PubMed Health⌕ Search

PubMed · 7724014

Urea kinetic modelling.

Abstract

The source did not provide an abstract. Follow the original record for more information.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

S W Smye, T Buur, E J Will. 1995. Urea kinetic modelling.. https://pubmed.ncbi.nlm.nih.gov/7724014/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Quantitative differentiation between BOLD models in fMRI.

Several gradient-echo fMRI blood oxygenation level-dependent (BOLD) effects are described in the literature: extravascular spin dephasing around capillaries and veins, intravascular phase changes, and transverse relaxation changes of blood. This work considers a series of tissue compartmentalized models incorporating each of these effects, and tries to determine the model which is most consistent with the data. To isolate the different tissue contributions, a series of multi-echo inversion recovery (IR) fMRI scans were performed. Visual stimulation experiments were performed at 1.5 T, one interleaved six-echo and two IR six-echo EPI scans (the latter to suppress gray matter (GM) and cerebrospinal fluid (CSF)). The tissue and vascular composition of activated areas was analyzed using independent spin-echo IR MRI experiments and MR venography, respectively. This information was used to fit the multi-echo fMRI data to the BOLD models. The activated areas almost always included a venous vessel visible on the venogram and consisted of GM and CSF. The fMRI signal changes were best described by extravascular dephasing effects in both GM and CSF around a venous vessel, in combination with intravascular effects. The role of spin dephasing around capillaries in GM appears to be insignificant. Magn Reson Med 45:233-246, 2001.

Body Fluid Compartments↗

Indirect pharmacodynamic models for responses with multicompartmental distribution or polyexponential disposition.

Basic indirect response models where drug alters the production (kin) of the response variable (R) based on the Hill function previously assumed one-compartment distribution of the response variable and simple first-order loss (kout) of R. These models were extended using convolution theory to consideration of two-compartment distribution of R and/or polyexponential loss of R. Theoretical equations and methods of data analysis were developed and simulations are provided to demonstrate expected response behavior based on biexponential response dissipation. The inhibition model was applied to our previous data for inhibition of circadian cortisol secretion by prednisolone. The presence of multicompartment response variables and/or polyexponential loss complicates the response patterns and resolution of pharmacologic parameters of indirect response models and requires careful experimental and data analysis approaches in order to properly evaluate such pharmacodynamic responses. The occurrence of these alternative distribution or disposition components does not alter the area under the effect curve (AUCE) which remains identical to the basic models. Model misselection was addressed by testing fittings comparing the basic and new models. Use of the former for these more complex models does not severely perturb the calculated cardinal dynamic parameters. These models may provide improved insights into indirect responses with complexities in distribution or disposition.

Body Fluid Compartments↗