Measurement Of Force Development Research Articles

Force Development Prediction Model for Constrained Lithium-Ion Pouch Cells

Mechanical stability of lithium-ion battery modules is crucial for the safety of electric vehicles. This is challenging to ensure as cells show irreversible thickness growth over lifetime. Therefore, mechanical bracing of cells and the consequent force on the module housing increases over lifetime. Furthermore, both too low and too high mechanical pressure on cells have been shown to have negative impact on their lifetime due to layer delamination and lithium plating, respectively [1]. Consequently, an integrated design should realize medium cell pressures over the entire lifetime. Thus, in order to properly design a module for a specific cell in a given installation space a force prediction model is necessary which may consider the potential addition of pressure pads. Unfortunately, both a comprehensive modeling technique as well as automotive module force development data over lifetime are unavailable in literature. Cell thickness growth is mainly attributed to solid electrolyte interface (SEI) growth on anode particles with consequent cycling [2]. Slightly grown particles cause the macroscopic electrode to expand upon mechanical reorganization of the microstructure caused by the cyclic swelling. Thus, cell thickness growth correlates directly with loss of active lithium to the SEI and – in the limited case – to the capacity loss of the cell [2]. A novel one-dimensional mechano-electrochemical model is presented which considers the cell stack in force equilibrium with its bracing module. For this, a fixed bracing stiffness and an aging-dependent cell stack stiffness is considered where the cell stack may consist of cells with or without pressure pads. Care is taken to implement the aging anode lithiation degrees in the graphite anode affected by lithium loss influencing the reversibility of SOC dependent swelling. The experimental data required for the model are the module dimensions, stiffness data of components and the cell thickness growth of cells over aging. The latter is measured in a constant-force cell aging experiment where the cell thickness evolution is measured. Based on this, the model may predict force development of the module over lifetime and can thus a priori validate designs or considered pressure pads. For model validation, automotive modules with and without pressure pads are aged in representative as well as accelerated aging conditions. The force development is determined at several points during aging by correlating 3D-deformations of module capping plates to a reference experiment. Such measurements of force development over lifetime in automotive modules have not been reported yet. Both accelerated and representative aging conditions show similar force evolution as correlated to capacity loss but not to energy throughput. Crucially, the predictions of the model are validated by the force evolution in the modules in both cases. As designed modules with pressure pads show significantly attenuated force development which is also successfully predicted by the model. Remaining errors exist at higher pressures which have to be investigated in detail in the future. The presented model is a powerful tool to quantitatively validate module and pressure pad designs as well as predict force evolution in given bracing conditions.

Gene-specific increase in the energetic cost of contraction in hypertrophic cardiomyopathy caused by thick filament mutations.

Disease mechanisms regarding hypertrophic cardiomyopathy (HCM) are largely unknown and disease onset varies. Sarcomere mutations might induce energy depletion for which until now there is no direct evidence at sarcomere level in human HCM. This study investigated if mutations in genes encoding myosin-binding protein C (MYBPC3) and myosin heavy chain (MYH7) underlie changes in the energetic cost of contraction in the development of human HCM disease. Energetic cost of contraction was studied in vitro by measurements of force development and ATPase activity in cardiac muscle strips from 26 manifest HCM patients (11 MYBPC3mut, 9 MYH7mut, and 6 sarcomere mutation-negative, HCMsmn). In addition, in vivo, the ratio between external work (EW) and myocardial oxygen consumption (MVO2) to obtain myocardial external efficiency (MEE) was determined in 28 pre-hypertrophic mutation carriers (14 MYBPC3mut and 14 MYH7mut) and 14 healthy controls using [(11)C]-acetate positron emission tomography and cardiovascular magnetic resonance imaging. Tension cost (TC), i.e. ATPase activity during force development, was higher in MYBPC3mut and MYH7mut compared with HCMsmn at saturating [Ca(2+)]. TC was also significantly higher in MYH7mut at submaximal, more physiological [Ca(2+)]. EW was significantly lower in both mutation carrier groups, while MVO2 did not differ. MEE was significantly lower in both mutation carrier groups compared with controls, showing the lowest efficiency in MYH7 mutation carriers. We provide direct evidence that sarcomere mutations perturb the energetic cost of cardiac contraction. Gene-specific severity of cardiac abnormalities may underlie differences in disease onset and suggests that early initiation of metabolic treatment may be beneficial, in particular, in MYH7 mutation carriers.

Nebivolol, bucindolol, metoprolol and carvedilol are devoid of intrinsic sympathomimetic activity in human myocardium.

1. The present study investigated whether or not there may be differences in the direct cardiac actions of the novel, highly beta(1)-selective adrenoceptor antagonist nebivolol (NEB) in comparison to metoprolol (MET), bisoprolol (BIS), carvedilol (CAR) and bucindolol (BUC) in human myocardium (n=9). 2. The rank order of beta(1)-selectivity as judged by competition experiments to (3)H-CGP 12.1777 in the presence of CGP 207.12 A (300 nmol l(-1), K(i)beta(2)) or ICI 118.551 (50 nmol l(-1), K(i)beta(1)) were NEB(K(i)beta(2)/K(i)beta(1): 40.7) > BIS(15.6) > MET(4.23) > CAR(0.73) > BUC(0.49). 3. The rank order of the negative inotropic potency of the beta-adrenoceptor antagonists measured in left ventricular trabeculae (dilated cardiomyopathy, DCM) as judged by the concentration needed to induce a 50% decrease in isoprenaline (1 micromol l(-1))-stimulated force (IC(50)) was: MET (0.6 micromol l(-1)) > CAR (4.1 micromol l(-1)) > NEB (7.0 micromol l(-1)). 4. NEB, BUC, MET and CAR did not not exert an intrinsic sympathomimetic activity (ISA) as determined by measurements of force development in forskolin (0.3 micromol l(-1)) pre-treated left ventricular trabeculae, nor by measuring adenylate cyclase activity in forskolin (0.3 micromol l(-1))-stimulated assays (crude membranes). This also holds true for radioligand binding assays with or without guanine nucleotide guanyl-5'-yl imidodiphosphate (Gpp(NH)p). 5. Although all studied beta-adrenoceptor antagonists lack intrinsic sympathomimetic activity (ISA), they differ in the beta(1)-selectivity as well as in their direct negative inotropic action. These differences as well as the mode of extracardiac action may have an impact on outcome of patients treated with beta-adrenoceptor antagonists.

Measurement of Platelet-Mediated Force Development During Plasma Clot Formation

We have developed an instrument that measures force development during clot retraction. Clots are formed between an aluminum plate and cup. The plate is coupled to a strain gauge transducer. Force generated by platelets is transmitted to the upper plate and the resulting voltage change is recorded. Calibration using standard weights allows conversion of the voltage signal to dynes/cm2. Study parameters include lag phase prior to force development, maximum rate of force development (MRFD), and maximum force generated (MFG). When controlled for platelet count, ionic strength (0.15), pH (7.4), calcium concentration (10mM), thrombin concentration (1.5 u/ml), temperature, and gap distance (1 mm), measurements are reproducible. Control of each variable is critical since clot retraction depends on platelet function and fibrin structure. At 37 degrees C and 26 x 10(3) platelets/microL, the lag phase was 300 seconds, the MRFD was 0.69 dynes/(cm2 sec), and the force at 1000 seconds (MFG) was 2450 dynes. At 7.5 x 10(4) platelets/microL, the lag phase was 160 seconds, the MRFD was 1.06 dyne/(cm2 sec), and the MFG was 4400 dynes. Decreasing the sample temperature from 37 degrees C to 27 degrees C (75 x 10(3) platelets/microL) increases the lag phase from 170 to 300 seconds, decreases MRFD from 1.06 to 0.66 dynes/(cm2 sec), and decreases the MFG at 1000 seconds from 4,400 to 2,800 dynes. At 15 degrees C, retraction is totally inhibited. This instrument provides a simple way to quantify the impact of altered fibrin structure and platelet function on clot retraction. Measurement of force development during clot retraction may offer a new approach to the study of qualitative platelet dysfunction.