| 1. |
- Ray, A. K., et al.
(författare)
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Damage resistance of a thermal barrier coated superalloy used in aero turbine blade under accelerated creep condition
- 2009
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Ingår i: High Temperature Materials and Processes. - 0334-6455 .- 2191-0324. ; 28:1-2, s. 35-53
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Tidskriftsartikel (refereegranskat)abstract
- This paper highlights the hot tensile and accelerated creep properties of a thermal barrier coated (TBC) AE 437A alloy used as a candidate blade material in aero engines. Acoustic emission technique has been utilised to characterise the ductile-brittle transition temperature of the bond coat. Results revealed that the DBTT (ductile to brittle transition temperature) of this bond coat is around 923 K, which is in close proximity to the value reported for NiCoCrAlY type of bond coat. Finite element technique used for analysing the equivalent stresses in the bond coat well within the elastic limit, revealed highest order of equivalent stress at 1073 K as the bond coat is ductile above 923 K. The lifetime of the TBC coated superai loy was superior to that of the bare substrate and that oxidation is likely the cause of the reduced life of the bare substrate as compared to the coated substrate while stress rupture or accelerated creep experiments are carried out in an oxidizing environment.. Delamination of the bond coat and that of the TBC at high stresses during accelerated creep was evident. During accelerated creep, the mode of fracture in the substrate at very high stresses was transgranular whereas that at low stresses was intergranular.
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| 4. |
- Tiwari, Swasti, et al.
(författare)
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Trafficking of ENaC subunits in response to acute insulin in mouse kidney
- 2007
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Ingår i: American Journal of Physiology - Renal Physiology. - : American Physiological Society. - 0363-6127 .- 1522-1466 .- 1931-857X. ; 293:1, s. F178-F185
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Tidskriftsartikel (refereegranskat)abstract
- Studies done in cell culture have demonstrated that insulin activates the epithelial sodium channel (ENaC) via a variety of mechanisms. However, to date, upregulation of ENaC in native renal tissue by in vivo administration of insulin has not been demonstrated. To address this, we injected 6-mo-old male C57BL/CBA mice (n = 14/group) intraperitoneally with vehicle or 0.5 U/kg body wt insulin and examined short-term (1-2 h) sodium excretion and kidney ENaC subunits (alpha, beta, and gamma) and serum and glucocorticoid-induced kinase (SGK-1) regulation. Insulin resulted in a significant reduction in urine sodium (by approximately 80%) that was restored by intraperitoneal administration of the ENaC antagonist, benzamil (1.4 mg/kg body wt). Differential centrifugation followed by Western blotting of whole kidney revealed significantly increased band densities (by 26-103%) for insulin- relative to vehicle-treated mice for alpha- and gamma-ENaC in the homogenate (H), and plasma membrane-enriched fraction (MF), with no difference in the vesicle-enriched fraction (VF). Similarly, beta-ENaC was significantly increased in MF (by 45%) but no change in the H. It was, however, significantly decreased in the VF (by 28%) with insulin. In agreement, immunoperoxidase labeling demonstrated relatively stronger apical, relative to cytosolic, localization of alpha-, beta-, and gamma-ENaC with insulin, whereas, with vehicle, labeling was fairly evenly dispersed throughout collecting duct principal cells. Furthermore, Western blotting showed insulin increased SGK-1 (by 75%) and phosphorylated-SGK band densities (by 30%) but only in the MF. These studies demonstrate novel in vivo regulation of renal ENaC activity and subunit proteins and SGK-1 by insulin in the acute time frame in the mouse.
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