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1.
  • Huang, Pan, et al. (creator_code:aut_t)
  • The ERK1/2 Signaling Pathway Is Involved in Sulfur Dioxide Preconditioning-Induced Protection against Cardiac Dysfunction in Isolated Perfused Rat Heart Subjected to Myocardial Ischemia/Reperfusion
  • 2013
  • record:In_t: International Journal of Molecular Sciences. - : MDPI. - 1661-6596 .- 1422-0067. ; 14:11, s. 22190-22201
  • swepub:Mat_article_t (swepub:level_refereed_t)abstract
    • Ischemia/reperfusion injury (IRI) occurs frequently during reperfusion of ischemic myocardium, and preconditioning has been regarded as one of the best strategies to prevent myocardial injury during the ischemia/reperfusion process. Our previous studies indicated that a small dose of sulfur dioxide (SO2) used as preconditioning exerts cardioprotection. However, the mechanisms underlying the cardioprotection remain unclear. The present study was designed to examine if the extracellular regulated protein kinases 1/2 (ERK1/2) signaling pathway mediated protection against cardiac dysfunction after SO2 preconditioning in isolated rat hearts subjected to ischemia/reperfusion (I/R). Langendorff heart perfusion was performed in vitro, where 56 male Wistar rats were randomly divided into seven groups: control group, 5 mol/L SO2 group (S5), 2-(2-Amino-3-methoxyphenyl)-4H-1-benzopyran-4-one (PD98059) + 5 mol/L SO2 (PD98059 + S5) group, PD98059 group, I/R group, 5 mol/L SO2 + I/R (S5 + I/R) group and PD98059 + 5 mol/L SO2 + I/R (PD98059 + S5 + I/R) group. Cardiac function and myocardial phosphorylated ERK1/2 protein were measured. We found that I/R in isolated rat heart resulted in cardiac dysfunction with a significant increase in phosphorylated ERK1/2 protein. SO2 preconditioning markedly suppressed phosphorylated ERK1/2 protein and improved cardiac function in isolated rat heart with I/R (p less than 0.05). However, pre-treatment with PD98059 could prevent the above effects of SO2 preconditioning. In conclusion, SO2 preconditioning protected against cardiac dysfunction in isolated rat heart subjected to I/R via suppression of the over-activation of the ERK1/2 signaling pathway.
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2.
  • Merino, Jordi, et al. (creator_code:aut_t)
  • Genome-wide meta-analysis of macronutrient intake of 91,114 European ancestry participants from the cohorts for heart and aging research in genomic epidemiology consortium
  • 2019
  • record:In_t: Molecular Psychiatry. - : Springer Science and Business Media LLC. - 1359-4184 .- 1476-5578. ; 24:12, s. 1920-1932
  • swepub:Mat_article_t (swepub:level_refereed_t)abstract
    • Macronutrient intake, the proportion of calories consumed from carbohydrate, fat, and protein, is an important risk factor for metabolic diseases with significant familial aggregation. Previous studies have identified two genetic loci for macronutrient intake, but incomplete coverage of genetic variation and modest sample sizes have hindered the discovery of additional loci. Here, we expanded the genetic landscape of macronutrient intake, identifying 12 suggestively significant loci (P < 1 × 10−6) associated with intake of any macronutrient in 91,114 European ancestry participants. Four loci replicated and reached genome-wide significance in a combined meta-analysis including 123,659 European descent participants, unraveling two novel loci; a common variant in RARB locus for carbohydrate intake and a rare variant in DRAM1 locus for protein intake, and corroborating earlier FGF21 and FTO findings. In additional analysis of 144,770 participants from the UK Biobank, all identified associations from the two-stage analysis were confirmed except for DRAM1. Identified loci might have implications in brain and adipose tissue biology and have clinical impact in obesity-related phenotypes. Our findings provide new insight into biological functions related to macronutrient intake.
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3.
  • Zeng, Jinyan, et al. (creator_code:aut_t)
  • 導論
  • 2022
  • record:In_t: 在幽昏中顯影 : 港中對話中國獨立紀錄片 2014-2020 - 港中對話中國獨立紀錄片 2014-2020. - 9781738705009 ; , s. 12-26
  • swepub:Mat_chapter_t (swepub:level_refereed_t)abstract
    • 《在幽昏中顯影:港中對話中國獨立紀錄片2014-2020》一書以導演、學者、觀眾對話的形式,討論了中國獨立紀錄片研究會(香港)2014至2020年期間展映、製片、發行的獨立電影。我們從中選擇了記錄較為完整的“叛逆中國”、“飛越瘋人院”、“情慾中國”三個展映單元的獨立紀錄片討論,以及針對夾邊溝右派農場倖存者記憶、維吾爾和新疆議題、三自教會、地下知識分子、前政府高官、工人抗爭等18部影片的映後交流文本或者導演訪談文本,形成本書“性、性別與女性主體”、“權利與政治”、“歷史與記憶”、“放逐與流亡”四個部分的主要內容。本書還收入研究會參與製片的《喊叫與耳語》首映對談,曾金燕對艾未未在跨國視野(流亡處境)下關於藝術(如《人流》)、社會行動和審查的兩次訪談,曾金燕對應亮半自傳劇情片《自由行》的訪談、曾金燕對艾曉明關於性別、紀錄片和社會行動的訪談、曾金燕與王月眉關於在香港八年“邊緣”經驗的筆談。額外收入的稿件中,除卻艾未未訪談,其餘四篇對話,回應獨立電影(本書中主要指紀錄片)的文化生產、策展交流,紀錄片作為社會行動,以及影像研究的智識與藝術傳統裡性別不對等的問題。後三篇回應香港在2014年雨傘運動、2019年反送中運動以及2020年引入國安法後,放逐、流亡到香港的創作者面臨的再次流亡的議題。流亡在這裡,既指內在的、思想的、立場上遠離權力中心的、處於社會邊緣批判既定結構的作者狀態,也指創作者主動或被迫選擇的肉身離開故土的流亡。“權利與政治”討論去政治化的紀錄片電影主流思考方式下,獨立紀錄片對中國社會現實在議題與美學方面的回應,以及關於人的尊嚴如何建構了紀錄片的人文關懷。 “歷史與記憶”章節裡,在通過控制記憶來控制歷史再現的環境中,紀錄片導演和觀眾共同探討了當歷史被壓抑、篡改時,如何找(不)到個人的語言來說(不)出個人的經歷,建構基於個體經驗的、被壓抑的、表演性的個人記憶和集體歷史。將在幽昏中被隱沒的聲音和形象帶到香港的華文世界以及英語世界關於中國的討論中。這,也許就是中國獨立紀錄片研究會在香港所做的工作以及本書的意義。「導論」可通過鏈接免費預覽。This book discusses the independent films screened, produced, and distributed by the China Independent Documentary Lab (Hong Kong) from 2014 to 2020, in conversations between directors, scholars and audiences. This collection has chosen to discuss the relatively well documented independent documentaries in the three screening sections of Rebel China, One Flew Over the Cuckoo's Nest and Desiring China. The book also includes 18 post-screening discussion texts or director interviews on issues on the survivors’ testimonies of Jiabiangou Rightist Labour Camp, Uyghur and Tibetan issues, the three self-churches, the underground intellectuals, former senior government officials, and workers' resistance. The book is composed of four sections: "Sexuality, Gender, and the Female Subjectivity", "Rights and Politics", "History and Memory", and "Banishment and Exile". The book also includes a conversation during the premiere of Outcry and Whisper, which was produced by the CIDL; two interviews by Zeng Jinyan with Ai Weiwei on art (e.g. Human Flow), activism, and censorship in a transnational/exile perspective; an interview by Zeng Jinyan with Ying Liang's semi-autobiographical fiction film Family Tour; an interview by Zeng Jinyan with Ai Xiaoming on gender and documentary film and activism; a written interview by Vivian Wang with Zeng Jinyan on Zeng’s eight years experiences in Hong Kong on the edge.Except the interview with Ai Weiwei, the remaining four conversations respond to the gender asymmetrical tradition of intellectual and art, in cultural production of independent film (mainly documentaries in this book), curatorial exchange, documentary as social action, and documentary studies. The latter three conversations respond to the topic of re-exile faced by artists who had exiled to Hong Kong, after the Umbrella Movement in 2014, the 2019 Hong Kong Protest, and the 2020 introduction of the National Security Law in Hong Kong. Exile in this context refers to both the internal, ideological, authorial state of being on the margins of society, far from the centre of power and critiquing established structures, as well as the physical exile of artists from their homeland, either of their own accord or by forced choice."Power and Politics" discusses the way in which independent documentaries respond to the social reality of China in terms of issues and aesthetics, and how the dignity of the human being constructs the humanistic concerns of documentary film in the context of a de-politicised way of thinking about documentary film. In the section "History and Memory", the documentary filmmaker and the audience discuss how (not able) to find the language of the individual to speak about personal experiences when history is suppressed and tampered with, and to construct a repressed, performative personal memory and collective history based on individual experiences, in a context of controlling the reproduction of history through the control of memory.Bringing the voices and images that have been hidden in the darkness of the dusk to the Chinese world in Hong Kong and to the discussions about China in the English-speaking world. This, perhaps, is what the China Independent Documentary Lab is doing in Hong Kong and the meaning-making of this book.The Introduction chapter can be read in the book free preview.
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4.
  • Berndt, Sonja I., et al. (creator_code:aut_t)
  • Meta-analysis of genome-wide association studies discovers multiple loci for chronic lymphocytic leukemia
  • 2016
  • record:In_t: Nature Communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 7
  • swepub:Mat_article_t (swepub:level_refereed_t)abstract
    • Chronic lymphocytic leukemia (CLL) is a common lymphoid malignancy with strong heritability. To further understand the genetic susceptibility for CLL and identify common loci associated with risk, we conducted a meta-analysis of four genome-wide association studies (GWAS) composed of 3,100 cases and 7,667 controls with follow-up replication in 1,958 cases and 5,530 controls. Here we report three new loci at 3p24.1 (rs9880772, EOMES, P = 2.55 x 10(-11)), 6p25.2 (rs73718779, SERPINB6, P = 1.97 x 10(-8)) and 3q28 (rs9815073, LPP, P = 3.62 x 10(-8)), as well as a new independent SNP at the known 2q13 locus (rs9308731, BCL2L11, P = 1.00 x 10(-11)) in the combined analysis. We find suggestive evidence (P<5 x 10(-7)) for two additional new loci at 4q24 (rs10028805, BANK1, P = 7.19 x 10(-8)) and 3p22.2 (rs1274963, CSRNP1, P = 2.12 x 10(-7)). Pathway analyses of new and known CLL loci consistently show a strong role for apoptosis, providing further evidence for the importance of this biological pathway in CLL susceptibility.
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5.
  • Cerhan, James R., et al. (creator_code:aut_t)
  • Genome-wide association study identifies multiple susceptibility loci for diffuse large B cell lymphoma
  • 2014
  • record:In_t: Nature Genetics. - : Springer Science and Business Media LLC. - 1061-4036 .- 1546-1718. ; 46:11, s. 1233-1238
  • swepub:Mat_article_t (swepub:level_refereed_t)abstract
    • Diffuse large B cell lymphoma (DLBCL) is the most common lymphoma subtype and is clinically aggressive. To identify genetic susceptibility loci for DLBCL, we conducted a meta-analysis of 3 new genome-wide association studies (GWAS) and 1 previous scan, totaling 3,857 cases and 7,666 controls of European ancestry, with additional genotyping of 9 promising SNPs in 1,359 cases and 4,557 controls. In our multi-stage analysis, five independent SNPs in four loci achieved genome-wide significance marked by rs116446171 at 6p25.3 (EXOC2; P = 2.33 x 10(-21)), rs2523607 at 6p21.33 (HLA-B; P = 2.40 x 10(-10)), rs79480871 at 2p23.3 (NCOA1; P = 4.23 x 10(-8)) and two independent SNPs, rs13255292 and rs4733601, at 8q24.21 (PVT1; P = 9.98 x 10(-13) and 3.63 x 10(-11), respectively). These data provide substantial new evidence for genetic susceptibility to this B cell malignancy and point to pathways involved in immune recognition and immune function in the pathogenesis of DLBCL.
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6.
  • Felix, Janine F, et al. (creator_code:aut_t)
  • Genome-wide association analysis identifies three new susceptibility loci for childhood body mass index.
  • 2016
  • record:In_t: Human molecular genetics. - : Oxford University Press (OUP). - 1460-2083 .- 0964-6906. ; 25:2, s. 389-403
  • swepub:Mat_article_t (swepub:level_refereed_t)abstract
    • A large number of genetic loci are associated with adult body mass index. However, the genetics of childhood body mass index are largely unknown. We performed a meta-analysis of genome-wide association studies of childhood body mass index, using sex- and age-adjusted standard deviation scores. We included 35 668 children from 20 studies in the discovery phase and 11 873 children from 13 studies in the replication phase. In total, 15 loci reached genome-wide significance (P-value < 5 × 10(-8)) in the joint discovery and replication analysis, of which 12 are previously identified loci in or close to ADCY3, GNPDA2, TMEM18, SEC16B, FAIM2, FTO, TFAP2B, TNNI3K, MC4R, GPR61, LMX1B and OLFM4 associated with adult body mass index or childhood obesity. We identified three novel loci: rs13253111 near ELP3, rs8092503 near RAB27B and rs13387838 near ADAM23. Per additional risk allele, body mass index increased 0.04 Standard Deviation Score (SDS) [Standard Error (SE) 0.007], 0.05 SDS (SE 0.008) and 0.14 SDS (SE 0.025), for rs13253111, rs8092503 and rs13387838, respectively. A genetic risk score combining all 15 SNPs showed that each additional average risk allele was associated with a 0.073 SDS (SE 0.011, P-value = 3.12 × 10(-10)) increase in childhood body mass index in a population of 1955 children. This risk score explained 2% of the variance in childhood body mass index. This study highlights the shared genetic background between childhood and adult body mass index and adds three novel loci. These loci likely represent age-related differences in strength of the associations with body mass index.
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7.
  • Flannick, Jason, et al. (creator_code:aut_t)
  • Data Descriptor : Sequence data and association statistics from 12,940 type 2 diabetes cases and controls
  • 2017
  • record:In_t: Scientific Data. - : Springer Science and Business Media LLC. - 2052-4463. ; 4
  • swepub:Mat_article_t (swepub:level_refereed_t)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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8.
  • Fuchsberger, Christian, et al. (creator_code:aut_t)
  • The genetic architecture of type 2 diabetes
  • 2016
  • record:In_t: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 536:7614, s. 41-47
  • swepub:Mat_article_t (swepub:level_refereed_t)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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9.
  • Joshi, Peter K, et al. (creator_code:aut_t)
  • Directional dominance on stature and cognition in diverse human populations
  • 2015
  • record:In_t: Nature. - : Springer Science and Business Media LLC. - 0028-0836 .- 1476-4687. ; 523:7561, s. 459-462
  • swepub:Mat_article_t (swepub:level_refereed_t)abstract
    • Homozygosity has long been associated with rare, often devastating, Mendelian disorders, and Darwin was one of the first to recognize that inbreeding reduces evolutionary fitness. However, the effect of the more distant parental relatedness that is common in modern human populations is less well understood. Genomic data now allow us to investigate the effects of homozygosity on traits of public health importance by observing contiguous homozygous segments (runs of homozygosity), which are inferred to be homozygous along their complete length. Given the low levels of genome-wide homozygosity prevalent in most human populations, information is required on very large numbers of people to provide sufficient power. Here we use runs of homozygosity to study 16 health-related quantitative traits in 354,224 individuals from 102 cohorts, and find statistically significant associations between summed runs of homozygosity and four complex traits: height, forced expiratory lung volume in one second, general cognitive ability and educational attainment (P < 1 × 10(-300), 2.1 × 10(-6), 2.5 × 10(-10) and 1.8 × 10(-10), respectively). In each case, increased homozygosity was associated with decreased trait value, equivalent to the offspring of first cousins being 1.2 cm shorter and having 10 months' less education. Similar effect sizes were found across four continental groups and populations with different degrees of genome-wide homozygosity, providing evidence that homozygosity, rather than confounding, directly contributes to phenotypic variance. Contrary to earlier reports in substantially smaller samples, no evidence was seen of an influence of genome-wide homozygosity on blood pressure and low density lipoprotein cholesterol, or ten other cardio-metabolic traits. Since directional dominance is predicted for traits under directional evolutionary selection, this study provides evidence that increased stature and cognitive function have been positively selected in human evolution, whereas many important risk factors for late-onset complex diseases may not have been.
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10.
  • Li, Man, et al. (creator_code:aut_t)
  • SOS2 and ACP1 Loci Identified through Large-Scale Exome Chip Analysis Regulate Kidney Development and Function
  • 2017
  • record:In_t: Journal of the American Society of Nephrology: JASN. - 1533-3450. ; 28:3, s. 981-994
  • swepub:Mat_article_t (swepub:level_refereed_t)abstract
    • Genome-wide association studies have identified >50 common variants associated with kidney function, but these variants do not fully explain the variation in eGFR. We performed a two-stage meta-analysis of associations between genotypes from the Illumina exome array and eGFR on the basis of serum creatinine (eGFRcrea) among participants of European ancestry from the CKDGen Consortium (nStage1: 111,666; nStage2: 48,343). In single-variant analyses, we identified single nucleotide polymorphisms at seven new loci associated with eGFRcrea (PPM1J, EDEM3, ACP1, SPEG, EYA4, CYP1A1, and ATXN2L; PStage1<3.7×10-7), of which most were common and annotated as nonsynonymous variants. Gene-based analysis identified associations of functional rare variants in three genes with eGFRcrea, including a novel association with the SOS Ras/Rho guanine nucleotide exchange factor 2 gene, SOS2 (P=5.4×10-8 by sequence kernel association test). Experimental follow-up in zebrafish embryos revealed changes in glomerular gene expression and renal tubule morphology in the embryonic kidney of acp1- and sos2-knockdowns. These developmental abnormalities associated with altered blood clearance rate and heightened prevalence of edema. This study expands the number of loci associated with kidney function and identifies novel genes with potential roles in kidney formation.
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