[ON THE ELASTICITY THEORY OF HIGHLY ELASTIC BODIES. COMPARISON BETWEEN CRYSTAL ELASTICITY AND RUBBER ELASTICITY].
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The microfibrillar protein (MFP) of foetal bovine ligamentum nuchae elastic fibres was prepared and used to produce a monospecific antiserum. Indirect immunofluorescence studies employing the specific antiserum demonstrated its selectivity for MFP associated with elastic fibres. The antiserum was demonstrated to react with vascular elastic tissue, perivascular connective tissue and reticular basement membranes in a variety of tissues. This evidence suggests that the MFP (or an immunologically related protein) is not confined to elastic fibres but is widely distributed in connective tissue being associated with both elastin and collagen fibres.
Numerous physical characterizations clearly demonstrate that the polypentapeptide of elastin (Val1-Pro2-Gly3-Val4-Gly5)n in water undergoes an inverse temperature transition. Increase in order occurs both intermolecularly and intramolecularly on raising the temperature from 20 to 40 degrees C. The physical characterizations used to demonstrate the inverse temperature transition include microscopy, light scattering, circular dichroism, the nuclear Overhauser effect, temperature dependence of composition, nuclear magnetic resonance (NMR) relaxation, dielectric relaxation, and temperature dependence of elastomer length. At fixed extension of the cross-linked polypentapeptide elastomer, the development of elastomeric force is seen to correlate with increase in intramolecular order, that is, with the inverse temperature transition. Reversible thermal denaturation of the ordered polypentapeptide is observed with composition and circular dichroism studies, and thermal denaturation of the crosslinked elastomer is also observed with loss of elastomeric force and elastic modulus. Thus, elastomeric force is lost when the polypeptide chains are randomized due to heating at high temperature. Clearly, elastomeric force is due to nonrandom polypeptide structure. In spite of this, elastomeric force is demonstrated to be dominantly entropic in origin. The source of the entropic elastomeric force is demonstrated to be the result of internal chain dynamics, and the mechanism is called the librational entropy mechanism of elasticity. There is significant application to the finding that elastomeric force develops due to an inverse temperature transition. By changing the hydrophobicity of the polypeptide, the temperature range for the inverse temperature transition can be changed in a predictable way, and the temperature range for the development of elastomeric force follows. Thus, elastomers have been prepared where the development of elastomeric force is shifted over a 40 degrees C temperature range from a midpoint temperature of 30 degrees C for the polypentapeptide to 10 degrees C by increasing hydrophobicity with addition of a single CH2 moiety per pentamer and to 50 degrees C by decreasing hydrophobicity.(ABSTRACT TRUNCATED AT 400 WORDS)
The traditional bulk elastic modulus approach to plant cell pressure-volume relations is inconsistent with its definition. The relationship between the bulk modulus and Young's modulus that forms the basis of their usual application to cell pressure-volume properties is demonstrated to be physically meaningless. The bulk modulus describes stress/strain relations of solid, homogeneous bodies undergoing small deformations, whereas the plant cell is best described as a thin-shelled, fluid-filled structure with a polymer base. Because cell walls possess a polymer structure, an alternative method of mechanical analysis is presented using polymer elasticity principles. This initial study presents the groundwork of polymer mechanics as would be applied to cell walls and discusses how the matrix and microfibrillar network induce nonlinear stress/strain relationships in the cell wall in response to turgor pressure. In subsequent studies, these concepts will be expanded to include anisotropic expansion as regulated by the microfibrillar network.
The action of two elastic activators (Bimler and Klammt) is studied in twenty Class II/1 malocclusions, with a mean age of 10.2 years and a treatment time of 2.7 years. Intercanine and intermolar widths, and "anterior arch height" (Korkhaus) were measured on models at the beginning and at the end of treatment. On lateral X-Ray films following parameters (Ricketts) were measured: facial axis, facial depth, convexity, lower facial height, and corpus axis. Conclusions are: both appliances have a good transverse response, Bimler's Gebissformer increase vertical growth, and Klammt's elastic activator decrease convexity by a more anterior mandibular positioning.
The first part of this review on entropic elastic processes in protein mechanisms (Urry, 1988) demonstrated with the polypentapeptide of elastin (Val1-Pro2-Gly3-Val4-Gly5)n that elastic structure develops as the result of an inverse temperature transition and that entropic elasticity is due to internal chain dynamics in a regular nonrandom structure. This demonstration is contrary to the pervasive perspective of entropic protein elasticity of the past three decades wherein a network of random chains has been considered the necessary structural consequence of the occurrence of dominantly entropic elastomeric force. That this is not the case provides a new opportunity for understanding the occurrence and role of entropic elastic processes in protein mechanisms. Entropic elastic processes are considered in two classes: passive and active. The development of elastomeric force on deformation is class I (passive) and the development of elastomeric force as the result of a chemical process shifting the temperature of a transition is class II (active). Examples of class I are elastin, the elastic filament of muscle, elastic force changes in enzyme catalysis resulting from binding processes and resulting in the straining of a scissile bond, and in the turning on and off of channels due to changes in transmembrane potential. Demonstration of the consequences of elastomeric force developing as the result of an inverse temperature transition are seen in elastin, where elastic recoil is lost on oxidation, i.e., on decreasing the hydrophobicity of the chain and shifting the temperature for the development of elastomeric force to temperatures greater than physiological. This is relevant in general to loss of elasticity on aging and more specifically to the development of pulmonary emphysema. Since random chain networks are not the products of inverse temperature transitions and the temperature at which an inverse temperature transition occurs depends on the hydrophobicity of the polypeptide chain, it now becomes possible to consider chemical processes for turning elastomeric force on and off by reversibly changing the hydrophobicity of the polypeptide chain. This is herein called mechanochemical coupling of the first kind; this is the chemical modulation of the temperature for the transition from a less-ordered less elastic state to a more-ordered more elastic state. In the usual considerations to date, development of elastomeric force is the result of a standard transition from a more-ordered less elastic state to a less-ordered more elastic state.(ABSTRACT TRUNCATED AT 400 WORDS)
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The aim of this study was to establish the long-term effect of graduated elastic compression on venous elasticity in patients with superficial or deep venous disease and to determine the possible relationship between elasticity and the duration of the disease. The elastic modulus of 29 patients, 19 with superficial vein incompetence and 10 with deep vein incompetence was assessed by the simultaneous measurement of calf volume (determined using strain gauge) and venous pressure (obtained via a dorsal foot vein) during venous occlusion. The measurements were obtained before and after 4 weeks of elastic compression stockings. The elastic modulus K, was defined as stress/strain when the veins were full and was calculated from the pressure/volume relationship. The results show a clear difference in elasticity before and after elastic stockings. Two groups of patients were identified: group 1 with increased elasticity and group 2 with decreased elasticity. There was a negative linear relationship (r = 0.88) between increase in elasticity after treatment and duration of venous disease.
OBJECTIVE: To quantify the influence of elastic and non-elastic external mesh support on para-anastomotic hypercompliance in end-to-end anastomoses (ex vivo). MATERIALS: Six end-to-end anastomoses prepared from ovine carotid arteries without mesh support and with external elastic and non-elastic dacron mesh support. METHODS: Compliance profiles of the anastomised arterial segments were measured successively, in the same anastomotic configuration without mesh support, with external elastic dacron mesh support and with external non-elastic dacron mesh support (randomized order). A pulsatile ex vivo perfusion system using a laser scan micrometer to monitor outer systolic and diastolic diameter was employed. RESULTS: Median pre-anastomotic and post-anastomotic hypercompliance without external mesh support were 1.45 and 1.19%/100 mmHg, respectively, above reference compliance. Use of the elastic mesh support significantly reduced the median hypercompliance to 0.68%/100 mmHg (pre-anastomotic) and to 0.34%/100 mmHg (post-anastomotic) above reference compliance. The non-elastic mesh support caused approximately the same significantly reduced median hypercompliance to 0.53%/100 mmHg (pre-anastomotic) and 0.43%/100 mmHg (post-anastomotic). CONCLUSIONS: Both elastic and non-elastic external mesh support significantly reduced pre- and post-anastomotic hypercompliance.
The elastic fibers in the skin and other organs can be affected in several disease processes. In this study, we have developed morphometric techniques that allow accurate quantitation of the elastic fibers in punch biopsy specimens of skin. In this procedure, the elastic fibers, visualized by elastin-specific stains, are examined through a camera unit attached to the microscope. The black and white images sensing various gray levels are then converted to binary images after selecting a threshold with an analog threshold selection device. The binary images are digitized and the data analyzed by a computer program designed to express the properties of the image, thus allowing determination of the volume fraction occupied by the elastic fibers. As an independent measure of the elastic fibers, alternate tissue sections were used for assay of desmosine, an elastin-specific cross-link compound, by a radioimmunoassay. The clinical applicability of the computerized morphometric analyses was tested by examining the elastic fibers in the skin of five patients with pseudoxanthoma elasticum or Buschke-Ollendorff syndrome. In the skin of 10 healthy control subjects, the elastic fibers occupied 2.1 +/- 1.1% (mean +/- SD) of the dermis. The volume fractions occupied by the elastic fibers in the lesions of pseudoxanthoma elasticum or Buschke-Ollendorff syndrome were increased as much as 6-fold, whereas the values in the unaffected areas of the skin in the same patients were within normal limits. A significant correlation between the volume fraction of elastic fibers, determined by computerized morphometric analyses, and the concentration of desmosine, quantitated by radioimmunoassay, was noted in the total material. These results demonstrate that computerized morphometric techniques are helpful in characterizing disease processes affecting skin. This methodology should also be applicable to other tissues that contain elastic fibers and that are affected in various heritable and acquired diseases.
Water-filled elastic shells present more complicated backscattered echoes when compared to evacuated shells and are less well understood. The objective here is to determine and explain features peculiar to such objects and to use these features to aid in object characterization. Towards that end, an acoustic background suitable for such targets in conjunction with "residual" partial wave analysis obtained from subtracting the background from the elastic response is used. This analysis is aided by the determination and comparison of plate modes and resonance locations of evacuated unloaded, evacuated loaded, and loaded water-filled shells. Analysis of water-filled shells suggests that there exist isolated narrow, uniformly spaced eigenmodes in addition to the elastic modes. The broader elastic modes appear split in comparison to their unloaded counterparts. Otherwise, the elastic modes are not greatly affected by the included eigenmodes. The isolated (included) eigenmodes are extremely well modeled by a water inclusion in an infinite elastic matrix composed of the elastic shell material. The splitting of elastic modes proves to be due to interference of the included eigenmodes and the elastic body resonances. This leads to what appear to be separate branches of dispersion curves related to the elastic modes. Because of the numerous and usually evenly spaced included eigenmodes, dispersion curves are dominated by the abundance of these modes. A clear picture of the physical processes emerges from this analysis that explains all features of this event. Simple sets of rules that lead to tractable calculations are introduced that facilitate analysis of this interesting physical process.
It is generally believed that the Fenn effect contradicts all visco-elastic models of muscle, including the new elastic body and the time-varying elastance models. Although it is clear that the new elastic body model can be discarded, the Fenn effect does not preclude the time-varying elastance model. Although no visco-elastic models can simulate the extra energy utilization for work above the level of the energy utilized for the maximal isometric contraction, the extra energy observed by Fenn is not generally observed, even in skeletal muscles. However, work-related extra energy utilization, above the isometric energy utilization at equivalent force (Mommaerts' unifying concept of the Fenn effect), is generally observed in both skeletal and cardiac muscles. This unifying concept of the Fenn effect in cardiac muscle can be simulated by a simple time-varying elastance model. This study demonstrates the essential difference in energetics between the new elastic body model and the time-varying elastance model.
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Elastic fibers in the extracellular matrix are an integral component of dermal connective tissue. The resilience and elasticity required for normal structure and function of the skin may be attributed to the network of elastic tissue. Advances in our understanding of elastic tissue physiology provide a foundation for studying the pathogenesis of elastic tissue disorders. Many acquired disorders are nevertheless poorly understood due to the paucity of reported cases. Several acquired disorders in which accumulation or elastotic degeneration of dermal elastic fibers produces prominent clinical and histopathologic features have recently been described. They include elastoderma, linear focal elastosis, and late-onset focal dermal elastosis and must be differentiated from better-known disorders, among them acquired pseudoxanthoma elasticum, elastosis perforans serpiginosa, and Favré-Racouchot syndrome. Learning objective At the conclusion of this learning activity, participants should understand the similarities and differences between acquired disorders of elastic tissue that are characterized by an increase in elastic tissue, as well as the spectrum of solar elastotic dermatoses.
Evolution of species has led to the appearance of circulatory systems including blood vessels and one or more pulsatile pumps, typically resulting in a low-pressurised open circulation in most invertebrates and a high-pressurised closed circulation in vertebrates. In both open and closed circulations, the large elastic arteries proximal to the heart damp out the pulsatile flow and blood pressure delivered by the heart, in order to limit distal shear stress and to allow regular irrigation of downstream organs. To achieve this goal, networks of resilient and stiff proteins adapted to each situation--i.e. low or high blood pressure--have been developed in the arterial wall to provide it with non-linear elasticity. In the low-pressurised circulation of some invertebrates, the mechanical properties of arteries can almost be entirely microfibril-based, whereas, in high-pressurised circulations, they are due to an interplay between a highly resilient protein, an elastomer in the octopus and elastin in most vertebrates, and the rather stiff protein collagen. In vertebrate development, elastin is incorporated in elastic fibres, on a earlier deposited scaffold of microfibrils. The elastic fibres are then arranged in functional concentric elastic lamellae and, with the smooth muscle cells, lamellar units. The microfibrils may also play a direct functional role in all mature arteries of high- and low-pressurised circulations. Finally, since blood pressure regularly increases with developmental stages, it appears possible that the early deposition of microfibrils, which are highly-conserved in evolution, corresponds, at least in part, to an early microfibril-driven elasticity in low-pressurised arteries, present across species. In vertebrates, when pressure developmentally rises above a threshold value, the vascular wall stress may turn on the expression of other resilient protein genes, including the elastin gene. Elastin would then be deposited on microfibrils and resulting in the elastic fibre network and elastic lamellae whose mechanical properties are adapted to allow for proper arterial work at higher pressures.
Scanning electron microscopy (SEM) was used to study the arrangement of elastic fibers in the canine saphenous vein as the basis for further studies of veins used in by-pass grafting operations. The elastic fiber arrangement in distended and non-distended veins was examined in both immersion-fixed and perfusion-fixed vessels. Transmission electron microscope (TEM) observation of the SEM samples confirmed the identity of these fibrillar structures as elastic fibers. In addition, specific stains for elastic fibers (Verhoeff's iron hematoxylin and orcein) were used. The elastic fibers forming the internal elastic lamina were arranged in a fishnet-like pattern. Large-diameter fibers, running longitudinally along the vascular wall, were interconnected by smaller oblique fibers. Together the fibers formed an elastic cylindrical network between the endothelium and the smooth muscle cells. The thicker longitudinal fibers were the same diameter in distended and non-distended veins. By contrast, the oblique fibers were thinner and more complexly branched in distended veins. The architecture of the elastic fiber network contributes to vascular flexibility and allows circumferential distension. The interconnecting oblique fibers presumably serve to distribute internal pressure equally around the venous wall.
Ball-racket interactions were investigated in a task where participants propelled a ball rhythmically into the air. The study contrasted two ball-racket conditions: (1) an elastic impact where the ball was able to rebound due to the elasticity of the colliding objects and participants bounced the ball, and (2) a non-elastic impact where the coefficient of restitution was zero and the ball did not rebound such that the participants had to throw the ball. The goal of the study was to contrast the situations where haptic information about the ball-racket interactions is either secondary (elastic bouncing) or becomes a primary factor for control (non-elastic propulsion). In the elastic condition, the performers controlled the parameters for ball-racket contact prior to contact: In agreement with the criteria for dynamical stability defined by a model, racket accelerations immediately before the contacts were negative, racket positions and velocities at the instant of the initial contact correlated negatively, contact durations were short (30+/-9 ms), and during the collision interval racket velocity and acceleration decreased monotonically. In the non-elastic condition, the parameters of ball release were primarily controlled during the collision phase: Racket accelerations before contact were positive, racket positions and velocities at initial contact showed weak correlations, and the contact intervals were significantly longer (116+/-15 ms) with a clear segmentation into two segments. Negative correlations were observed between the integrals of the velocity and acceleration computed over the two consecutive segments, giving evidence that in the non-elastic condition the CNS is able to introduce corrections during the very short collision interval. The results are discussed with respect to physiological mechanisms of movement corrections available during such short time intervals.