Development Of Tortuosity Research Articles

Thermochemical stability of Y2Si2O7 in high‐temperature water vapor

AbstractThe thermochemical stability of Y2Si2O7 was assessed in a high‐temperature high‐velocity water vapor environment to improve the understanding of the mechanisms that lead to SiO2 depletion. Spark plasma sintered Y2Si2O7 specimens were exposed in a steam‐jet furnace at 1000°C and 1200°C for 3‐250 hours, steam velocities of 131‐174 m/s and at 1 atm H2O pressure. These exposures resulted in the selective volatilization of SiO2 to form volatile Si(OH)4 and porous Y2SiO5. Microstructural evolution from fine rectangular pores at short times to larger rounded pores at longer times was observed. Mechanisms contributing to the overall depletion reaction kinetics were evaluated and include the interface reaction to form Y2SiO5 and Si(OH)4 (g), Y2SiO5 coarsening, development of tortuosity in the pore network and diffusion of H2O (g) and Si(OH)4 (g) through pores by molecular diffusion and/or Knudsen diffusion. SiO2 depletion was found to follow parabolic volatilization kinetics (kp = 0.38 µm2/h) at 1200°C indicating the reaction is limited by a diffusion process, most likely the outward diffusion of Si(OH)4 (g) through pores. Results are utilized to assess the viability of Y2Si2O7 and other rare‐earth silicates as environmental barrier coating (EBC) materials for SiC ceramic matrix composites (CMCs).

Partial Off-Loading of Longitudinal Tension Induces Arterial Tortuosity

Arterial tortuosity is a frequent manifestation of vascular disease and collateral vessel growth, but its causes are poorly understood. This study was designed to assess the relationship between the development of tortuosity and the mechanical forces that are imposed on arterial tissue. Axial strain in rabbit carotid arteries was reduced from 62+/-2% to 33+/-2% by implanting an interposition graft, prepared from the contralateral carotid, at the downstream end of the artery. Axial strain remained unchanged for 12 weeks; however, all vessels became tortuous because of tissue growth and remodeling. After 7 days, there was a marked elevation in proliferation rates of endothelial and smooth muscle cells; however, increased apoptosis was also detected, and no net accumulation of DNA was observed. Significant accumulations of elastin (24%) and total collagen (26%) occurred by 5 weeks. Gelatin zymography detected upregulation and activation of matrix metalloproteinase-2 (MMP-2), and confocal microscopy revealed enlargement of fenestrae in the internal elastic lamina. MMP inhibition by treatment with doxycycline prevented enlargement of fenestrae and development of tortuosity, and it enabled normalization of axial strain by 5 weeks. These findings indicate that substantial axial strain is necessary to sustain the morphological stability of arteries, and that a reduction in strain results in arterial tortuosity attributable to aberrant MMP activity.

Rabbit Aneurysm Model Mediated by the Application of Elastase

The concentrations and application methods of elastase in the rabbit aneurysm model were optimized to control the initiation of aneurysms and to cause rupture in a stepwise, controlled fashion. The common carotid artery of male Japanese albino rabbits was exposed. No aneurysm was generated if the adventitia was not dissected. After gentle removal of the adventitia, a two-fold dilution series of elastase was applied to the lesion and observed over a period of 2 hours. Various stages of aneurysmal lesions, from spindle-shaped enlargement to rupture, were produced in proportion to the elastase concentration. Application of elastase stock solution (5 U/mg of type I porcine pancreatic elastase) resulted in rupture within 30 minutes in all six animals. Elastase 1:2 solutions caused oozing in all animals, but subsequent rupture in only three of six animals. Histological examination found serious destruction of the internal elastic lamina and media, with expansion of the very thin wall. Elastase 1:4 to 1:16 solutions caused spindle-like distention of the entire artery and the development of tortuosity at the lesion. Elastase 1:32 or weaker solutions caused only localized dilatations. Overall, the destruction of the tunica media became less severe with decreased elastase concentration. Furthermore, the bursting pressure of the aneurysms decreased with increasing elastase concentrations. In particular, aneurysms produced by the elastase 1:2 solution ruptured at less than 150 mmHg, whereas aneurysms induced by the elastase 1:4 or weaker solutions did not rupture within the physiological range of blood pressure. The present aneurysm model requires shorter preparation time and enables accurate control of aneurysm development and rupture.