Three-dimensional random Voronoi tessellations: From cubic crystal lattices to Poisson point processes

We perturb the SC, BCC, and FCC crystal structures with a spatial Gaussian noise whose adimensional strength is controlled by the parameter a, and analyze the topological and metrical properties of the resulting Voronoi Tessellations (VT). The topological properties of the VT of the SC and FCC crystals are unstable with respect to the introduction of noise, because the corresponding polyhedra are geometrically degenerate, whereas the tessellation of the BCC crystal is topologically stable even against noise of small but finite intensity. For weak noise, the mean area of the perturbed BCC and FCC crystals VT increases quadratically with a. In the case of perturbed SCC crystals, there is an optimal amount of noise that minimizes the mean area of the cells. Already for a moderate noise (a>0.5), the properties of the three perturbed VT are indistinguishable, and for intense noise (a>2), results converge to the Poisson-VT limit. Notably, 2-parameter gamma distributions are an excellent model for the empirical of of all considered properties. The VT of the perturbed BCC and FCC structures are local maxima for the isoperimetric quotient, which measures the degre of sphericity of the cells, among space filling VT. In the BCC case, this suggests a weaker form of the recentluy disproved Kelvin conjecture. Due to the fluctuations of the shape of the cells, anomalous scalings with exponents >3/2 is observed between the area and the volumes of the cells, and, except for the FCC case, also for a->0. In the Poisson-VT limit, the exponent is about 1.67. As the number of faces is positively correlated with the sphericity of the cells, the anomalous scaling is heavily reduced when we perform powerlaw fits separately on cells with a specific number of faces

Discovery of Calcium, Indium, Tin, and Platinum Isotopes

Currently, twenty-four calcium, thirty-eight indium, thirty-eight tin and thirty-nine platinum isotopes have been observed and the discovery of these isotopes is discussed here. For each isotope a brief synopsis of the first refereed publication, including the production and identification method, is presented.Comment: to be published in At. Data Nuclear Data Tables, This updated paper combines manuscripts: 1004.4934 (Calcium), 1004.5266 (Indium), 1003.5127 (Tin), and 1006.4033 (Platinum

Influence Of The Kcl Concentration On Rat Sinus Node Recovery Time In Vitro.

The influence of changes in the KCl concentration of the bath fluid ([KCl]o) on the corrected sinus node recovery time (CSNRT) was studied using the continuous pacing method (M1) and the method of stimulation with premature pulses (M2). M1 and M2 were compared in Krebs-Henseleit solution containing normal (4.6 mM), low (3.1 mM, LoKCl) and high (6.1 mM, HiKCl) [KCl]o. The results revealed that HiKCl increased CSNRT (P less than 0.01) and changed the prematurity-CSNRT relationship (P less than 0.01), whereas LoKCl did not change CSNRT. M1 and M2 were different (P less than 0.01) regardless of [KCl]o, except for pacing intervals near the spontaneous cycle length.22680380

Influence Of Stimulatory Parameters On Sinus Node Recovery Time: An In Vitro Study.

The effects of pacing frequency, overdrive duration and stimulus amplitude on the sinus node recovery time (SNRT) were studied in the isolated right atrium of the rat. A positive relationship between pacing frequency and the SNRT was observed, whereas overdrive duration and stimulus amplitude did not affect SNRT. There was no significant interaction among the factors studied. The effect of frequency upon SNRT probably does not involve neurotransmitter release due to stimulation, since in vitro pretreatment with atropine plus propranolol does change the SNRT-frequency relation.2151079108

Temperature And Relative Contributions Of Ca Transport Systems In Cardiac Myocyte Relaxation

The relative contributions of the different Ca transport systems involved in cardiac relaxation were evaluated at 25 and 35°C in isolated rabbit, ferret, and cat ventricular myocytes during twitches, caffeine-induced contractures in normal Tyrode solution, and caffeine-induced contractures in Na- and Ca-free solution. The time course of intracellular [Ca] decline during these contractions in rabbit ventricular myocytes allowed estimates of the relative contributions of the sarcoplasmic reticulum (SR) Ca pump, Na/Ca exchange, sarcolemmal Ca pump, and the mitochondrial calcium uniporter (with the latter two considered together as 'slow mechanisms'). The percent contributions of the SR Ca pump, the Na/Ca exchange, and the slow mechanisms were 70, 27, and 3% at 25°C and 74, 23, and 3% at 35°C. Warming from 25 to 35°C decreases twitch contractions in rabbit and ferret myocytes and caffeine-induced contractures in normal Tyrode solution and Na- and Ca-free solution in all species. In contrast, in cat myocytes warming increased twitches, possibly because of a stronger effect of temperature on Ca influx. We conclude that increased temperature accelerates all of the Ca transport systems involved in relaxation. Despite large changes in each Ca transport system with warming, the relative contributions during relaxation remain similar at physiological temperature.2705 39-5H1772H1778Bassani, J.W.M., Bassani, R.A., Bers, D.M., Relaxation in rabbit and rat cardiac cells: Species-dependent differences in cellular mechanisms (1994) J. Physiol. Lond., 476, pp. 279-293Bassani, J.W.M., Yuan, W., Bers, D.M., Fractional SR Ca release is regulated by trigger Ca and SR Ca content in cardiac myocytes (1995) Am. J. Physiol., 268, pp. C1313-C1329. , Cell Physiol. 37Bassani, R.A., Bassani, J.W.M., Bers, D.M., Relaxation in ferret ventricular myocytes: Role of the sarcolemmal Ca ATPase (1995) Pfluegers Arch., 430, pp. 573-578Bassani, R.A., Bassani, J.W.M., Bers, D.M., Relaxation in ferret ventricular myocytes: Unusual interplay among calcium transport systems (1994) J. Physiol. Lond., 476, pp. 295-308Bassani, R.A., Bassani, J.W.M., Bers, D.M., Mitochondrial and sarcolemmal Ca2+ transport reduce [Ca]1 during caffeine contractures in rabbit cardiac myocytes (1992) J. Physiol. Lond., 453, pp. 591-608Bers, D.M., (1991) Excitation-Contraction Coupling and Cardiac Contractile Force, p. 258. , Dordrecht, The Netherlands: Kluwer AcademicBers, D.M., Berlin, J.R., The kinetics of [Ca]1 decline in cardiac myocytes depends on peak [Ca]i (1995) Am. J. Physiol., 268, pp. C271-C277. , Cell Physiol. 37Bers, D.M., Bridge, J.H.B., Relaxation of rabbit ventricular muscle by Na-Ca exchange and sarcoplasmic reticulum calcium pump. Eyanodine and voltage sensitivity (1989) Circ. Res., 65, pp. 334-342Bers, D.M., Bridge, J.H.B., Spitzer, K.W., Intracellular Ca2+ transients during rapid cooling contractures in guinea-pig ventricular myocytes (1989) J. Physiol. Lond., 417, pp. 537-553Bersohn, M.M., Vemuri, R., Schuil, D.W., Weiss, R.S., Philipson, K.D., Effect of temperature on sodium-calcium exchange in sarcolemma from mammalian and amphibian hearts (1991) Biochim. Biophys. Acta, 1062, pp. 19-23Blinks, J.R., Koch-Weser, J., Physical factors in the analysis of the action of drugs on myocardial contractility (1963) Pharmacol. Rev., 15, pp. 531-599Briggs, G.M., Bers, D.M., Role of calcium current in hypothermie inotropy in myocytes isolated from rabbit ventricles (1990) Biophys. J, 57, p. 346Cavalié, A., McDonald, T.F., Pelzer, D., Trautwein, W., Temperature-induced transitory and steady-state changes in the calcium current of guinea pig ventricular myocytes (1985) Pfluegers Arch., 405, pp. 294-296Chapman, R.A., Sodium/calcium exchange and intracellular calcium buffering in ferret myocardium: An ion-sensitive microelectrode study (1986) J. Physiol. Lond., 373, pp. 163-179Debetto, P., Cusinato, F., Luciani, S., Temperature dependence of Na+/Ca2+ exchange activity in beef-heart sarcolemmal vesicles and proteoliposomes (1990) Arch. Biochem. Biophys., 278, pp. 205-210Delbridge, L.M., Bassani, J.W.M., Bers, D.M., Steadystate twitch Ca fluxes and cytosolic Ca buffering in rabbit ventricular myocytes (1996) Am. J. Physiol., 270, pp. C192-C199. , Cell Physiol. 39Grynkiewicz, G., Poenie, M., Tsien, R.Y., A new generation of Ca2+ indicators with greatly improved fluorescence properties (1985) J. Biol. Chem., 250, pp. 3440-3450Harrison, S.M., Bers, D.M., Influence of temperature on the calcium sensitivity of the myofilaments of skinned ventricular muscle from the rabbit (1989) J. Gen. Physiol., 93, pp. 411-428Hove-Madsen, L., Bers, D.M., Passive Ca buffering and SR Ca uptake in permeabilized rabbit ventricular myocytes (1993) Am. J. Physiol., 264, pp. C677-C686. , Cell Physiol. 33Hryshko, L.V., Stiffel, V.M., Bers, D.M., Rapid cooling contractures as an index of sarcoplasmic reticulum calcium content in rabbit ventricular myocytes (1989) Am. J. Physiol., 257, pp. H1369-H1377. , Heart Circ. Physiol. 26Kimura, J., Miyamae, S., Noma, A., Identification of sodium-calcium exchange current in single ventricular cells of guinea-pig (1987) J. Physiol. Lond., 384, pp. 199-222Kruta, V., Sur l'activité rythmique du muscle cardiaque. II. Variations, en fonction de la température, des relations entre la réponse mécanique et le rythme (1938) Arch. Int. Physiol., 47, pp. 35-62Lipp, P., Pott, L., Callewaert, G., Carmeliet, E., Simultaneous recording of indo-1 fluorescence and Na+/Ca2+ exchange current reveals two components of Ca2+ release from sarcoplasmic retieulum of cardiac atrial myocytes (1990) FEBS Lett., 275, pp. 181-184Mattiazzi, A.R., Nilsson, E., The influence of temperature on time course of the mechanical activity in rabbit papillary muscle (1976) Acta Physiol. Scand., 97, pp. 310-318Negretti, N., O'Neill, S.C., Eisner, D.A., The relative contributions of different intracellular and sarcolemmal systems to relaxation in rat ventricular myocytes (1993) Cardiouasc. Res., 27, pp. 1826-1830Niggli, E., Lederer, W.J., Activation of Na-Ca exchange current by photolysis of "caged calcium" (1993) Biophys. J, 65, pp. 882-891Shattock, M.J., Bers, D.M., Inotropic response to hypothermia and the temperature-dependence of ryanodine action in isolated rabbit and rat ventricular muscle: Implications for the excitation-contraction coupling (1987) Circ. Res., 61, pp. 761-771Shikegawa, M., Finegan, J.M., Katz, A.M., Calcium transport ATPase of canine cardiac sarcoplasmic reticulum (1976) J. Biol. Chem., 251, pp. 6894-6900Sitsapesan, R., Montgomery, R.A., MacLeod, K.T., Williams, A.J., Sheep cardiac sarcoplasmic reticulum calcium-release channels: Modification of conductance and gating by temperature (1991) J. Physiol. Lond., 434, pp. 469-488Zhou, Z., Lipsius, S.L., Na+-Ca2+ exchange current in latent pacemaker cells isolated from cat right atrium (1993) J. Physiol. Lond., 466, pp. 263-28

Plastic flow in a composite: a comparison of nonlocal continuum and discrete dislocation predictions

A two-dimensional model composite with elastic reinforcements in a crystalline matrix subject to macroscopic shear is considered using both discrete dislocation plasticity and a nonlocal continuum crystal plasticity theory. Only single slip is permitted in the matrix material. The discrete dislocation results are used as numerical experiments and we explore the extent to which the nonlocal crystal plasticity theory can reproduce their behavior. In the nonlocal theory, the hardening rate depends on a particular strain gradient that provides a measure of plastic (or elastic) incompatibility. This nonlocal formulation preserves the classical structure of the incremental boundary value problem. Two composite morphologies are considered; one gives rise to relatively high composite hardening and a dependence of the stress-strain response on size, while the other exhibits nearly ideally plastic composite response and size independence. The predictions of the two plasticity models fo..

Rupture of blood clots: Mechanics and pathophysiology

© 2020 The Authors. Fibrin is the three-dimensional mechanical scaffold of protective blood clots that stop bleeding and pathological thrombi that obstruct blood vessels. Fibrin must be mechanically tough to withstand rupture, after which life-threatening pieces (thrombotic emboli) are carried downstream by blood flow. Despite multiple studies on fibrin viscoelasticity, mechanisms of fibrin rupture remain unknown. Here, we examined mechanically and structurally the strain-driven rupture of human blood plasma-derived fibrin clots where clotting was triggered with tissue factor. Toughness, i.e., resistance to rupture, quantified by the critical energy release rate (a measure of the propensity for clot embolization) of physiologically relevant fibrin gels was determined to be 7.6 ± 0.45 J/m2. Finite element (FE) simulations using fibrin material models that account for forced protein unfolding independently supported this measured toughness and showed that breaking of fibers ahead the crack at a critical stretch is the mechanism of rupture of blood clots, including thrombotic embolization