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Träfflista för sökning "hsv:(NATURVETENSKAP) hsv:(Matematik) hsv:(Beräkningsmatematik) ;pers:(Wennberg Bernt 1961)"

Sökning: hsv:(NATURVETENSKAP) hsv:(Matematik) hsv:(Beräkningsmatematik) > Wennberg Bernt 1961

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1.
  • Adiels, Martin, 1976, et al. (författare)
  • Overproduction of VLDL1 driven by hyperglycemia is a dominant feature of diabetic dyslipidemia
  • 2005
  • Ingår i: Arterioscler Thromb Vasc Biol. - 1524-4636 .- 1079-5642. ; 25:8, s. 1697-703
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: We sought to compare the synthesis and metabolism of VLDL1 and VLDL2 in patients with type 2 diabetes mellitus (DM2) and nondiabetic subjects. METHODS AND RESULTS: We used a novel multicompartmental model to simultaneously determine the kinetics of apolipoprotein (apo) B and triglyceride (TG) in VLDL1 and VLDL2 after a bolus injection of [2H3]leucine and [2H5]glycerol and to follow the catabolism and transfer of the lipoprotein particles. Our results show that the overproduction of VLDL particles in DM2 is explained by enhanced secretion of VLDL1 apoB and TG. Direct production of VLDL2 apoB and TG was not influenced by diabetes per se. The production rates of VLDL1 apoB and TG were closely related, as were the corresponding pool sizes. VLDL1 and VLDL2 compositions did not differ in subjects with DM2 and controls, and the TG to apoB ratio of newly synthesized particles was very similar in the 2 groups. Plasma glucose, insulin, and free fatty acids together explained 55% of the variation in VLDL1 TG production rate. CONCLUSIONS: Insulin resistance and DM2 are associated with excess hepatic production of VLDL1 particles similar in size and composition to those in nondiabetic subjects. We propose that hyperglycemia is the driving force that aggravates overproduction of VLDL1 in DM2.
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  • Anguelova, Milena, 1978, et al. (författare)
  • On analytic and algebraic observability of nonlinear delay systems
  • 2010
  • Ingår i: Automatica. - : Elsevier BV. - 0005-1098. ; 46:4, s. 682-686
  • Tidskriftsartikel (refereegranskat)abstract
    • The observability of nonlinear delay systems has previously been defined in an algebraic setting by a rank condition on modules over noncommutative rings. We introduce an analytic definition of observability to ensure the local uniqueness of state and initial conditions that correspond to a given input-output behaviour. It is shown that an algebraically observable delay system can be reformulated as a system of ordinary differential equations. Analytic observability is then decided by the local uniqueness of solutions to a boundary value problem for this ODE system. (C) 2010 Elsevier Ltd. All rights reserved.
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  • Anguelova, Milena, 1978, et al. (författare)
  • State elimination and identifiability of the delay parameter for nonlinear time-delay systems
  • 2008
  • Ingår i: Automatica. - : Elsevier BV. - 0005-1098. ; 44:5, s. 1373-1378
  • Tidskriftsartikel (refereegranskat)abstract
    • The identifiability of the delay parameter for nonlinear systems with a single constant time delay is analyzed. We show the existence of input–output equations and relate the identifiability of the delay parameter to their form. Explicit criteria based on rank calculations are formulated. The identifiability of the delay parameter is shown not to be directly related to the well-characterized identifiability/observability of the other system parameters/states.
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  • Berglund, Martin, 1980, et al. (författare)
  • Investigations of a compartmental model for leucine kinetics using non-linear mixed effects models with ordinary and stochastic differential equations.
  • 2012
  • Ingår i: Mathematical Medicine and Biology. - : Oxford University Press (OUP). - 1477-8599 .- 1477-8602. ; 29:4, s. 361-384
  • Tidskriftsartikel (refereegranskat)abstract
    • Non-linear mixed effects (NLME) models represent a powerful tool to simultaneously analyse data from several individuals. In this study, a compartmental model of leucine kinetics is examined and extended with a stochastic differential equation to model non-steady-state concentrations of free leucine in the plasma. Data obtained from tracer/tracee experiments for a group of healthy control individuals and a group of individuals suffering from diabetes mellitus type 2 are analysed. We find that the interindividual variation of the model parameters is much smaller for the NLME models, compared to traditional estimates obtained from each individual separately. Using the mixed effects approach, the population parameters are estimated well also when only half of the data are used for each individual. For a typical individual, the amount of free leucine is predicted to vary with a standard deviation of 8.9% around a mean value during the experiment. Moreover, leucine degradation and protein uptake of leucine is smaller, proteolysis larger and the amount of free leucine in the body is much larger for the diabetic individuals than the control individuals. In conclusion, NLME models offers improved estimates for model parameters in complex models based on tracer/tracee data and may be a suitable tool to reduce data sampling in clinical studies.
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  • Henriksson, J., et al. (författare)
  • A Model of Sympatric Speciation Through Reinforcement
  • 2010
  • Ingår i: Kinetic and Related Models. - : American Institute of Mathematical Sciences (AIMS). - 1937-5093 .- 1937-5077. ; 3:1, s. 143-163
  • Tidskriftsartikel (refereegranskat)abstract
    • Sympatric speciation, i.e. the evolutionary split of one species into two in the same environment, has been a highly troublesome concept. It has been a questioned if it is actually possible. Even though there have been a number of reported results both in the wild and from controlled experiments in laboratories, those findings are both hard to get and hard to analyze, or even repeat. In the current study we propose a mathematical model which addresses the question of sympatric speciation and the evolution of reinforcement. Our aim has been to capture some of the essential features such as: phenotype, resources, competition, heritage, mutation, and reinforcement, in as simple a way as possible. Still, the resulting model is not too easy to grasp with purely analytical tools, so we have also complemented those studies with stochastic simulations. We present a few results that both illustrates the usefulness of such a model, but also rises new biological questions about sympatric speciation and reinforcement in particular.
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  • Resultat 1-10 av 16

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