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Aging research on P. anserina and other model systems involves the identification of cellular pathways which contribute to an increased functional period of time ('healthspan') [ 3, 6].
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We show here how model systems involving large-scale molecular dynamics simulations can be used to study the dynamics of spreading.
However, in experimental model systems involving myelination, overall observations point to Abs synthesized following CNS injuries as being potentially therapeutic, and these examples are reviewed.
The above results utilized various in vitro model systems involving CEA/CEACAM6 transfectants and could therefore have given findings that do not apply in vivo.
Furthermore, much work remains to determine the generalizability of the behavior in these model systems involving young tissue to behavior of cartilage in vivo in older humans.
Until recently, inorganic arsenic in rodents was generally not carcinogenic except in model systems involving co-administration with known carcinogenic agents (Germolec et al. 1998; Rossman et al. 2004).
Model systems involving three direct-acting alkylating carcinogens, two organ sites, and two species have been employed to elucidate the relationships between carcinogenic etiology, tissue specificity, and activation of known and novel oncogenes.
Our model system involves a panel of peptide aptamers that recognise specific protein partners of the cyclin-dependent kinase (CDK) family.
This model system involves serial propagation in mice of tissue explants and avoids cell culture on Petri dishes.
While our model system involves increased IGF-1R activity due to receptor overexpression, it must be noted that increased IGF-1R signaling in clinical breast cancer might also arise from mechanisms involving abnormally high IGF-2 expression or from derangements in IGF-binding protein physiology [ 42].
This concept was experimentally studied in the present work by developing a model system involving DLC coatings with FGI based on theoretical finite element analysis (FEA) predictions.
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