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At least 595 records · Page 33Linked to original sources
PubMed1987

Elastosis in breast carcinoma: II. Association of protease inhibitors with immature elastic fibres.

The elastosis of 11 invasive ductal and infiltrative lobular carcinomas of the breast was specifically immunostained for the plasma protease inhibitors alpha-1 antitrypsin, alpha-1 antichymotrypsin, alpha-2 macroglobulin, inter alpha trypsin inhibitor and C1 esterase inhibitor. None of these components was detected in the elastic fibres of normal ducts or blood vessels in the breast. The elastosis in breast carcinomas was also stained by Concanavalin A and Triticum vulgaris lectins. Such lectin staining probably represents binding to the microfibrillar component of elastic fibres, which is increased in immature elastic fibres, thus suggesting that the elastotic fibres of breast carcinoma are recently synthesised. It is suggested that the presence of protease inhibitors may influence the metabolism of elastic fibres, facilitating elastic fibre proliferation by the inhibition of elastinolytic enzymes.

Adult↗
PubMed1997

AFM imaging and elasticity measurements on living rat liver macrophages.

The authors investigated the morphology and the elastic properties of living cultured rat liver macrophages (Kupffer cells) with an atomic force microscope (AFM). Continuous imaging and elasticity mapping of individual cells in physiological buffer was carried out for several hours without damaging the cells as judged by their persistent undisturbed morphology. Dynamic events such as protrusive activity were observed in time course. The importance of the cytoskeleton for the mechanical properties of the cell has been investigated by measuring the cell's elasticity as a function of position. Chemical disassembly of the actin network by applying 10 microgram/ml cytochalasin B decreased the cell's average elastic modulus seven-fold within less than 40 minutes. Treating the cells with 0.1 micrograms/ml latrunculin A resulted in a two-fold decrease in the elastic modulus merely in the perinuclear region after 40 minutes, whereas other parts of the cell were not affected.

Animals↗
PubMed2000

Sequence-dependent elastic properties of DNA.

Harmonic elastic constants of 3-11 bp duplex DNA fragments were evaluated using four 5 ns unrestrained molecular dynamics simulation trajectories of 17 bp duplexes with explicit inclusion of solvent and counterions. All simulations were carried out with the Cornell et al. force-field and particle mesh Ewald method for long-range electrostatic interactions. The elastic constants including anisotropic bending and all coupling terms were derived by analyzing the correlations of fluctuations of structural properties along the trajectories. The following sequences have been considered: homopolymer d(ApA)(n) and d(GpG)(n), and alternating d(GPC)(n) and d(APT)(n). The calculated values of elastic constants are in very good overall agreement with experimental values for random sequences. The atomic-resolution molecular dynamics approach, however, reveals a pronounced sequence-dependence of the stretching and torsional rigidity of DNA, while sequence-dependence of the bending rigidity is smaller for the sequences considered. The earlier predicted twist-bend coupling emerged as the most important cross-term for fragments shorter than one helical turn. The calculated hydrodynamic relaxation times suggest that damping of bending motions may play a role in molecular dynamics simulations of long DNA fragments. A comparison of elasticity calculations using global and local helicoidal analyses is reported. The calculations reveal the importance of the fragment length definition. The present work shows that large-scale molecular dynamics simulations represent a unique source of data to study various aspects of DNA elasticity including its sequence-dependence.

Algorithms↗
PubMed1999

Non-elastic deformation of myocardium in low-flow ischemia and reperfusion: ultrastructure-function relations.

This study tested the hypothesis that regional low-flow ischemia and reperfusion alter myocardial material properties by causing non-elastic deformation. Twenty-two anesthetized, open-chest pigs were studied. Pigs underwent 90 min of regional low-flow ischemia (anterior LV subendocardial blood flow 29+/-7% of baseline) followed by 90 min reperfusion. LV pressure and regional subendocardial segment length were recorded to derive end-diastolic pressure vs segment length (EDP vs EDL) and preload-recruitable stroke work (PRSW) relations. In vivo, non-elastic myocardial deformation was inferred from increases in minimally loaded myocardial dimensions: the EDL at zero EDP (L0) and the EDL at which no regional external work was performed (Lw, the PRSW intercept). In 15 pigs, ultrastructural confirmation of non-elastic deformation was obtained from sarcomere dimensions measured by transmission electron microscopy after in situ perfusion fixation under non-ischemic conditions, after 90 min ischemia, or after 90 min ischemia plus 90 min reperfusion. Ischemia increased L0 and Lw to 1.17+/-0.05 and 1. 13+/-0.04 times baseline, respectively. After reperfusion, L0 and Lw remained increased to 1.09+/-0.03 and 1.15+/-0.02 times baseline (all P<0.05). After reperfusion, PRSW slope was not different from baseline, but regional external work remained depressed (0.38+/-0.03 times baseline) due to the persistent increase in Lw. Neither L0 nor Lw changed in the posterior (non-ischemic) region. In hearts fixed after ischemia or after ischemia plus reperfusion, sarcomere length was significantly greater and transverse distance between thick myofilaments was significantly smaller in the anterior (ischemic) subendocardium than in the posterior (non-ischemic) subendocardium (P<0.01). We conclude that regional low-flow ischemia and reperfusion cause non-elastic deformation of myocardium, manifest in vivo by increased minimally loaded myocardial dimensions (L0 and Lw) and ultrastructurally by increased sarcomere length and decreased transverse interfilament distance. Non-elastic deformation of myocardium may contribute to contractile dysfunction in low-flow ischemia and reperfusion.

Animals↗
PubMed1977

The morphogenesis of elastic fibers.

Elastic fibers have been shown to contain two proteins, insoluble elastin and the elastic fiber microfibril, a glycoprotein. The microfibril has been suggested to play a morphogenetic role in determining the presumptive shape and direction of the forming elastic fiber. The principal alteration seen in individuals with the disease Pseudoxanthoma Elasticum is in insoluble elastin which loses its amorphous appearance and affinity for anionic stains, and takes on a finely granular appearance and shows increased affinity for cationic stains. Normal elastic fiber microfibrils are sometimes associated with this material; although, in general, these structures are not present in the elastic fibers that are markedly altered in this disease.

Animals↗
PubMed1977

The ultrastructure and mechanics of elastic ligaments.

The major central part of elastic ligaments is constituted by longitudinally orientated elastic fibres, each surrounded by a sheath of spirally orientated collagen fibrils with an intervening thin layer of microfibrils. In the terminal region of such ligaments the orientation of the collagen fibrils is longitudinal and the elastic fibres end within the ligament without any attachment to bone. The ligament response to a first, unphysiologically high load produces a continuous stress-strain curve. On the other hand the curve becomes biphasic after repeated application of such loads. It is suggested that three factors are involved in this mechanical response, namely, frictional forces between elastic fibres and their sheaths, compressive forces exerted upon elastic fibres by their sheaths, and intre-sheath friction due to rearrangement of the constituent collagen fibrils.

Animals↗
PubMed1997

Time course of tissue elasticity and fluidity in vasogenic brain edema.

We examined chronological changes in regional tissue elasticity (stiffness) and fluidity (1/viscosity) of the white matter during the development and resolution of vasogenic brain edema. Cryogenic injury was created in the cortex of cat brain, and the brain was prepared for measurement of regional tissue elasticity and fluidity. The results were then compared with the histology and tissue water content. Vasogenic edema developed in the white matter under the lesioned cortex (4-24 h) and was resolved by day 10. Regional tissue elasticity decreased significantly during the initial 24 h (45.3 +/- 32.5% of the control (mean +/- S.D.), and then increased to 158.6 +/- 32.3% of the control level at day 10. Regional tissue fluidity increased to 376.7 +/- 240.4% of the control level during the initial 24 h decreased to 77.7 +/- 17.9% of the control level at day 10. Histological examination of the white matter revealed widening of the inter-fiber space at 4-24 h after lesioning and astrocytosis at day 10. Thus vasogenic edema causes an increase of tissue fluidity with a decrease of tissue elasticity. Reactive astrocytosis after the resolution of edema causes an increase of tissue elasticity with mild decrease in tissue fluidity.

Animals↗
PubMed1981

Ultrastructure of elastic cartilage in the rat external ear.

The structure of elastic cartilage in the external ear of the rat was investigated by transmission and scanning electron microscopy. The narrow subperichondrial, boundary zone contains predominantly ovoid cells rich in cell organelles: mitochondria, Golgi complex, granular endoplasmic reticulum and small (40--100 nm) vesicles. Scarce glycogen granules and bundles of 6--7 nm cytoplasmic filaments are also present. Deeper in the boundary zone, one or more cytoplasmic lipid droplets appear and cytofilaments become more abundant. Fully differentiated chondrocytes in the central zone of the cartilage plate resemble white adipose cells. They are globular and contain a single, large cytoplasmic lipid droplet. The cytoplasm is reduced to a thin peripheral rim; it contains a flattened nucleus, few cytoplasmic organelles and abundant, densely packed, cytoplasmic filaments. The intercellular matrix is very sparse. The pericellular ring consists of collagen fibrils about 20 nm in diameter and a proteoglycan cartilage matrix in the form of a "stellate reticulum". The complex of these two structures appears in the scanning electron micrographs as a a network of randomly oriented, ca 100 nm thick fibrils. Spaces between pericellular rings of matrix also contain thick elastic fibers or plates, apparently devoid of microfibrils. In scanning electron micrographs elastic fibers could be detected only in a few areas, in which they were not obscured by other constituents of the matrix. Immature forms of elastic fibers, oxytalan (pre-elastic) and elaunin fibers, were found in the perichondrial and boundary zones.

Animals↗
PubMed1993

Endothelial cell connecting filaments anchor endothelial cells to the subjacent elastic lamina in the developing aortic intima of the mouse.

The ultrastructural association of endothelial cells with the subjacent elastic lamina was investigated in the developing mouse aorta by electron microscopy. In the 5-day postnatal aorta, extensive filament bundles extend along the subendothelial matrix connecting the endothelial cells to the underlying elastic lamina. The connecting filaments form lateral associations with the abluminal surface of the endothelial cells in regions of membrane occupied by membrane-associated dense plaques. On the intracellular face of each plaque, the termini of stress fibers penetrate and anchor to the cell membrane in alignment with the extracellular connecting filaments. Both the stress fibers and the connecting filaments are oriented parallel to the longitudinal axis of the vessel. High magnification electron micrographs of individual endothelial cell connecting filaments reveal features similar to those of elastin-associated microfibrils. Each connecting filament consists of a 9-10 nm linear core with an electron-lucent center and peripheral spike-like projections. From the filaments, small thread-like extensions span laterally, linking the filaments into a loose bundle and anchoring them to the endothelial cell membrane and the surface of the elastic lamina. The filaments also appear heavily coated with electron-dense material; often with some degree of periodicity along the filament length. During development, the number of endothelial cell connecting filaments decreases as the elastic lamina expands and the subendothelial matrix is reduced. In the aortic intima of mature mice, the elastic lamina is closely apposed to the abluminal surface of the endothelial cell and no connecting filaments are seen.(ABSTRACT TRUNCATED AT 250 WORDS)

Actin Cytoskeleton↗
PubMed1976

In vitro elastic fiber formation by aggregated arotic cells of newborn rabbits.

Cells isolated enzymatically from the aortas of newborn rabbits were aggregated and grown in organ culture. Bundles of microfibrils, some of them with an amouphous core (elastin), were evident in 3-day-old aggregates. Furthermore, droplets of elastin surrounded by darker dots and short filaments, corresponding to the elastic units were observed. In 6-day-old aggregates the number of elastic fibers composed of bundles of microfibrils with deposited elastin increased. Elastic elements which probably resulted from a coalescence of elastic units were also present. These two ways of elastic fiber formation in aggregates are compared with those described in papers on aortic development.

Animals↗
PubMed1983

Fluorescence microscopical visualization of elastic fibres using basic fuchsin.

We show that fluorescence microscopy after staining of tissue sections with basic fuchsin (BF) can be used successfully for the demonstration of elastic fibres. Using double staining with BF and antibodies reacting with microfibrils of elastic fibres (anti-SAP) we showed that BF reacts with the elastin core of elastic fibres and the elastin poor terminal branches of the subepidermal elastic fibre system. Small amounts of bound BF were easily seen by fluorescence microscopy (FL) but not by ordinary light microscopy. Both frozen sections and sections of paraffin embedded tissues could be stained. The BF-FL staining procedure is simple to perform and, due to its selectivity, it may be useful for detecting elastic fibres in various tissues at the light microscopical level.

Elastic Tissue↗
PubMed1986

Cytochemical visualization of anions in collagenous and elastic fiber-associated connective tissue matrix in neonatal and adult rat lungs using iron-containing stains.

The cytochemical reactivity of pulmonary connective tissue matrix component in neonatal and adult rat was evaluated using high iron diamine (HID) to detect sulfate ester end groups and dialyzed iron (DI) to detect sulfated and carboxylated end groups of complex carbohydrates, including glycoproteins and glycosaminoglycans at the ultrastructural level. The HID reaction product, in the form of discrete 5-12 nm silver particles following appropriate intensification with thiocarbohydrazide-silver proteinate, was found associated with cell surfaces, the elastin component of elastic fibers, and at regular intervals along the length of collagen fibers in large airways and deep lung interstitium. Staining was similar in adult and neonatal rats, except in areas where connective tissues were presumably still rapidly developing in the neonatal animals. Here large gaps or spaces containing filamentous structures were observed between collagen and elastic fibers. The distribution of DI-reactive sites was similar to that seen with HID with the exception of elastic fibers in which only the microfibrillar portion stained. The collagen-associated reaction was not regularly disposed like that stained with HID, but rather it formed a tight continuous density around the fiber. These results indicated the presence and location of glycoproteins and glycosaminoglycans in connective tissue ground substance regions prior to the full development of elastic and collagenous elements in neonatal pulmonary airways and parenchyma. They also demonstrate cytochemically the presence of a sulfate ester-containing complex sugar found associated with the elastin component of elastic fibers in the lung.

Aging↗
PubMed1985

Ultrastructural visualization of elastic fibres with a tannate--metal salt method.

A modification of the tannic acid-metal salt method was applied as an ultrastructural stain for elastin. Thin sections of glutaraldehyde-fixed, embedded rat aorta and rabbit elastic cartilage, with and without osmication, were examined. Raising the pH of the tannic acid solution from 2.7 to 9.0 progressively increased the electron-density of elastic fibres and collagen fibrils in osmicated and unosmicated specimens. The maximum tannic acid staining of elastic fibres was observed in the pH range 7.0-9.0. Collagen staining, although less intense than that of elastic fibres, was also greatest in this pH range. Elastic fibres in osmicated specimens demonstrated the strongest tannic acid staining with a minimal increase in density of collagen and cell nuclei when compared to the unosmicated specimens. Sequential treatments of osmicated specimens with tannic acid pH 7.0-9.0, and uranyl acetate, pH 4.1, enhanced the density of the elastin intensely, increased collagen staining moderately, but hardly increased the density of nuclei and microfibrils. In elastase-digested osmicated specimens, all tannic acid (pH 7.0)-uranyl acetate-reactive elastin was selectively removed. These results demonstrate that all the neutral and alkaline tannic acid-uranyl acetate methods can be used as a postembedment stain for elastin specimens fixed in glutaraldehyde and osmium tetroxide.

Animals↗
PubMed1989

Estimation of elastic properties in the urethral flow controlling zone by signal analysis of urodynamic pressure/flow data.

When urethral flow is treated as a lossless flow through an elastic tube, the relationship between the detrusor pressure and the urinary flow can be related to the elasticity of the flow-controlling zone of the urethra. A recent analytical method of describing urethral elasticity is implemented on a computer. The function p(Q) = pmo + LmQm is fitted to the recorded pressure/flow data. p(Q) is the detrusor pressure, Q the flow and pmo, m and Lm parameters. The elastic properties are then obtained as p(A) = pmo + KnAn, where p(A) is the static pressure, A the cross-sectional area of the flow-controlling zone and n and Kn calculated parameters. The urodynamic methods used and the computer implementation of the analytical method are described. In obstructed and unobstructed men without neurological symptoms, the elastic properties could be estimated in 94 per cent of the micturitions. The method makes it possible to describe urethral flow properties with Griffiths' model in a standardised way and compare results obtained by different investigators. It is recommended for quantification of urethral obstruction in research and for assessment of borderline cases of obstruction in clinical practice.

Biomechanical Phenomena↗
PubMed1993

Estimation of left ventricular myocardial elasticity and viscosity by a thick-walled spherical model.

The authors measured the transfer function (TF) of the left ventricle (LV) in an isolated canine preparation. Here TF indicates the ratio of induced vibration in LV to input vibration when an external mechanical oscillation is applied. TF had a single peak the frequency of which changed from 40 Hz to 80 Hz when LV pressure (LVP) increased from 6 mm Hg to 96 mm Hg. A mathematical model was formulated to estimate the viscoelasticity of the spherical shell. This model was constructed of the material points, elastic components which connected all the material points, and viscous components placed in series with elastic components. Theoretical TF can be computed if the viscoelastic values are given. The value of viscoelasticity at which the theoretical TF best fitted the experimental TF was considered to be the viscoelasticity of the model. The validity of this approach was verified using a silicone spherical shell. The estimated myocardial elasticity was 40 kPa when LVP was 6 mm Hg, 160-170 kPa when LVP was 96 mm Hg and was approximately proportional to LVP, whereas viscosity showed small change. The inclination of elasticity was consistent with previous reports. These results proved that myocardial elasticity can be estimated by analysing the transfer function of the left ventricle.

Animals↗
PubMed2002

Determination of the elasticity parameters of the human periodontal ligament and the location of the center of resistance of single-rooted teeth a study of autopsy specimens and their conversion into finite element models.

MATERIAL AND METHODS: The aim of this study was to determine the elasticity parameters of the human periodontal ligament by measuring three-dimensionally the initial buccolingual tooth displacements of eight single-rooted teeth in human jaw specimens, using a noninvasive method. Subsequently the specimens were used to develop finite element models presenting the same individual geometry as the respective autopsy material. These models formed the basis for computerized movement simulations, whose characteristic was brought into line with the experimentally registered movements by adapting the elasticity parameters of the periodontal ligament. Using the individual elasticity parameters determined in this way, with which the displacement of the computer models could be realistically calculated, the centers of resistance of the examined teeth were determined by simulating the effects of different force systems. RESULTS: The nonlinear character of the initial tooth movement could be effectively simulated by using a bilinear parameter set for the elasticity of the periodontal ligament and by determining a critical expansion value for the transition from the validity range of the first Young's modulus to the second. The mean Young's modulus of the first phase of movement was 0.05 MPa, that of the second phase 0.28 MPa, and the critical expansion 7.5% (Poisson's ratio mu = 0.3). The centers of resistance of single-rooted teeth were found to be at approximately 42% of the alveolar height from the alveolar crest to the apex, irrespective of root length and direction of loading. CONCLUSION: The elasticity parameters were found to be on a similar scale to those determined in previous studies on multi-rooted pig teeth.

Biomechanical Phenomena↗
PubMed1999

Abnormalities of elastin and elastic fibers in infantile hypertrophic pyloric stenosis.

Infantile hypertrophic pyloric stenosis (IHPS) is characterized by hypertrophy of the pyloric muscle, causing pyloric-channel narrowing and elongation. The rigidity of the muscle is increased, which is characterized as an "olive." Elastin is an insoluble protein that forms the major structural component of the elastic fibers and maintains the tensile strength of the tissues. To understand the possible histologic and molecular basis of the elasticity of the hypertrophic muscle in IHPS, we determined the distribution of the elastic fibers and elastin expression using Victoria blue van Gieson (VVG) staining and immunohistochemistry. In IHPS, the number of elastic fibers in the connective tissue was significantly increased in the thickened connective-tissue septa (CTS) compared with normal control specimens. In normal pyloric muscle, weak to moderate elastin immunoreactivity was observed in the CTS while no immunoreactivity was observed among the muscle fibers. In IHPS, strong immunoreactivity of elastin was observed in the CTS and moderate immunoreactivity among the hypertrophic smooth-muscle fibers. Our findings suggest that the increase on elastic fibers and elastin expression in the pyloric muscle in IHPS may play an important role in the development of pyloric-muscle rigidity, causing pyloric-canal obstruction.

Elasticity↗
PubMed2001

Muscle efficiency: the controversial role of elasticity and mechanical energy conversion in stretch-shortening cycles.

The analysis of muscle efficiency was performed on a variety of simulated muscle stretch-shortening cycles of in situ rat gastrocnemius muscle. The processes of biochemical energy conversions (phosphorylation and contraction-coupling) and mechanical conversions (internal work to external work) were incorporated in the efficiency calculations. Metabolic cost was determined using a simple linear model. Special attention was drawn to the interacting roles of series elastic compliance and contraction dynamics. The results showed that series elastic compliance affected the efficiency of muscle contraction to a great extent. Stiff muscle was well designed to perform efficient contractions in which muscle merely shortened while active. Compliant muscle performed best in true stretch-shortening contractions utilising the storage and release of series elastic energy effectively. However, both stiff and compliant series elastic elements showed similar optimal muscle efficiency values in shortening contractions and stretch-shortening contractions, respectively. The findings indicate that the storage and re-utilisation of series elastic energy does not enhance overall muscle efficiency, but that optimal efficiency is obtained by a proper design of the muscle with regard to the dynamics of the movement task. Furthermore, it was found that although biochemical efficiency determined the feasible range of muscle efficiency, mechanical work conversions had the strongest influence on the exact value of overall muscle efficiency in stretch-shortening contractions.

Animals↗