SwePub
Sök i SwePub databas

  Extended search

Träfflista för sökning "WFRF:(Motyka R) "

Search: WFRF:(Motyka R)

  • Result 1-5 of 5
Sort/group result
   
EnumerationReferenceCoverFind
1.
  • Rosendahl, J, et al. (author)
  • Genome-wide association study identifies inversion in the CTRB1-CTRB2 locus to modify risk for alcoholic and non-alcoholic chronic pancreatitis
  • 2018
  • In: Gut. - : BMJ. - 1468-3288 .- 0017-5749. ; 67:10, s. 1855-1863
  • Journal article (peer-reviewed)abstract
    • Alcohol-related pancreatitis is associated with a disproportionately large number of hospitalisations among GI disorders. Despite its clinical importance, genetic susceptibility to alcoholic chronic pancreatitis (CP) is poorly characterised. To identify risk genes for alcoholic CP and to evaluate their relevance in non-alcoholic CP, we performed a genome-wide association study and functional characterisation of a new pancreatitis locus.Design1959 European alcoholic CP patients and population-based controls from the KORA, LIFE and INCIPE studies (n=4708) as well as chronic alcoholics from the GESGA consortium (n=1332) were screened with Illumina technology. For replication, three European cohorts comprising 1650 patients with non-alcoholic CP and 6695 controls originating from the same countries were used.ResultsWe replicated previously reported risk loci CLDN2-MORC4, CTRC, PRSS1-PRSS2 and SPINK1 in alcoholic CP patients. We identified CTRB1-CTRB2 (chymotrypsin B1 and B2) as a new risk locus with lead single-nucleotide polymorphism (SNP) rs8055167 (OR 1.35, 95% CI 1.23 to 1.6). We found that a 16.6 kb inversion in the CTRB1-CTRB2 locus was in linkage disequilibrium with the CP-associated SNPs and was best tagged by rs8048956. The association was replicated in three independent European non-alcoholic CP cohorts of 1650 patients and 6695 controls (OR 1.62, 95% CI 1.42 to 1.86). The inversion changes the expression ratio of the CTRB1 and CTRB2 isoforms and thereby affects protective trypsinogen degradation and ultimately pancreatitis risk.ConclusionAn inversion in the CTRB1-CTRB2 locus modifies risk for alcoholic and non-alcoholic CP indicating that common pathomechanisms are involved in these inflammatory disorders.
  •  
2.
  •  
3.
  • Jung, Hannes, et al. (author)
  • What HERA may provide?
  • 2008
  • In: Proceedings, 16th International Workshop on Deep Inelastic Scattering and Related Subjects (DIS 2008): London, UK, April 7-11, 2008. - Amsterdam : Science Wise Publishing. ; , s. 17-17
  • Conference paper (other academic/artistic)
  •  
4.
  • Kreiss, C. M., et al. (author)
  • Ocean warming and acidification modulate energy budget and gill ion regulatory mechanisms in Atlantic cod (Gadus morhua)
  • 2015
  • In: Journal of Comparative Physiology B-Biochemical Systemic and Environmental Physiology. - : Springer Science and Business Media LLC. - 0174-1578. ; 185:7, s. 767-781
  • Journal article (peer-reviewed)abstract
    • Ocean warming and acidification are threatening marine ecosystems. In marine animals, acidification is thought to enhance ion regulatory costs and thereby baseline energy demand, while elevated temperature also increases baseline metabolic rate. Here we investigated standard metabolic rates (SMR) and plasma parameters of Atlantic cod (Gadus morhua) after 3-4 weeks of exposure to ambient and future PCO2 levels (550, 1200 and 2200 A mu atm) and at two temperatures (10, 18 A degrees C). In vivo branchial ion regulatory costs were studied in isolated, perfused gill preparations. Animals reared at 18 A degrees C responded to increasing CO2 by elevating SMR, in contrast to specimens at 10 A degrees C. Isolated gills at 10 A degrees C and elevated PCO2 (a parts per thousand yen1200 A mu atm) displayed increased soft tissue mass, in parallel to increased gill oxygen demand, indicating an increased fraction of gill in whole animal energy budget. Altered gill size was not found at 18 A degrees C, where a shift in the use of ion regulation mechanisms occurred towards enhanced Na+/H+-exchange and HCO3 (-) transport at high PCO2 (2200 A mu atm), paralleled by higher Na+/K+-ATPase activities. This shift did not affect total gill energy consumption leaving whole animal energy budget unaffected. Higher Na+/K+-ATPase activities in the warmth might have compensated for enhanced branchial permeability and led to reduced plasma Na+ and/or Cl- concentrations and slightly lowered osmolalities seen at 18 A degrees C and 550 or 2200 A mu atm PCO2 in vivo. Overall, the gill as a key ion regulation organ seems to be highly effective in supporting the resilience of cod to effects of ocean warming and acidification.
  •  
5.
  • Makita, M., et al. (author)
  • Femtosecond phase-transition in hard x-ray excited bismuth
  • 2019
  • In: Scientific Reports. - : NATURE PUBLISHING GROUP. - 2045-2322. ; 9
  • Journal article (peer-reviewed)abstract
    • The evolution of bismuth crystal structure upon excitation of its A(1g) phonon has been intensely studied with short pulse optical lasers. Here we present the first-time observation of a hard x-ray induced ultrafast phase transition in a bismuth single crystal at high intensities (similar to 10(14) W/cm(2)). The lattice evolution was followed using a recently demonstrated x-ray single-shot probing setup. The time evolution of the (111) Bragg peak intensity showed strong dependence on the excitation fluence. After exposure to a sufficiently intense x-ray pulse, the peak intensity dropped to zero within 300 fs, i.e. faster than one oscillation period of the A(1g) mode at room temperature. Our analysis indicates a nonthermal origin of a lattice disordering process, and excludes interpretations based on electron-ion equilibration process, or on thermodynamic heating process leading to plasma formation.
  •  
Skapa referenser, mejla, bekava och länka
  • Result 1-5 of 5

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 Close

Copy and save the link in order to return to this view