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Computational inelasticity of fibrous biological tissues with a focus on viscoelasticity, damage and rupture

Başlık çevirisi mevcut değil.

  1. Tez No: 583755
  2. Yazar: OSMAN GÜLTEKİN
  3. Danışmanlar: Prof. Dr. GERHARD A. HOLZAPFEL
  4. Tez Türü: Doktora
  5. Konular: Biyomühendislik, Biyoteknoloji, Bioengineering, Biotechnology
  6. Anahtar Kelimeler: Belirtilmemiş.
  7. Yıl: 2018
  8. Dil: İngilizce
  9. Üniversite: Graz Unıversıty Of Technology
  10. Enstitü: Yurtdışı Enstitü
  11. Ana Bilim Dalı: Belirtilmemiş.
  12. Bilim Dalı: Belirtilmemiş.
  13. Sayfa Sayısı: Belirtilmemiş.

Özet

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Özet (Çeviri)

Practical and ethical limitations generally impede the purely experimental characterization of the relations between the mechanical loads acting on cells, tissues, organs and the nonlinear inelastic phenomena, such as damage and fracture, thereby favoring the use of numerical modeling and simulations. The subsequent chapters deliver a dissemination of the extensive efforts to model the inelastic mechanical response occurring in human cardiovascular tissue, such as viscoelasticity, damage and rupture associated with the human myocardial and arterial wall under hemodynamic loads. Anisotropic fracture of arterial walls are evident from the intrinsic structure of the wall conferred by the collagen fibers embedded in an otherwise isotropic, thick–walled solid. The first two contributions aim at developing a computational framework capable of handling the anisotropic fracture. To this end, the crack phase–field approach is blended with a novel energy–based anisotropic criterion, in other words, the crack driving source term based on the distinction of the isotropic and anisotropic failure process. In addition, an anisotropic crack surface density function is introduced within the context of fibrous tissue modeling which orients the crack propagation parallel to the direction of fibers. The crack phase–field approach is, in principle, hinged on the gradient damage models with the inherent ingredients of fracture mechanics, e.g., the critical energy release rate. The third study investigates the interesting case of aortic dissection from a numerical viewpoint. A simplistic model of a human aorta with a prescribed initial tear is presented where the incipient propagation of the aortic dissection around the initial tear tracks the mean orientation of a single family of fibers when subjected to a supra–physiological loading, thereby manifesting a helical growth in the wall which is in line with clinical observations. The results also imply the significance of systematic experimental analyses of the aortic tissue, enabling the constituent (elastin, collagen) and layer (intima, media, adventitia) specific rupture properties of the wall. Further, an orthotropic viscoelastic model for the human passive myocardium is presented which captures the strong hystereses and stress relaxation behavior observed upon the biaxial extension and triaxial shear experiments on human test specimens. Of equal importance is the accuracy of the computational models mimicking the quasi–incompressible behavior of soft biological tissues under mechanical loading which is covered in a systematic way in the final study.

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