Mechanism Of Shape Change Research Articles

Structural Mechanisms of High-Temperature Shape Changes in Titanium-Nickel Alloys After Low-Temperature Thermomechanical Treatment

High-Temperature Shape Memory Effect (HTSME) in Ti-Ni alloys and corresponding structural and internal stress changes were studied using dilatometry, in situ electron microscopy and X-ray diffractometry. The HTSME induced by the Low Temperature Thermomechanical Treatment (LTMT) consists of two stages. The temperature range of the first stage is limited to 250°C, while the second stage extends to 400-500°C. The first stage is caused by the oriented reverse martensite transformation. The heterogeneous residual stress field causes a different thermal stability for the different martensite orientations. During the reverse transformation an anisotropic shift of martensite and austenite X-ray lines is observed that can be due to a relaxation of the orientated stresses and to changes in the martensite lattice. The second stage of HTSME is caused by internal stress relaxation during recovery and polygonization of austenite that are not typical shape memory mechanisms. The possible reasons for the martensite stabilization induced by LTMT will be discussed.On a étudié l'effet de mémoire de forme à haute température (HTSME) des alliages Ti-Ni et les changements correspondants de structures et de contraintes internes. On a utilisé la dilatométrie, la microscopie électronique in situ et la diffractométrie à rayons x. Le HTSME induit par le traitement thermomécanique à basse température (LTMT) est constitué de deux stades. Le domaine de température du premier stade est limité à 250°C alors que le second stade s'étend de 400 à 500°C. Le premier stade est causé par la transformation orientée inverse de la martensite. Le champ de contraintes résiduelles hétérogènes produit une stabilité thermale différente pour les différentes orientations de martensite. Lors de la transformation inverse, on observe un déplacement d'anisotropie des lignes de rayon x de la martensite et de l'austénite, qui peut être dû à une relaxation des contraintes orientées et à des changements dans le réseau de martensite. Le second stade de HTSME est causé par la relaxation de contraintes internes lors de la restauration et de la polygonisation de l'austénite, qui ne sont pas typiques des mécanismes de mémoire de forme. On discute des raisons possibles de stabilisation de la martensite induite par le LTMT.

Surface and interface properties of alumina via model studies of microdesigned interfaces

The ability to produce controlled-geometry, controlled-crystallography internal voids in ceramics has made possible several new model experiments for studying the high-temperature properties of surfaces and interfaces in ceramics. Recent advances have enabled the production of more complex microdesigned internal defect structures, and have exploited new means of examining them, thus, broadening the range of problems that can be addressed. A particular topic of concern is the effect of surface energy anisotropy on both the driving force for and the mechanism of shape changes. This paper reviews and previews recent research focussing on improving our understanding of surface diffusion in ceramics. Rayleigh instabilities provide one means of examining morphological evolution. The modelling of Rayleigh instabilities in materials with surface energy anisotropy is reviewed, and the results of experiments utilizing microdesigned pore arrays in sapphire are summarized. In a material with anisotropic surface energy and a facetted Wulff shape, the driving force for shape changes hinges on both the absolute and relative surface energies. Microdesigned pore structures have been used to determine the stable surfaces in both undoped and doped sapphire and to provide the relative values of the energies of these stable surfaces. Nonequilibrium shape, controlled-crystallography cavities have been introduced into undoped sapphire, and the effect of crystallographic orientation on their morphological evolution has been studied. Comparisons of the results with predictions of models of surface-diffusion-controlled evolution indicate that surface-attachment-limited kinetics (SALK) play an important role.

INTEGRATING DEVELOPMENTAL EVOLUTIONARY PATTERNS AND MECHANISMS: A CASE STUDY USING THE GASTROPOD RADULA.

Determining the connection between ontogeny and phylogeny continues to be a major theme in biology. However, few studies have combined dissection of pattern and process that lead to transformation of complex morphological structures. Here we examine the patterns and processes of shape change in a model system-the gastropod radula. This system is a simple one having only two processes: initial secretion and postsecretional movement of teeth. However, it produces a tremendous amount of shape variability and fusion patterns. To determine both pattern and mechanism of shape change in an evolutionary context, we use three complementary approaches and datasets. First, we use a phylogenetic hypothesis to determine the polarity of developmental events. Second, we perform a morphometric analysis of shape change using relative warp analysis that allows us to locate and compare the direction and magnitude of ontogenetic and phylogenetic shape divergence. These comparisons are the basis for testing hyptheses of heterochrony and heterotopy, and we show how our results do not conform to expectations of pure heterochrony. The rejection of heterochrony as a hypothesis is based on empirically demonstrating (1) initial shape differs in each taxon; (2) a single dimension of shape variability does not simultaneously describe ontogenetic and evolutionary shape changes; and (3) a significantly different shape and size covariance between taxa. This rejection is probably based on spatial changes in initial conditions and not spatial changes caused by the process itself. Finally, we construct a mechanistic model that explains how shape change happens based on the sequence of events during ontogeny. By using the parameters in the model as characters in the phylogenetic dataset, we show that different parts of the system have arisen at different times and become co-opted into the process. By integrating our analyses together we show that spatial process parameters can be responsible for our nonspatial patterns and that different ontogenetic processes can create similar end morphologies.

P–103 - Mechanism of shape change induced by theonezolide-A in rabbit platelet

P–103 - Mechanism of shape change induced by theonezolide-A in rabbit platelet

Mechanism of endothelial cell shape change and cytoskeletal remodeling in response to fluid shear stress.

Endothelium exposed to fluid shear stress (FSS) undergoes cell shape change, alignment and microfilament network remodeling in the direction of flow by an unknown mechanism. In this study we explore the role of tyrosine kinase (TK) activity, intracellular calcium ([Ca2+]i), mechanosensitive channels and cytoskeleton in the mechanism of cell shape change and actin stress fiber induction in bovine aortic endothelium (BAE). We report that FSS induces beta-actin mRNA in a time- and magnitude-dependent fashion. Treatment with quin2-AM to chelate intracellular calcium release and herbimycin A to inhibit TK activity abolished BAE shape change and actin stress fiber induction by FSS, while inhibition of protein kinase C with chelerythrine had no effect. Altering intermediate filament structure with acrylamide did not affect alignment or F-actin induction by FSS. Examining the role of the BAE cytoskeleton revealed a critical role for microtubules (MT). MT disruption with nocodazole blocked both FSS-induced morphological change and actin stress fiber induction. In contrast, MT hyperpolymerization with taxol attenuated the cell shape change but did not prevent actin stress fiber induction under flow. Mechanosensitive channels were found not to be involved in the FSS-induced shape change. Blocking the shear-activated current (IK.S) with barium and the stretch-activated cation channels (ISA) with gadolinium had no effect on the shear-induced changes in morphology and cytoskeleton. In summary, FSS has a profound effect on endothelial shape and F-actin network by a mechanism which depends on TK activity, intracellular calcium, and an intact microtubule network, but is independent of protein kinase C, intermediate filaments and shear- and stretch-activated mechanosensitive channels.

Mechanism of Shape Change in Chilled Human Platelets

The so-called cold activation of platelets that precludes refrigeration of platelets for storage has long been recognized, but its mechanism has remained a mystery. Cooling of discoid resting platelets to temperatures below 15 degrees C causes shape distortions, and the chilled cells rewarmed to above 25 degrees C are spheres rather than discs. As platelet shape change responsive to receptor activation at normal temperatures requires the remodeling of an actin scaffolding (Hartwig JH, 1992, J Cell Biol 118:1421-1442), we examined the role of actin in the morphologic changes induced by cooling. The addition of actin monomers onto the fast-exchanging (barbed) ends of actin filaments accompanies the initial physiologic platelet shape changes, and a key control point in this growth is the removal of proteins (caps) from the filament ends. This uncapping of actin filament ends is mediated by polyphosphoinositide aggregates in vitro, suggesting that cold-induced phase changes in membrane lipids might uncap actin filaments and thereby account for actin assembly-mediated shape alterations during cooling. Consistent with this hypothesis, reversible inhibition of actin assembly with cytochalasin B prevented the distortions in shape, although cooled platelets had increased actin nucleation sites and became spherical. Another step in normal platelet shape changes requires the severing of actin filaments that maintain the resting platelet. The proteins that sever initially bind to the broken filament ends, and uncapping of these fragmented filaments provides numerous nucleation sites for growth of actin filaments to fill in spreading filopodia and lamellae. Actin filament fragmentation requires a rise in intracellular calcium, and we showed that chilling platelets from 37 degrees C to 4 degrees C increases free cytosolic calcium levels from 80 nmol/L to approximately 200 nmol/L in minutes, thus providing an explanation for the spherical shape of cooled, rewarmed platelets. Blocking the calcium transient with nanomolar concentrations of the permeant calcium chelators Quin-2 and Fura-2 prevented the increase in nucleation sites and the sphering, but not the other shape changes of chilled and rewarmed platelets. However, a combination of micromolar cytochalasin B and millimolar intracellular calcium chelators preserved the discoid shapes of chilled and rewarmed platelets. After removal of cytochalasin B and addition of sufficient extracellular calcium, these platelets responded with normal morphologic alterations to glass and thrombin activation.

Sodium selenite as modulator of red cell shape

Addition of sodium selenite to human red cells, under ATP deplete conditions, induces a rapid oxidation of both glutathione and protein sulphydryl groups. Selenite also inhibits the discocyte-echinocyte shape transformation and stops the process before completion. Parallel to the effect on shape, selenite reduces the dephosphorylation of phosphatidylinositol 4,5-bisphosphate and phosphatidylinositol 4-monophosphate. Therefore our results support a shape change mechanism based on the metabolism of phosphoinositides and compatible with the bilayer-couple hypothesis.

Cell shape changes induced by sulphate in the cloudman mouse melanoma cell line

The mechanism of cell shape changes and haematogenous translocations (metastases) in mouse malignant melanoma cells induced by phorbol esters and protein kinase C (PKC) is reported as adhesion "downregulation", exocytosis and motility. However, PKC activation also produces intracellular alkalinization, a causal factor in plasma membrane internalization, cell rounding and detachment that does not necessarily implicate specific cell adhesion downregulation. We show here that Cloudman mouse malignant melanoma cells can be induced to round up and detach with concomitant intracellular alkalinization by simple inorganic sulphate treatment, thereby suggesting an alternative explanation to the reported phenomena.

Mechanisms of cell shape change: the cytomechanics of cellular response to chemical environment and mechanical loading.

Processes such as cell locomotion and morphogenesis depend on both the generation of force by cytoskeletal elements and the response of the cell to the resulting mechanical loads. Many widely accepted theoretical models of processes involving cell shape change are based on untested hypotheses about the interaction of these two components of cell shape change. I have quantified the mechanical responses of cytoplasm to various chemical environments and mechanical loading regimes to understand better the mechanisms of cell shape change and to address the validity of these models. Measurements of cell mechanical properties were made with strands of cytoplasm submerged in media containing detergent to permeabilize the plasma membrane, thus allowing control over intracellular milieu. Experiments were performed with equipment that generated sinusoidally varying length changes of isolated strands of cytoplasm from Physarum polycephalum. Results indicate that stiffness, elasticity, and viscosity of cytoplasm all increase with increasing concentration of Ca2+, Mg2+, and ATP, and decrease with increasing magnitude and rate of deformation. These results specifically challenge assumptions underlying mathematical models of morphogenetic events such as epithelial folding and cell division, and further suggest that gelation may depend on both actin cross-linking and actin polymerization.

Shape changes in isolated outer hair cells: measurements with attached microspheres

Shape changes can be induced in isolated outer hair cells by various stimuli and quantified from digitized video-images. While overall changes in length between base and apex are easily measured, changes in defined segments of the cell require fixed landmarks on the cell body. The problem of locating such landmarks makes it difficult to assess if a change in length is uniform or largely confined to a particular segment of the cell. This information is important in identifying the location of a contractile apparatus and the elucidation of mechanisms of motility. We demonstrate here that microspheres can serve as reference points for such measurements. By attaching microspheres to cells we determined that, when outer hair cells increased their volume upon K +-depolarization, their middle segment shortened more significantly (14 ± 6%) than either the basal (10 ± 5%) or apical section (7 ± 6%; P < 0.01). In contrast, when cortical contractions were induced by elevating intracellular Ca 2+, the elongation of the cells was more pronounced in their basal (8 ± 2%) than their apical (6 ± 2%; P = 0.06) or middle region (6 ± 3%). This study provides further insight into the mechanisms of shape changes in isolated outer hair cells and illustrates a method to analyze localized changes in the absence of internal landmarks.

Zinc Electrode Shape Change: II . Process and Mechanism

The process and mechanism of zinc electrode shape change is investigated with the radiotracer technique. It is shown that during repeated cycling of the nickel oxide/zinc battery zinc material is transported over the zinc electrode via the battery electrolyte. During charge as well as during discharge zinc material is transported over the electrode. The direction of the zinc material transport during charge is opposite its direction during discharge. The amount of zinc material displaced over the electrode during charge is smaller than during discharge, so that after one charge‐discharge cycle the net zinc material transport is observed in the direction as found during discharge. A new model for shape change is presented: the density gradient model. The model is based on the occurrence of an electrolyte flow during repeated charge‐discharge cycling of the zinc secondary battery, which transports zinc material over the electrode. During battery cycling this electrolyte flow arises as a result of density gradients in the solution layer adjacent to the zinc electrode and of volume variations of the battery electrolyte.

Modulation of the delayed rectifier K+ current by isoprenaline in bull-frog atrial myocytes.

1. The effects of isoprenaline (ISO) on the calcium current (ICa) and delayed rectifier K+ current (IK) were examined using a tight-seal whole-cell voltage-clamp technique in single cells from bull-frog atrium to examine the ionic mechanism(s) of catecholamine-induced action potential shape changes. 2. The effects of ISO on the action potential were dose-dependent. Very low doses (5 x 10(-9) M) prolonged the action potential. Higher doses (10(-6) M) of ISO increased the plateau height, but shortened the action potential by accelerating the early repolarization phase. 3. ISO increased IK and ICa in a dose-dependent fashion. Both of these effects were blocked by a beta-receptor antagonist, propranolol (3 x 10(-7) M). In contrast IK1, the inwardly rectifying K+ current, was not changed significantly by ISO. 4. The ISO-induced increase in IK was observed in the presence of CdCl2 (3 x 10(-4) M), indicating that this effect is not due to a Ca2(+)-activated potassium current. 5. The reversal potential of IK in normal Ringer solution (-83 +/- 2 mV) was not significantly changed by ISO. Thus, stimulation of the Na(+)-K+ pump and a consequent hyperpolarizing shift in EK are not responsible for the increase in IK. 6. In the presence of ISO (10(-6) M) the steady-state activation curve (n infinity) for IK was consistently shifted to more negative values (by approximately 10 mV). The activation and deactivation kinetics of IK were also changed by ISO: activation was accelerated, deactivation was slowed. These ISO-induced changes in IK result in an increase in IK at voltages corresponding to the plateau of the action potential. 7. ISO (10(-6) M) increased ICa dramatically, approximately 6-fold at 0 mV. At the same time, the time constant of ICa inactivation decreased significantly (34 +/- 4 ms control; 23 +/- 4 ms ISO). 8. These results confirm that low doses of sympathetic agonists acting via beta-receptors increase ICa. Relatively high doses of beta-receptor agonists increase both ICa and IK, but these two effects appear to be generated by different biophysical mechanisms. 9. These dose-dependent changes in ICa and IK can explain the observed ISO-induced changes in action potential shape. At doses of approximately 10(-8) M ICa is increased, resulting in a more depolarized plateau and small lengthening of the action potential.(ABSTRACT TRUNCATED AT 400 WORDS)

Mechanism of endothelial cell shape change in oxidant injury

Changes in endothelial cell morphology induced by neutrophil-generated hydrogen peroxide (H 2O 2) may account for the capillary leak of the adult respiratory distress syndrome (ARDS). The relationship of H 2O 2 effects on the concentration of intracellular Ca 2+([Ca 2+] i) and ATP to changes in microfilaments and microtubules, important determinants of cell shape, was examined. Bovine pulmonary artery endothelial cells were injured over a 2-hr time course with a range of H 2O 2 doses (0–20 m M). The higher concentrations of H 2O 2 consistently produced contraction and rounding of >50–75% of cells by 1–2 hr. The range of 1–20 m M H 2O 2 produced rapid, significant reductions in endothelial ATP levels over the time course of injury. Although there were significant increases in mean endothelial [Ca 2+] i in response to 5, 10, and 20 m M H 2O 2, 1 m MH 2O 2 did not affect the [Ca 2+] i. Fluorescence microscopy revealed that microfilament disruption occurred as ATP levels fell and preceded depolymerization of microtubules which developed after [Ca 2+] 1 approached 1 × 10 −6 M. H 2O 2 at 1 m M injury caused microfilament disruption but did not depolymerize microtubules. Microfilament disruption occurred without oxidant exposure, when ATP levels were reduced by glucose depletion and mitochondrial inhibition with oligomycin (650 n M). If a Ca 2+ ionophore, ionomycin (5 μ M), was then added, [Ca 2+] i rose to > 1 × 10 −6 M, microtubules fragmented and depolymerized, and cell contraction and rounding very similar to that induced by H 2O 2 occurred. These results suggest that endothelial cell dysfunction and capillary leak in ARDS may be due to H 2O 2-mediated changes in cellular ATP and [Ca 2+] i.

Pasted‐Rolled Zinc Electrodes Containing Calcium Hydroxide for Use in Zn / NiOOH Cells

This paper discusses work to evaluate the durability of pasted‐rolled zinc electrodes prepared from a water‐based process in 26 Ah size zinc‐nickel oxide cells in 20 weight percent . An optimum Ca/Zn ratio of 0.58 was selected based upon data obtained using a potentiodynamic discharge technique and a specially designed small test cell to simulate a full size cell, experimental zinc electrodes with Ca/Zn ratios ranging from 0 to 0.8, SEM data, and zincate solubility considerations. The cells reached 400 to 550 cycles to 70% of the theoretical cell capacity. The loss in cell capacity seemed to be related mostly to a loss in utilization of the zinc electrode, and the shape change mechanism.

一次血小板機能異常症の形態と形態変化

In order to clarify the relationship between the platelet shape and the disease abnormality, the circualting form and its change in response to agonists were examined in various primary platelet abnormalities. Patients consisted of thrombashenia (T) 3, essential athrombia (E) 2, Bernard-Soulier syndrome (BS) 1, May-Hegglin anomaly (MH) 2, Hermansky-Pudlak syndrome (HP) 1, platelet cyclo-oxygenase deficiency (CD) 1, release mechanism abnormality characterized by defective A23187-aggregation (A) 1, and aspirin-ingested volunteers (AS) . The circulating form was examined by our method using light microscopy. Shape change was induced by incubation of native platelet suspension from the subjects with various concentrations of either ADP (-10-5M, 1min), thrombin (-2-1U/ml, 30sec) or arachidonate (-2-1mM, 2min).Striking spherification and pseudopod formation were noted in circulating form in BS, a mild one in some of T and E, and a slight spherification in MH, whereas not in the others. Shape change induced by ADP was inhibited in none, and that by arachidonate was completely inhibited in CD (as previously reported 14), AS, HP and 2 out of 11 normal subjects. Thrombin-induced change was inhibited only in BS probably in agreement with its defect of glycoprotein Ib as a possible receptor of thrombin.Thus the circulating form and its change response to some agonists differed among various platelet abnormalities. This indicates the necessities for clarifying the mechanism of shape change and for investigating clinical usefulness of shape (change) determination.

A study of the kinetics of ADP-triggered platelet shape change

The rapid transformation of human blood platelets from inert discoid cells to spheroechinocytes that is induced by adenosine diphosphate (ADP) has been followed by right-angle light scattering intensity measurements using a laser light source and a sensitive photomultiplier. Two steps have been observed, and their rate constants have been determined as a function of pH and [ADP] and in the presence and absence of calcium for both platelet-rich plasma and gel-filtered platelets. Both steps are significantly faster in the presence of physiologic levels of calcium. Platelets were fixed prior to and during activation, then examined by phase-contrast and scanning electron microscopy. The light scattering and morphological changes support a model in which, under physiologic conditions of pH, temperature, ionic strength, and calcium concentration, the initial rapid event in platelet shape change is the loss of discoid shape, with a decay time of two to three seconds, leading to an intermediate with short pseudopods. The slower extension of long pseudopods occurs next, with a time constant of approximately seven to eight seconds. These results may help to resolve the contradictory descriptions of the mechanism of platelet shape change that have recently appeared in the literature.

A Study of the Kinetics of ADP-Triggered Platelet Shape Change

The rapid transformation of human blood platelets from inert discoid cells to spheroechinocytes that is induced by adenosine diphosphate (ADP) has been followed by right-angle light scattering intensity measurements using a laser light source and a sensitive photomultiplier. Two steps have been observed, and their rate constants have been determined as a function of pH and [ADP] and in the presence and absence of calcium for both platelet-rich plasma and gel-filtered platelets. Both steps are significantly faster in the presence of physiologic levels of calcium. Platelets were fixed prior to and during activation, then examined by phase-contrast and scanning electron microscopy. The light scattering and morphological changes support a model in which, under physiologic conditions of pH, temperature, ionic strength, and calcium concentration, the initial rapid event in platelet shape change is the loss of discoid shape, with a decay time of two to three seconds, leading to an intermediate with short pseudopods. The slower extension of long pseudopods occurs next, with a time constant of approximately seven to eight seconds. These results may help to resolve the contradictory descriptions of the mechanism of platelet shape change that have recently appeared in the literature.

The role of ankyrin in shape and deformability change of human erythrocyte ghosts

Human erythrocyte membranes (ghosts) from acid/citrate/dextrose preserved blood were digested with trypsin (protein/trypsin  100:1) under hypotonic conditions and then analyzed by SDS-polyacrylamide gel electrophoresis. After digestion for about 20–30 s at 0°C, only ankyrin had disappeared and other bands including spectrin, actin, band 4.1 and band 3 remained intact. This observation was supported by electron micrographs showing that the horizontally disposed, filamentons structure was a little apart from the lipid bilayer and its components were not destroyed. In contrast to intact ghosts, treatment with chlorpromazine, or Mg-ATP did not induce shape change in these trypsin-treated ghosts. The number of transformable cells correlated closely with the amount of remaining ankyrin in the SDS-polyacrylamide gel electrophoresis pattern. Furthermore, the chlorpromazine- and Mg-ATP-induced decreases in viscosity of suspensions of erythrocyte ghosts were also prevented by trypsin treatment for 20–30 s at 0°C. These findings suggest that ankyrin plays an important role in the change in shape and deformability of erythrocyte ghosts. The molecular mechanism of drug-induced shape change and the role of undermembrane structure in regulating erythrocyte shape and deformability are discussed.

Effects of Local Anesthetics on Human Platelets: Filopodial Suppression and Endogenous Proteolysis

Agents that affect platelet shape may be useful in understanding the mechanism of shape change; for this reason the effects of local anesthetics are worthy of further study. Local anesthetics cause platelets to retract filopodia. At short time intervals (up to about 30 min) and low concentrations of the drugs, the filopodia are reextended when the platelets are gel filtered with eluant free of anesthetic. At longer time intervals (1-2 hr) or higher drug concentrations, the retraction becomes irreversible. When the polypeptide composition of the total platelet lysate was examined on SDS gels, proteolysis of two high molecular weight bands was seen when the suppression became irreversible. These polypeptides, estimated as 250,000 and 230,000 daltons, were major components of a precipitate that formed when platelets were lysed at low ionic strength and were also enriched in a "cytoskeletal" preparation made by lysing platelets attached to glass beads and analyzing the adherent residue. Electron micrographs of platelets lysed on surfaces showed an intermeshed network of filaments to be a major component of the residue. The results suggest that the proteins comprised of these bands may be part of the cytoskeletal system and that their integrity may be necessary for the platelet to reextend filopodia following suppression.

Effects of local anesthetics on human platelets: filopodial suppression and endogenous proteolysis

Agents that affect platelet shape may be useful in understanding the mechanism of shape change; for this reason the effects of local anesthetics are worthy of further study. Local anesthetics cause platelets to retract filopodia. At short time intervals (up to about 30 min) and low concentrations of the drugs, the filopodia are reextended when the platelets are gel filtered with eluant free of anesthetic. At longer time intervals (1–2 hr) or higher drug concentrations, the retraction becomes irreversible. When the polypeptide composition of the total platelet lysate was examined on SDS gels, proteolysis of two high molecular weight bands was seen when the suppression became irreversible. These polypeptides, estimated as 250,000 and 230,000 daltons, were major components of a precipitate that formed when platelets were lysed at low ionic strength and were also enriched in a “cytoskeletal” preparation made by lysing platelets attached to glass beads and analyzing the adherent residue. Electron micrographs of platelets lysed on surfaces showed an intermeshed network of filaments to be a major component of the residue. The results suggest that the proteins comprised of these bands may be part of the cytoskeletal system and that their integrity may be necessary for the platelet to reextend filopodia following suppression.