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Träfflista för sökning "WFRF:(Flanagan A M) srt2:(2005-2009)"

Sökning: WFRF:(Flanagan A M) > (2005-2009)

  • Resultat 1-6 av 6
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1.
  • Flanagan, K. T., et al. (författare)
  • Nuclear Spins and Magnetic Moments of Cu-71,Cu-73,Cu-75 : Inversion of pi 2p(3/2) and pi 1f(5/2) Levels in Cu-75
  • 2009
  • Ingår i: Physical Review Letters. - 0031-9007 .- 1079-7114. ; 103:14, s. 142501-
  • Tidskriftsartikel (refereegranskat)abstract
    • We report the first confirmation of the predicted inversion between the pi 2p(3/2) and pi 1f(5/2) nuclear states in the nu g(9/2) midshell. This was achieved at the ISOLDE facility, by using a combination of in-source laser spectroscopy and collinear laser spectroscopy on the ground states of Cu-71,Cu-73,Cu-75, which measured the nuclear spin and magnetic moments. The obtained values are mu(Cu-71)=+2.2747(8)mu(N), mu(Cu-73)=+1.7426(8)mu(N), and mu(Cu-75)=+1.0062(13)mu(N) corresponding to spins I=3/2 for Cu-71,Cu-73 and I=5/2 for Cu-75. The results are in fair agreement with large-scale shell-model calculations.
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  • Beurskens, M. N. A., et al. (författare)
  • Pedestal width and ELM size identity studies in JET and DIII-D; implications for ITER
  • 2009
  • Ingår i: Plasma Physics and Controlled Fusion. - : IOP Publishing. - 0741-3335 .- 1361-6587. ; 51:12, s. 124051-
  • Tidskriftsartikel (refereegranskat)abstract
    • The dependence of the H-mode edge transport barrier width on normalized ion gyroradius (rho* = rho/a) in discharges with type I ELMs was examined in experiments combining data for the JET and DIII-D tokamaks. The plasma configuration as well as the local normalized pressure (beta), collisionality (nu*), Mach number and the ratio of ion and electron temperature at the pedestal top were kept constant, while rho* was varied by a factor of four. The width of the steep gradient region of the electron temperature (T-e) and density (n(e)) pedestals normalized to machine size showed no or only a weak trend with rho*. A rho(1/2) or rho(1) dependence of the pedestal width, given by some theoretical predictions, is not supported by the current experiments. This is encouraging for the pedestal scaling towards ITER as it operates at lower rho* than existing devices. Some differences in pedestal structure and ELM behaviour were, however, found between the devices; in the DIII-D discharges, the n(e) and T-e pedestal were aligned at high rho* but the ne pedestal shifted outwards in radius relative to T-e as rho* decreases, while on JET the profiles remained aligned while rho* was scanned by a factor of two. The energy loss at an ELM normalized to the pedestal energy increased from 10% to 40% as rho* increased by a factor of two in the DIII-D discharges but no such variation was observed in the case of JET. The measured pedestal pressures and widths were found to be consistent with the predictions from modelling based on peeling-ballooning stability theory, and are used to make projections towards ITER
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5.
  • Tchkonia, T, et al. (författare)
  • Identification of depot-specific human fat cell progenitors through distinct expression profiles and developmental gene patterns
  • 2007
  • Ingår i: American journal of physiology. Endocrinology and metabolism. - : American Physiological Society. - 0193-1849 .- 1522-1555. ; 292:1, s. E298-E307
  • Tidskriftsartikel (refereegranskat)abstract
    • Anatomically separate fat depots differ in size, function, and contribution to pathological states, such as the metabolic syndrome. We isolated preadipocytes from different human fat depots to determine whether the basis for this variation is partly attributable to differences in inherent properties of fat cell progenitors. We found that genome-wide expression profiles of primary preadipocytes cultured in parallel from abdominal subcutaneous, mesenteric, and omental fat depots were distinct. Interestingly, visceral fat was not homogeneous. Preadipocytes from one of the two main visceral depots, mesenteric fat, had an expression profile closer to that of subcutaneous than omental preadipocytes, the other main visceral depot. Expression of genes that regulate early development, including homeotic genes, differed extensively among undifferentiated preadipocytes isolated from different fat depots. These profiles were confirmed by real-time PCR analysis of preadipocytes from additional lean and obese male and female subjects. We made preadipocyte strains from single abdominal subcutaneous and omental preadipocytes by expressing telomerase. Depot-specific developmental gene expression profiles persisted for 40 population doublings in these strains. Thus, human fat cell progenitors from different regions are effectively distinct, consistent with different fat depots being separate mini-organs.
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6.
  • Richard, Ann-Marie T, et al. (författare)
  • Tissue-dependent loss of phosphofructokinase-M in mice with interrupted activity of the distal promoter : impairment in insulin secretion
  • 2007
  • Ingår i: American Journal of Physiology. Endocrinology and Metabolism. - : American Physiological Society. - 0193-1849 .- 1522-1555. ; 293:3, s. E794-801
  • Tidskriftsartikel (refereegranskat)abstract
    • Phosphofructokinase is a key enzyme of glycolysis that exists as homo- and heterotetramers of three subunit isoforms: muscle, liver, and C type. Mice with a disrupting tag inserted near the distal promoter of the phosphofructokinase-M gene showed tissue-dependent differences in loss of that isoform: 99% in brain and 95-98% in islets, but only 50-75% in skeletal muscle and little if any loss in heart. This correlated with the continued presence of proximal transcripts specifically in muscle tissues. These data strongly support the proposed two-promoter system of the gene, with ubiquitous use of the distal promoter and additional use of the proximal promoter selectively in muscle. Interestingly, the mice were glucose intolerant and had somewhat elevated fasting and fed blood glucose levels; however, they did not have an abnormal insulin tolerance test, consistent with the less pronounced loss of phosphofructokinase-M in muscle. Isolated perifused islets showed about 50% decreased glucose-stimulated insulin secretion and reduced amplitude and regularity of secretory oscillations. Oscillations in cytoplasmic free Ca(2+) and the rise in the ATP/ADP ratio appeared normal. Secretory oscillations still occurred in the presence of diazoxide and high KCl, indicating an oscillation mechanism not requiring dynamic Ca(2+) changes. The results suggest the importance of phosphofructokinase-M for insulin secretion, although glucokinase is the overall rate-limiting glucose sensor. Whether the Ca(2+) oscillations and residual insulin oscillations in this mouse model are due to the residual 2-5% phosphofructokinase-M or to other phosphofructokinase isoforms present in islets or involve another metabolic oscillator remains to be determined.
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