20 research outputs found
Layout Optimisation of Wave Energy Converter Arrays
No full textThis paper proposes an optimisation strategy for the layout design of wave energy converter (WEC) arrays. Optimal layouts are sought so as to maximise the absorbed power given a minimum q-factor, the minimum distance between WECs, and an area of deployment. To guarantee an efficient optimisation, a four-parameter layout description is proposed. Three different optimisation algorithms are further compared in terms of performance and computational cost. These are the covariance matrix adaptation evolution strategy (CMA), a genetic algorithm (GA) and the glowworm swarm optimisation (GSO) algorithm. The results show slightly higher performances for the latter two algorithms; however, the first turns out to be significantly less computationally demanding
Techno-Economic Modelling of Tidal Energy Converter Arrays in the Tacoma Narrows
No full textHydrokinetic tidal energy converter (TEC) technology is yet to become cost competitive with other renewable energy sources. Understanding the interaction between energy production and the costs incurred harvesting that energy may unlock the economic potential of this technology. Although hydrodynamic simulation of TEC arrays has matured over time, including demonstration of how small and large arrays affect the resource, integration of cost modelling is often limited. The advanced ocean energy array techno-economic modelling tool ‘DTOcean’ enables designers to calculate and improve the levelised cost of energy (LCOE) of an array through parametric simulation of the energy extraction, design of the electrical network, moorings and foundations, and simulation of the installation and lifetime operations and maintenance of the array. This work presents a verification of DTOcean’s ability to simulate the techno-economic performance of TEC arrays by reproducing the hypothetical RM1 reference model, a semi-analytical model of a TEC array based in the Tacoma Narrows of Washington state, U.S.A. It is demonstrated that DTOcean can produce a reasonable estimate to the LCOE predicted by the reference model, giving (in Euro cents per kiloWatt hour) 36.69 ¢/kWh against the reference model’s 34.612 ¢/kWh for 10 TECs, while for 50 TECs, DTOcean calculated 20.34 ¢/kWh compared to 17.34 ¢/kWh for the reference model
BIOMECHANICAL STUDY OF THE MECHANICAL AND STRUCTURAL PROPERTIES OF ADHERENT CELLS
No full textA cell is a biological complex system and its understanding requires a combination of various approaches including biomechanics. Like engineering materials, cells deform when external forces act on them. There is evidence that many normal and diseased conditions of cells are dependent on, or regulated by the way cells mechanically interact with the environment.
A major interest in cell mechanics is the regulation of cellular function by mechanical forces, which is determined by the composition and structures of cells. While the exact structural mechanisms involved in force transmission inside the cells are not well understood, computational cell modelling can yield important insights. This may contribute to build up a structure- function relationship of different adherent cell types. One approach to studying the mechanosensing processes is to understand the mechanical properties of cells’ constitutive components individually.
For this purpose, a representative 3D finite element model of a single adherent cell was developed based on the internal structures of the cytoskeleton that provide the cells with their mechanical properties. The results indicate which cytoskeleton components are targeted to respond to specific loading conditions, such as compression and stretching. More specifically, actin cortex and microtubules are targeted to respond to compressive loads, while actin bundles and microtubules are major components in maintaining cell forces during stretching.
This approach clarifies the effects of cytoskeletal heterogeneity and regional variations on the interpretation of force-deformation measurements. With a sensitivity study of the material properties of the different cellular components, the model shows how these properties differ to define cell rigidity across different cell types. Cell force is mainly affected by changes in cortex
thickness, cortex Young’s modulus and rigidity of the cytoplasm. Changes in rigidity of actin bundles and number of microtubules influence cell response to shear loads, while the number of actin bundles deeper in the interior of the cell, affect cell response to compression.
The time dependent responses observed following a power-law are remarkably similar to those reported for a variety of measurements with atomic force microscopy, suggesting this model is a consensus description of the fundamental principles defining cell mechanics. Simulations of the dynamic response of a single cell suggest that the origin of different force-relaxation times is linked to the structural architecture of the cell. The results also suggest that it is important to consider the viscoelastic properties of the cortex, other than the cytoplasm, to properly define the time-dependent response of the cell to compressive loads.
The FE single-cell model includes the three parameters defining the fundamental principles defining cell mechanics: rigidity, prestress and time-dependence deformation following a power-law behaviour. This thesis con- tributes to understand the mechanical interaction and properties across different cell components, responsible for cell behaviour, that will ultimately lead to functional adaptation or pathological conditions
Numerical analysis of the influence of micro-voids on fretting fatigue crack initiation lifetime
No full text[EN] In this paper, the influence of the heterogeneity in the predicted crack initiation lifetime under fretting fatigue conditions is analysed for a regular and a random distribution of micro-voids. A critical plane analysis with two multiaxial damage criteria is performed to assess the crack initiation lifetime. The predicted initiation lifetime in the heterogeneous material is compared with the results obtained in the homogeneous case. The numerical results show that the heterogeneity has a noticeable influence on the predicted initiation lifetime. Furthermore, the numerical model suggests that a crack may firstly initiate at the upper edge of the micro-voids located close to the contact edge, leading to a mean reduction of the predicted crack initiation lifetime. However, in some cases, the introduction of micro-voids reduces the stress intensity at the contact edge and thus decreasing the predicted crack initiation lifetime.The authors gratefully acknowledge the financial support given by the Spanish Ministry of Economy and Competitiveness and the FEDER program through the projects DPI2017-89197-C2-1-R, DPI2017-89197-C2-2-R and the FPI subprogram with the reference BES-2015-072070. The support of the Generalitat Valenciana, Programme PROMETEO 2016/007, is also acknowledged.r The last author would like to acknowledge the financial support of the Research Foundation-Flanders (FWO), The Luxembourg National Research Fund (FNR) and Slovenian Research Agency (ARRS) in the framework of the FWO Lead Agency project: G018916N 'Multi-analysis of fretting fatigue using physical and virtual experiments'.Infante-García, D.; Giner Maravilla, E.; Miguélez, MH.; Wahab, MA. (2019). Numerical analysis of the influence of micro-voids on fretting fatigue crack initiation lifetime. Tribology International. 135:121-129. https://doi.org/10.1016/j.triboint.2019.02.032S121129135Hills, D. A., & Nowell, D. (2014). Mechanics of fretting fatigue—Oxford’s contribution. Tribology International, 76, 1-5. doi:10.1016/j.triboint.2013.09.015Hojjati-Talemi, R., Wahab, M. A., Giner, E., & Sabsabi, M. (2013). Numerical Estimation of Fretting Fatigue Lifetime Using Damage and Fracture Mechanics. Tribology Letters, 52(1), 11-25. doi:10.1007/s11249-013-0189-8Nowell, D., Dini, D., & Hills, D. A. (2006). Recent developments in the understanding of fretting fatigue. Engineering Fracture Mechanics, 73(2), 207-222. doi:10.1016/j.engfracmech.2005.01.013Amargier, R., Fouvry, S., Chambon, L., Schwob, C., & Poupon, C. (2010). Stress gradient effect on crack initiation in fretting using a multiaxial fatigue framework. International Journal of Fatigue, 32(12), 1904-1912. doi:10.1016/j.ijfatigue.2010.06.004PROUDHON, H., FOUVRY, S., & BUFFIERE, J. (2005). A fretting crack initiation prediction taking into account the surface roughness and the crack nucleation process volume. International Journal of Fatigue, 27(5), 569-579. doi:10.1016/j.ijfatigue.2004.09.001Pereira, K., & Abdel Wahab, M. (2017). Fretting fatigue crack propagation lifetime prediction in cylindrical contact using an extended MTS criterion for non-proportional loading. Tribology International, 115, 525-534. doi:10.1016/j.triboint.2017.06.026Hojjati-Talemi, R., Abdel Wahab, M., De Pauw, J., & De Baets, P. (2014). Prediction of fretting fatigue crack initiation and propagation lifetime for cylindrical contact configuration. Tribology International, 76, 73-91. doi:10.1016/j.triboint.2014.02.017Noraphaiphipaksa, N., Manonukul, A., & Kanchanomai, C. (2017). Fretting Fatigue with Cylindrical-On-Flat Contact: Crack Nucleation, Crack Path and Fatigue Life. Materials, 10(2), 155. doi:10.3390/ma10020155NAVARRO, C., MUNOZ, S., & DOMINGUEZ, J. (2008). On the use of multiaxial fatigue criteria for fretting fatigue life assessment. International Journal of Fatigue, 30(1), 32-44. doi:10.1016/j.ijfatigue.2007.02.018Bhatti, N. A., & Abdel Wahab, M. (2017). A numerical investigation on critical plane orientation and initiation lifetimes in fretting fatigue under out of phase loading conditions. Tribology International, 115, 307-318. doi:10.1016/j.triboint.2017.05.036Sabsabi, M., Giner, E., & Fuenmayor, F. J. (2011). Experimental fatigue testing of a fretting complete contact and numerical life correlation using X-FEM. International Journal of Fatigue, 33(6), 811-822. doi:10.1016/j.ijfatigue.2010.12.012Szolwinski, M. P., & Farris, T. N. (1998). Observation, analysis and prediction of fretting fatigue in 2024-T351 aluminum alloy. Wear, 221(1), 24-36. doi:10.1016/s0043-1648(98)00264-6Gong, H., Rafi, K., Gu, H., Starr, T., & Stucker, B. (2014). Analysis of defect generation in Ti–6Al–4V parts made using powder bed fusion additive manufacturing processes. Additive Manufacturing, 1-4, 87-98. doi:10.1016/j.addma.2014.08.002RAJASEKARAN, B., GANESHSUNDARARAMAN, S., JOSHI, S., & SUNDARARAJAN, G. (2009). Effect of grinding on plain fatigue and fretting fatigue behaviour of detonation gun sprayed Cu–Ni–In coating on Al–Mg–Si alloy. International Journal of Fatigue, 31(4), 791-796. doi:10.1016/j.ijfatigue.2008.03.003Chan, L. C., Lu, X. Z., & Yu, K. M. (2015). Multiscale approach with RSM for stress–strain behaviour prediction of micro-void-considered metal alloy. Materials & Design, 83, 129-137. doi:10.1016/j.matdes.2015.05.064Bhatti, N. A., & Abdel Wahab, M. (2018). Fretting fatigue crack nucleation: A review. Tribology International, 121, 121-138. doi:10.1016/j.triboint.2018.01.029Marco, M., Infante-García, D., Díaz-Álvarez, J., & Giner, E. (2019). Relevant factors affecting the direction of crack propagation in complete contact problems under fretting fatigue. Tribology International, 131, 343-352. doi:10.1016/j.triboint.2018.10.048Muñoz, S., Navarro, C., & Domínguez, J. (2007). Application of fracture mechanics to estimate fretting fatigue endurance curves. Engineering Fracture Mechanics, 74(14), 2168-2186. doi:10.1016/j.engfracmech.2006.10.010Giner, E., Sabsabi, M., Ródenas, J. J., & Javier Fuenmayor, F. (2014). Direction of crack propagation in a complete contact fretting-fatigue problem. International Journal of Fatigue, 58, 172-180. doi:10.1016/j.ijfatigue.2013.03.001Kumar, D., Biswas, R., Poh, L. H., & Wahab, M. A. (2017). Fretting fatigue stress analysis in heterogeneous material using direct numerical simulations in solid mechanics. Tribology International, 109, 124-132. doi:10.1016/j.triboint.2016.12.033Mayer, H., Papakyriacou, M., Zettl, B., & Stanzl-Tschegg, S. . (2003). Influence of porosity on the fatigue limit of die cast magnesium and aluminium alloys. International Journal of Fatigue, 25(3), 245-256. doi:10.1016/s0142-1123(02)00054-3Taylor, D. (2008). The theory of critical distances. Engineering Fracture Mechanics, 75(7), 1696-1705. doi:10.1016/j.engfracmech.2007.04.007Araújo, J. (2002). The effect of rapidly varying contact stress fields on fretting fatigue. International Journal of Fatigue, 24(7), 763-775. doi:10.1016/s0142-1123(01)00191-8McDiarmid, D. L. (1991). A GENERAL CRITERION FOR HIGH CYCLE MULTIAXIAL FATIGUE FAILURE. Fatigue & Fracture of Engineering Materials and Structures, 14(4), 429-453. doi:10.1111/j.1460-2695.1991.tb00673.xSocie, D. (1987). Multiaxial Fatigue Damage Models. Journal of Engineering Materials and Technology, 109(4), 293-298. doi:10.1115/1.3225980Gates, N., & Fatemi, A. (2016). Multiaxial variable amplitude fatigue life analysis including notch effects. International Journal of Fatigue, 91, 337-351. doi:10.1016/j.ijfatigue.2015.12.011El Haddad, M. H., Dowling, N. E., Topper, T. H., & Smith, K. N. (1980). J integral applications for short fatigue cracks at notches. International Journal of Fracture, 16(1), 15-30. doi:10.1007/bf00042383Kim, J., Gao, X., & Srivatsan, T. S. (2004). Modeling of void growth in ductile solids: effects of stress triaxiality and initial porosity. Engineering Fracture Mechanics, 71(3), 379-400. doi:10.1016/s0013-7944(03)00114-0Fatemi, A., & Socie, D. F. (1988). A CRITICAL PLANE APPROACH TO MULTIAXIAL FATIGUE DAMAGE INCLUDING OUT-OF-PHASE LOADING. Fatigue & Fracture of Engineering Materials and Structures, 11(3), 149-165. doi:10.1111/j.1460-2695.1988.tb01169.xLykins, C. (2001). Combined experimental–numerical investigation of fretting fatigue crack initiation. International Journal of Fatigue, 23(8), 703-711. doi:10.1016/s0142-1123(01)00029-
The Limits of Reduced Order Current Energy Converter Modeling
No full textPublisher Copyright: © 2020, Offshore Technology Conference.Reduced-order models for mesoscale current energy converter (CEC) modeling allow for tractablecomputation times for investigations of array configurations on power performance and environmentaleffects to support design optimization. The CEC representation in these models take the form of actuatordiscs in codes such as SNL-Delft3D-CEC-FM treating the rotating CEC blades as momentum sinks. Inthe first-of-its-kind, whole-plant optimization software, DTOcean, the hydrodynamic modelling of CECsis reduced one step further by superimposing wake models based on normalized CFD simulations onto aset of pre-computed velocity fields, to provide power estimates. DTOcean is a new tool and the amountof verification and validation evidence gathered is presently limited. To gain additional confidence andindustry buy-in to the software penetration, this study investigated a primary component of levelized cost ofelectricity (LCOE) calculation, annual energy production (AEP), through an analytic calculation of powerusing the results of an identical simulation in SNL-Delt3D-CEC-FM. Three configurations of an 8-turbinearray are studied with DTOcean where two rows of 4-turbines are spaced (unstaggered) 5-, 10-, and 20-Diameters apart and the AEP was calculated; The energy calculation in SNL-Delft3D-CEC-FM were morecomputationally expensive for the mesoscale domain making the optimization of solely an arrays powerproduction using the wake superposition method implemented DTOcean attractive. The codes however arecomplementary as SNL-Delft3D-CEC-FM simultaneously investigates environmental effects of varyingarray configurations while DTOcean considers all aspects of array costs through its lifetime to optimizeLCOE from a whole-plant perspective.Sandia National Laboratories is a multimission laboratory managed and operated by National Technology & Engineering Solutions of Sandia, LLC, a wholly owned subsidiary of Honeywell International Inc., for the U.S. Department of Energy's National Nuclear Security Administration under contract DE-NA0003525.Peer reviewe
TNF-α modulates the Na+-K+ ATPase and the Na+K+2Cl- symporter in LLC-PK1 cells
No full textBackground Tumour necrosis factor alpha (TNF-α) has been implicated in the development of diabetic nephropathy and the accompanying increase in sodium retention. Inhibition of renal Na+-K+ ATPase was reported to accompany cell death. As TNF is known to induce both apoptosis and cell survival, this work investigated the effect and mechanism of action of TNF-α on the Na+-K+ ATPase and the Na +K+2Cl- symporter using LLC-PK1 cells, a porcine renal proximal tubules cell line. Materials and methods Cells were incubated for 2 h with TNF-α in presence and absence of pyrrolidinedithiocarbamate, SP600125 and FK009, respective inhibitors of the transcription factor nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), c-Jun N-terminal kinase (JNK) and caspases. The activity of the pump was assayed by measuring the ouabain-inhibitable release of inorganic phosphate. Changes in its expression and the expression of the symporter were monitored by western blot analysis. Results TNF-α up-regulated both transporters. NF-κB, JNK and the caspases were all mediators of the cytokine action. TNF up-regulated the Na+-K+ pump by stimulating JNK which in turn, activated NF-κB and inhibited the caspases. TNF effect on the cotransporter was also mediated via activation of JNK which however inhibited NF-κB and by so doing prevented activation of caspases. As caspases were demonstrated to down-regulate the two transporters, their inhibition by TNF is responsible for the observed up-regulatory effect. Conclusions It was concluded that the Na+-K+ ATPase and Na+K+2Cl- are both targets of TNF-α and the effect of the cytokine favours cell survival over cell death. © 2009 Stichting European Society for Clinical Investigation Journal Foundation.AMSLER K, 1985, J CELL PHYSIOL, V123, P257, DOI 10.1002-jcp.1041230216; Arrebola F, 2005, J CELL PHYSIOL, V204, P500, DOI 10.1002-jcp.20306; BARLETBAS C, 1991, J BIOL CHEM, V268, P11512; Bazzoni F, 1996, NEW ENGL J MED, V334, P1717; Bortner CD, 2001, J BIOL CHEM, V276, P4304, DOI 10.1074-jbc.M005171200; BRADFORD MM, 1976, ANAL BIOCHEM, V72, P54; Dempsey PW, 2003, CYTOKINE GROWTH F R, V14, P193, DOI 10.1016-S1359-6101(03)00021-2; DiPetrillo K, 2004, KIDNEY INT, V65, P1676, DOI 10.1111-j.1523-1755.2004.00606.x; DiPetrillo K, 2003, AM J PHYSIOL-RENAL, V284, pF113, DOI 10.1152-ajprenal.00026.2002; Farokhzad OC, 1999, J CELL PHYSIOL, V181, P489, DOI 10.1002-(SICI)1097-4652(199912)181:3489::AID-JCP133.0.CO;2-7; Feraille E, 2001, PHYSIOL REV, V81, P345; GREGER R, 1985, PHYSIOL REV, V65, P760; Haas M, 1998, J BIOENERG BIOMEMBR, V30, P161, DOI 10.1023-A:1020521308985; Hughes FM, 1997, J BIOL CHEM, V272, P30567, DOI 10.1074-jbc.272.48.30567; Jensen BS, 1997, BBA-BIOMEMBRANES, V1329, P1, DOI 10.1016-S0005-2736(97)00148-X; JORGENSEN PL, 1980, PHYSIOL REV, V60, P864; Kalantarinia K, 2003, KIDNEY INT, V64, P1208, DOI 10.1046-j.1523-1755.2003.00237.x; KILLANDE.D, 1965, EXP CELL RES, V40, P12, DOI 10.1016-0014-4827(65)90285-5; LINGREL JB, 1994, J BIOL CHEM, V269, P19659; Lorz C, 2008, J AM SOC NEPHROL, V19, P904, DOI 10.1681-ASN.2007050581; LYTLE C, 1992, J BIOL CHEM, V267, P25438; Matsuda T, 1996, J NEUROCHEM, V66, P511; Moriwaki Y, 2003, METABOLISM, V52, P605, DOI 10.1053-meta.2003.50096; NAVARRO JF, 2005, KIDNEY INT S99, V68, pS98, DOI 10.1111-j.1523-1755.2005.09918.x; Navarro JF, 2006, CYTOKINE GROWTH F R, V17, P441, DOI 10.1016-j.cytogfr.2006.09.011; Navarro-Gonzalez JF, 2008, J AM SOC NEPHROL, V19, P433, DOI 10.1681-ASN.2007091048; NORBY JG, 1988, METHOD ENZYMOL, V156, P116; Olej B, 1998, BIOSCIENCE REP, V18, P1, DOI 10.1023-A:1022259832207; PARIS S, 1986, J BIOL CHEM, V261, P6177; PAYNE JA, 1995, CURR OPIN CELL BIOL, V7, P493, DOI 10.1016-0955-0674(95)80005-0; Russell JM, 2000, PHYSIOL REV, V80, P211; Shaulian E, 2002, NAT CELL BIOL, V4, P131; SMYTH MJ, 1990, J CELL PHYSIOL, V145, P531, DOI 10.1002-jcp.1041450320; Sun D, 1997, AM J PHYSIOL-CELL PH, V272, pC1829; Topper JN, 1997, J CLIN INVEST, V99, P2941, DOI 10.1172-JCI119489; Trimarchi JR, 2002, AM J PHYSIOL-CELL PH, V282, pC588; Vinciguerra M, 2005, J AM SOC NEPHROL, V16, P2576, DOI 10.1681-ASN.2005040448; Wajant H, 2003, CELL DEATH DIFFER, V10, P45, DOI 10.1038-sj.cdd.4401189; WEDER AB, 1994, AM J MED SCI, V307, pS5333
Novel methods for fatigue data editing for horizontal axis wind turbine blades
No full textWind turbine blades are the most critical components of wind turbines. Full-scale blade fatigue testing is required to verify that the blades possess the strength and service life specified in the design. Unfortunately, the test must be run for a long time period. This problem led the blade testing laboratories to accelerate fatigue testing time. To achieve the objective, this thesis proposes two novel methods called STFT- and WT-based fatigue damage part extracting methods which are based on short-time Fourier transform (STFT) and wavelet transform (WT), respectively. For WT, different wavelet functions which are Morl, Meyr, Dmey, Mexh and DB30 are studied.
An aerodynamic computer code, HAWTsimulator, based on blade element momentum theory has been developed. This code is used to generate the sets of aerodynamic loads acting along the span of a ‘SERI-8 wind turbine blade’ in the range of wind speed from cut-in to cut-out. SERI-8 blades are installed on 65 kW wind turbines. Each set of aerodynamic loads is applied on the finite element model of the SERI-8 blade in structural software (ANSYS) to generate a plot of von Mises stress at the critical point on the blade versus wind speed. By relating this relationship to the wind speed data, the stress-time history at the critical point on the SERI-8 blade can be generated. It has the same sampling rate and length as the wind speed data.
A concept of applying accumulative power spectral density (AccPSD) distribution with time to identify fatigue damage events contained in the stress-time history has been introduced in this thesis. For STFT, AccPSD is the sum of power spectral density (PSD) of each frequency band at each time interval in the spectrogram. For WT, AccPSD is the sum of PSD of wavelet coefficients of each scale at each time interval in the scalogram. It has been found that the locations of AccPSD spikes imply where the fatigue damage events are. Based on an appropriate AccPSD level called a cutoff level, the fatigue damage events can be identified at time location of the stress-time history.
A fatigue computer code, HAWTfatigue, based on stress-life approach and Miner’s linear cumulative damage rule has been developed. Basically, the code is used for evaluating the fatigue damage and service lifetime of horizontal axis wind turbine blade. In addition, the author has implemented STFT- and WT-based fatigue damage part extracting methods into the code. Fatigue damage parts are extracted from the stress time history and they are concatenated to form the edited stress-time history. The effectiveness of STFT- and WTbased algorithms is performed by comparing the reduction in length and the difference in fatigue damage per repetition of the edited stress-time histories generated by STFT and WT to those of the edited stress-time history generated by an existing method, Time Correlated Fatigue Damage (TCFD) used by commercial software.
The findings of this research project are as follows:
1. The comparison of the reduction in length of the edited stress-time histories generated by TCFD, STFT and WT indicates that WT with the Mexh wavelet has the maximum reduction of 20.77% in length with respect to the original length, followed by Meyr (20.24%), Dmey (19.70%), Morl (19.66%), DB30 (19.19%), STFT (15.38%), and TCFD (10.18%), respectively.
2. The comparison of the retained fatigue damage per repetition in the edited stress-time histories generated by TCFD, STFT and WT indicates that TCFD has the retained fatigue damage per repetition less than the original fatigue damage per repetition by 0.076%, followed by Mexh (0.068%), DB30 (0.063%), STFT (0.045%), Meyr (0.032%), Dmey (0.014%), and Morl (0.013%), respectively.
3. Both comparison of reduction in length and comparison in the retained fatigue damage per repetition of the edited stress-time histories suggest that WT is the best method for extracting fatigue damage parts from the given stress-time history. It has also been indicated that not only do STFT and WT improve accuracy of fatigue damage per repetition retained in the edited stress-time histories, but also they provide the length of the edited stress-time histories shorter than TCFD does. Thus, STFT and WT are useful methods for performing accelerated fatigue tests.
4. It has been found that STFT is controlled by two main factors which are window size and cutoff level. Also, WT is controlled by three main factors which are wavelet decomposition level, cutoff level and wavelet type.
To conclude, the edited stress-time history can be used by blade testing laboratories to accelerate fatigue testing time. STFT- and WT-based fatigue damage part extracting methods proposed in this thesis are suggested as alternative methods in accelerating fatigue testing time, especially for the field of wind turbine engineering
Phantoms of Anglo-Confederate commerce : an historical and archaeological investigation of American civil war blockade running
No full textDuring the American Civil War Wilmington, North Carolina and the
Bermudian ports of St. Georges and Hamilton served as vital links in a
complex trading network that developed to facilitate the exchange of southern
agricultural products for war materials and civilian merchandise through a
Union blockade of the Confederacy. Although that material contributed
significantly to the Confederate war effort, Anglo-Confederate blockade
running has received limited scholarly attention. Much of the associated
literature is based on memoirs rather than scholarship and does not accurately,
reflect that necessarily clandestine trade. The primary goal of this thesis is to
produce a more comprehensive and detailed picture of blockade running, the
cargoes carried through the Union blockade and the powerful steam vessels
that made Anglo-Confederate commerce possible. Unlike previous treatments,
this thesis combines the results of both archival and archaeological research.
The results illustrate the evolution of strategies involved in both establishing
and maintaining the blockade and those developed for running the blockade.
Assessment of the vessel remains and historical data associated with the
construction and procurement of steamers identifies the vessel types and
confirms that blockade runners adapted extant technology. Contrary to the
popularly held impression, no technological innovations were specifically
developed to address the demands of the trade. The spatial distribution of
wrecks and the minimal amount of cultural material surviving in association
with them, provides strong evidence that cargoes were more valuable than the
vessels. That premise influenced the strategy adopted by blockade runners.
While Confederate salvors left little evidence of cargo, historical research
revealed a wealth of new insight into the specific nature of that material. This
new evidence provides a more accurate and detailed picture of Anglo-
Confederate blockade running and the strategies, ships and cargoes that made
blockade running between Wilmington and Bermuda a success
Antiinflammatory therapy with canakinumab for atherosclerotic disease
No full textBackground: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.
Thromboelastographic assessment of the efficacy of rFVIIa in vitro and in vivo
No full textHaemorrhage is a leading cause of death in both the military and civilian environs and blood loss from sites which are not easily accessible or do not lend themselves to direct physical compression to reduce blood loss contribute hugely to the haemorrhage mortality rate, particularly in the face of delay before surgical intervention. A number of agents aimed at controlling non-compressible haemorrhage are currently under evaluation, including activated recombinant factor Vila (rFVIIa), a drug injected intravenously. rFVIIa is an attractive option to control blood loss in this population of patients since the drug can be injected at any site, the effects of rFVIIa targeted to where they are required. A number of clinical case reports and case series have demonstrated a beneficial effect of rFVIIa in trauma victims, when used as a last resort. These anecdotal reports are yet to be corroborated by adequately powered clinical trials. Animal studies have yielded conflicting results, some demonstrating a clear effect of rFVIIa on survival and others finding no benefit, or effect only on parameters such as blood product usage. Further research is required to firmly establish the efficacy of rFVIIa in trauma patients. The in vivo animal study from which blood samples for the present study were obtained provided a model of haemorrhage followed by progressive haemodilution associated with intravenous fluid resuscitation. The main aim of the in vitro study that forms the experimental work for this thesis was to compare the ability of rFVIIa with placebo to enhance clotting under the effects of progressive haemodiltion. A further aim was to establish whether a second dose of rFVIIa under these conditions had any effect. The study utilised an established technique called thromboelastography (TEG) to compare clotting in blood samples treated in vitro with rFVIIa and placebo
