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PubMed2004

Atomic dynamics and Marangoni films during liquid-metal spreading.

Despite its apparent simplicity, spreading of liquid metals at high temperatures has defied description and generalization. Wetting at high temperature is usually accompanied by interdiffusion and chemical reaction, but the forces that drive reactive spreading and the mechanisms that control its kinetics have been very poorly understood. The unsolved challenge has been to link macroscopic measurements such as the dynamic contact angle or the speed of a moving liquid front to phenomena occurring at the microscopic and even atomic level in the vicinity of the triple solid-liquid-vapour junction. We have taken a big step towards meeting this challenge. Our systematic analysis of the spreading of metal-metal systems with varying degrees of mutual solubility allows us to report on the fundamental differences between the mechanisms controlling spreading of organic liquids and liquid metals and on formation of Marangoni films driven by surface-tension gradients in high-temperature systems.

Computer Simulation↗
PubMed2006

Spreading of silent chromatin: inaction at a distance.

One of the oldest unsolved problems in genetics is the observation that gene silencing can 'spread' along a chromosome. Although spreading has been widely perceived as a process of long-range assembly of heterochromatin proteins, such 'oozing' might not apply in most cases. Rather, long-range silencing seems to be a dynamic process, involving local diffusion of histone-modifying enzymes from source binding sites to low-affinity sites nearby. Discontinuous silencing might reflect looping interactions, whereas the spreading of continuous silencing might be driven by the processive movement of RNA or DNA polymerases. We review the evidence for the spreading of silencing in many contexts and organisms and conclude that multiple mechanisms have evolved that silence genes at a distance.

Animals↗
PubMed1999

Laminin mediates tethering and spreading of colon cancer cells in physiological shear flow.

Under the physiological shear condition, cultured colon cancer cells bound to laminin (LM), but not to fibronectin or vitronectin. Most of the tethered cells did not roll, but arrested immediately and spread within 10-30 min on LM under the continuous presence of shear flow. The tethering of Colo201 was partially inhibited by monoclonal antibodies (mAbs) to alpha6 integrin and a combination of mAbs to beta1 and beta4 integrins, but not by mAb to 67KD laminin receptor. Some Colo201 cells still tethered at 4 degrees C. This suggests that alpha6beta1 and alpha6beta4 integrins participate in Colo201 tethering on LM, although other non-integrin molecules play roles. In contrast, the spread of Colo201 was effectively inhibited by the mAbs to integrin alpha2, alpha6 and beta1 chains. The effect of anti-alpha2 plus anti-alpha6 mAbs was almost equal to anti-beta1, suggesting that Colo201 cells mainly use alpha2beta1 and alpha6beta1 integrins for spreading on LM. When the cells were perfused on subconfluent endothelial cells (HUVEC) cultured on LM, they did not tether on HUVEC but did on coated LM exposed at intercellular gap area. Immunohistochemistry revealed that LM abundantly existed in the cytosol of human portal and hepatic vein endothelial cells. These data suggest that LM can mediate from tethering to spreading of colon cancer cells under the blood flow and plays an essential role in haematogeneous metastasis.

Antibodies, Monoclonal↗
PubMed1998

Rho-dependent cell spreading activated by E.coli cytotoxic necrotizing factor 1 hinders apoptosis in epithelial cells.

Cell-cell and cell-matrix interactions play a pivotal role in numerous cell functions including cell survival and death. In this work, we report evidence that the Rho-dependent cell spreading activated by a protein toxin from E. coli, the cytotoxic necrotizing factor 1 (CNF1), is capable of hindering apoptosis in HEp-2 cells. In addition to the promotion of cell spreading, CNF1 protects cells from the experimentally-induced rounding up and detachment and improves the ability of cells to adhere to each other and to the extracellular matrix by modulating the expression of proteins related to cell adhesion. In particular, the expression of integrins such as alpha 5, alpha 6 and alpha v, as well as of some heterotypic and homotypic adhesion-related proteins such as the Focal Adhesion Kinase, E-cadherin, alpha and beta catenins were significantly increased in cells exposed to CNF1. Our results suggest, however, that the promotion of Rho-dependent cell spreading is the key mechanism in protecting cells against apoptosis rather than cell adhesion per se. A toxin inducing cell spreading without activating Rho, such as Cytochalasin B, was in fact ineffective in favouring cell survival. These data are of relevance (i) for the understanding of the role of the actin-dependent and especially Rho-dependent cellular activities involved in apoptosis regulation and (ii) in providing some clues to understanding the mechanisms by which bacteria, by controlling cell fate, might exert their pathogenic activity.

Actins↗
PubMed2005

Listeria monocytogenes exploits ERM protein functions to efficiently spread from cell to cell.

Cell-to-cell spread is a fundamental step in the infection cycle of Listeria monocytogenes that strictly depends on the formation of bacteria-induced protrusions. Since Listeria actin tails in the protrusions are tightly associated with the plasma membrane, we hypothesised that membrane-cytoskeleton linkers would be required for initiating and sustaining their formation and the subsequent cell-to-cell spread. We have found that ezrin, a member of the ezrin, radixin and moesin (ERM) family that functions as a key membrane-cytoskeleton linker, accumulates at Listeria protrusions. The ability of Listeria to induce protrusions and effectively spread between adjacent cells depends on the interaction of ERM proteins with both a membrane component such as CD44 and actin filaments. Interfering with either of these interactions or with ERM proteins phosphorylation not only reduces the number of protrusions but also alters their morphology, resulting in the formation of short and collapsed protrusions. As a consequence, Listeria cell-to-cell spread is severely impaired. Thus, ERM proteins are exploited by Listeria to escape the host immune response and to succeed in the development of the infection.

Actin Cytoskeleton↗
PubMed2002

Paxillin null embryonic stem cells are impaired in cell spreading and tyrosine phosphorylation of focal adhesion kinase.

Paxillin is a focal-adhesion associated protein implicated in the regulation of integrin signaling and organization of the actin cytoskeleton. Paxillin associates with numerous signaling molecules including adaptor molecules (p130Cas, CRK), kinases (FAK, Pyk2, PAK and SRC), tyrosine phosphatases (PTP-PEST), ARF-GAP proteins (p95pkl, PAG3) and papillomavirus E6 oncoproteins. Although paxillin is tyrosine phosphorylated in cellular processes such as cell attachment and spreading, little direct evidence is available about paxillin's role in these events. Targeted gene disruption was used to generate paxillin null mouse embryonic stem (ES) cells and paxillin null differentiated cells. Paxillin null ES cells exhibit delayed spreading on integrin binding substrates fibronectin and laminin, and there is reduced tyrosine phosphorylation of Focal Adhesion Kinase (FAK). Both of these phenotypes are recovered in paxillin knockout cells upon exogenous re-expression of paxillin. The individual LD motifs of paxillin that are binding sites for FAK, vinculin and ARF-GAP proteins, as well as tyrosine residues that when phosphorylated create binding sites for CRK family members, are dispensable for FAK phosphorylation and early cell spreading. These results demonstrate that paxillin contributes to attachment-dependent tyrosine phosphorylation of FAK and early cell spreading in ES cells.

Amino Acid Motifs↗
PubMed2001

Sulphatides trigger polymorphonuclear granulocyte spreading on collagen-coated surfaces and inhibit subsequent activation of 5-lipoxygenase.

Sulphatides are sulphate esters of galactocerebrosides that are present on the surfaces of many cell types and act as specific ligands to selectins. The present study was undertaken to investigate the effect of sulphatides on polymorphonuclear granulocyte (PMN) attachment, spreading and 5-lipoxygenase (5-LO) metabolism. Sulphatides, but not non-sulphated galactocerebrosides, dose-dependently enhanced attachment to collagen, as measured by the myeloperoxidase assay. Studies with blocking antibodies indicated that the increased attachment was mediated by CD11b/CD18 (Mac-1) beta 2 integrin. Scanning electron microscopy indicated that sulphatides also greatly enhanced the degree of cell spreading. In PMNs treated in suspension, sulphatides had no effect on the ionophore A23187-stimulated release of arachidonic acid and the synthesis of 5-LO metabolites. In contrast, in PMNs attached to collagen, the enzymic conversion of arachidonic acid by 5-LO was inhibited by sulphatides. Inhibition of 5-LO metabolism by sulphatides was observed even in the presence of exogenous substrate, suggesting that sulphatides directly inhibited 5-LO action. Consistent with this, sulphatides interfered with ionophore-induced translocation of the 5-LO to the nuclear envelope. Substances competing with sulphatide binding to cells, like dextran sulphate, or a strong inhibitor of cell spreading, like the actin-polymerizing agent jasplakinolide, prevented the effects of sulphatides on PMN attachment and spreading and leukotriene synthesis. We conclude that shape changes occurring in response to sulphatides specifically impair PMN leukotriene synthesis by inhibiting translocation of 5-LO.

Animals↗
PubMed2005

Regulation of FAK Ser-722 phosphorylation and kinase activity by GSK3 and PP1 during cell spreading and migration.

In addition to tyrosine sites, FAK (focal adhesion kinase) is phosphorylated on multiple serine residues. In the present study, the regulation of two of these sites, Ser-722 (S1) and Ser-911 (S4), was investigated. Phosphorylation of S1 (but not S4) decreased in resuspended cells, and recovered during spreading on fibronectin, indicating adhesion-dependent regulation. GSK3 (glycogen synthase kinase 3) inhibitors decreased S1 phosphorylation, and siRNA (short interfering RNA) silencing indicated further the involvement of GSK3beta. Furthermore, GSK3beta was found to become activated during cell spreading on fibronectin, and to physically associate with FAK. S1 phosphorylation was observed to decrease in wounded cell monolayers, while GSK3beta underwent inactivation and later was observed to increase to the original level within 24 h. Direct phosphorylation of S1, requiring pre-phosphorylation of Ser-726 in the +4 position, was demonstrated using purified GSK3 and a synthetic peptide containing FAK residues 714-730. An inhibitory role for S1 phosphorylation in FAK signalling was indicated by findings that both alanine substitution for S1 and dephosphorylation of S1 by PP1 (serine/threonine protein phosphatase type-1) resulted in an increase in FAK kinase activity; likewise, this role was also shown by cell treatment with the GSK3 inhibitor LiCl. The inhibitory role was confirmed by the finding that cells expressing FAK with alanine substitution for S1 displayed improved cell spreading and faster migration in wound-healing and trans-well assays. Finally, the finding that S1 phosphorylation increased in cells treated with the PP1 inhibitor okadaic acid indicated targeting of this site by PP1. These results indicate an additional mechanism for regulation of FAK activity during cell spreading and migration, involving Ser-722 phosphorylation modulated through the competing actions of GSK3beta and PP1.

Amino Acid Sequence↗
PubMed2003

Factors affecting the spread of bupivacaine in the adult thoracic paravertebral space.

Factors affecting the spread of bupivacaine in the paravertebral space were investigated in patients undergoing paravertebral nerve blocks for the treatment of chronically painful conditions. Injections of bupivacaine 0.5%, 10-15 ml mixed with depomedrone up to 80 mg were repeated at 2-wk intervals up to a maximum of four times. A blinded observer mapped out the subsequent distribution of sensory loss to cold on both sides of the torso at 5-min intervals after each injection. Age, sex, height and weight did not correlate with the block; nor did injectate volume, mass of bupivacaine, previous posterolateral thoractomy and spread of radiocontrast. Injections repeated at 2-wk intervals in the same patient resulted in different degrees of spread that were unrelated to one another. Time to peak onset of blockade was 40 min in 95% of patients. A single bolus of bupivacaine produces a safe but unpredictable block. Yet to be defined physical properties and anatomical factors are probably key determinants of the spread of bupivacaine in the paravertebral space. This single bolus technique may be better supplanted by a reversion to the older multiple level injection technique.

Adult↗
PubMed2002

In situ ablation of experimental liver metastases delays and reduces residual intrahepatic tumour growth and peritoneal tumour spread compared with hepatic resection.

BACKGROUND: The aim of this study was to evaluate the influence of in situ ablation and hepatic resection of experimental liver metastases on residual intrahepatic tumour growth and macroscopic peritoneal tumour spread. METHODS: Two colonic carcinomas (CC 531) were implanted into 90 WAG rat livers, one in the right liver lobe (untreated tumour) and one in the left liver lobe (treated tumour) of each rat. The animals were randomized into two test groups and a sham-operated control group. Animals in group 1 received in situ ablation (laser-induced thermotherapy) of the treated tumour. Rats in group 2 were submitted to partial hepatectomy. Untreated tumour volumes were calculated and the incidence of macroscopic peritoneal spread was determined at different times. RESULTS: After 21 days median (95 per cent confidence interval) volumes of untreated tumours were 507 (282) mm(3) in group 1, 2096 (994) mm(3) in group 2 and 1896 (755) mm(3) in group 3. Compared with values obtained before treatment, growth of the untreated tumours had increased significantly after 4 days in group 2, after 7 days in group 3 and after 10 days in group 1. Macroscopic peritoneal tumour spread was detected in six of 30 animals in group 1 (laser), in 20 of 30 in group 2, and in 24 of 30 in group 3. CONCLUSION: Compared with hepatic resection, in situ ablation of experimental liver metastases delays and reduces residual intrahepatic tumour growth and macroscopic peritoneal tumour spread.

Animals↗
PubMed2000

Survival of Salmonella in peanut butter and peanut butter spread.

In 1996, the first documented outbreak of salmonellosis associated with the consumption of peanut butter was reported. This study was undertaken to determine survival characteristics of high (5.68 log10 cfu g(-1)) and low (1.51 log10 cfu g(-1)) inocula of a five-serotype mixture of Salmonella in five commercial peanut butters and two commercial peanut butter spreads. Populations in samples inoculated with 5.68 log10 cfu g(-1) and stored for 24 weeks at 21 or 5 degrees C decreased 4.14-4.50 log10 cfu g(-1) and 2.86-4.28 log10 cfu g(-1), respectively, depending on the formulation. The order of retention of viability was: peanut butter spreads > traditional (regular) and reduced sugar, low-sodium peanut butters > natural peanut butter. Differences in rates of inactivation are attributed to variation in product composition as well as size and stability of water droplets in the colloidal matrix, which may influence nutrient availability. With the exception of natural peanut butter, products initially inoculated with 1.51 log10 cfu of Salmonella g(-1) (32 cfu g(-1)) were positive for the pathogen after storage for 24 weeks at 5 degrees C. At 21 degrees C, however, with the exception of one peanut butter spread, all products were negative for Salmonella after storage for 24 weeks. Post-process contamination of peanut butter and spreads with Salmonella may to result in survival in these products for the duration of their shelf life at 5 degrees C and possibly 21 degrees C, depending on the formulation.

Arachis↗
PubMed1996

Identification and characterization of ispA, a Shigella flexneri chromosomal gene essential for normal in vivo cell division and intracellular spreading.

The virulent phenotype of Shigella requires loci on the chromosome as well as on the large virulence plasmid, and is regulated via a complex web of interactions amongst various chromosomal and large plasmid genes. To further investigate the role of chromosomal loci in virulence, we performed random Tn10 mutagenesis in Shigella flexneri YSH6000T, and isolated an avirulent mutant (V3404) incapable of spreading throughout an epithelial cell monolayer. Although V3404 initially spread intercellularly at the same rate as the wild-type, it gradually slowed down and ceased spreading as a result of increasing defects in cell division, leading to the formation of long filamentous bacteria lacking septa, trapped within cells. In addition, the mutation affected the ability of V3404 to polymerize actin, a prerequisite for intra- and inter-cellular spreading ability. Sequencing of Tn10-flanking DNA revealed that the mutated gene, designated ispA (intracellular septation), was equivalent to a previously sequenced but uncharacterised gene of Escherichia coli located between trp and tonB. Using E. coli sequence data, we cloned the ispA gene from the YSH6000T chromosome and found that it complemented the V3404 mutation. Nucleotide sequencing and in vitro expression experiments revealed that ispA coded for a small (21 kDa), very hydrophobic protein. These results thus show that ispA is an essential virulence gene affecting several functions of the virulence process.

Actins↗
PubMed2002

Restricted specificity of intermolecular spreading to endogenous La (SS-B) and 60 kDa Ro (SS-A) in experimental autoimmunity.

Intermolecular spreading of humoral autoimmunity to different components of the Ro (SS-A) and La (SS-B) ribonucleoprotein (RNP) complex has been reported following immunization with a single component of the complex. Although the immune response to the immunizing antigen is polyclonal and diversified, little is known about the specificity of the recruited autoimmune responses to the endogenous Ro and La antigens which drive B-cell spreading. To determine the specificity of intermolecular spreading to La, we examined sera from 52 kDa Ro (Ro52)- and 60 kDa Ro (Ro60)-immunized C3H/HeJ mice for reactivity with recombinant fragments spanning endogenous mouse (m)La by enzyme-linked immunosorbent assay (ELISA) and immunoblotting. Sera from mice primed and boosted with recombinant Ro52 and Ro60 showed reactivity restricted to the COOH-terminal fragment of mLa (aa361-415). The recruited anti-La response was species-specific, cross-reacting weakly with the corresponding region on the human La molecule, and was abrogated by the preabsorption of the Ro-immune sera with mLa 361-415. Analogous experiments using recombinant mRo60 fragments spanning the mRo60 molecule revealed a similar pattern of oligoclonality in the specificity of anti-Ro60 autoimmunity following active immunization with La and Ro52. These results suggest that intermolecular-intrastructural T-B help is limiting in this model, and reveal unsuspected immunodominance of selected Ro-La epitopes in the spreading of the autoantibody response to these structures. The focusing of the recruited autoantibody response to these COOH-terminal regions of the Ro and La polypeptides may also reflect the surface accessibility of these regions in La-Ro RNP.

Animals↗
PubMed2000

Perineural spread leading to orbital invasion from skin cancer.

Orbital and intracranial invasion from skin cancer is an uncommon but serious consequence of skin cancer located around the orbit, particularly the forehead. Perineural spread is an aggressive manifestation of skin cancer similar to lymph node metastases. Such spread can provide access to the orbit and squamous cell carcinoma is the most common histology reported. Treatment should be directed at preventing such orbital spread. Adjuvant radiotherapy is strongly recommended. Disease may present in an advanced state within the orbit or beyond the orbital apex and involve the cavernous sinus. Palliative radiotherapy should be considered in such advanced cases. Presented are the cases of four patients treated for advanced orbital and intracranial spread from periorbital skin cancer.

Aged↗
PubMed2000

Functional connections and epileptic spread between hippocampus, entorhinal cortex and amygdala in a modified horizontal slice preparation of the rat brain.

The hippocampus, the entorhinal cortex and the amygdala are interconnected structures of the limbic system that are implicated in memory and emotional behaviour. They demonstrate synaptic plasticity and are susceptible to development of temporal lobe epilepsy, which may lead to emotional and psychological disturbances. Their relative anatomical disposition has limited the study of neurotransmission and epileptic spread between these three regions in previous in vitro preparations. Here we describe a novel, modified-horizontal slice preparation that includes in the same plane the hippocampus, entorhinal cortex and amygdala. We found that, following application of bicuculline, each region in our preparation could generate spontaneous bursts that resembled epileptic interictal spikes. This spontaneous activity initiated in the hippocampal CA3/2 region, from where it propagated and controlled the activity in the entorhinal cortex and the amygdala. We found that this spontaneous bursting activity could spread via two different pathways. The first pathway comprises the well-known subiculum-entorhinal cortex-perirhinal cortex-amygdala route. The second pathway consists of a direct connection between the CA1 region and perirhinal cortex, through which the hippocampal bursting activity can spread to the amygdala while bypassing the entorhinal cortex. Thus, our experiments provide a new in vitro model of initiation and spread of epileptic-like activity in the ventral part of the limbic system, which includes a novel, fast and functional connection between the CA1 region and perirhinal cortex.

Action Potentials↗
PubMed1998

A comparison of the spread of three formulations of botulinum neurotoxin A as determined by effects on muscle function.

The purpose of these experiments was to compare the spread of three formulations of botulinum neurotoxin A. A gelatin/phosphate buffer (C), DysportR (D {0.5 U}, BotoxR (B {0.167 U}), or a purified preparation of botulinum neurotoxin A [Bont A] (BA {0.5 U}) was injected into the tibialis anterior of male, Wistar rats. After 4 days, the adjacent extensor digitorum longus muscle was isolated in situ and the nerve was maximally stimulated to determine contractile properties and the rate of fatigue. There were no differences in body or muscle weights between any of the groups after 4 days of treatment. Maximal twitch and tetanic tensions were decreased reverse similar 25% (p < 0.05) in all treatment groups compared to C. In addition, rate of tension development was significantly less in all treatment groups compared to C but one-half relaxation time and time to peak tension were not different between any groups. Fatigue of the muscle was significantly faster in all groups compared to C but there was no difference between treatment groups. These data indicated that botulinum toxin A injected intramuscularly was likely to spread to adjacent muscles but that the spread was not different between the three formulations tested. The effect of the spread ranged from a slight to a severe reduction in maximal tension but this did not occur in all animals studied. Copyright Rapid Science Ltd

Journal Article↗
PubMed1999

[The extracapsular spread of cervical lymph node metastases: the diagnostic value of computed tomography].

OBJECTIVE: To assess the value of computed tomography in the determination of extracapsular neoplastic spread and soft tissue infiltration of cervical lymph nodes. MATERIALS AND METHODS: Prospectively 165 CT reports of patients with squamous cell carcinoma in the head-neck region were compared with the histologic specimens after neck dissection. RESULTS: CT reached a sensitivity of 80.9% in the determination of extra-capsular neoplastic spread. The infiltration of cervical muscles and the jugular vein was always determined but-often diagnosed false-positive. Therefore, the overall specificity in determining extracapsular neoplastic spread was low with 72.7%. CONCLUSIONS: The accuracy of computed tomography (76.3%) in the determination of extracapsular neoplastic spread, infiltration of cervical muscles and the jugular vein is only partially satisfying.

Carcinoma, Squamous Cell↗
PubMed1999

Spreading of a surfactant monolayer on a thin liquid film: Onset and evolution of digitated structures.

We describe the response of an insoluble surfactant monolayer spreading on the surface of a thin liquid film to small disturbances in the film thickness and surfactant concentration. The surface shear stress, which derives from variations in surfactant concentration at the air-liquid interface, rapidly drives liquid and surfactant from the source toward the distal region of higher surface tension. A previous linear stability analysis of a quasi-steady state solution describing the spreading of a finite strip of surfactant on a thin Newtonian film has predicted only stable modes. [Dynamics in Small Confining Systems III, Materials Research Society Symposium Proceedings, edited by J. M. Drake, J. Klafter, and E. R. Kopelman (Materials Research Society, Boston, 1996), Vol. 464, p. 237; Phys. Fluids A 9, 3645 (1997); O. K. Matar Ph.D. thesis, Princeton University, Princeton, NJ, 1998]. A perturbation analysis of the transient behavior, however, has revealed the possibility of significant amplification of disturbances in the film thickness within an order one shear time after the onset of flow [Phys. Fluids A 10, 1234 (1998); "Transient response of a surfactant monolayer spreading on a thin liquid film: Mechanism for amplification of disturbances," submitted to Phys. Fluids]. In this paper we describe the linearized transient behavior and interpret which physical parameters most strongly affect the disturbance amplification ratio. We show how the disturbances localize behind the moving front and how the inclusion of van der Waals forces further enhances their growth and lifetime. We also present numerical solutions to the fully nonlinear 2D governing equations. As time evolves, the nonlinear system sustains disturbances of longer and longer wavelength, consistent with the quasi-steady state and transient linearized descriptions. In addition, for the parameter set investigated, disturbances consisting of several harmonics of a fundamental wavenumber do not couple significantly. The system eventually singles out the smallest wavenumber disturbance in the chosen set. The summary of results to date seems to suggest that the fingering process may be a transient response which nonetheless has a dramatic influence on the spreading process since the digitated structures redirect the flux of liquid and surfactant to produce nonuniform surface coverage. (c) 1999 American Institute of Physics.

Journal Article↗