Numerous Protrusions Research Articles

Relation between breakdown voltage and prebreakdown current in vacuum gap

Two different surface treatments (mechanical polishing, thin film deposition) were performed on cathode surfaces, and the field emission currents from the cathodes were measured with a microchannel plate. In order to discuss the relationship between the breakdown voltage and prebreakdown current in the vacuum gap, the breakdown voltage was measured after field emission measurement. The V–I characteristics of the field emission and breakdown voltage were influenced by surface treatment, and the breakdown voltages of mechanical polished cathodes were lower than those of the thin film deposited cathodes. It was found that the probability of breakdown increased when the field emission current reached 10–11 A. Atomic force microscope (AFM) measurements showed numerous protrusions on the cathode surface in the case of thin film deposition treatment, but we estimated by the finite element method that these protrusions make the field enhancement effect low. It was inferred that the breakdown voltage in vacuum gaps could be increased by the thin film deposition method. © 2000 Scripta Technica, Electr Eng Jpn, 131(4): 11–18, 2000

Dorsoventral compartmentalization of mesoderm in heart-forming area of chick embryo.

In early chick development (stages 5-8) the seemingly homogeneous mesoderm in the heart-forming area splits to somatic and splanchnic cardiogenic layers. Little is known about dorsoventral compartmentalization before splitting. Electron microscopic analysis shows the early dorsoventral polarization of precardiomyocytes. The dorsal compartment has epithelial and the ventral compartment mesenchymal features with numerous protrusions. At stage 5+-6 staining for wheat germ agglutinine (WGA) transiently demarcates the ventral part of mesoderm. The glycosomes (beta-glycogen) show a dorsoventral gradient in the mesoderm of the cardiogenic field during the initial step of the compaction. The differential expression of glycosomes depends on the activity of glycogen synthase kinase 3-beta, a component of the wnt-signaling pathway, and might in this spatiotemporal developmental window be involved in the commitment of presumptive cardiogenic and somatic cells. To verify this hypothesis simulation experiments with LiCl in vitro were carried out. The normal splitting of the mesoderm and the development of heart primordia were disturbed. Blocking the receptors of WGA by WGA in vitro at stage 5-5+ perturbs the migration of mesoderm to anterio-medial direction. It appears that early specification of dorsal and ventral compartments of the mesoderm in the heart-forming area correlates with the gradient of glycosomes. Our results suggest that the target of LiCl action (glycogen synthase kinase 3-beta) might be involved in the specification of heart primordia and that WGA receptors mediate the migration of mesoderm to the anteriomedial direction.

Transforming power of immunosuppression: experimental mirage or clinical mirror to the future

Malignancy is a common and dreaded complication after organ transplantation. The high incidence of neoplasm and its aggressive progression, which are associated with immunosuppressive therapy, are thought to be due to the resulting impairment of the organ recipient's immune-surveillance system. Here we report a mechanism for the heightened malignancy that is independent of host immunity. We show that ryclosporine (cyclosporin A), an immunosuppressant that has had a major impact on improving patient outcome following organ transplantation, induces phenotypic changes, including invasiveness of non-transformed cells, by a cell-autonomous mechanism. Our studies show that ryclosporine treatment of adenocarcinoma cells results in striking morphological alterations, including membrane ruing and numerous pseudopodial protrusions, increased cell motility, and anchorage-independent (invasive) growth. These changes are prevented by treatment with monoclonal antibodies directed at transforming growth factor-β (TGF-β). In vivo, cyclosporine enhances tumor growth in immunodeficient SCID-beige mice; anti-TGF-(3 monoclonal antibodies but not control antibodies prevent the cyclosporine-induced increase in the number of metastases. Ourfindings suggest that immunosuppressants like cyclosporine can promote cancer progression by a direct cellular effect that is independent of its effect on the host's immune cells, and that ryclosporine-induced TGF-8 production is involved in this.

Transforming Power of Immunosuppression: Experimental Mirage or Clinical Mirror to the Future.

Abstract Malignancy is a common and dreaded complication after organ transplantation. The high incidence of neoplasm and its aggressive progression, which are associated with immunosuppressive therapy, are thought to be due to the resulting impairment of the organ recipient's immune-surveillance system. Here we report a mechanism for the heightened malignancy that is independent of host immunity. We show that ryclosporine (cyclosporin A), an immunosuppressant that has had a major impact on improving patient outcome following organ transplantation, induces phenotypic changes, including invasiveness of non-transformed cells, by a cell-autonomous mechanism. Our studies show that ryclosporine treatment of adenocarcinoma cells results in striking morphological alterations, including membrane ruing and numerous pseudopodial protrusions, increased cell motility, and anchorage-independent (invasive) growth. These changes are prevented by treatment with monoclonal antibodies directed at transforming growth factor-β (TGF-β). In vivo, cyclosporine enhances tumor growth in immunodeficient SCID-beige mice; anti-TGF-(3 monoclonal antibodies but not control antibodies prevent the cyclosporine-induced increase in the number of metastases. Ourfindings suggest that immunosuppressants like cyclosporine can promote cancer progression by a direct cellular effect that is independent of its effect on the host's immune cells, and that ryclosporine-induced TGF-8 production is involved in this.

Cyclosporine Induces Cancer Progression by a Cell-Autonomous Mechanism

Malignancy is a common and dreaded complication following organ transplantation. The high incidence of neoplasm and its aggressive progression, which are associated with immunosuppressive therapy, are thought to be due to the resulting impairment of the organ recipient's immune-surveillance system. Here we report a mechanism for the heightened malignancy that is independent of host immunity. We show that cyclosporine (cyclosporin A), an immunosuppressant that has had a major impact on improving patient outcome following organ transplantation, induces phenotypic changes, including invasiveness of non-transformed cells, by a cell-autonomous mechanism. Our studies show that cyclosporine treatment of adenocarcinoma cells results in striking morphological alterations, including membrane ruffling and numerous pseudopodial protrusions, increased cell motility, and anchorage-independent (invasive) growth. These changes are prevented by treatment with monoclonal antibodies directed at transforming growth factor-beta (TGF-beta). In vivo, cyclosporine enhances tumour growth in immunodeficient SCID-beige mice; anti-TGF-beta monoclonal antibodies but not control antibodies prevent the cyclosporine-induced increase in the number of metastases. Our findings suggest that immunosuppressants like cyclosporine can promote cancer progression by a direct cellular effect that is independent of its effect on the host's immune cells, and that cyclosporine-induced TGF-beta production is involved in this.

Cyclosporine induces cancer progression by a cell-autonomous mechanism.

Malignancy is a common and dreaded complication following organ transplantation. The high incidence of neoplasm and its aggressive progression, which are associated with immunosuppressive therapy, are thought to be due to the resulting impairment of the organ recipient's immune-surveillance system. Here we report a mechanism for the heightened malignancy that is independent of host immunity. We show that cyclosporine (cyclosporin A), an immunosuppressant that has had a major impact on improving patient outcome following organ transplantation, induces phenotypic changes, including invasiveness of non-transformed cells, by a cell-autonomous mechanism. Our studies show that cyclosporine treatment of adenocarcinoma cells results in striking morphological alterations, including membrane ruffling and numerous pseudopodial protrusions, increased cell motility, and anchorage-independent (invasive) growth. These changes are prevented by treatment with monoclonal antibodies directed at transforming growth factor-beta (TGF-beta). In vivo, cyclosporine enhances tumour growth in immunodeficient SCID-beige mice; anti-TGF-beta monoclonal antibodies but not control antibodies prevent the cyclosporine-induced increase in the number of metastases. Our findings suggest that immunosuppressants like cyclosporine can promote cancer progression by a direct cellular effect that is independent of its effect on the host's immune cells, and that cyclosporine-induced TGF-beta production is involved in this.

Tunic morphology and cellulosic components of pyrosomas, doliolids, and salps (thaliacea, urochordata).

The morphology and cellulosic composition of the tunic was studied in pelagic tunicates (3 pyrosomas, 2 doliolids, and 13 salps). The tunic is transparent and gelatinous, consisting of an electron-dense cuticular layer with a fibrous tunic matrix. The thickness and density of the cuticular layer and of the tunic matrix differ from species to species. In some salps, the cuticular layer has numerous minute protrusions that are structurally identical to those found in several ascidians. Free mesenchymal cells (tunic cells) are distributed in the tunic. Whereas the number of tunic cells in the pyrosomas is similar to that in ascidians, there are many fewer tunic cells in doliolids and salps. These differences may be caused by the different functions of the tunic in each group. The existence of cellulose in the tunic was confirmed using electron diffraction in all of the species studied thus far. Their diffractograms indicate that the cellulose microfibrils consist of nearly pure I{beta} of the allomorph. These results show that tunic morphology and cellulosic composition are similar in ascidians and thaliaceans (pyrosomas, doliolids, and salps). The tunic is considered to be a homologous tissue in these animals, and their most recent common ancestor would have possessed this tissue.

Adenosine A3 Receptors and Viability of Astrocytes.

We investigated the role of the A3 adenosine receptor in cells of the astroglial lineage (both rat primary astrocytes and human astrocytoma ADF cells) by means of the selective A3 agonists N6-(3-iodobenzyl)-adenosine-5'-N-methyluronamide (IB-MECA) and CI-IB-MECA, and by utilizing the selective A3 receptor antagonist MRS1191. Exposure of ADF cells to μM concentrations of either agonist resulted in reduction of cell number, likely due to cell death. In both rat astrocytes and human astrocytoma cells, at concentrations 2-3 orders of magnitude lower (which were not associated with cytotoxicity), these same agonists induced a marked reorganization of the cytoskeleton, with appearance of stress fibers and numerous cell protrusions. Functionally, these morphological changes were associated with cell protection, as demonstrated by a significant reduction of spontaneous apoptosis in A3 agonist-treated cells. To confirm a role for the A3 receptor in this effect, MRS1191 completely counteracted CI-IB-MECA-induced reduction of spontaneous apoptosis. In ADF cells, A3 agonists also induced changes in the intracellular distribution of the anti-apoptotic protein Bcl-XL, which became localized in cell protrusions. Also, this effect was specifically antagonized by MRS1191. These dual actions of A3 agonists in vitro may have important in vivo implications. For example, a robust and acute activation of the A3 receptor following massive adenosine release during ischemia may contribute to brain cell death; conversely, a subthreshold activation of this receptor prior to ischemia may trigger protective mechanisms (i.e., induction of stress fibers and of a Bcl-XL-dependent reorganization of cytoskeleton) making the brain more resistant to subsequent insults ("ischemic tolerance").

How significant is fetal Doppler velocimetry in the obstetrical management?

<dm:abstracts xmlns:dm="http://www.elsevier.com/xml/dm/dtd"><ce:abstract xmlns:ce="http://www.elsevier.com/xml/common/dtd" view="all" class="author" id="aep-abstract-id1"><ce:section-title>Publisher Summary</ce:section-title><ce:abstract-sec view="all" id="aep-abstract-sec-id1"><ce:simple-para id="fsabs018" view="all">This chapter discusses materno-fetal nutrient transfer, particularly focusing on syntrophoblast, which constitutes the main materno-fetal barrier and the main site of placental nutrient metabolism later in pregnancy. The maternally facing side (microvillous membrane, MVM) of the syntrophoblast has numerous cell protrusions (microvilli) while the fetal side (basal membrane, 8M) is relatively smooth. Due to this structural difference, the ratio of microvillous membrane to basal membrane surface areas is typically about 6: 1. The glucose transporter 1 (GLUT1) is active at both sides of the syntrophoblast cell layer. This transporter mediates the transfer of both glucose and galactose, but not of other sugars to any significant extent. The placenta preferentially transports essential polyunsaturated fatty acids, in particular arachidonic acid and docosahexaenoic acid. A wide range of fatty acids is taken up from maternal circulation with lipoproteins. Amino acids are used extensively by the fetus, and by the placenta itself, as building blocks for protein and peptide synthesis and as an important energy source. Amino acid metabolism in the placenta is very active, providing energy and protein precursors for the growth and sustenance of this crucial organ. The placenta is also the major site for synthesis of glycine from serine, both from maternal and fetal circulation.</ce:simple-para></ce:abstract-sec></ce:abstract></dm:abstracts>

Fibronectin: structure, assembly, and cardiovascular implications.

In the past 2 decades, it has been appreciated that the functions of the extracellular matrix (ECM) are not entirely structural. ECM components interact with specific adhesion receptors on cell surfaces and regulate various cellular functions, including differentiation, proliferation, migration, and apoptosis. Fibronectin (FN) is a paradigm adhesive protein, nonreactive with adhesion receptors in its soluble state but highly adhesive when insoluble. Polymerization of FN into the ECM must be tightly regulated to ensure that the adhesive information in the ECM is appropriate. FN exists in a soluble protomeric form in micromolar concentration in blood plasma and in an insoluble multimeric form in the ECM.1 2 Unlike fibrillar or basement membrane collagens, laminins, actin, and tubulin, circulating FN does not self-polymerize in physiologically relevant solutions. Furthermore, there is little passive accumulation of FN in preexisting ECM. Rather, assembly of FN takes place at specialized areas on the cell surface.3 FN is especially abundant in the ECM of embryonic and regenerating or injured tissues, although it can be found in most ECMs, including basement membranes. FN interacts with cells through integrins, heterodimeric transmembrane receptors linking the ECM to the intracellular cytoskeleton and signaling pathways. The aim of this review is to describe the mechanisms and consequences of FN deposition and give a brief overview of the significance of FN for selected areas of cardiovascular research. In the first section we describe important features of the FN molecule that account for its multiple functions. Next, we focus on the assembly process, ie, the conversion of soluble FN to its active, adhesive, insoluble form. Finally, we discuss several areas of cardiovascular research in which FN may have an important role, exemplifying how the adhesive information of FN can drive pathophysiological processes. Soluble FN is a dimeric glycoprotein. Each subunit is a …

Effect of Collagenase on Surface Expression of Immunoreactive Fibronectin and Laminin in Freshly Isolated Cardiac Myocytes

The extracellular glycoproteins fibronectin (FN) and laminin (LMN) are ubiquitously expressed in myocardial tissue. These glycoproteins are important for cellular attachment and differentiation of the cardiac myocytes. Utilizing specific antibodies for the detection of FN and LMN, respectively, the distribution of these extracellular proteins was examined in enzymatically isolated adult cardiac myocytes. Immunofluorescence staining of rod-shaped cardiac myocytes revealed only remnants of immunoreactive FN on the cellular surface and in the transverse tubular membrane system. LMN expression, however, was preserved in a raster-like pattern in the cardiac myocytes. In order to study the distribution of these glycoproteins at high resolution, scanning electron microscopy using the backscattered electron mode was combined with immunogold staining and silver-enhancement. In addition, to confirm the immunofluorescence microscopic observations it was shown that FN labelling was restricted to ill-defined extracellular material and that LMN was absent from the intercalated discs of the cardiac myocytes. The hypercontracted cells were characterized by numerous surface protrusions devoid of immunoreactive LMN. Thus, these results indicate that FN and LMN are differently affected by collagenase treatment, and that these changes of glycoprotein expression may influence the normal function of the cardiac myocytes as well as the membrane stability during the development of irreversible cellular lesions.

The A3Adenosine Receptor Mediates Cell Spreading, Reorganization of Actin Cytoskeleton, and Distribution of Bcl-xL: Studies in Human Astroglioma Cells

The pathophysiological role of the adenosine A3receptor in the central nervous system is largely unknown. We have investigated the effects of the selective A3receptor agonist 2-chloro-N6-(3-iodobenzyl)-adenosine, Cl-IB-MECA, in cells of the astroglial lineage (human astrocytoma ADF cells). A marked reorganization of the cytoskeleton, with appearance of stress fibers and numerous cell protrusions, was found following exposure of cells to low (nM) concentrations of Cl-IB-MECA. These “trophic” effects were accompanied by induction of the expression of Rho, a small GTP-binding protein, which was virtually absent in control cells, and by changes of the intracellular distribution of the antiapoptotic protein Bcl-xL, that, in agonist-exposed cells, became specifically associated to cell protrusions. This is the first demonstration that the intracellular organization of Bcl-xLcan be modulated by the activation of a G-protein-coupled membrane receptor, such as the A3adenosine receptor. Moreover, modulation of the astrocytic cytoskeleton by adenosine may have intriguing implications in both nervous system development and in the response of the brain to trauma and ischemia.

High-resolution backscatter electron detection of cell surface molecules on human platelets using the double-layer coating method and cryo field emission scanning electron microscopy.

A model system utilizing cryo scanning electron microscopy (SEM) for the detection of putative cell adhesion molecule(s) on the surface of human platelets is described. Plunge freezing was used for cryoimmobilization of unactivated and activated platelets after prefixation. Extracellular ice was removed by sublimation to expose the surface of the platelet membrane. Cryosamples were coated by the double-layer method, in which undirectional shadowing is performed at an angle of 45 degrees with 2 nm of platinum by thermal evaporation, followed by evaporation of 5 nm of carbon at an angle of 90 degrees for stabilization of the platinum film. The topography of the extracellular surface of the unstimulated platelet membrane was dominated by small spherical protrusions, while that of the activated platelet had not only similar spherical projections, but also possessed numerous rod-like protrusions, presumably representing the upregulation of the cell adhesion molecule, P-selectin, from intracellular a granules. These results clearly demonstrate that cryo field-emission SEM can detect molecular topography on the extracellular surface of cells consistent with the dimensions and shape of membrane cell adhesion molecules.

A New Species of Phoreiobothrium (Cestoidea: Tetraphyllidea) from the Great Hammerhead Shark Sphyrna mokarran and Its Implications for the Evolution of the Onchobothriid Scolex

Phoreiobothrium manirei n. sp. is described from the spiral intestines of 3 immature individuals of the great hammerhead shark Sphyrna mokarran collected off of the west coast of Florida. This cestode is unusual in that it possesses 4 muscular papillae on the anterior margin of the accessory sucker. Numerous small protrusions with central cilium-like projections were conspicuous throughout the posterior margin of each bothridium. This species possesses the unique combination of bothridia posteriorly subdivided into subloculi and hooks with extended bases and 2 rather than 3 prongs. In fact, the hooks are strikingly like those of species in the genera Dicranobothrium and Platybothrium. This combination of characters suggests that the bifid hook condition is plesiomorphic with respect to the trifid hook condition within the Onchobothriidae. These data further suggest that the triloculated bothridial condition is plesiomorphic relative to the biloculated condition.

Ultrastructural characterization of the postnatal development of the thalamic ventrobasal and reticular nuclei in the rat.

Electron microscopy has been employed to analyze the normal maturational sequence that characterizes the postnatal development of synaptic circuits in the ventrobasal (VB) and reticular (Rt) thalamic nuclei of rats at different ages (from birth to the end of the third postnatal week). Throughout the first postnatal week, similar signs of immaturity are observed in both nuclei, mainly consisting in scarcity of cytoplasmic organelles, presence of wide extracellular spaces, and absence of myelinated fibers. Several synaptic terminals are however present from birth, thus indicating that some of the afferents have already reached and contacted their thalamic target during embryonic life. Most of the terminals are small and contain only a few round, clear vesicles, and therefore their cytological features do not allow the identification of their origin. In particular, in both nuclei, terminals with flat vesicles and symmetric specialization are only rarely observed, and in VB the ascending terminals are not distinguishable from terminals of other sources as they are in adults. During the second postnatal week, progressive maturational changes in VB and Rt lead to neurons having well-developed cytoplasmic organelles and to an elaborate neuropil containing myelinated fibers and synaptic terminals that are morphologically heterogeneous and resemble the adult ones. The permanence of growth cone-like profiles and of numerous somatic and dendritic protrusions, often contacted by synaptic terminals, indicates that a certain degree of reorganization is still taking place in both nuclei. By the end of the third postnatal week the synaptic organization of VB and Rt is indistinguishable from that observed in adults. This ultrastructural study shows that the appearance of the neuropil of VB and Rt and the morphological complexity of the synaptic arrangements characteristic of the adult rat are not present in neonates, but are gradually acquired during the first three postnatal weeks, and that they result from progressive modifications in circuit organization involving both pre- and postsynaptic elements.

Mutagenesis of ser41 to ala inhibits the association of GAP-43 with the membrane skeleton of GAP-43-deficient PC12B cells: effects on cell adhesion and the composition of neurite cytoskeleton and membrane.

To investigate the molecular basis for GAP-43 function in axon outgrowth, we produced a mutant, GAP-43 (Ala41), whose interaction with calmodulin in vitro was unaffected by increasing Ca2+ concentrations, and stably transfected it into GAP-43-deficient PC12B cells. Several lines that expressed wild-type or mutant protein at levels that resembled endogenous GAP-43 expression in PC12 controls were subcloned and characterized. GAP-43 (Ala41) was significantly more extractable with Nonidet P-40 and less tightly associated with the membrane skeleton than the wild-type protein. Furthermore, GAP-43 (Ala41) expression by PC12B cells profoundly affected their phenotype: First, observation of living cells using video-enhanced microscopy revealed irregular plasma membranes with numerous blebs and protrusions and neurites that appeared thin and varicose. Second, both the cells' ability to remain attached to laminin substrates and the amount of alpha 1 beta 1 integrin expressed on the cell surface was significantly decreased. Finally, peripherin transport, which is abnormal in PC12B cells, could be rescued by transfection of wild-type GAP-43 but not the GAP-43 (Ala41) mutant. The phenotypic abnormalities resemble other cell types in which membrane skeleton/plasma membrane interactions have been functionally decoupled, and our results are consistent with the notion that these interactions may be abnormal in GAP-43 (Ala41)-expressing PC12B cells, either as a direct consequence of the mutation or arising secondarily to the altered availability of calmodulin in the growing neurite.

3-Aminobenzamide Induces Cytoskeleton Rearrangement in M14 Melanoma-Cells

3-aminobenzamide (3-ABA) is an inhibitor of poly-ADP-ribose-polymerase, an enzyme involved in numerous subcellular processes including cell death. With the aim of contributing to clarify the mode of action of the drug, which is still poorly understood, its effects on cultured melanoma cells M14 have been assessed. In particular, an impairment of cell growth accompanied by the formation of long and numerous dendritic-like protrusions has been detected. This finding appears to be due to a specific effect of the drug on some cytoskeletal elements and could be associated with its differentiating capability. This finding, together with previous data from our group - Biochem. Biophys. Res. Commun., (1994) 199, 525-530 and 1250-1255 - suggests that cytoskeleton is an important target of 3-ABA.

Nucleation of diamond particles by hot filament chemical vapour deposition

Diamond particles have been synthesized on an abraded silicon substrate from a gas mixture of methane and hydrogen by hot filament chemical vapour deposition. The nucleation and growth process of the diamond particles have been studied by varying the deposition time. The intermediate layer between the diamond particle clusters and the substrate was observed by scanning electron microscopy of the films deposited for 60 and 120 min. By micro-IR absorption measurements, absorptions were detected between 2800 cm −1 and 3000 cm −1 for the intermediate layer, while for the diamond particle clusters little absorption was observed in the same region. Raman spectra from the intermediate layer displayed the broad peak lying between 1300 cm −1 and 1600 cm −1, indicating amorphous carbon. The intermediate layer was found to be a hydrogenated amorphous carbon (a-C:H) film. Atomic force microscopy (AFM) studies have been performed on the surfaces of films deposited for 30, 60 and 120 min. AFM observations revealed that the surface of the intermediate a-C:H layer in the films deposited for 60 min was covered with numerous protrusions and in the films deposited for 120 min these protrusions were developed to layered triangular pyramids. Several aggregates of triangular pyramids were found in the a-C:H layer, suggesting a precursor to the diamond particles. However, the surfaces of the films deposited for only 30 min were not covered with the protrusions, but were covered with particle-like features. It is proposed that a-C:H films are initially formed on the substrate and that diamond nuclei are created in the a-C:H films and grow to be diamond particles.

Transplantation of colon carcinoma into granulation tissue induces an invasive morphotype

The stroma surrounding many malignant tumors resembles granulation tissue. To test the hypothesis that such stroma stimulates tumor invasiveness, we compared, by electron microscopy and immunohistochemistry, the growth patterns of CC531 rat colon adenocarcinoma in 2 experimental situations: (i) after transplantation into the undisturbed subcutaneous connective tissue of rats, and (ii) after transplantation into experimentally induced subcutaneous granulation tissue in rats. For the latter experimental situation, a subcutaneous "tissue chamber" was designed allowing fragments of tumor tissue to be transplanted into the very center of developing granulation tissue. In the undisturbed subcutaneous tissue, the whole tumor was generally encapsulated, and the tumor cells were arranged in compact groups with a strong tendency to form acini. In the pre-formed granulation tissue, on the other hand, the tumor tissue closely matched descriptions of invasive colon carcinomas in the literature and met the criteria for the "invasive morphotype". In this situation, the tumor consisted of thin, unorganized, widely dispersed strands of irregular tumor cells with numerous protrusions that deeply penetrated the surrounding matrix. Our results show that an invasive morphotype can be evoked by pre-inducing granulation tissue at the transplantation site.

Shape-from-shading is independent of visual attention and may be a 'texton'

Shading was used to generate the appearance of an obliquely illuminated surface with spherical indentations and protrusions. The "pop-out" of an apparent indentation among numerous apparent protrusions served as a psychophysical assay for shape-from-shading. Detectability of the pop-out varied with the direction of apparent illumination, a finding which is characteristic for shape-from-shading and which demonstrated the appropriateness of this assay. Observers were able to concurrently detect two shape-from-shading pop-outs in different parts of the display, demonstrating that shape-from-shading is a parallel process. In another experiment, visual attention was engaged by a letter discrimination task. Nevertheless, observers were able to detect a shape-from-shading pop-out concurrently in the unattended part of the display, suggesting that shape-from-shading is independent of visual attention. Thus, shape-from-shading shares some of the characteristics of Julesz' textural stimulus dimensions ('textons').