SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Tsao PS) "

Sökning: WFRF:(Tsao PS)

  • Resultat 1-50 av 58
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
1.
  •  
2.
  •  
3.
  •  
4.
  •  
5.
  •  
6.
  •  
7.
  •  
8.
  •  
9.
  •  
10.
  •  
11.
  •  
12.
  •  
13.
  •  
14.
  •  
15.
  •  
16.
  •  
17.
  •  
18.
  •  
19.
  •  
20.
  •  
21.
  • Lim, C, et al. (författare)
  • Linking single nucleotide polymorphisms to signaling blueprints in abdominal aortic aneurysms
  • 2022
  • Ingår i: Scientific reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 12:1, s. 20990-
  • Tidskriftsartikel (refereegranskat)abstract
    • Abdominal aortic aneurysms (AAA) is a multifactorial complex disease with life-threatening consequences. While Genome-wide association studies (GWAS) have revealed several single nucleotide polymorphisms (SNPs) located in the genome of individuals with AAA, the link between SNPs with the associated pathological signals, the influence of risk factors on their distribution and their combined analysis is not fully understood. We integrated 86 AAA SNPs from GWAS and clinical cohorts from the literature to determine their phenotypical vulnerabilities and association with AAA risk factors. The SNPs were annotated using snpXplorer AnnotateMe tool to identify their chromosomal position, minor allele frequency, CADD (Combined Annotation Dependent Depletion), annotation-based pathogenicity score, variant consequence, and their associated gene. Gene enrichment analysis was performed using Gene Ontology and clustered using REVIGO. The plug-in GeneMANIA in Cytoscape was applied to identify network integration with associated genes and functions. 15 SNPs affecting 20 genes with a CADD score above ten were identified. AAA SNPs were predominantly located on chromosome 3 and 9. Stop-gained rs5516 SNP obtained high frequency in AAA and associated with proinflammatory and vascular remodeling phenotypes. SNPs presence positively correlated with hypertension, dyslipidemia and smoking history. GO showed that AAA SNPs and their associated genes could regulate lipid metabolism, extracellular matrix organization, smooth muscle cell proliferation, and oxidative stress, suggesting that part of these AAA traits could stem from genetic abnormalities. We show a library of inborn SNPs and associated genes that manifest in AAA. We uncover their pathological signaling trajectories that likely fuel AAA development.
  •  
22.
  •  
23.
  •  
24.
  •  
25.
  • Maegdefessel, L, et al. (författare)
  • Micromanaging abdominal aortic aneurysms
  • 2013
  • Ingår i: International journal of molecular sciences. - : MDPI AG. - 1422-0067. ; 14:7, s. 14374-14394
  • Tidskriftsartikel (refereegranskat)
  •  
26.
  •  
27.
  •  
28.
  •  
29.
  •  
30.
  •  
31.
  • Maegdefessel, L, et al. (författare)
  • miR-24 limits aortic vascular inflammation and murine abdominal aneurysm development
  • 2014
  • Ingår i: Nature communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 5, s. 5214-
  • Tidskriftsartikel (refereegranskat)abstract
    • Identification and treatment of abdominal aortic aneurysm (AAA) remain among the most prominent challenges in vascular medicine. MicroRNAs (miRNAs) are crucial regulators of cardiovascular pathology and represent intriguing targets to limit AAA expansion. Here we show, by using two established murine models of AAA disease along with human aortic tissue and plasma analysis, that miR-24 is a key regulator of vascular inflammation and AAA pathology. In vivo and in vitro studies reveal chitinase 3-like 1 (Chi3l1) to be a major target and effector under the control of miR-24, regulating cytokine synthesis in macrophages as well as their survival, promoting aortic smooth muscle cell migration and cytokine production, and stimulating adhesion molecule expression in vascular endothelial cells. We further show that modulation of miR-24 alters AAA progression in animal models, and that miR-24 and CHI3L1 represent novel plasma biomarkers of AAA disease progression in humans.
  •  
32.
  •  
33.
  • Maegdefessel, L, et al. (författare)
  • Pathogenesis of abdominal aortic aneurysms: microRNAs, proteases, genetic associations
  • 2014
  • Ingår i: Annual review of medicine. - : Annual Reviews. - 1545-326X .- 0066-4219. ; 65, s. 49-62
  • Tidskriftsartikel (refereegranskat)abstract
    • Abdominal aortic aneurysm (AAA) disease is a common, morbid, and highly lethal pathology. Extraordinary efforts have been launched to determine the molecular and pathophysiological characteristics of AAAs. Although surgery is highly effective in preventing death by rupture for larger AAAs, no guidance or preventive therapy is currently available for the >90% of patients whose aneurysms are below the surgical threshold. Predictive animal models of AAA as well as human pathological samples have revealed a complex circuit of AAA formation and progression. The proteolytic destruction of matrix components of the aorta by different proteases has been extensively studied over many years. Recently, a novel class of small noncoding RNAs, called microRNAs, was identified as “fine-tuners” of the translational output of target genes; they act by promoting mRNA degradation. Their therapeutic potential in limiting AAA development appears very intriguing. Further, current studies assessing genetic and heritable associations for AAA disease have provided great insight into its pathogenesis, potentially enabling us to better clinically manage affected patients.
  •  
34.
  •  
35.
  • Mishra, A, et al. (författare)
  • Diminishing benefits of urban living for children and adolescents' growth and development
  • 2023
  • Ingår i: Nature. - : Springer Science and Business Media LLC. - 1476-4687 .- 0028-0836. ; 615:7954, s. 874-883
  • Tidskriftsartikel (refereegranskat)abstract
    • Optimal growth and development in childhood and adolescence is crucial for lifelong health and well-being1–6. Here we used data from 2,325 population-based studies, with measurements of height and weight from 71 million participants, to report the height and body-mass index (BMI) of children and adolescents aged 5–19 years on the basis of rural and urban place of residence in 200 countries and territories from 1990 to 2020. In 1990, children and adolescents residing in cities were taller than their rural counterparts in all but a few high-income countries. By 2020, the urban height advantage became smaller in most countries, and in many high-income western countries it reversed into a small urban-based disadvantage. The exception was for boys in most countries in sub-Saharan Africa and in some countries in Oceania, south Asia and the region of central Asia, Middle East and north Africa. In these countries, successive cohorts of boys from rural places either did not gain height or possibly became shorter, and hence fell further behind their urban peers. The difference between the age-standardized mean BMI of children in urban and rural areas was <1.1 kg m–2 in the vast majority of countries. Within this small range, BMI increased slightly more in cities than in rural areas, except in south Asia, sub-Saharan Africa and some countries in central and eastern Europe. Our results show that in much of the world, the growth and developmental advantages of living in cities have diminished in the twenty-first century, whereas in much of sub-Saharan Africa they have amplified.
  •  
36.
  •  
37.
  •  
38.
  •  
39.
  •  
40.
  •  
41.
  •  
42.
  •  
43.
  •  
44.
  •  
45.
  •  
46.
  • Spin, JM, et al. (författare)
  • Non-coding RNAs in aneurysmal aortopathy
  • 2019
  • Ingår i: Vascular pharmacology. - : Elsevier BV. - 1879-3649 .- 1537-1891. ; 114, s. 110-121
  • Tidskriftsartikel (refereegranskat)
  •  
47.
  •  
48.
  •  
49.
  •  
50.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 1-50 av 58

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy