Significant Reduction In Wall Thickness Research Articles

Condition assessment of damaged elbow in subsea pipelines

The evaluation of the performance of aged structures is essential in the oil and gas industry, where inaccurate predictions of structural performance may lead to significant hazardous consequences. Elbows are critical structures subject to continuous corrosion that can lead to a burst or collapse. It is important to be able to predict both burst strength in continually corroding structures and the behaviour of the structures after critical corrosion takes place. Structural failures due to a significant reduction in wall thickness make it very complicated for pipeline operators to maintain pipeline serviceability. This paper discusses the plastic limit pressure of elbows without defects and with several local thinned areas. Finite element analysis (FEA) and the Goodall formula were used to evaluate the new formula. The results of the FEA show that the limit load of elbows under internal pressure differs with position and depth of damage. An empirical formula for the limit load of elbows with local thinned areas is proposed. Eight sizes of elbow were considered in this study, with Rm/t of 5, 6, 7.5, 9, 12, 15, 20 and 25. This range covers most of the piping used in high-pressure environments, such as nuclear and subsea situations. The method of numerical analysis was validated by experiment and with FEA results from the literature. The results of the study can be applied to both the operation and assessment of pipelines. A formula to predict the maximum burst strength of damaged elbows is presented, which will enable more accurate estimates of the time until pipelines need to be replaced or repaired.

Burst strength behaviour of an aging subsea gas pipeline elbow in different external and internal corrosion-damaged positions

Evaluation of the performance of aging structures is essential in the oil and gas industry, where the inaccurate prediction of structural performance can have significantly hazardous consequences. The effects of structure failure due to the significant reduction in wall thickness, which determines the burst strength, make it very complicated for pipeline operators to maintain pipeline serviceability. In other words, the serviceability of gas pipelines and elbows needs to be predicted and assessed to ensure that the burst or collapse strength capacities of the structures remain less than the maximum allowable operation pressure. In this study, several positions of the corrosion in a subsea elbow made of API X42 steel were evaluated using both design formulas and numerical analysis. The most hazardous corrosion position of the aging elbow was then determined to assess its serviceability. The results of this study are applicable to the operational and elbow serviceability needs of subsea pipelines and can help predict more accurate replacement or repair times.

Decellularized ovine arteries as small-diameter vascular grafts

Atherosclerosis and its complications still represent the leading cause of death in the developed countries. While autologous blood vessels may be regarded as the best solution for peripheral and coronary bypass, they are unavailable in most patients. Even though tissue engineering techniques are often applied to the development of small-diameter vascular grafts, limiting factors of this approach are represented by the lack of essential extracellular matrix proteins and/or poor biomechanical properties of the scaffolds used. Along these lines, the aim of this study was to develop a decellularization protocol for ovine carotids to be used as suitable small-diameter vascular grafts. Samples were treated either with sodium dodecyl sulphate (SDS) or with Trypsin and Triton X-100; a final nuclease digestion was performed for both protocols. Morphological analyses demonstrate complete removal of nuclei and cellular components in treated vessels, also confirmed by significant reduction in wall thickness and DNA content. Essential extracellular matrix proteins such as collagen, elastin, and fibronectin are well preserved after decellularization. From a mechanical point of view, Trypsin and Triton X-100 treated arteries show elastic modules and compliance comparable to native carotids, whereas the use of SDS makes samples stiffer, with a significant decrease in the compliance mean value and an increase in longitudinal and circumferential Young’s modules. It is demonstrated that the treatment where Trypsin and Triton X-100 are combined guarantees complete decellularization of carotids, with no significant alteration of biomechanical and structural properties, thus preserving a suitable environment for adhesion, proliferation, and migration of cells.

Locally advanced rectal cancer: histopathological correlation and predictive accuracy of serial MRI after neoadjuvant chemotherapy

The accuracy of MRI after long-course chemoradiotherapy (CRT) in locally advanced rectal cancer (LARC) has been questioned. We have evaluated our experience of sequential MRI to assess pre-operative downstaging with histopathology correlation. 17 patients with LARC had three MRI scans: MRI 1, before treatment; MRI 2, 6 weeks post-CRT; and MRI 3, pre-operatively. MRI T and N staging were reported, with T3 subdivided into T3a (<5 mm through wall), T3b (1-5 mm), T3c (5-15 mm) and T3d (>15 mm). The maximal wall measurements and a prediction of vascular involvement were also correlated with histopathology. Histopathological agreement with MRI 3 was high: T 82%; N 88% and vascular 73%. Statistically significant (p<0.01) T downstaging was shown in MRI 2 and MRI 3 groups. In the 6 weeks post-CRT scan, T downstaging occurred in 6% of patients, with a further 29.4% showing T3c to T3b downsizing. 41% showed N stage improvement. In the third MRI group pre-surgery, 41.2% showed an MRI T stage improvement, with a further T3 downsizing in 17.6% of patients. 50% of these responders had shown no T stage improvement on their second scan. The sequential scans also showed significant reduction in wall thickness (p<0.01). In conclusion, the pre-operative MRI showed ongoing response to CRT up to 12 weeks post-CRT, which has important clinical implications regarding the most appropriate time to operate. Improved agreement between MRI 3 and histopathology compared with previous studies including only one post-treatment MRI was also demonstrated.

Evaluation of Methods for Detecting and Monitoring of Corrosion Damage in Risers

Offshore pipeline failure statistics have been collected for more than 30 years now and illustrate that the riser predominantly fails as a result of corrosion. The consistent wetting and drying in the splash zone combined with defects in the coatings are the usual contributors to the problem. Risers are inspected at some determined frequency and can be done by internal and external methods. Inspecting by either means brings into account caveats and limitations from the technology used as well as human factors. For example, external inspections can be inefficient and inaccurate with some tools missing defects in areas of coating disbondment. In addition, internal inspections sometimes create false positives and can miss defects. These inaccuracies in the technologies or the techniques used may miss defects that eventually lead to failure. On the other hand, using corrosion mapping and fitness-for-service (FFS) assessment from the data collected, along with the inherent conservatism of this data from limited measurement accuracy, may result in the premature replacement of risers. A literature search is being conducted to review existing riser inspection methods and identify candidate nondestructive methods for riser inspection. These methods should be capable of detecting and monitoring general corrosion, localized corrosion pitting, and stress-corrosion cracking (sulfide or hydrogen induced) as external or internal corrosion damage. Thus far, this search has found that assessing the remaining service life of aging risers is largely dependent on the accuracy of analyzing corrosion damage to the riser surface in the atmospheric, splash (tidal), submerged, and buried environmental zones. The accuracy of each technology was analyzed. The capabilities and limitations of each method/technique used for riser inspection are summarized. The investigation is focused on long- and short-range ultrasonic techniques used for initial screening and corrosion mapping. These techniques can be deployed to detect a significant reduction in wall thickness using guided and torsional waves or to map accurately a corrosion damage using single/multiple transducers and phased-array probes in manual or automated mode. A pulsed eddy-current technique that uses a stepped or pulsed input signal for the detection of corrosion areas under insulation (CUI) is also being evaluated. This allows the detection of wall-thinning areas in the riser without removing the outside coatings. In addition, it is found that filmless, real-time, and digital radiography can be used to find internal and external corrosion defects in an insulated splash zone while the riser remains in service. A survey of nondestructive evaluation (NDE) manufacturing companies, NDE inspection companies, and operating companies was completed to collect information about current instrumentation and inspection/operators’ experience for riser inspection. Examples of advanced riser inspection instrumentation and field results are included. The ability of the candidate technologies to be adapted to riser variations, the stage of standardization, and costs are also discussed.

Nitric Oxide Synthase 3-Dependent Vascular Remodeling and Circulatory Dysfunction in Cirrhosis

Vascular remodeling is an active process that consists in important modifications in the vessel wall. Endothelium-derived nitric oxide (NO) plays a major role in this phenomenon. We assessed wall thickness (WT), total wall area (TWA), lumen diameter, and total nuclei number/cross-section (TN) in cirrhotic rats with ascites and in control rats. A second group of cirrhotic rats received the NO synthesis inhibitor, L-NAME, or vehicle daily for 11 weeks and systemic hemodynamics, arterial compliance, aortic NO synthase 3 (NOS3) protein expression, and vascular morphology were analyzed. Cirrhotic vessels showed a significant reduction in WT, TWA, and TN as compared to control vessels. Long-term inhibition of NOS activity in cirrhotic rats resulted in a significant increase in WT, TWA, and TN as compared to cirrhotic rats receiving vehicle. NOS3 protein abundance was higher in aortic vessels of nontreated cirrhotic animals than in controls. This difference was abolished by chronic treatment with L-NAME. NOS inhibition in cirrhotic rats resulted in higher arterial pressure and peripheral resistance and lower arterial compliance than cirrhotic rats receiving vehicle. Therefore, vascular remodeling in cirrhosis with ascites is a generalized process with significant functional consequences that can be negatively modulated by long-term inhibition of NOS activity.

Effect of heparin on adaptation of vein grafts to arterial circulation.

We studied the effect of heparin on wall thickening in balloon-injured carotid arteries and vein grafts in rabbits. Heparin (0.3 mg/kg of body weight/hour) reduced intimal cross-sectional area in balloon-injured carotid arteries at 2 weeks (0.20 +/- 0.05 mm2 vs. 0.05 +/- 0.02 mm2, p = 0.02). Autoradiography after a single pulse of tritiated thymidine revealed no labeling in the few intimal cells present in heparin-treated animals, whereas control smooth muscle cells (SMC) had a 10% labeling index. Heparin did not affect medial proliferation, suggesting that the decrease in intimal thickening was largely due to inhibition of SMC migration into the intima. Heparin caused a slight reduction in intimal cross-sectional area at 2 weeks in vein grafts (0.17 +/- 0.03 mm2 vs. 0.09 +/- 0.02 mm2, p = 0.03) but no significant reduction in wall thickness at any other time and no reduction in SMC proliferation rate (thymidine labeling index). DNA content per surface area or dry weight was the same in control and heparin-treated vein grafts at 4 weeks, implying that SMC content and the amount of matrix made by individual SMC was not affected. These data suggest that either SMC in veins are less susceptible to heparin than SMC in arteries, or the mechanism of thickening is substantially different. Heparin may not block all forms of SMC proliferation and may only be a weak inhibitor in processes that primarily are in response to changes in pressure.