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1.
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2.
  • Klionsky, Daniel J., et al. (författare)
  • Guidelines for the use and interpretation of assays for monitoring autophagy
  • 2012
  • Ingår i: Autophagy. - : Landes Bioscience. - 1554-8635 .- 1554-8627. ; 8:4, s. 445-544
  • Forskningsöversikt (refereegranskat)abstract
    • In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field.
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3.
  • Feitosa, Mary F., et al. (författare)
  • Novel genetic associations for blood pressure identified via gene-alcohol interaction in up to 570K individuals across multiple ancestries
  • 2018
  • Ingår i: PLoS ONE. - : Public library science. - 1932-6203. ; 13:6
  • Tidskriftsartikel (refereegranskat)abstract
    • Heavy alcohol consumption is an established risk factor for hypertension; the mechanism by which alcohol consumption impact blood pressure (BP) regulation remains unknown. We hypothesized that a genome-wide association study accounting for gene-alcohol consumption interaction for BP might identify additional BP loci and contribute to the understanding of alcohol-related BP regulation. We conducted a large two-stage investigation incorporating joint testing of main genetic effects and single nucleotide variant (SNV)-alcohol consumption interactions. In Stage 1, genome-wide discovery meta-analyses in approximate to 131 K individuals across several ancestry groups yielded 3,514 SNVs (245 loci) with suggestive evidence of association (P <1.0 x 10(-5)). In Stage 2, these SNVs were tested for independent external replication in individuals across multiple ancestries. We identified and replicated (at Bonferroni correction threshold) five novel BP loci (380 SNVs in 21 genes) and 49 previously reported BP loci (2,159 SNVs in 109 genes) in European ancestry, and in multi-ancestry meta-analyses (P < 5.0 x 10(-8)). For African ancestry samples, we detected 18 potentially novel BP loci (P< 5.0 x 10(-8)) in Stage 1 that warrant further replication. Additionally, correlated meta-analysis identified eight novel BP loci (11 genes). Several genes in these loci (e.g., PINX1, GATA4, BLK, FTO and GABBR2 have been previously reported to be associated with alcohol consumption. These findings provide insights into the role of alcohol consumption in the genetic architecture of hypertension.
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4.
  • Sung, Yun J., et al. (författare)
  • A Large-Scale Multi-ancestry Genome-wide Study Accounting for Smoking Behavior Identifies Multiple Significant Loci for Blood Pressure
  • 2018
  • Ingår i: American Journal of Human Genetics. - : Cell Press. - 0002-9297 .- 1537-6605. ; 102:3, s. 375-400
  • Tidskriftsartikel (refereegranskat)abstract
    • Genome-wide association analysis advanced understanding of blood pressure (BP), a major risk factor for vascular conditions such as coronary heart disease and stroke. Accounting for smoking behavior may help identify BP loci and extend our knowledge of its genetic architecture. We performed genome-wide association meta-analyses of systolic and diastolic BP incorporating gene-smoking interactions in 610,091 individuals. Stage 1 analysis examined similar to 18.8 million SNPs and small insertion/deletion variants in 129,913 individuals from four ancestries (European, African, Asian, and Hispanic) with follow-up analysis of promising variants in 480,178 additional individuals from five ancestries. We identified 15 loci that were genome-wide significant (p < 5 x 10(-8)) in stage 1 and formally replicated in stage 2. A combined stage 1 and 2 meta-analysis identified 66 additional genome-wide significant loci (13, 35, and 18 loci in European, African, and trans-ancestry, respectively). A total of 56 known BP loci were also identified by our results (p < 5 x 10(-8)). Of the newly identified loci, ten showed significant interaction with smoking status, but none of them were replicated in stage 2. Several loci were identified in African ancestry, highlighting the importance of genetic studies in diverse populations. The identified loci show strong evidence for regulatory features and support shared pathophysiology with cardiometabolic and addiction traits. They also highlight a role in BP regulation for biological candidates such as modulators of vascular structure and function (CDKN1B, BCAR1-CFDP1, PXDN, EEA1), ciliopathies (SDCCAG8, RPGRIP1L), telomere maintenance (TNKS, PINX1, AKTIP), and central dopaminergic signaling MSRA, EBF2).
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5.
  • Sung, Yun Ju, et al. (författare)
  • A multi-ancestry genome-wide study incorporating gene-smoking interactions identifies multiple new loci for pulse pressure and mean arterial pressure
  • 2019
  • Ingår i: Human Molecular Genetics. - : Oxford University Press. - 0964-6906 .- 1460-2083. ; 28:15, s. 2615-2633
  • Tidskriftsartikel (refereegranskat)abstract
    • Elevated blood pressure (BP), a leading cause of global morbidity and mortality, is influenced by both genetic and lifestyle factors. Cigarette smoking is one such lifestyle factor. Across five ancestries, we performed a genome-wide gene–smoking interaction study of mean arterial pressure (MAP) and pulse pressure (PP) in 129 913 individuals in stage 1 and follow-up analysis in 480 178 additional individuals in stage 2. We report here 136 loci significantly associated with MAP and/or PP. Of these, 61 were previously published through main-effect analysis of BP traits, 37 were recently reported by us for systolic BP and/or diastolic BP through gene–smoking interaction analysis and 38 were newly identified (P < 5 × 10−8, false discovery rate < 0.05). We also identified nine new signals near known loci. Of the 136 loci, 8 showed significant interaction with smoking status. They include CSMD1 previously reported for insulin resistance and BP in the spontaneously hypertensive rats. Many of the 38 new loci show biologic plausibility for a role in BP regulation. SLC26A7 encodes a chloride/bicarbonate exchanger expressed in the renal outer medullary collecting duct. AVPR1A is widely expressed, including in vascular smooth muscle cells, kidney, myocardium and brain. FHAD1 is a long non-coding RNA overexpressed in heart failure. TMEM51 was associated with contractile function in cardiomyocytes. CASP9 plays a central role in cardiomyocyte apoptosis. Identified only in African ancestry were 30 novel loci. Our findings highlight the value of multi-ancestry investigations, particularly in studies of interaction with lifestyle factors, where genomic and lifestyle differences may contribute to novel findings.
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6.
  • Ablikim, M., et al. (författare)
  • Amplitude analysis of the KSKS system produced in radiative J /psi decays
  • 2018
  • Ingår i: Physical Review D. - : AMER PHYSICAL SOC. - 2470-0010 .- 2470-0029. ; 98:7
  • Tidskriftsartikel (refereegranskat)abstract
    • An amplitude analysis of the KSKS system produced in radiative J/psi decays is performed using the (1310.6 +/- 7.0) x 10(6) nip decays collected by the BESIII detector. Two approaches are presented. A mass-dependent analysis is performed by parametrizing the KSKS invariant mass spectrum as a sum of Breit-aligner line shapes. Additionally, a mass-independent analysis is performed to extract a piecewise function that describes the dynamics of the KSKS system while making minimal assumptions about the properties and number of poles in the amplitude. The dominant amplitudes in the mass-dependent analysis include the f(0)(1710), f(0)(2200), and f(2)'(1525). The mass-independent results, which are made available as input for further studies, are consistent with those of the mass-dependent analysis and are useful for a systematic study of hadronic interactions. The branching fraction of radiative J/psi decays to KSKS is measured to be (8.1 +/- 0.4) x 10(-4), where the uncertainty is systematic and the statistical uncertainty is negligible.
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7.
  • Ablikim, M., et al. (författare)
  • Branching fraction measurement of J/ψ→KSKL and search for J/ψ→KSKS
  • 2017
  • Ingår i: Physical Review D. - 2470-0010 .- 2470-0029. ; 96:11
  • Tidskriftsartikel (refereegranskat)abstract
    • Using a sample of 1.31 x 10(9) J/Psi events collected with the BESIII detector at the BEPCII collider, we study the decays of J/Psi -> KSKL and KSKS. The branching fraction of J/Psi -> KSKL is determined to be B(J/Psi -> KSKL) = (1.93 +/- 0.01 (stat) +/- 0.05 (syst)) x 10(-4), which significantly improves on previous measurements. No clear signal is observed for the J/Psi -> KSKS process, and the upper limit at the 95% confidence level for its branching fraction is determined to be B(J/Psi -> KSKS) < 1.4 x 10(-8), which improves on the previous searches by 2 orders in magnitude and reaches the order of the Einstein-Podolsky-Rosen expectation.
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8.
  • Ablikim, M., et al. (författare)
  • Branching fraction measurements of psi (3686) -> gamma chi(cJ)
  • 2017
  • Ingår i: Physical Review D. - 2470-0010 .- 2470-0029. ; 96:3
  • Tidskriftsartikel (refereegranskat)abstract
    • Using a sample of 106 million psi(3686) decays, the branching fractions of psi(3686) -> gamma chi(c0), psi(3686) -> gamma chi(c1), and psi(3686) -> gamma chi(c2) are measured with improved precision to be (9.389 +/- 0.014 +/- 0.332) %, (9.905 +/- 0.011 +/- 0.353) %, and (9.621 +/- 0.013 +/- 0.272) %, respectively, where the first uncertainties are statistical and the second ones are systematic. The product branching fractions of (psi 3686) -> gamma chi(c1), chi(c1) -> gamma J/psi (3686) -> gamma chi(c2), chi(c2) -> gamma J/psi and the branching fractions of chi(c1) -> gamma J/psi and chi(c2) -> gamma J/psi are also presented.
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9.
  • Ablikim, M., et al. (författare)
  • Confirmation of a charged charmoniumlike state Z(c)(3885)(-/+) in e(+)e(-) -> pi(+/-) (D(D)over-bar*)(-/+) with double D tag
  • 2015
  • Ingår i: Physical Review D. - 1550-7998 .- 1550-2368. ; 92:9
  • Tidskriftsartikel (refereegranskat)abstract
    • We present a study of the process e(+)e(-) -> pi(+/-) (D (D) over bar*)(-/+) using data samples of 1092 pb(-1) at root s = 4.23 GeV and 826 pb(-1) at root s = 4.26 GeV collected with the BESIII detector at the BEPCII storage ring. With full reconstruction of the D meson pair and the bachelor pi(+) in the final state, we confirm the existence of the charged structure Z(c) (3885)(-/+) in the (D (D) over bar*)(-/+) system in the two isospin processes e(+)e(-) -> pi(+DD)-D-0*(-) and e(+)e(-) -> pi+D-D*(0). By performing a simultaneous fit, the statistical significance of Zc(3885)(-/+) signal is determined to be greater than 10 sigma, and its pole mass and width are measured to be M-pole = (3881.7 +/- 1.6(stat) +/- 1.6(syst)) MeV/c(2) and Gamma(pole) = (26.6 +/- 2.0(stat) +/- 2.1(syst)) MeV, respectively. The Born cross section times the (D (D) over bar*)(-/+) branching fraction (sigma(e(+)e(-) -> pi(+/-)Z(c)(3885)(-/+)) x Br(Z(c)(3885)(-/+) -> (D (D) over bar*)(-/+) )) is measured to be (141.6 +/- 7.9(stat) +/- 12.3(syst)) pb at root s = 4.23 GeV and (108.4 +/- 6.9(stat) +/- 8.8(syst)) pb at root s = 4.26 GeV. The polar angular distribution of the pi(+) - Z(c)(3885)(-/+) system is consistent with the expectation of a quantum number assignment of J(P) = 1(+) for Z(c)(3885)(-/+).
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10.
  • Ablikim, M., et al. (författare)
  • Evidence for e+e−→γηc(1S) at center-of-mass energies between 4.01 and 4.60 GeV
  • 2017
  • Ingår i: Physical Review D. - 2470-0010 .- 2470-0029. ; 96:5
  • Tidskriftsartikel (refereegranskat)abstract
    • We present first evidence for the process e(+)e(-) -> gamma eta(c)(1S) at six center-of-mass energies between 4.01 and 4.60 GeV using data collected by the BESIII experiment operating at BEPCII. We measure the Born cross section at each energy using a combination of twelve eta(c)(1S) decay channels. We also combine all six energies under various assumptions for the energy-dependence of the cross section. If the process is assumed to proceed via the Y(4260), we measure a peak Born cross section sigma(peak)(e(+)e(-) -> gamma eta(c)(1S)) = 2.11 +/- 0.49 (stat.) +/- 0.36 (syst.) pb with a statistical significance of 4.2 sigma.
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