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PubMed2000

Microstructure and dynamic surface properties of surfactant protein SP-B/dipalmitoylphosphatidylcholine interfacial films spread from lipid-protein bilayers.

Suspensions of dipalmitoylphosphatidylcholine (DPPC) bilayers containing 5, 10 or 20% (w/w) surfactant protein SP-B have been reconstituted and spread at air-liquid interfaces. Compression isotherms of DPPC/SP-B monolayers spread from these preparations were qualitatively comparable to the isotherms of the corresponding DPPC/SP-B monolayers spread from solvents. SP-B was squeezed-out at higher pressures from vesicle-spread films than from solvent-spread monolayers. SP-B caused a marked decrease on the rate of relaxation of DPPC collapse phases to equilibrium pressures in all the lipid/protein films assayed. This stabilizing effect was higher in vesicle-spread than in solvent-spread monolayers. Inclusion in the films of traces of the fluorescent probe NBD-PC (1 mol%) and use of a fluorescent derivative of SP-B labeled with a rhodamine derivative, Texas Red, allowed for direct observation of protein and lipid domains at the interface by epifluorescence microscopy. Upon compression, SP-B altered the packing of phospholipids in the bilayer-spread films, observed as a SP-B-induced reduction of the area of liquid-condensed domains, in a way similar to its effect in solvent-spread monolayers. SP-B was not associated with condensed regions of the films. Fluorescence images from vesicle-spread films showed discrete fluorescent aggregates that could be consistent with the existence of lipid-protein vesicles in close association with the monolayer. Both the retention of SP-B at higher surface pressures and the greater stability of collapse phases of DPPC/SP-B films prepared by spreading from liposomes in comparison to those spread from solvents can be interpreted as a consequence of formation of complex bilayer-monolayer interacting systems.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1990

Spreading of B16 F1 cells on laminin and its proteolytic fragments P1 and E8: involvement of laminin carbohydrate chains.

The properties of EHS laminin and its proteolytic fragments E8 and P1 to promote spreading of B16 F1 murine melanoma cells were studied in short-term adhesion assays. The cells exhibited similar attachment rates but distinct spread morphologies on laminin, P1, and E8 fragments. The extent of spreading and the shape of the cells were quantitatively defined by two geometrical parameters: the surface and the form factor. These parameters were computed with an automatic image analyzer. Wheat germ agglutinin (WGA), applied to laminin-coated substrates, totally blocked cell spreading, but did not modify attachment percentages. Under similar conditions, WGA partially inhibited cell spreading on the E8 fragment and had no effect on the P1 fragment. In Western blot analysis, P1 fragment, contrary to laminin and E8, did not bind WGA. Laminin galactosylation and cell treatment with alpha-lactalbumin, which should prevent cell galactosyltransferase (GalTase) from binding to N-acetylglucosamine (GlcNAc) residues of the substrate, had no effect on the spreading ability of B16 F1 cells. The role of laminin N-linked carbohydrate chains in the induction of B16 F1 cell spreading was studied further after endoglycosidase F (Endo F) treatment of the substrates. The loss of carbohydrate chains was estimated by the reduction of iodinated lectin binding and by SDS-PAGE. Endo F treatment of laminin (85% of WGA binding inhibition) and E8 (40-50%) had no effect on cell spreading. In contrast, Endo F treatment of P1 fragment (85% of Con A binding inhibition) reduced both cell surface and form factor of B16 F1 cells. These results suggest that: (i) other spreading systems may act in concert with or in place of GalTase/GlcNAc interactions, (ii) the N-linked sugar chains of P1, which are not recognized by WGA, are involved in the spreading process of B16 F1 cells on this fragment, (iii) the epitopes of E8 fragment and E8 domain in laminin which are responsible for spreading are differently masked by WGA, (iv) the binding of WGA to laminin may impair cell spreading by steric hindrance.

Animals↗
PubMed1987

Platelet thrombospondin mediates attachment and spreading of human melanoma cells.

Human platelet thrombospondin adsorbed on plastic promotes attachment and spreading of human G361 melanoma cells. Attachment is rapid, and spreading is maximal by 90 min with 60-90% of the attached cells spread. In contrast, thrombospondin promotes attachment but not spreading of human C32 melanoma cells, which attach and spread only on laminin substrates. The specificity of these interactions and the regions of the thrombospondin molecule involved in attachment and spreading were examined using proteolytic fragments of thrombospondin and by inhibition studies. The sulfated fucan, fucoidan, and monoclonal antibody A2.5, which is directed against the heparin-binding domain of thrombospondin, selectively inhibit spreading but only weakly inhibit attachment. Monoclonal antibodies against some other domains of thrombospondin, however, are potent inhibitors of attachment. The amino-terminal heparin-binding domain of thrombospondin does not promote attachment. Large fragments lacking the heparin-binding domain support attachment but not spreading of G361 cells. Attachment activity is lost following removal of the 18-kD carboxyl-terminal domain. These results suggest that at least two melanoma ligands are involved in cell attachment and spreading on thrombospondin. The carboxyl-terminal region and perhaps other regions of the molecule bind to receptor(s) on the melanoma surface that promote initial attachment but not cell spreading. Interaction of the heparin-binding domain with sulfated glycoconjugates on melanoma surface proteoglycans and/or sulfated glycolipids mediates spreading. Monoclonal antibodies A2.5 and C6.7 also reverse spreading of G361 cells growing on glass culture substrates, suggesting that binding to thrombospondin mediates attachment of these melanoma cells in culture.

Adsorption↗
PubMed1993

Moving and stationary actin filaments are involved in spreading of postmitotic PtK2 cells.

We have investigated spreading of postmitotic PtK2 cells and the behavior of actin filaments in this system by time-lapse microscopy and photoactivation of fluorescence. During mitosis PtK2 cells round up and at cytokinesis the daughter cells spread back to regain their interphase morphology. Normal spreading edges are quite homogenous and are not comprised of two distinct areas (lamellae and lamellipodia) as found in moving edges of interphase motile cells. Spreading edges are connected to a network of long, thin, actin-rich fibers called retraction fibers. A role for retraction fibers in spreading was tested by mechanical disruption of fibers ahead of a spreading edge. Spreading is inhibited over the region of disruption, but not over neighboring intact fibers. Using photoactivation of fluorescence to mark actin filaments, we have determined that the majority of actin filaments move forward in spreading edges at the same rate as the edge. As far as we are aware, this is the first time that forward movement of a cell edge has been correlated with forward movement of actin filaments. In contrast, actin filaments in retraction fibers remain stationary with respect to the substrate. Thus there are at least two dynamic populations of actin polymer in spreading postmitotic cells. This is supported by the observation that actin filaments in some spreading edges not only move forward, but also separate into two fractions or broaden with time. A small fraction of postmitotic cells have a spreading edge with a distinct lamellipodium. In these edges, marked actin polymer fluxes backward with respect to substrate. We suggest that forward movement of actin filaments may participate in generating force for spreading in postmitotic cells and perhaps more generally for cell locomotion.

Actin Cytoskeleton↗
PubMed1993

Requirement for diacylglycerol and protein kinase C in HeLa cell-substratum adhesion and their feedback amplification of arachidonic acid production for optimum cell spreading.

Release of arachidonic acid (AA) and subsequent formation of a lipoxygenase (LOX) metabolite(s) is an obligatory signal to induce spreading of HeLa cells on a gelatin substratum (Chun and Jacobson, 1992). This study characterizes signaling pathways that follow the LOX metabolite(s) formation. Levels of diacylglycerol (DG) increase upon attachment and before cell spreading on a gelatin substratum. DG production and cell spreading are insignificant when phospholipase A2 (PLA2) or LOX is blocked. In contrast, when cells in suspension where PLA2 activity is not stimulated are treated with exogenous AA, DG production is turned on, and inhibition of LOX turns it off. This indicates that the formation of a LOX metabolite(s) from AA released during cell attachment induces the production of DG. Consistent with the DG production is the activation of protein kinase C (PKC) which, as with AA and DG, occurs upon attachment and before cell spreading. Inhibition of AA release and subsequent DG production blocks both PKC activation and cell spreading. Cell spreading is also blocked by the inhibition of PKC with calphostin C or sphingosine. The inhibition of cell spreading induced by blocking AA release is reversed by the direct activation of PKC with phorbol ester. However, the inhibition of cell spreading induced by PKC inhibition is not reversed by exogenously applied AA. In addition, inhibition of PKC does not block AA release and DG production. The data indicate that there is a sequence of events triggered by HeLa cell attachment to a gelatin substratum that leads to the initiation of cell spreading: AA release, a LOX metabolite(s) formation, DG production, and PKC activation. The data also provide evidence indicating that HeLa cell spreading is a cyclic feedback amplification process centered on the production of AA, which is the first messenger produced in the sequence of messengers initiating cell spreading. Both DG and PKC activity that are increased during HeLa cell attachment to a gelatin substratum appear to be involved. DG not only activates PKC, which is essential for cell spreading, but is also hydrolyzed to AA. PKC, which is initially activated as consequence of AA production, also increases more AA production by activating PLA2.

Arachidonic Acid↗
PubMed2004

Bioeconomics of managing the spread of exotic pest species with barrier zones.

Exotic pests are serious threats to North American ecosystems; thus, economic analysis of decisions about eradication, stopping, or slowing their spread may be critical to ecosystem management. The proposed bioeconomic model assumes that the rate of population expansion can be reduced (even to negative values in a case of eradication) if certain management actions are taken along the population front. The area of management can be viewed as a dynamic barrier zone that moves together with the population front. The lower is the target rate of spread, the higher would be both benefits and costs of the project. The problem is to find the optimal target rate of spread at which the present value of net benefits from managing population spread reaches its maximum value. If a population spreads along an infinite habitat strip, the target rate of spread is optimal if the slope of the cost function versus the rate of spread is equal to the ratio of the average pest-related damage per unit time and unit area to the discount rate. In a more complex model where the potential area of expansion is limited, two local maxima of net benefits may exist: one for eradication and another for slowing the spread. If both maxima are present, their heights are compared and the strategy that corresponds to a higher value of net benefits is selected. The optimal strategy changes from eradication to slowing the spread and finally to doing nothing as the area occupied by the species increases. The model shows that slowing the spread of pest species generates economic benefits even if a relatively small area remains uninfested. The cost of slowing the spread can be estimated from a model of population expansion via establishment of isolated colonies beyond the moving front. The model is applied to managing the spread of the gypsy moth (Lymantria dispar) populations in the United States.

Animals↗
PubMed1985

The spreading of human normal glial and malignant glioma cells in culture. Studies on standard culture conditions.

Using three lines of human normal glial cells and four established lines of human malignant glioma cells we have studied cell spreading following seeding onto glass and plastic substrata. The cells were detached with EDTA and trypsin, suspended in EMEM with 10% calf serum and studied with time-lapse, phase-contrast cinematography in suspension and during attachment and spreading. Cells were fixed and prepared for light microscopy while in suspension and during the spreading process. They were also prepared for scanning and transmission electron microscopy at different times during spreading. The projected areas of stained cells, in suspension and at different stages of spreading, were measured morphometrically and the results compared statistically. The glial cells in suspension were often found to retain somewhat their shape from the previous monolayer. They spread radially outwards with even lamellar cytoplasm and peripheral ruffling, as a group more quickly than the malignant glioma cells. They also became polarized and started to translocate in a shorter time. The glioma cells were spherical in suspension and characterized by pronounced blebbing of the cell surface. Blebbing continued during spreading and was finally replaced by ruffling at the edge. The cells spread like the glial cells radially outwards but the lamellar cytoplasm was occasionally somewhat irregular. Cells from the glioma lines spread as groups slower than the glial cells but with individual rates for the different lines. One of the glioma lines appeared to spread more thinly than the glial cells. Cells which sedimented on top of other cells could not spread. Aggregations of cells spread and became polarized more quickly than single cells in all cases.

Cell Adhesion↗
PubMed1999

Spreads enriched with plant sterols, either esterified 4,4-dimethylsterols or free 4-desmethylsterols, and plasma total- and LDL-cholesterol concentrations.

In a 9-week study seventy-six healthy adult volunteers with an average age of 44 (SD 11) years, with baseline plasma total cholesterol levels below 8 mmol/l, received in a balanced, double-blind, crossover design, a total of three different table spreads for personal use. Two spreads were fortified either with free (non-esterified) vegetable-oil sterols, mainly from soyabean oil (31 g sterol equivalents/kg; 0.8 g/d) or sheanut-oil sterols (133 g sterol equivalents/kg; 3.3 g/d). One spread was not fortified (control). Average intake of spread was 25 g/d for 3 weeks. None of the spreads induced changes in blood clinical chemistry or haematology. Plasma total- and LDL-cholesterol concentrations were statistically significantly reduced by 3.8% and 6% (both 0.19 mmol/l) respectively, for the spread enriched with free soyabean-oil sterols compared with the control spread. The spread enriched with sheanut-oil sterols did not lower plasma total- and LDL-cholesterol levels. None of the plant-sterol-enriched spreads affected plasma HDL-cholesterol concentrations. Plasma-lipid-standardized concentrations of alpha- plus beta-carotene were not statistically significantly affected by the soyabean-oil sterol spread in contrast to lipid-standardized plasma lycopene levels which showed a statistically significant decrease (9.5%). These findings indicate that a daily intake of free soyabean-oil sterols as low as 0.8 g added to a spread is effective in lowering blood total- and LDL-cholesterol levels with limited effects on blood carotenoid levels. The lowering in total- and LDL-cholesterol blood levels due to consumption of the vegetable-oil-sterol-enriched spread may be helpful in reducing the risk of CHD for the population.

Adult↗
PubMed1988

Spreading depression and central nervous system pharmacology.

Spreading depression is a reversible response of brain tissue to a local insult. It has been postulated to be the physiological substrate for the aura phase of classic migraine. The properties and mechanisms of spreading depression were studied in the parietal neocortex of the alfentanil-anesthesized rat, by using a cup electrode that provided close control of the electrical stimulus while allowing specific ion (K+) and potential recordings to be made directly beneath the cathode, the region of origin of the stimulus-induced spreading depression. Cathodal stimulation caused the extracellular K+ concentration to rise, and spreading depressions were observed when this concentration exceeded 8-12 mM in the upper 100-200 microns of cortex. In some experiments extracellular [K+] continued to increase for 5-10 sec after termination of the stimulus, without detectable after-discharge in the potential record, before subsiding. While spreading depression could easily be induced by pressure on the cortex, local damage incidental to opening the dura rarely induced spreading depression. This suggests that a local (1-mm2) neurovascular injury is not likely to induce spreading depression--at least in normal cortex--and so is probably not the source of the spreading depression postulated to generate the aura of classic migraine. Mechanisms of spreading depression, and drugs that influence spreading depression, are reviewed, and possible uses of spreading depression in the pharmacology of the central nervous system are considered.

Animals↗
PubMed2000

Effects of chloride transport inhibition and chloride substitution on neuron function and on hypoxic spreading-depression-like depolarization in rat hippocampal slices.

Chloride fluxes play a crucial role in synaptic inhibition, cell pH regulation, as well as in cell volume control. In many neuropathological processes, cell swelling is a pivotal parameter, since cell volume changes and the dimension of the interstitial space critically modulate synchronized neuronal activity as well as the tissue's susceptibility to seizures or spreading depression. This study therefore focuses on the effects of different Cl(-) transport inhibitors and Cl(-) substitution on neuronal function and hypoxia-induced changes in rat hippocampal tissue slices. Orthodromically evoked focal excitatory postsynaptic potentials were depressed by furosemide (2mM), 4,4'-diisothiocyanatostilbene-2, 2'-disulfonic acid (1mM) and Cl(-) substitution by methylsulfate, but were enhanced by 4,4'-dinitrostilbene-2,2'-disulfonic acid (1mM). All four treatments induced multiple population spike firing in response to single orthodromic volleys, suggesting reduced synaptic inhibition. Antidromic population spikes increased following Cl(-) withdrawal, were unaffected in the presence of furosemide and 4, 4'-dinitrostilbene-2,2'-disulfonic acid, but were abolished by 4, 4'-diisothiocyanatostilbene-2,2'-disulfonic acid. The amplitude of the hypoxic spreading-depression-like extracellular potential shift was reduced by furosemide, 4,4'-diisothiocyanatostilbene-2, 2'-disulfonic acid and Cl(-) withdrawal, i.e. by the same treatments that depressed orthodromically evoked postsynaptic potentials. Furosemide prolonged the time to onset and the duration of the spreading-depression-like extracellular potential shift, while 4, 4'-dinitrostilbene-2,2'-disulfonic acid shortened the time to onset. Spreading-depression-related cell swelling was recorded as the shrinkage of relative interstitial space, which was measured as tetramethylammonium-chloride space. Neither the Cl(-) transport inhibitors nor Cl(-) withdrawal had any detectable effect on spreading-depression-related cell swelling. CA1 pyramidal neurons usually hyperpolarized during drug application and their input resistance decreased. Cl(-) withdrawal increased their input resistance and caused spontaneous burst firing. Hypoxia caused the expected spreading-depression-like rapid, near complete depolarization of single pyramidal neurons and drastically reduced their input resistance. The three Cl(-) transport inhibitors and Cl(-) withdrawal delayed the onset of the hypoxic depolarization. In low Cl(-) solutions, the apparent threshold potential at which spreading depression was triggered shifted to more positive membrane potentials. The final voltage of the hypoxic depolarization was, however, not affected. It appears from these results that the reduction in the hypoxic spreading-depression-like extracellular potential shifts by Cl(-) transport inhibitors is at least partially attributable to desynchronization of depolarization, not to decreased depolarization in individual cells. Other contributing factors could be changes in recording conditions, depression of swelling-induced amino acid release from glial cells and unspecific side-effects of the applied drugs. Desynchronization could also account for the delayed spreading-depression onset. It is concluded that Cl(-) fluxes play a role in the triggering of spreading depression, but the spreading-depression-like depolarization itself or its self-regenerative character is not mediated by Cl(-).

Animals↗
PubMed2006

Delayed ischaemic neurological deficits after subarachnoid haemorrhage are associated with clusters of spreading depolarizations.

Progressive ischaemic damage in animals is associated with spreading mass depolarizations of neurons and astrocytes, detected as spreading negative slow voltage variations. Speculation on whether spreading depolarizations occur in human ischaemic stroke has continued for the past 60 years. Therefore, we performed a prospective multicentre study assessing incidence and timing of spreading depolarizations and delayed ischaemic neurological deficit (DIND) in patients with major subarachnoid haemorrhage (SAH) requiring aneurysm surgery. Spreading depolarizations were recorded by electrocorticography with a subdural electrode strip placed on cerebral cortex for up to 10 days. A total of 2110 h recording time was analysed. The clinical state was monitored every 6 h. Delayed infarcts after SAH were verified by serial CT scans and/or MRI. Electrocorticography revealed 298 spreading depolarizations in 13 of the 18 patients (72%). A clinical DIND was observed in seven patients 7.8 days (7.3, 8.2) after SAH. DIND was time-locked to a sequence of recurrent spreading depolarizations in every single case (positive and negative predictive values: 86 and 100%, respectively). In four patients delayed infarcts developed in the recording area. As in the ischaemic penumbra of animals, delayed infarction was preceded by progressive prolongation of the electrocorticographic depression periods associated with spreading depolarizations to >60 min in each case. This study demonstrates that spreading depolarizations have a high incidence in major SAH and occur in ischaemic stroke. Repeated spreading depolarizations with prolonged depression periods are an early indicator of delayed ischaemic brain damage after SAH. In view of experimental evidence and the present clinical results, we suggest that spreading depolarizations with prolonged depressions are a promising target for treatment development in SAH and ischaemic stroke.

Adult↗
PubMed2005

Arrested spread of vesicular stomatitis virus infections in vitro depends on interferon-mediated antiviral activity.

A quantitative understanding of the innate immune response will enable its recruitment against emerging, poorly characterized, or weaponized viral pathogens. To gain insights into how the innate responses can limit viral spread, we used quantitative focal infections to study how the spread of recombinant vesicular stomatitis viruses (VSV) on baby hamster kidney (BHK) and delayed brain tumor (DBT) cell monolayers is affected by innate cellular antiviral responses. We observed that rates of infection spread correlated with one-step growth rankings for four ectopic VSV strains: N1, N2, N3, and N4. However, this correlation was lost for M51R, a recombinant VSV mutant that lacks the ability to shut-off host gene expression. In BHK cells, M51R spread at two-thirds the rate of the recombinant control virus, XK3.1, even though their one-step growth was comparable. In DBT cells, M51R infections failed to spread beyond the site of inoculation. Addition of anti-interferon antibody restored M51R spread and one-step growth to wild-type levels. Interestingly, the antibody enhanced the spread of wild-type virus but not its growth. These results suggest that while the rate of viral spread generally correlates with the rate of viral growth, the induction of cellular antiviral activities can be in some cases, the overriding factor in both spread and growth. In summary, focal infections enabled us to visualize and quantify how viral spread was inhibited by cellular antiviral activities. This study demonstrates a mechanism for quantifying how innate cellular responses can mitigate infection spread in vitro.

Animals↗
PubMed2003

A new method for improving metaphase chromosome spreading.

BACKGROUND: The success of complex molecular cytogenetic studies depends on having properly spread chromosomes. However, inconsistency of optimum chromosome spreading remains a major problem in cytogenetic studies. METHODS: The metaphase spreading process was carefully timed to identify the most critical phase of chromosome spreading. The effects of dropping height of cell suspension, slide condition, drying time, fixative ratio, and relative humidity on the quality of metaphase spreads were studied by quantitative examination of metaphase chromosome spreads. Normal and immortalized human epithelial ovarian cells, neuroblastoma cells, and normal lymphocytes were tested. RESULTS: Humidity over the slide was the most important variable affecting the quality of chromosome spreads. Consistent improvement in chromosome spreading (larger metaphase area, less chromosome overlaps, or lower frequencies of broken metaphases) was obtained for all cell types if dynamic cell rehydration, occurring as fixative absorbs moisture from air, was made to coincide with the prompt fixation of spread chromosomes to the slide. This was achieved by dropping cells on dry glass slides placed in a shallow metal tray and then quickly lowering the tray into a covered 50 degrees C water bath for slide drying. CONCLUSIONS: A new and simple method for improving metaphase chromosome spreading was developed based on our study on the characteristics of chromosome spreading.

Cell Line, Tumor↗
PubMed2006

Relative risk of spread of symptoms among the focal onset primary dystonias.

Adult-onset primary torsion dystonia (PTD) may spread to multiple body parts, but the relative risk of spread by site of onset of dystonia has not been well characterized. We retrospectively identified 602 patients with PTD out of 1,500 dystonia patients in our electronic database and extracted age at onset, site of onset, family history, and spread. Survival analyses were performed for groups based on site of onset, and hazard ratios compared relative risk of spread across groups. Patients with adult-onset blepharospasm were more likely to spread (31% past the head) than those with dystonia starting in the neck (9%), larynx (12%), or upper extremities (16%). Hazard ratios proved that the blepharospasm group had the greatest relative risk of spread. The rate of spread after onset varied significantly between the different groups. Most spread occurred in the first 1 to 2 years after onset of blepharospasm, whereas the risk of spread was relatively constant over time in cervical and laryngeal dystonia. Different sites of onset of PTD confer different risks of spread, important for clinical prognosis. Different risks of spread may provide clues about underlying pathogenesis of adult-onset primary dystonias.

Adult↗
PubMed1983

Characterization of the spreading process in human T lymphocytes.

Substratum-bound concanavalin A (conA) caused attachment and spreading of human T lymphocytes identified by monoclonal anti-T cell antibodies and sheep erythrocyte rosette formation. The simultaneous presence of conA in the medium increased the spreading, whereas preincubation of the cells with conA inhibited spreading. The tendency of conA to induce spreading was dependent on the concentration used, the higher the conA concentration the more pronounced was the spreading. For example, conA at 10 micrograms ml-1 triggered the formation of prominent substratum-attached filopodia with a length of 1-10 micron in 60-80% of T-enriched lymphocytes obtained from separate individuals. At the same conA dose the filopodia were, in 10-20% of the lymphocytes, accompanied by development of lamellipodia. With conA at 100 micrograms ml-1 the number of cells that underwent pronounced spreading was 55-90% in separate individuals. Observation of T-enriched cells fixed at different times after initiation of spreading induced by conA at 100 micrograms ml-1 indicated that filopodia formation represented the initial morphological alteration during the spreading process. This process thereafter proceeded with development of lamellipodia, extensive cytoplasmic spreading and flattening of the central cell mass. Quiescent and mitogen-activated cells exhibited the same sequence of changes during spreading. Spreading led to disappearance of the microvilli with a length of 0.1-0.7 micron present on lymphocytes in suspension, although some microvilli persisted over the cell center.

Cell Movement↗
PubMed2004

Nanometer analysis of cell spreading on matrix-coated surfaces reveals two distinct cell states and STEPs.

When mouse embryonic fibroblasts in suspension contact a matrix-coated surface, they rapidly adhere and spread. Using total internal reflection fluorescence microscopy of dye-loaded fibroblasts to quantify cell-substrate contact, we found that increasing the surface matrix density resulted in faster spreading initiation whereas lamellipodial dynamics during spreading were unaltered. After spreading initiation, most cells spread in an anisotropic manner through stochastic, transient extension periods (STEPs) with approximately 30 STEPs over 10 min to reach an area of 1300 micro m(2) +/- 300 micro m(2). A second mode of spreading, increased in serum-deprived cells, lacked STEPs and spread in a rapid, isotropic manner for 1-4 min. This isotropic mode was characterized by a high rate of area increase, 340 micro m(2)/min with 78% of the cell edge extending. Anisotropic cells spread slower via STEPs, 126 micro m(2)/min with 34% of the edge extending. During the initial 2-4 min of fast, isotropic spreading, centripetal flow of actin was low (0.8 micro m/min) whereas in anisotropic cells it was high from early times (4.7 micro m/min). After initial isotropic spreading, rearward actin movement increased and isotropic cells displayed STEPs similar to anisotropic cells. Thus, the two cell states display dramatically different spreading whereas long-term motility is based on STEPs.

Actinin↗
PubMed2004

Non-aqueous phase liquid spreading during soil vapor extraction.

Many non-aqueous phase liquids (NAPLs) are expected to spread at the air-water interface, particularly under non-equilibrium conditions. In the vadose zone, this spreading should increase the surface area for mass transfer and the efficiency of volatile NAPL recovery by soil vapor extraction (SVE). Observations of spreading on water wet surfaces led to a conceptual model of oil spreading vertically above a NAPL pool in the vadose zone. Analysis of this model predicts that spreading can enhance the SVE contaminant recovery compared to conditions where the liquid does not spread. Experiments were conducted with spreading volatile oils hexane and heptane in wet porous media and capillary tubes, where spreading was observed at the scale of centimeters. Within porous medium columns up to a meter in height containing stagnant gas, spreading was less than ten centimeters and did not contribute significantly to hexane volatilization. Water film thinning and oil film pinning may have prevented significant oil film spreading, and thus did not enhance SVE at the scale of a meter. The experiments performed indicate that volatile oil spreading at the field scale is unlikely to contribute significantly to the efficiency of SVE.

Air↗
PubMed2006

Effect of fortified spread on homocysteine concentration in apparently healthy volunteers.

OBJECTIVE: To determine the effect of folic acid, vitamin B(6) and B(12) fortified spreads on the blood concentrations of these vitamins and homocysteine. DESIGN AND SETTING: A 6-week randomized, double-blinded, placebo-controlled, parallel trial carried out in a clinical research center. SUBJECTS: One hundred and fifty healthy volunteers (50% males). INTERVENTIONS: For 6 weeks, the subjects consumed the test spreads (20 g/day): containing per 20 g (1) 200 microg folic acid, 2 microg vitamin B(12) and 1 mg vitamin B(6), or (2) 400 microg folic acid, 2 microg vitamin B(12) and 1 mg vitamin B(6) or (3) no B-vitamins (control spread). RESULTS: The B-vitamin status increased on using the test spreads, with the largest effect on the serum folate concentration: 48% in men and 58% in women on spread 1 and 92 and 146%, respectively, on spread 2 (P-values all <0.05). The plasma homocysteine decreased in the groups treated with the fortified spreads as compared to the control group. Average decreases were for males: 0.7+/-1.5 micromol/l (6.8%) on spread 1 and 1.7+/-1.7 micromol/l (17.6%) on spread 2 and for females: 1.4+/-1.2 micromol/l (14.2%) and 2.4+/-2.0 micromol/l (23.3%), respectively (P-values all <0.05). CONCLUSIONS: Consumption of a spread fortified with folic acid, vitamin B(6) and vitamin B(12) for 6 weeks significantly increases the blood concentrations of these vitamins and significantly decreases the plasma concentration of homocysteine. Fortified staple foods like spreads can contribute to the lowering of homocysteine concentrations.

Adolescent↗