Simulation of peak tension loads in Subsea power cables during installation

At present, most of the insurance claims in the offshore wind industry are due to cable failures where a large percentage occurs during the installation of the array and export cables. As the reliability of the cables depends on the location and installation method, it is important to map the risks involved, which can compromise the cable’s integrity in individual projects. This paper presents sensitivity analyses conducted on crucial parameters in the cable laying process, with an objective of successful installation of subsea power cables without any damages to the cable. The analyses focus on the peak tension loads with reference to key parameters as cable self-weight and laying geometry, as well as the cable deployment position on the installation vessel. Finite element analyses were conducted with both static forces and dynamic forces for irregular vessel motions, by the aid of the well-tested software OrcaFlex.

Cardiac Inotropic Effect of Long-Term Administration of Oral Thymoquinone

Back Ground. Long-term administration of Nigella sativa showed cardiac hypertrophic and positive inotropic effects. Thymoquinone (TQ) is an active ingredient in Nigella sativa. Therefore, we aimed to test the cardiac effects of long-term TQ administration. Materials and Methods. Twenty adult Wistar rats weighing (150-250 g) were divided into two groups: control and TQ. A TQ-olive oil solution was administered orally to the TQ group (dose 10 mg/kg) for two months. An equivalent volume of olive oil was given to the control group. Langendorff isolated hearts were studied. Peak tension, time to peak tension, half relaxation time, and myocardial flow rate were determined. Heart and left ventricle weights and ratios were recorded. Results. The TQ group exhibited significantly higher peak tension than the control group. There were no significant differences between the two groups in time to peak tension, half relaxation time, and myocardial flow rate. Likewise, there were no signs of cardiac hypertrophy. Conclusions. Long-term administration of oral TQ induced a positive inotropic effect in the form of an increase in peak tension. TQ administration did not result in cardiac hypertrophy or an increased cardiac metabolic demand at the studied dose. TQ may be a promising inotropic agent.

Experimental Investigation of the Anchoring Effect of Two Different Types of Rock Bolts on Fractured Rock

A deep understanding of the anchoring effect of rock bolts on fractured rock is essential for support design in rock engineering. In this paper, cubic specimens containing a single preexisting flaw with different inclination angles were made by high-strength gypsum; uniaxial compression tests were conducted on bolted and unbolted specimens to study the anchoring effect of the fully bonded bolt and the prestressed bolt on fractured rock. The mechanical parameters and failure characteristics of bolted and unbolted specimens were compared and analyzed in detail. The results indicated that both the prestressed and fully bonded bolt had a significant influence on the mechanical behavior of fractured rock. The average value of E, σi, σp, and σr of bolted specimens all increased due to the effect of the rock bolt. The increase degree was the greatest for the specimens with flaw inclination angle of 45°. The increase in residual strength, σr, was the most significant among all the mechanical parameters. The mechanical parameters of specimens anchored with a prestressed bolt increased with an increase in pretension stress. Besides, the reinforcement effect of the two types of rock bolts was different for different mechanical parameters. The bolted specimens displayed different failure characteristics compared to the unbolted specimens. Variation of tension stress in the prestressed bolt during the loading process was divided into three different stages. With an increase in the inclination angle from 30° to 60°, the peak tension stress value first increased and then decreased and obtained the maximum value at inclination angle of 45°. Besides, the peak tension stress value increased with pretension stress.

A Crane Overload Protection Controller for Blade Lifting Operation Based on Model Predictive Control

Lifting is a frequently used offshore operation. In this paper, a nonlinear model predictive control (NMPC) scheme is proposed to overcome the sudden peak tension and snap loads in the lifting wires caused by lifting speed changes in a wind turbine blade lifting operation. The objectives are to improve installation efficiency and ensure operational safety. A simplified three-dimensional crane-wire-blade model is adopted to design the optimal control algorithm. A crane winch servo motor is controlled by the NMPC controller. The direct multiple shooting approach is applied to solve the nonlinear programming problem. High-fidelity simulations of the lifting operations are implemented based on a turbulent wind field with the MarIn and CaSADi toolkit in MATLAB. By well-tuned weighting matrices, the NMPC controller is capable of preventing snap loads and axial peak tension, while ensuring efficient lifting operation. The performance is verified through a sensitivity study, compared with a typical PD controller.

Timing and magnitude of systolic stretch affect myofilament activation and mechanical work

Dyssynchronous activation of the heart leads to abnormal regional systolic stretch. In vivo studies have suggested that the timing of systolic stretch can affect regional tension and external work development. In the present study, we measured the direct effects of systolic stretch timing on the magnitude of tension and external work development in isolated murine right ventricular papillary muscles. A servomotor was used to impose precisely timed stretches relative to electrical activation while a force transducer measured force output and strain was monitored using a charge-couple device camera and topical markers. Stretches taking place during peak intracellular Ca2+ statistically increased peak tension up to 270%, whereas external work due to stretches in this interval reached values of 500 J/m. An experimental analysis showed that time-varying elastance overestimated peak tension by 100% for stretches occurring after peak isometric tension. The addition of the force-velocity relation explained some effects of stretches occurring before the peak of the Ca2+ transient but had no effect in later stretches. An estimate of transient deactivation was measured by performing quick stretches to dissociate cross-bridges. The timing of transient deactivation explained the remaining differences between the model and experiment. These results suggest that stretch near the start of cardiac tension development substantially increases twitch tension and mechanical work production, whereas late stretches decrease external work. While the increased work can mostly be explained by the time-varying elastance of cardiac muscle, the decreased work in muscles stretched after the peak of the Ca2+ transient is largely due to myofilament deactivation.

Abstract 209: Different Reaction To Lactate Between The Atrial And The Ventricular Muscle In Excitation-contraction Coupling

Background: The effect of a metabolic change on excitation-contraction (EC) coupling is poorly understood in the atrial myocardium, while the previous studies have mainly focused on EC coupling in the ventricular myocardioum. Although the myocardium mostly uses fatty acid as an energy source, we have reported that metabolic substrate, includes lactate, can be used for energy production and that the metabolomic profile is different between the atria and the ventricles in mouse heart. In addition, it is still under discussion whether lactate can be an energy source for muscles. In the present study, we aimed to investigate the effect of lactate exposure on EC coupling in the atrial and the ventricular myocardium. Methods: We micro-injected aequorin (a Ca2+-sensitive photoprotein) into superficial cells of the left atrium and/or the left ventricular papillary muscle isolated from mice (C57/BL6, 12 - 17 weeks of age), and simultaneously measured intracellular Ca2+ concentration and tension (1 Hz at 36 °C). We added lactate (~10 mM) into HEPES-Tyrode solution (pH was adjusted at 7.4) and observed the changes in the peak tension and the peak Ca2+ concentration. Results and Conclusion: Lactate at a concentration of 10 mM significantly decreased the peak tension (61.7±6.0%; n = 3; P < 0.05.) and the peak Ca2+ concentration (78.8±4.8%; n = 3; P < 0.05.) in the atrial myocardium. Although we observed similar effect of lactate on the ventricular papillary muscle, it was modest compared with the atrial myocardium (72.8±5.6%, 91.6±13.5%, peak tension and Ca2+, respectively; n = 3; no significance). Our results suggest that the atrium has different characteristic of EC coupling from the ventricles in response to an increase in lactate, of which condition is often observed in myocardial ischemia. Moreover, lactate did not seem to contribute to make energy in terms of the tension in the heart. Simultaneous measurement of tension and intracellular Ca2+ concentration can be useful to analyze the atrial physiological property.

Lengthening-contractions in isolated myocardium impact force development and worsen cardiac contractile function in the mdx mouse model of muscular dystrophy

Lengthening-contractions exert eccentric stress on myofibers in normal myocardium. In congestive heart failure caused by a variety of diseases, the impact of lengthening-contractions of myocardium likely becomes more prevalent and severe. The present study introduces a method to investigate the role of stretching imposed by repetitive lengthening-contractions in myocardium under near-physiological conditions. By exerting various stretch-release ramps while the muscle is contracting, consecutive lengthening-contractions and their potential detrimental effect on cardiac function can be studied. We tested our model and hypothesis in age-matched (young and adult) mdx and wild-type mouse right ventricular trabeculae. These linear and ultrathin muscles possess all major cardiac cell types, and their contractile behavior very closely mimics that of the whole myocardium. In the first group of experiments, 10 lengthening-contractions at various magnitudes of stretch were performed in trabeculae from 10-wk-old mdx and wild-type mice. In the second group, 100 lengthening-contractions at various magnitudes were conducted in trabeculae from 10- and 20-wk-old mice. The peak isometric active developed tension (Fdev, in mN/mm2) and kinetic parameters time to peak tension (TTP, in ms) and time from peak tension to half-relaxation (RT50, in ms) were measured. Our results indicate lengthening-contractions significantly impact contractile behavior, and that dystrophin-deficient myocardium in mdx mice is significantly more susceptible to these damaging lengthening-contractions. The results indicate that lengthening-contractions in intact myocardium can be used in vitro to study this emerging contributor to cardiomyopathy.

The O2 cost of the tension-time integral in isolated single myocytes during fatigue

One proposed explanation for the V̇o2 slow component is that lower-threshold motor units may fatigue and develop little or no tension but continue to use O2, thereby resulting in a dissociation of cellular respiration from force generation. The present study used intact isolated single myocytes with differing fatigue resistance profiles to investigate the relationship between fatigue, tension development, and aerobic metabolism. Single Xenopus skeletal muscle myofibers were allocated to a fast-fatiguing (FF) or a slow-fatiguing (SF) group, based on the contraction frequency required to elicit a fall in tension to 60% of peak. Phosphorescence quenching of a porphyrin compound was used to determine Δ intracellular Po2 (PiO2; a proxy for V̇o2), and developed isometric tension was monitored to allow calculation of the time-integrated tension (TxT). Although peak ΔPiO2 was not different between groups ( P = 0.36), peak tension was lower ( P < 0.05) in SF vs. FF (1.97 ± 0. 17 V vs. 2. 73 ± 0.30 V, respectively) and time to 60% of peak tension was significantly longer in SF vs. FF (242 ± 10 s vs. 203 ± 10 s, respectively). Before fatigue, both ΔPiO2 and TxT rose proportionally with contraction frequency in SF and FF, resulting in ΔPiO2/TxT being identical between groups. At fatigue, TxT fell dramatically in both groups, but ΔPiO2 decreased proportionately only in the FF group, resulting in an increase in ΔPiO2/TxT in the SF group relative to the prefatigue condition. These data show that more fatigue-resistant fibers maintain aerobic metabolism as they fatigue, resulting in an increased O2 cost of contractions that could contribute to the V̇o2 slow component seen in whole body exercise.

Regulation of atrial contraction by PKA and PKC during development and regression of eccentric cardiac hypertrophy

ANG II plays a major role in development of cardiac hypertrophy through its AT1 receptor subtype, whereas angiotensin-converting enzyme (ACE) inhibitors are effective in reversing effects of ANG II on the heart. The objective of this study was to investigate the role of PKA and PKC in the contractile response of atrial tissue during development and ACE inhibitor-induced regression of eccentric hypertrophy induced by aortocaval shunt. At 1 wk after surgery, sham and shunt rats were divided into captopril-treated and untreated groups for 2 wk. Then isometric contraction was assessed by electrical stimulation of isolated rat left atrial preparations superfused with Tyrode solution in the presence or absence of specific inhibitors KT-5720 (for PKA) and Ro-32-0432 (for PKC) and high Ca2+. Peak tension developed was greater in shunt than in sham hearts. However, when expressed relative to tissue mass, hypertrophied muscle showed weaker contraction than muscle from sham rats. In sham rats, peak tension developed was more affected by PKC than by PKA inhibition, whereas this differential effect was reduced in the hypertrophied heart. Treatment of shunt rats with captopril regressed left atrial hypertrophy by 67% and restored PKC-PKA differential responsiveness toward sham levels. In the hypertrophied left atria, there was an increase in the velocity of contraction and relaxation that was not evident when expressed in specific relative terms. Treatment with ACE inhibitor increased the specific velocity of contraction, as well as its PKC sensitivity, in shunt rats. We conclude that ACE inhibition during eccentric cardiac hypertrophy produces a negative trophic and a positive inotropic effect, mainly through a PKC-dependent mechanism.