extremely rare; only 11 novel recoding sites were uncovered. Thirty single nucleotide polymorphisms from genome-wide association studies were associated with RNA editing; one that influences type 2 diabetes (rs2028299) was associated with editing in ARPIN. Twenty-five genes, including LRP11 and PLIN5, had editing sites that were associated with plasma lipid levels. Our findings provide new insights into the genetic regulation of RNA editing and establish a rich catalogue for further exploration of this process.
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127.
  • Gill, Dipender, et al. (författare)
  • ACE inhibition and cardiometabolic risk factors, lung ACE2 and TMPRSS2 gene expression, and plasma ACE2 levels : a Mendelian randomization study
  • 2020
  • Ingår i: Royal Society Open Science. - : ROYAL SOC. - 2054-5703. ; 7:11
  • Tidskriftsartikel (refereegranskat)abstract
    • Angiotensin-converting enzyme 2 (ACE2) and serine protease TMPRSS2 have been implicated in cell entry for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus responsible for coronavirus disease 2019 (COVID-19). The expression of ACE2 and TMPRSS2 in the lung epithelium might have implications for the risk of SARS-CoV-2 infection and severity of COVID-19. We use human genetic variants that proxy angiotensin-converting enzyme (ACE) inhibitor drug effects and cardiovascular risk factors to investigate whether these exposures affect lung ACE2 and TMPRSS2 gene expression and circulating ACE2 levels. We observed no consistent evidence of an association of genetically predicted serum ACE levels with any of our outcomes. There was weak evidence for an association of genetically predicted serum ACE levels with ACE2 gene expression in the Lung eQTL Consortium (p = 0.014), but this finding did not replicate. There was evidence of a positive association of genetic liability to type 2 diabetes mellitus with lung ACE2 gene expression in the Gene-Tissue Expression (GTEx) study (p = 4 x 10(-4)) and with circulating plasma ACE2 levels in the INTERVAL study (p = 0.03), but not with lung ACE2 expression in the Lung eQTL Consortium study (p = 0.68). There were no associations of genetically proxied liability to the other cardiometabolic traits with any outcome. This study does not provide consistent evidence to support an effect of serum ACE levels (as a proxy for ACE inhibitors) or cardiometabolic risk factors on lung ACE2 and TMPRSS2 expression or plasma ACE2 levels.
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128.
  • Hao, Yanfen, et al. (författare)
  • Air monitoring of polychlorinated biphenyls, polybrominated diphenyl ethers and organochlorine pesticides in West Antarctica during 2011-2017 : Concentrations, temporal trends and potential sources
  • 2019
  • Ingår i: Environmental Pollution. - : Elsevier. - 0269-7491 .- 1873-6424. ; 249, s. 381-389
  • Tidskriftsartikel (refereegranskat)abstract
    • Annual air samples were collected at various sites in the Fildes Peninsula, West Antarctica from December 2010 to January 2018 using XAD-2 resin passive air samplers to investigate concentrations, temporal trends and potential sources of persistent organic pollutants (POPs) in Antarctic air. Relatively low concentrations of polychlorinated biphenyls (PCBs) (Σ19PCBs: 1.5-29.7 pg/m3), polybrominated diphenyl ethers (PBDEs) (Σ12PBDEs: 0.2-2.9 pg/m3) and organochlorine pesticides (OCPs) (Σ13OCPs: 101-278 pg/m3) were found in the atmosphere of West Antarctica. PCB-11, BDE-47 and hexachlorobenzene (HCB) were the predominant compounds in the atmosphere. The concentrations of PCBs, HCHs, DDTs and endosulfans were found to show decreasing temporal trends, whereas uniform temporal trends were observed for HCB. The atmospheric half-life values for PCBs, HCHs, DDTs and endosulfans in Antarctic air were estimated for the first time, using regressions of the natural logarithm of the concentrations versus the number of years, obtaining the values of 2.0, 2.0, 2.4 and 1.2 year, respectively. An increasing ratio of α-HCH/γ-HCH indicated long residence time for α-HCH and possible transformation of γ-HCH to α-HCH in the atmosphere. The ratios of p,p'-DDT/p,p'-DDE were mostly lower than unity in this study, which could be attributed to aged sources. It was found that long-range atmospheric transport was still considered to be the main contributing factor to the atmospheric levels of the POPs in West Antarctica whereas the contribution of human activities at the Chinese Great Wall Station was minor. The results of this study give a view on the most recent temporal trends and provide new insights regarding the occurrence of various POPs in the Antarctic atmosphere.
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129.
  • Ingelsson, Erik, et al. (författare)
  • Detailed Physiologic Characterization Reveals Diverse Mechanisms for Novel Genetic Loci Regulating Glucose and Insulin Metabolism in Humans
  • 2010
  • Ingår i: Diabetes. - 0012-1797 .- 1939-327X. ; 59:5, s. 1266-1275
  • Konferensbidrag (refereegranskat)abstract
    • OBJECTIVE-Recent genome-wide association studies have revealed loci associated with glucose and insulin-related traits. We aimed to characterize 19 such loci using detailed measures of insulin processing, secretion, and sensitivity to help elucidate their role in regulation of glucose control, insulin secretion and/or action. RESEARCH DESIGN AND METHODS-We investigated associations of loci identified by the Meta-Analyses of Glucose and Insulin-related traits Consortium (MAGIC) with circulating proinsulin, measures of insulin secretion and sensitivity from oral glucose tolerance tests (OGTTs), euglycemic clamps, insulin suppression tests, or frequently sampled intravenous glucose tolerance tests in nondiabetic humans (n = 29,084). RESULTS-The glucose-raising allele in MADD was associated with abnormal insulin processing (a dramatic effect on higher proinsulin levels, but no association with insulinogenic index) at extremely persuasive levels of statistical significance (P = 2.1 x 10(-71)). Defects in insulin processing and insulin secretion were seen in glucose-raising allele carriers at TCF7L2, SCL30A8, GIPR, and C2CD4B. Abnormalities in early insulin secretion were suggested in glucose-raising allele carriers at MTNR1B, GCK, FADS1, DGKB, and PROX1 (lower insulinogenic index; no association with proinsulin or insulin sensitivity). Two loci previously associated with fasting insulin (GCKR and IGF1) were associated with OGTT-derived insulin sensitivity indices in a consistent direction. CONCLUSIONS-Genetic loci identified through their effect on hyperglycemia and/or hyperinsulinemia demonstrate considerable heterogeneity in associations with measures of insulin processing, secretion, and sensitivity. Our findings emphasize the importance of detailed physiological characterization of such loci for improved understanding of pathways associated with alterations in glucose homeostasis and eventually type 2 diabetes. Diabetes 59:1266-1275, 2010
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130.
  • Ingelsson, Erik, et al. (författare)
  • Detailed physiologic characterization reveals diverse mechanisms for novel genetic Loci regulating glucose and insulin metabolism in humans
  • 2010
  • Ingår i: Diabetes. - : American Diabetes Association. - 0012-1797 .- 1939-327X. ; 59:5, s. 1266-1275
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE Recent genome-wide association studies have revealed loci associated with glucose and insulin-related traits. We aimed to characterize 19 such loci using detailed measures of insulin processing, secretion, and sensitivity to help elucidate their role in regulation of glucose control, insulin secretion and/or action. RESEARCH DESIGN AND METHODS We investigated associations of loci identified by the Meta-Analyses of Glucose and Insulin-related traits Consortium (MAGIC) with circulating proinsulin, measures of insulin secretion and sensitivity from oral glucose tolerance tests (OGTTs), euglycemic clamps, insulin suppression tests, or frequently sampled intravenous glucose tolerance tests in nondiabetic humans (n = 29,084). RESULTS The glucose-raising allele in MADD was associated with abnormal insulin processing (a dramatic effect on higher proinsulin levels, but no association with insulinogenic index) at extremely persuasive levels of statistical significance (P = 2.1 x 10(-71)). Defects in insulin processing and insulin secretion were seen in glucose-raising allele carriers at TCF7L2, SCL30A8, GIPR, and C2CD4B. Abnormalities in early insulin secretion were suggested in glucose-raising allele carriers at MTNR1B, GCK, FADS1, DGKB, and PROX1 (lower insulinogenic index; no association with proinsulin or insulin sensitivity). Two loci previously associated with fasting insulin (GCKR and IGF1) were associated with OGTT-derived insulin sensitivity indices in a consistent direction. CONCLUSIONS Genetic loci identified through their effect on hyperglycemia and/or hyperinsulinemia demonstrate considerable heterogeneity in associations with measures of insulin processing, secretion, and sensitivity. Our findings emphasize the importance of detailed physiological characterization of such loci for improved understanding of pathways associated with alterations in glucose homeostasis and eventually type 2 diabetes.
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