Cari Amici,
non avendo gli indirizzi e-mail adeguati allo scopo, vi pregherei la
cortesia di diffondere l'avviso che segue nelle vostre strutture, tra
i dottorandi, e comunque tra i possibile interessati.
Grazie e cordiali saluti,
Hugo B.V.
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AVVISO DI SEMINARIO:
Conferenziere: Prof. ANNE M. ROBERTSON (Department of Mechanical
Engineering and Materials Science -- University of Pittsburgh)
Titolo: A STRUCTURAL MULTI-MECHANISM MODEL FOR CEREBRAL
ARTERIAL TISSUE WITH DAMAGE
Data: Venerdi 13 Febbraio, ore 15:30
Locale: Dipartimento di Matematica Applicata
"U.Dini", via F. Buonarroti 1
ABSTRACT: Intracranial arteries (ICA) are abnormal saccular
dilations of cerebral arteries, commonly found at apices of arterial
bifurcations and curved segments of arteries at the base of the
brain. If untreated, an ICA can continue to expand until rupture,
resulting in hemorrhage which is followed by death or severe
disability in the majority of patients. Screening and preventative
treatment strategies are notably absent in the clinical handling of
this disease. This is in stark contrast to other diseases such as
atherosclerosis, in which detailed knowledge of the pathobiology is
instrumental in establishing screening procedures and developing
effective pharmaceutical treatments such as statins.
This talk will focus on research directed at modeling the development
of ICA from a segment of arterial tissue. Early stage cerebral
aneurysms are characterized by the disruption of the internal elastic
lamina (IEL). The cause of this breakdown is still not understood,
but it has been conjectured to be caused by fatigue failure or
alternatively by a breakdown in homeostatic mechanisms in the wall
arising from some aspect of the local hemodynamics and wall tension.
We propose to model this disruption using a structural damage model
in which the damage arises from both mechanical and hemodynamic
factors. It builds on a previously introduced nonlinear, inelastic
multi-mechanism model for cerebral arteries (Wulandana, Robertson,
2005), as well as a recent generalization to include the wall
anisotropy (Li, Robertson, 2009). In the multi-mechanism model,
elastin and collagen fibers are treated as separate components
(mechanisms) of the artery. The aniostropic material response of the
wall is introduced through the collagen mechanism which is composed
of helically distributed families of fibers. The orientation of
these families is described using either a finite number of fiber
orientations or using a fiber distribution function. The current
model includes subfailure damage of elastin, represented by changes
in tissue mechanical properties and unloaded reference length. A
structural model is used to characterize gradual degradation, failure
of elastin and recruitment of anisotropic collagen fibers. The
collagen fibers are arranged in two helically oriented families with
dispersion in their orientation. Inelastic experimental data for
cerebral arteries are used to evaluate the constitutive model.