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PubMed1976

The spread of blood-borne metastases in malignant lymphomas of man.

An autopsy study was performed on 190 cases with Hodgkin's disease and on 134 cases with reticulum cell sarcomas. It was found that a cascade spread of metastases, as opposed to a random spread, was detectable in patients with Hodgkin's disease, but not in patients with reticulum cell sarcoma. Metastatic key-sites for both lymphomas are defined as those organs whose chance of being seeded by the primary tumor is the highest; these sites are the spleen, liver, bone marrow and lungs. This study could not demonstrate in Hodgkin's cases that metastases in the liver and bone marrow were spleen dependent, but rather it showed that the spleen, liver and bone marrow acted as three independent sources of generalized metastases. Explanations proposed to account for the different metastatic spread in Hodgkin's disease and reticulum cell sarcomas, included different intrinsic cellular characteristics of the two lymphomas. the different location of the primary tumor either because of nodal, or of extra nodal origin, or because the primary tumor was located either in the upper or in the lower torso or in both areas. Malignant cells in the kidney, central nervous system and endocrine system were either released by the spleen via the lungs, or released by the liver and the lungs, or they were bone marrow dependent. The cascade spread of metastases hold true only for Hodgkin's disease. In cases with reticulum cell sarcomas, metastases appeared to spread at random from the primary tumor throughout the body, with rare exceptions such as metastases in the central nervous system, which originated either in the liver or in the spleen, lungs, kidney and bones.

Bone Marrow Diseases↗
PubMed1981

Spread of contraction in rabbit ear artery preparations in response to stimulation by norepinephrine.

To investigate the spread of contraction in the rabbit ear artery, changes in segment diameter were measured after local stimulation. No spread of contraction was produced by direct current or local application of norepinephrine (NE). Repetitive electrical stimulation caused contraction which spread far from the point of excitation. Since 2 x 10(-7) g/ml tetrodotoxin (TTX) or 10(-5) M phentolamine prevented this spread of contraction, we concluded that it depends on normal function of periarterial nerves and of the alpha-adrenergic receptors at the site of the smooth muscle cells. To check this conclusion and exclude the possibility of myogenic propagation, which normally is due to the conduction of action potentials, the relation between membrane potential of smooth muscle cells and the rapid phase of the contractile response after rapid addition of NE was investigated. In both polarized and depolarized tissues NE induces a biphasic contractile response with no difference in latency. Membrane potential does not change during mechanical latency after the rapid addition of 5 x 10(-9) - 5 x 10(-6) g/ml NE. There are only slight differences in contraction amplitude and maximum rate of tension development when strips from polarized and depolarized tissues incubated in Ca2+-free solution are stimulated by NE. These findings support the conclusion that spread of contraction is not due to myogenic propagation.

Animals↗
PubMed1995

The influence of serum for spreading of tumor cells on synthetic glycolipid films.

Adhesion and spreading of tumor cells to the films of a galactose-, glucose-, or phosphatidylcholine-bearing lipid was studied. Human adenocarcinoma Hela cells, B16 mouse melanoma cells, and HuH-7 human hepatoma cells selectively adhered and spread on galactose-bearing lipid in serum-containing medium, but not in serum-free medium. The spreading of the tumor cells in serum-containing medium was inhibited in the presence of lactose, but not in the presence of maltose. Cell spreading also occured on the galactose-bearing glycolipid film pre-treated with serum. From quantitative analysis for the the adsorption of serum components by a quartz-crystal microbalance, the surfaces of the lipid films were found to be entirely covered with serum components. These results suggested that serum components pre-adsorbed on the galactose-bearing lipid influence the cell spreading.

Adenocarcinoma↗
PubMed2006

Dynamic texture spreading: probing the mechanisms of surface interpolation.

Dynamic texture spreading is a filling-in phenomenon where a colored pattern perceptually spreads onto an area confined by virtual contours in a multi-aperture motion display. The spreading effect is qualitatively similar to static texture spreading but widely surpasses it in strength, making it particularly suited for quantitative studies of visual interpolation processes. We first carried out two experiments to establish with objective tasks that texture spreading is a genuine representation of surface qualities and thus goes beyond mere contour interpolation. Two subsequent experiments serve to relate the phenomenon to ongoing discussions about potentially responsible mechanisms for spatiotemporal integration. With a phenomenological method, we examined to what extent simple sensory persistence might be causally involved in the effect under consideration. Most of our findings are consistent with the idea of sensory persistence, and indicate that information fragments are integrated over a time window of about 100 to 180 ms to form a complete surface representation.

Adaptation, Ocular↗
PubMed2006

Inhibition of human retinal pigment epithelial cell attachment, spreading, and migration by alkylphosphocholines.

PURPOSE: To investigate the effect of alkylphosphocholines (APCs) on human retinal pigment epithelium (RPE) attachment, spreading, migration, and microfilament assembly in vitro. METHODS: Cultured RPE cells of five human donors were treated with one of four APCs (C18:1-PC, C20:1-PC, C21:1-PC, or C22:1-PC) in the presence of fetal calf serum. Cell viability was tested by the trypan blue exclusion assay. Attachment was assessed after a 2-hour incubation of RPE cells on coated 96-well-plates and subsequent MTT testing. Cellular spreading is characterized by cytoplasmic halo formation and was quantified by counting four separate fields of RPE cells allowed to spread on coated 24-well plates for 4 hours. Migration was measured by a modification of the Boyden chamber method in microchemotaxis chambers with polycarbonated filters. Microfilament assembly was assessed by immunofluorescence analysis after incubation with rhodamine-phalloidin. RESULTS: All four APCs inhibited RPE cell attachment by more than 70% of their IC50 (C18:1-PC: 30 microM; C20:1-PC: 10 microM; C21:1-PC: 10 microM; and C22:1-PC: 10 microM). Also, APCs inhibited RPE cell spreading by more than 80% and migration by more than 90% at similar concentrations. Trypan blue staining revealed a toxicity within control limits within the concentration interval tested. Microfilament organization was significantly disturbed after incubation of RPE cells with one of the four APCs close to its IC50. CONCLUSIONS: APCs inhibit RPE cell attachment and spreading in vitro at nontoxic concentrations. As a possible mechanism of action, APCs disturb microfilament assembly, since they are known to interfere with protein kinase C (PKC) function. This could represent a novel method of preventing even early stages of proliferative vitreoretinal diseases like proliferative vitreoretinopathy (PVR).

Actin Cytoskeleton↗
PubMed2002

Tr1 cell-dependent active tolerance blunts the pathogenic effects of determinant spreading.

Experimental autoimmune encephalomyelitis (EAE) is a T cell-mediated autoimmune disease of the CNS. The current study shows that even in an acute episode of disease the autoimmune response spreads from one determinant on myelin basic protein (MBP) to the other linked determinant and that this spread plays a functional role in the pathogenesis of disease. The soluble form of each determinant could be used to induce Ag-specific T cell tolerance and reverse an ongoing disease. We show that the rapid effect of soluble peptide therapy is due to repolarization of autoimmune T cells undergoing activation. We suggest that at least two different types of regulatory T cells participate in the induction of active tolerance. The first, yet to be fully characterized, functions in an IL-4-dependent manner. The second produces high levels of IL-10 and low levels of IL-4 (Tr1). We bring about completing evidence showing that these Tr1 cells play a pivotal role in the regulation of T cell tolerance during determinant spread and that soluble peptide therapy with the determinant to which the autoimmune response spreads amplifies a de novo regulatory mechanism aimed to reduce the pathological consequences of determinant spreading.

Animals↗
PubMedDate not supplied

Metastatic spread and common symptoms. Part One: Introduction, bladder cancer, and brain cancer.

This is the first of a multi-part series detailing the metastatic spread and natural history of 18 common tumors. The introduction summarizes (1) the concept of symptom/problem anticipation and early identification; (2) the process of cancer metastasis; and (3) the 18 tumors that each cause more than 6,000 deaths per year in the United States. Bladder cancer is discussed, with information included on tumor types, metastatic spread and invasion, and common symptoms. Obstructive uropathy is the oncologic emergency most commonly associated with bladder cancer. Sites of spread, resulting problems, and assessment parameters are presented as a table. Brain cancer (and brain metastasis) is discussed, with information included on tumor types, invasion (the primary means of spread in primary brain cancer), and common symptoms. Increased intracranial pressure and, to a lesser extent, spinal cord compression are the oncologic emergencies most commonly associated with brain cancer. Sites of spread, resulting problems (including site-specific symptoms), and assessment parameters are presented as a table.

Brain Neoplasms↗
PubMed2002

Possible use of spreads as a FOODlet for improving the diets of infants and young children.

Spreads are high-viscosity fat products prepared by mixing dried powdered ingredients with a vegetable fat chosen for its viscosity. Spreads are not traditionally used for feeding infants or young children and were initially proposed for feeding severely malnourished children during the recovery phase. The advantages of these products include a high energy and nutrient density, a very good acceptability, and resistance to bacterial contamination. Adapted spreads could be designed to boost the nutritional density of diets of young children from poor communities. Spreads could be mixed with the meals or porridges traditionally given to infants or eaten by themselves as snacks. Formulation of spread products is flexible, and acceptability and efficacy trials are required to optimize their composition and fortification levels and to select the best-adapted ingredients for each setting.

Arachis↗
PubMed2003

The evolving applications of spreads as a FOODlet for improving the diets of infants and young children.

Action is needed to reduce the burden of micronutrient malnutrition in developing countries, and because low-income populations are vulnerable to deficiencies of multiple micronutrients, we need to move beyond approaches that comprise only single nutrients. The normal and evolutionary manner in which to consume nutrients is in the context of foods, both snacks and meals. Spreads are high-viscosity-fat products prepared by mixing dried powdered ingredients with a vegetable fat chosen for its viscosity. Spreads are not traditionally used for feeding infants or young children and were initially proposed as a way to treat children recovering from severe malnutrition. In preparation for the International Research Group on Infant Supplementation (IRIS) III intervention, a sequel to the IRIS I study (which was the focus of a workshop in Lima, Peru, from May 30-June 1, 2001), the feasibility of preparing a FOODlet for feeding infants and young children was explored. Within the spectrum of intervention tools for micronutrient supplementation, tablets are a pharmaceutical form, fortified spreads are a food, and sprinkles are an intermediate approach. The issues still to be discussed and resolved with regard to creating such a spread include its specific micronutrient formulation, the capacity of young children to consume the required amounts (from either the FOODlet alone or the FOODlet mixed with other foods), the iron content and overall antioxidant protection of the spread matrix and its vitamins, potential allergenicity of proteins, and the economic implications of using such a FOODlet in low-income societies.

Child↗
PubMed1977

The automated classification of mitotic phase for human chromosome spreads.

A system has been developed that automatically recognizes the mitotic phase of human chromosome spreads for karyotyping. Suitable spreads are classified into one of five subphases of mitosis. Classification is performed on the basis of summed chromosome length and most probable chromosome width. Classification requires 100-500 msec. A television camera scans the spread through microscope optics; computer and special purpose electronics process the video signals to generate run length histograms. The histograms are used to determine mitotic phase. Unbanded spreads, 133, were classified with a 4.5% error rate. One hundred banded spreads were classified with a 15% error rate.

Autoanalysis↗
PubMed2005

Phylogenetic analyses suggest reverse splicing spread of group I introns in fungal ribosomal DNA.

BACKGROUND: Group I introns have spread into over 90 different sites in nuclear ribosomal DNA (rDNA) with greater than 1700 introns reported in these genes. These ribozymes generally spread through endonuclease-mediated intron homing. Another putative pathway is reverse splicing whereby a free group I intron inserts into a homologous or heterologous RNA through complementary base-pairing between the intron and exon RNA. Reverse-transcription of the RNA followed by general recombination results in intron spread. Here we used phylogenetics to test for reverse splicing spread in a taxonomically broadly sampled data set of fungal group I introns including 9 putatively ancient group I introns in the rDNA of the yeast-like symbiont Symbiotaphrina buchneri. RESULTS: Our analyses reveal a complex evolutionary history of the fungal introns with many cases of vertical inheritance (putatively for the 9 introns in S. buchneri) and intron lateral transfer. There are several examples in which introns, many of which are still present in S. buchneri, may have spread through reverse splicing into heterologous rDNA sites. If the S. buchneri introns are ancient as we postulate, then group I intron loss was widespread in fungal rDNA evolution. CONCLUSION: On the basis of these results, we suggest that the extensive distribution of fungal group I introns is at least partially explained by the reverse splicing movement of existing introns into ectopic rDNA sites.

Alternative Splicing↗
PubMed2006

Testicular seminoma--unusual histology and staging with sub epithelial spread of seminoma along the vas deferans.

BACKGROUND: The route of local and metastatic spread of testicular seminoma is well recognised and accepted. The spread is via lymphatics to the paraaortic nodes. CASE PRESENTATION: We present a case report of testicular seminoma in a 56 year old man with previously unreported histological findings. In this case seminoma tumour cells did not appear to have spread by the expected lymphatic route. There was no involvement of retro-peritoneal para-aortic lymph nodes. The tumour appeared to have spread directly along the vas deferans in the sub epithelial plane to the mesenteric lymph nodes. CONCLUSION: This type of seminoma tumour spread has not previously been described and it is not a recognised route for metastasis by seminoma tumour. In this case the macroscopic clinical appearance was of a stage I tumour with normal tumour markers. However, the pathological stage of the tumour was surprisingly increased to stage III on the basis of histology and CT radiological findings. We present the unusual histological findings. In view of this unusual histological finding we reinforce the need for accurate staging and for resection of the spermatic cord close to the deep inguinal ring. Accurate staging is crucial in planning the treatment and follow up of seminoma and determines the prognosis.

Epithelium↗
PubMed2006

Mycobacteria directly induce cytoskeletal rearrangements for macrophage spreading and polarization through TLR2-dependent PI3K signaling.

Macrophage migration and adhesion are important for the control of mycobacterial infection and are critically dependent on the reorganization of the cytoskeleton. Mycobacteria elicit rapid morphological changes, such as cell spreading, a process relevant to in vivo changes of macrophage shape during extravasation and migration. In this study, we investigated the BCG mycobacteria-induced signaling events leading to macrophage cytoskeletal rearrangements employing specific pharmacological inhibitors to suppress distinct kinase pathways known to be elicited by infection. Viable or lysed mycobacteria, as well as purified cell wall lipoprotein p19, TLR2 agonist, induced RAW264.7 cells to extend actin-rich pseudopods, which impart radial spreading within 3 h, leading later to persistent cell polarization. BCG induced rapid activation of phosphatidylinositol 3-kinase, PI3K, activation that was recruited to the activated TLR2 receptor. TLR2- neutralizing antibody inhibited macrophage spreading and PI3K activation induced by p19. Additionally, BCG induced spreading and polarization of bone marrow-derived macrophages from TLR2- expressing mice in contrast to their TLR2-knockout counterparts. Neither MEK1/ERK, p38 MAPK, nor NF-kappaB activation were important for the early cytoskeletal rearrangements observed, although suppression of these pathways is known to inhibit chemokine secretion by activated macrophages. Beta2-integrins blockade with a corresponding antibody inhibited macrophage spreading and polarization but had no effect on pseudopodia protrusions demonstrating the downstream position of integrin-mediated adhesion in PI3K- dependent signaling pathway leading to the motility phenotype. The obtained data demonstrate that the direct effect of mycobacteria on macrophage shape might be mediated through TLR2-dependent PI3K activation.

Animals↗
PubMed1998

Spreading of the immune response from 52 kDaRo and 60 kDaRo to calreticulin in experimental autoimmunity.

Calreticulin (CR) is widely recognized as a new human autoantigen but there are conflicting data concerning its relationship with the Ro(SS-A) ribonucleoprotein (RNP). Recent evidence suggests that CR binds to 52 kDaRo (Ro52) by a protein/protein interaction and binds to hY RNA and rubella virus RNA. Other studies have shown that initiation of immunity to either Ro52 or 60 kDaRo (Ro60) can lead to reciprocal spreading of autoimmunity to Ro60 or Ro52, respectively, and induce anti-La autoantibodies in some strains of mice. These findings support a physical association of these polypeptides in Ro/La complexes. To test the hypothesis that CR is physically associated with Ro52 and/or Ro60 we examined the sera of Ro52-, Ro60- and La-immunized mice for intermolecular spreading to CR. Immune sera from BALB/c and C3H/HeJ mice immunized with recombinant 6xHis-mouse Ro52, 6xHis-human Ro60 or 6xHis-human La were tested for reactivity by ELISA and immunoblotting with a full-length human CR protein expressed as a soluble maltose binding protein fusion protein (CR-MBP). Five of the six Ro52-immunized C3H/HeJ mice sera and all six Ro60-immunized C3H/HeJ mice sera reacted with the CR-MBP (but not a MBP control) on ELISA. In the BALB/c group, the responder rate was lower with one in six of the Ro52-immunized and one in five of the Ro60-immunized mice spreading to CR. In contrast, none of the BALB/c or C3H/HeJ mice which was immunized with La showed evidence of a recruited anti-CR antibody response. Immunoblotting of the different recombinant proteins with immune sera from the C3H/HeJ mice confirmed the specificity of the initial and recruited antibody responses. The spreading of immunity from Ro52 and Ro60 to CR in Ro-immunized mice suggests that a subpopulation of CR or CR-like molecules must associate under certain circumstances with Ro52 and Ro60 polypeptides in vivo, possibly as Ro/CR complexes concentrated in surface membrane blebs of apoptotic cells. The lack of spreading to CR in La-immunized mice suggests that CR may be associated with a subpopulation of Ro particles from which La has already dissociated.

Animals↗
PubMed2005

FGF signalling and the mechanism of mesoderm spreading in Drosophila embryos.

FGF signalling is needed for the proper establishment of the mesodermal cell layer in Drosophila embryos. The activation of the FGF receptor Heartless triggers the di-phosphorylation of MAPK in the mesoderm, which accumulates in a graded fashion with the highest levels seen at the dorsal edge of the mesoderm. We have examined the specific requirement for FGF signalling in the spreading process. We show that only the initial step of spreading, specifically the establishment of contact between the ectoderm and the mesoderm, depends upon FGF signalling, and that unlike the role of FGF signalling in the differentiation of heart precursors this function cannot be replaced by other receptor tyrosine kinases. The initiation of mesoderm spreading requires the FGF receptor to possess a functional kinase domain, but does not depend upon the activation of MAPK. Thus, the dispersal of the mesoderm at early stages is regulated by pathways downstream of the FGF receptor that are independent of the MAPK cascade. Furthermore, we demonstrate that the activation of MAPK by Heartless needs additional cues from the ectoderm. We propose that FGF signalling is required during the initial stages of mesoderm spreading to promote the efficient interaction of the mesoderm with the ectoderm rather than having a long range chemotactic function, and we discuss this in relation to the cellular mechanism of mesoderm spreading.

Animals↗
PubMed2002

Src family tyrosine kinases regulate adhesion-dependent tyrosine phosphorylation of 5'-inositol phosphatase SHIP2 during cell attachment and spreading on collagen I.

Inositol phosphatases play an important role in regulation of cellular levels of lipid second messengers. Recently we have reported a novel function for SHIP2 in cell adhesion and spreading. In this study, we further characterize the adhesion-dependent tyrosine phosphorylation of SHIP2 and examine the role of Src family tyrosine kinases in the regulation of SHIP2 function. SHIP2 was tyrosine phosphorylated during cell attachment and spreading on collagen I, but not on fibronectin, collagen IV, laminin or poly-L-lysine. SHIP2 tyrosine phosphorylation, induced by plating on a collagen-I-coated surface but not by epidermal growth factor or insulin treatment of cells, was completely blocked by small molecule inhibitors of Src family kinases. SHIP2 could be phosphorylated in vitro by recombinant Src kinase and tyrosines 986-987 in the NPXY motif of SHIP2 appear to be the major sites of phosphorylation for Src both in vitro and in vivo. An activated form of Src induced strong tyrosine phosphorylation of SHIP2 while a dominant-negative form decreased collagen-I-dependent SHIP2 phosphorylation. SHIP2 associated with the adapter protein Shc via its NPXY motif during cell spreading on collagen I in a Src activity-dependent manner. Expression of SHIP2 with mutated NPXY motif caused deregulation of lamellipodia formation during spreading on collagen I. These observations indicate that SHIP2 is regulated by Src family kinases during cell attachment and spreading on collagen I and suggest an important role for SHIP2 as a part of a signaling pathway that regulates actin cytoskeleton remodeling.

Adaptor Proteins, Signal Transducing↗
PubMed2003

EphrinA1 inactivates integrin-mediated vascular smooth muscle cell spreading via the Rac/PAK pathway.

Interactions between the Eph receptor tyrosine kinase and ephrin ligands transduce short-range signals regulating axon pathfinding, development of the cardiovascular system, as well as migration and spreading of neuronal and non-neuronal cells. Some of these effects are believed to be mediated by alterations in actin dynamics. The members of the small Rho GTPase family elicit various effects on actin structures and are probably involved in Eph receptor-induced actin modulation. EphrinA1 is proposed to contribute to angiogenesis as it is strongly expressed at sites of neovascularization. Moreover, angiogenic factors induce the expression of ephrinA1 in endothelial cells. In this study, using rat vascular smooth muscle cells (VSMCs), we investigated the contribution of the small Rho GTPases in ephrinA1-induced integrin inactivation. EphrinA1 did not significantly affect early adhesion of VSMCs on purified laminin or fibronectin, but strongly impaired cell spreading. The Rho kinase inhibitor Y-27632 partly reversed the ephrinA1 effect, suggesting involvement of Rho in this model. However, inhibition of RhoA synthesis with short interfering (si)RNA had a modest effect, suggesting that RhoA plays a limited role in ephrinA1-mediated inhibition of spreading in VSMCs. The ephrinA1-mediated morphological alterations correlated with inhibition of Rac1 and p21-activated kinase 1 (PAK1) activity, and were antagonized by the expression of a constitutively active Rac mutant. Moreover, repression of Rac1 synthesis with siRNA amplifies the ephrinA1-induced inhibition of spreading. Finally, sphingosine-1-phosphate (S1P), a lipid mediator known to inhibit Rac activation in VSMCs amplifies the ephrinA1 effect. In conclusion, our results emphasize the role of the Rac/PAK pathway in ephrinA1-mediated inhibition of spreading. In this way, ephrinA1, alone or in synergy with S1P, can participate in blood vessel destabilization, a prerequisite for angiogenesis.

Animals↗
PubMed1993

Endothelial cell attachment and spreading on human tenascin is mediated by alpha 2 beta 1 and alpha v beta 3 integrins.

Human umbilical vein endothelial cells were found to attach and partially spread on human tenascin. The attachment of endothelial cells to tenascin results in elongated cells with interconnecting processes and is distinct from the flattened appearance of endothelial cells on fibronectin, collagen, vitronectin or laminin substrata, suggesting a role for tenascin in modulating cell adhesion and motility. Endothelial attachment to tenascin was partially inhibitable by the SRRGDMS peptide derived from human tenascin and completely inhibitable by anti-integrin antibodies to alpha 2 beta 1 and alpha v beta 3. Endothelial cell attachment to tenascin could be inhibited up to 80% with anti-alpha 2 and anti-beta 1 monoclonal antibodies P1E6 and P4C10, respectively, and this was associated with a complete loss in cell spreading. In contrast, pretreatment of endothelial cells with the anti-alpha v beta 3 monoclonal antibody LM609, resulted in a 35% inhibition in cell attachment but did not alter cell spreading. In combination the anti-alpha 2 and anti-alpha v beta 3 antibodies, could completely abrogate cell spreading and attachment to tenascin-coated surfaces. Affinity purification of 125I-labeled endothelial cell extract on a tenascin matrix column followed by immunoprecipitation with monoclonal antibodies to different integrin alpha and beta subunits resulted in the identification of alpha 2 beta 1 and alpha v beta 3 integrins, respectively, as tenascin binding receptors. Collagen affinity-purified alpha 2 beta 1 receptor from endothelial cells bound not only to collagen and laminin but also to tenascin in a radio receptor binding assay. The results demonstrate that alpha 2 beta 1 and alpha v beta 3 mediate distinct endothelial cell interactions with tenascin; cell spreading and cell binding, respectively. Binding by alpha v beta 3 is mediated by the SRRGDMS site on tenascin, whereas the alpha 2 beta 1 binding site remains undefined. The interaction of alpha 2 beta 1 and alpha v beta 3 with tenascin may be regulated in a cell type-specific manner as evidenced by the binding of endothelial cell alpha 2 beta 1 and alpha v beta 3 to tenascin, and the lack of binding by the same receptors on osteosarcoma MG63 to tenascin.

Amino Acid Sequence↗