SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Thorell N. E.) "

Sökning: WFRF:(Thorell N. E.)

  • Resultat 1-15 av 15
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
1.
  •  
2.
  •  
3.
  •  
4.
  • Tai, F, et al. (författare)
  • Abdominal Wall Miscellaneous
  • 2015
  • Ingår i: Hernia : the journal of hernias and abdominal wall surgery. - 1248-9204. ; 19 Suppl 1, s. S5-S12
  • Tidskriftsartikel (refereegranskat)
  •  
5.
  •  
6.
  • Li, Q., et al. (författare)
  • Obesity and hyperinsulinemia drive adipocytes to activate a cell cycle program and senesce
  • 2021
  • Ingår i: Nature Medicine. - : Springer Science and Business Media LLC. - 1078-8956 .- 1546-170X. ; 27, s. 1941-1953
  • Tidskriftsartikel (refereegranskat)abstract
    • Obesity is considered an important factor for many chronic diseases, including diabetes, cardiovascular disease and cancer. The expansion of adipose tissue in obesity is due to an increase in both adipocyte progenitor differentiation and mature adipocyte cell size. Adipocytes, however, are thought to be unable to divide or enter the cell cycle. We demonstrate that mature human adipocytes unexpectedly display a gene and protein signature indicative of an active cell cycle program. Adipocyte cell cycle progression associates with obesity and hyperinsulinemia, with a concomitant increase in cell size, nuclear size and nuclear DNA content. Chronic hyperinsulinemia in vitro or in humans, however, is associated with subsequent cell cycle exit, leading to a premature senescent transcriptomic and secretory profile in adipocytes. Premature senescence is rapidly becoming recognized as an important mediator of stress-induced tissue dysfunction. By demonstrating that adipocytes can activate a cell cycle program, we define a mechanism whereby mature human adipocytes senesce. We further show that by targeting the adipocyte cell cycle program using metformin, it is possible to influence adipocyte senescence and obesity-associated adipose tissue inflammation. Studies in mature human adipocytes demonstrate that obesity and hyperinsulinemia can induce reentry into the cell cycle and induce senescence.
  •  
7.
  • Källström, Claes, et al. (författare)
  • Adaptive Autopilots for Large Tankers
  • 1978
  • Ingår i: 7th Triennial World Congress of the IFAC : A Link Between Science and Applications of Automatic Control, Helsinki, Finland, 12-16 June - A Link Between Science and Applications of Automatic Control, Helsinki, Finland, 12-16 June. - 1474-6670. ; 11:1, s. 477-484
  • Konferensbidrag (refereegranskat)abstract
    • The adaptive autopilots are based on velocity scheduling, a self-tuning regulator for steady state course keeping, a high gain turning regulator with variable structure, and a Kalman filter. Results from simulations and full-scale experiments on three different tankers are presented. The autopilots are shown to work excellently under different loads, speed and weather conditions.
  •  
8.
  •  
9.
  • Källström, Claes G., et al. (författare)
  • Adaptive Autopilots for Tankers
  • 1979
  • Ingår i: Automatica. - : Elsevier BV. - 0005-1098. ; 15:3, s. 241-254
  • Tidskriftsartikel (refereegranskat)abstract
    • Two adaptive autopilots for ships are designed, The autopilots are based on velocity scheduling, a self-tuning regulator for steady state course keeping, a high gain turning regulator with variable structure and a Kalman filter.Methods for design of the autopilots are discussed. Results from simulations and full-scale experiments with three different tankers are presented. The autopilots are shown to work excellently under different load, speed, and weather conditions.
  •  
10.
  • LeBlanc, K, et al. (författare)
  • Quality of Life after Hernia Surgery
  • 2015
  • Ingår i: Hernia : the journal of hernias and abdominal wall surgery. - 1248-9204. ; 19 Suppl 1, s. S127-31
  • Tidskriftsartikel (refereegranskat)
  •  
11.
  • Mileti, E, et al. (författare)
  • Human White Adipose Tissue Displays Selective Insulin Resistance in the Obese State
  • 2021
  • Ingår i: Diabetes. - : American Diabetes Association. - 1939-327X .- 0012-1797. ; 70:7, s. 1486-1497
  • Tidskriftsartikel (refereegranskat)abstract
    • Selective hepatic insulin resistance is a feature of obesity and type 2 diabetes. Whether similar mechanisms operate in white adipose tissue (WAT) of those with obesity and to what extent these are normalized by weight loss are unknown. We determined insulin sensitivity by hyperinsulinemic euglycemic clamp and insulin response in subcutaneous WAT by RNA sequencing in 23 women with obesity before and 2 years after bariatric surgery. To control for effects of surgery, women postsurgery were matched to never-obese women. Multidimensional analyses of 138 samples allowed us to classify the effects of insulin into three distinct expression responses: a common set was present in all three groups and included genes encoding several lipid/cholesterol biosynthesis enzymes; a set of obesity-attenuated genes linked to tissue remodeling and protein translation was selectively regulated in the two nonobese states; and several postobesity-enriched genes encoding proteins involved in, for example, one-carbon metabolism were only responsive to insulin in the women who had lost weight. Altogether, human WAT displays a selective insulin response in the obese state, where most genes are normalized by weight loss. This comprehensive atlas provides insights into the transcriptional effects of insulin in WAT and may identify targets to improve insulin action.
  •  
12.
  • Musi, N., et al. (författare)
  • Metformin increases AMP-activated-protein-kinase activity in skeletal of subjects with type 2 diabetes
  • 2002
  • Ingår i: Diabetes. - Alexandra, VA, USA : American Diabetes Association Inc.. - 0012-1797 .- 1939-327X. ; 51:7, s. 2074-2081
  • Tidskriftsartikel (refereegranskat)abstract
    • Metformin is an effective hypoglycemic drug that lowers blood glucose concentrations by decreasing hepatic glucose production and increasing glucose disposal in skeletal muscle; however, the molecular site of metformin action is not well understood. AMP-activated protein kinase (AMPK) activity increases in response to depletion of cellular energy stores, and this enzyme has been implicated in the stimulation of glucose uptake into skeletal muscle and the inhibition of liver gluconeogenesis. We recently reported that AMPK is activated by metformin in cultured rat hepatocytes, mediating the inhibitory effects of the drug on hepatic glucose production. In the present study, we evaluated whether therapeutic doses of metformin increase AMPK activity in vivo in subjects with type 2 diabetes. Metformin treatment for 10 weeks significantly increased AMPK α2 activity in the skeletal muscle, and this was associated with increased phosphorylation of AMPK on Thr172 and decreased acetyl-CoA carboxylase-2 activity. The increase in AMPK α2 activity was likely due to a change in muscle energy status because ATP and phosphocreatine concentrations were lower after metformin treatment. Metformin-induced increases in AMPK activity were associated with higher rates of glucose disposal and muscle glycogen concentrations. These findings suggest that the metabolic effects of metformin in subjects with type 2 diabetes may be mediated by the activation of AMPK α2.
  •  
13.
  •  
14.
  • Thorell, Kaisa, 1983, et al. (författare)
  • The Helicobacter pylori Genome Project: insights into H. pylori population structure from analysis of a worldwide collection of complete genomes
  • 2023
  • Ingår i: Nature Communications. - 2041-1723. ; 14:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Helicobacter pylori, a dominant member of the gastric microbiota, shares co-evolutionary history with humans. This has led to the development of genetically distinct H. pylori subpopulations associated with the geographic origin of the host and with differential gastric disease risk. Here, we provide insights into H. pylori population structure as a part of the Helicobacter pylori Genome Project (HpGP), a multi-disciplinary initiative aimed at elucidating H. pylori pathogenesis and identifying new therapeutic targets. We collected 1011 well-characterized clinical strains from 50 countries and generated high-quality genome sequences. We analysed core genome diversity and population structure of the HpGP dataset and 255 worldwide reference genomes to outline the ancestral contribution to Eurasian, African, and American populations. We found evidence of substantial contribution of population hpNorthAsia and subpopulation hspUral in Northern European H. pylori. The genomes of H. pylori isolated from northern and southern Indigenous Americans differed in that bacteria isolated in northern Indigenous communities were more similar to North Asian H. pylori while the southern had higher relatedness to hpEastAsia. Notably, we also found a highly clonal yet geographically dispersed North American subpopulation, which is negative for the cag pathogenicity island, and present in 7% of sequenced US genomes. We expect the HpGP dataset and the corresponding strains to become a major asset for H. pylori genomics.
  •  
15.
  • Thorpe, H. A., et al. (författare)
  • Repeated out-of-Africa expansions of Helicobacter pylori driven by replacement of deleterious mutations
  • 2022
  • Ingår i: Nature Communications. - : Springer Science and Business Media LLC. - 2041-1723. ; 13:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Helicobacter pylori lives in the human stomach and has a population structure resembling that of its host. However, H. pylori from Europe and the Middle East trace substantially more ancestry from modern African populations than the humans that carry them. Here, we use a collection of Afro-Eurasian H. pylori genomes to show that this African ancestry is due to at least three distinct admixture events. H. pylori from East Asia, which have undergone little admixture, have accumulated many more non-synonymous mutations than African strains. European and Middle Eastern bacteria have elevated African ancestry at the sites of these mutations, implying selection to remove them during admixture. Simulations show that population fitness can be restored after bottlenecks by migration and subsequent admixture of small numbers of bacteria from non-bottlenecked populations. We conclude that recent spread of African DNA has been driven by deleterious mutations accumulated during the original out-of-Africa bottleneck.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 1-15 av 15

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