Failure Prevention through Life Assessment of Structural Components and Equipment

2021 ◽  
pp. 51-68
Author(s):  
Daniel J. Benac

Abstract Life assessment of structural components is used to avoid catastrophic failures and to maintain safe and reliable functioning of equipment. The failure investigator's input is essential for the meaningful life assessment of structural components. This article provides an overview of the structural design process, the failure analysis process, the failure investigator's role, and how failure analysis of structural components integrates into the determination of remaining life, fitness-for-service, and other life assessment concerns. The topics discussed include industry perspectives on failure and life assessment of components, structural design philosophies, the role of the failure analyst in life assessment, and the role of nondestructive inspection. They also cover fatigue life assessment, elevated-temperature life assessment, fitness-for-service life assessment, brittle fracture assessments, corrosion assessments, and blast, fire, and heat damage assessments.

2014 ◽  
Vol 627 ◽  
pp. 45-48
Author(s):  
Cristian Sorin Nes ◽  
Angelica Enkelhardt ◽  
Lucian Bogdan ◽  
Nicolae Faur

Objectives: This paper presents a numerical fatigue life assessment of a self-expandable Nitinol stent. The analysis was performed using the ANSYS 11 software. Methods: Stent durability is an issue which must be addressed during the design of implants. Given the corrosive properties of blood and the cyclic loads that are applied on the stent (the cyclic variation of blood pressure), the determination of fracture parameters and fatigue characteristics of the implant is highly recommended. Breaking of the stent’s wire is particularly dangerous because it can cause the dislocation of a piece of stenotic plaque, which in turn can block a smaller artery, causing a heart attack. On the other hand, any discontinuity in stent structure acts as an accumulating place for stenosis particles, significantly shortening the life of the implant. The stent consists of a cylindrical tube 22.42 mm long, with a diameter of 8.3 millimeters. The wire section is square, 0.2x0.2 millimeters. The stent is only subjected to the pressure generated by the stenoted arterial wall. This evenly distributed pressure is defined at the outer surface of the stent and has a value of 2.5 MPa, corresponding to a 56% blood vessel stenosis. This way, the most severe loading conditions for the stent could be simulated. The stress distribution was then used to asses the fatigue life of the stent. Results and conclusions: The results showed that, in normal conditions (with the maximal internal pressure of 139 mm Hg = 18533 Pa), no damage appears on the stent after 107 cycles.


2008 ◽  
Vol 15 (4) ◽  
pp. 311-331 ◽  
Author(s):  
Jaganathan Swaminathan ◽  
Krishna Guguloth ◽  
Manojkumar Gunjan ◽  
Prabirkumar Roy ◽  
Rabindranath Ghosh

2009 ◽  
Vol 16 (4) ◽  
pp. 1314-1323 ◽  
Author(s):  
R.F. Martins ◽  
C. Moura Branco ◽  
A.M. Gonçalves-Coelho ◽  
Edgar C. Gomes

2014 ◽  
Vol 224 ◽  
pp. 112-117 ◽  
Author(s):  
Michał Böhm ◽  
Adam Niesłony

The paper presents a new formula for fatigue life determination with the use of the spectral method for fatigue life assessment on the basis of fatigue strain characteristics. The spectral method is widely used together with the stress characteristics, but the literature does not contain a case where it is used together with strain characteristics. The paper shows the theoretical assumptions as well as the derived analytical formula for fatigue life determination. The presented formula is using constants gained from the Manson-Coffin-Basquin strain characteristic. Due to the popularity of strain characteristics, the formula may be widely used in the engineering practice.


2021 ◽  
Author(s):  
Bin Qiang ◽  
Xin Wang

Abstract In this paper, the recent progress on the determination of welding residual stresses in Q345qD steel welded structural components and their effects on stress intensity factors for semi-elliptical surface cracks has been reviewed. Two different welded structural components: butt-welded steel plate and orthotropic steel deck (OSD) are considered. First, we summarize the results from recent studies on the experimental measurements and numerical simulations of the surface and through-thickness residual stress in the welded plate and OSD; the complete longitudinal and transverse residual stress distributions are discussed. Then, the effects of the obtained welding residual stresses on the SIFs for surface cracks in the weldments are quantified. The loading conditions considered are the combinations of service loading and residual stresses on the butt-welded plate and OSD. Semi-elliptical surface cracks with a wide range of aspect ratios and relative depths are investigated. In particular, both 3D FEA and weight function method are used for the determination of SIFs for surface cracks. The effects of welding residual stresses on SIFs are illustrated thoroughly. The current results are very important for the appropriate fatigue life assessment for welded structural components.


1987 ◽  
Vol 26 (01) ◽  
pp. 1-6 ◽  
Author(s):  
S. Selvaraj ◽  
M. R. Suresh ◽  
G. McLean ◽  
D. Willans ◽  
C. Turner ◽  
...  

The role of glycoconjugates in tumor cell differentiation has been well documented. We have examined the expression of the two anomers of the Thomsen-Friedenreich antigen on the surface of human, canine and murine tumor cell membranes both in vitro and in vivo. This has been accomplished through the synthesis of the disaccharide terminal residues in both a and ß configuration. Both entities were used to generate murine monoclonal antibodies which recognized the carbohydrate determinants. The determination of fine specificities of these antibodies was effected by means of cellular uptake, immunohistopathology and immunoscintigraphy. Examination of pathological specimens of human and canine tumor tissue indicated that the expressed antigen was in the β configuration. More than 89% of all human carcinomas tested expressed the antigen in the above anomeric form. The combination of synthetic antigens and monoclonal antibodies raised specifically against them provide us with invaluable tools for the study of tumor marker expression in humans and their respective animal tumor models.


1981 ◽  
Author(s):  
M Yamamoto ◽  
K Watanabe ◽  
Y Ando ◽  
H Iri ◽  
N Fujiyama ◽  
...  

It has been suggested that heparin caused potentiation of aggregation induced by ADP or epinephrine. The exact mechanism of heparin-induced platelet activation, however, remained unknown. In this paper, we have investigated the role of anti-thrombin III ( AT ) in heparin-induced platelet activation using purified AT and AT depleted plasma. When ADP or epinephrine was added to citrated PRP one minute after addition of heparin ( 1 u/ml, porcine intestinal mucosal heparin, Sigma Co. USA ), marked enhancement of platelet aggregation was observed, compared with the degree of aggregation in the absence of heparin. However, in platelet suspensions prepared in modified Tyrode’s solution, heparin exhibited no potentiating effect on platelet aggregation induced by epinephrine or ADP. Potentiation of epinephrine- or ADP-induced platelet aggregation by heparin was demonstrated when purified AT was added to platelet suspensions at a concentration of 20 μg/ml. AT depleted plasma, which was prepared by immunosorption using matrix-bound antibodies to AT, retained no AT, while determination of α1-antitrypsinα2- macroglobulin and fibrinogen in AT depleted plasma produced values which corresponded to those of the original plasma when dilution factor was taken into account. The activities of coagulation factors were also comparable to those of the original plasma. Heparin exhibited potentiating effect on ADP- or epinephrine-induced aggregation of platelets in original plasma, but no effect in AT depleted plasma. When purified AT was added back to AT depleted plasma at a concentration of 20 μg/ml, potentiation of platelet aggregation by heparin was clearly demonstrated.Our results suggest that effect of heparin on platelet aggregation is also mediated by anti-thrombin III.


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