Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Spreading”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 739 records · Page 41Linked to original sources
PubMedDate not supplied

Nasopharyngeal carcinoma with intracranial spread: CT and MR characteristics.

PURPOSE: Nasopharyngeal carcinoma (NPC) frequently spreads intracranially. We compare CT and MRI in identifying intracranial spread and reexamine the route of infiltration. METHOD: One hundred fourteen consecutive patients with proven NPC were evaluated prospectively with T1-, T2-weighted, contrast-enhanced MRI and CT. RESULTS: MRI showed 35 (31%) patients with middle cranial fossa involvement. Twenty-nine (25%) patients had cavernous sinus infiltration, while six (5%) showed only dural thickening. The most common route of spread is through the foramen ovale (FO) (12/35 patients, 34%), followed by skull base destruction (6/35 patients, 17%), foramen lacerum (FL) (6/35 patients, 17%), sphenoid sinus (6/35 patients, 17%), and combined FO and FL (5/35 patients, 14%). Using MRI as a standard, CT demonstrated the following involvement: cavernous sinus in 26 of 29 (90%) patients, FO in 9 of 12 patients, skull base in 6 of 6 patients, FO and FL in 3 of 5 patients, FL in 6 of 6 patients, sphenoid sinus in 6 of 6 patients and dura in 0 of 18 patients. CONCLUSION: It is believed that NPC most commonly spreads intracranially via the FL or by direct erosion. Perineural spread through the FO is an important route, which explains why with CT evidence of cavernous sinus involvement there may be no skull base erosion. These findings are best seen on MRI.

Brain↗
PubMed2002

Epidemic spreading in a variety of scale free networks.

We have shown that the epidemic spreading in scale-free networks is very sensitive to the statistics of degree distribution characterized by the index gamma, the effective spreading rate lambda, the social strategy used by individuals to choose a partner, and the policy of administrating a cure to an infected node. Depending on the interplay of these four factors, the stationary fractions of infected population F(gamma) as well as the epidemic threshold properties can be essentially different. We have given an example of the evolutionary scale-free network which is disposed to the spreading and the persistence of infections at any spreading rate lambda>0 for any gamma. Probably, it is impossible to obtain a simple immunization program that can be simultaneously effective for all types of scale-free networks. We have also studied the dynamical solutions for the evolution equation governed by the epidemic spreading in scale-free networks and found that for the case of vanishingly small cure rate delta<<1 the initial configuration of infected nodes would feature the solution for very long times.

Journal Article↗
PubMed2005

Quantifying fluctuations in market liquidity: analysis of the bid-ask spread.

Quantifying the statistical features of the bid-ask spread offers the possibility of understanding some aspects of market liquidity. Using quote data for the 116 most frequently traded stocks on the New York Stock Exchange over the two-year period 1994-1995, we analyze the fluctuations of the average bid-ask spread S over a time interval deltat. We find that S is characterized by a distribution that decays as a power law P[S>x] approximately x(-zeta(S) ), with an exponent zeta(S) approximately = 3 for all 116 stocks analyzed. Our analysis of the autocorrelation function of S shows long-range power-law correlations, (S(t)S(t + tau)) approximately tau(-mu(s)), similar to those previously found for the volatility. We next examine the relationship between the bid-ask spread and the volume Q, and find that S approximately ln Q; we find that a similar logarithmic relationship holds between the transaction-level bid-ask spread and the trade size. We then study the relationship between S and other indicators of market liquidity such as the frequency of trades N and the frequency of quote updates U, and find S approximately ln N and S approximately ln U. Lastly, we show that the bid-ask spread and the volatility are also related logarithmically.

Journal Article↗
PubMed2005

Numerical investigation of the spreading-receding cycle in a concentration-dependent lattice gas automaton diffusion model.

This work forms the second part of a numerical study about the dynamics of diffusive fronts in concentration-dependent diffusion processes. We previously demonstrated that one-dimensional spreading of a density front in a concentration-dependent microscopically heterogeneous, macroscopically homogeneous isotropic lattice gas automaton (LGA) substantially deviates from the t(1/2) relation expected from Fick's law over large periods of time. The time exponent was found to be larger than 1/2 , i.e., spreading of the density front is enhanced with respect to standard Fickian diffusion. In this note, we specifically investigate the dynamics of receding by using the same LGA model. We show here that the receding process essentially scales as t(1/2). The LGA simulations of diffusive fronts thus lead to the paradoxical result of Fick's-compatible receding and anomalous superdiffusive spreading for the same microscopic random structure and the same boundary conditions. The results also suggest that hysteresis of the spreading-receding cycle could arise from the contrasted dynamics between spreading and receding. A conceptual model of "offer and demand" which includes both the diffusivity gradient dD(rho)/d(rho) and the conditions applied at boundaries as main parameters is proposed to tentatively account for the dynamics of diffusive fronts in concentration-dependent diffusion processes.

Journal Article↗
PubMed2004

Molecular motion in a spreading precursor film.

Spreading of a polymer drop on a solid substrate was monitored with molecular resolution. Three characteristic rates, i.e., the spreading rate of the precursor film D(spread)=(3.9+/-0.2)x10(3) nm(2)/s, the flow-induced diffusion rate of molecules within the film D(induced)=1.3+/-0.1 nm(2)/s, and the thermal diffusion coefficient of single molecules D(therm)</=0.10+/-0.03 nm(2)/s, were independently measured. Since D(spread)>>D(induced), the plug flow of polymer chains was identified as the main mass-transport mechanism of spreading with an insignificant contribution from the molecular diffusion.

Journal Article↗
PubMed1990

Local and systemic spread of tobacco mosaic virus in transgenic tobacco.

Expression of a chimeric gene encoding the coat protein (CP) of tobacco mosaic virus (TMV) in transgenic tobacco plants confers resistance to infection by TMV. We investigated the spread of TMV within the inoculated leaf and throughout the plant following inoculation. Plants that expressed the CP gene [CP(+)] and those that did not [CP(-)] accumulated equivalent amounts of virus in the inoculated leaves after inoculation with TMV-RNA, but the CP(+) plants showed a delay in the development of systemic symptoms and reduced virus accumulation in the upper leaves. Tissue printing experiments demonstrated that if TMV infection became systemic, spread of virus occurred in the CP(+) plants essentially as it occurred in the CP(-) plants although at a reduced rate. Through a series of grafting experiments, we showed that stem tissue with a leaf attached taken from CP(+) plants prevented the systemic spread of virus. Stem tissue without a leaf had no effect on TMV spread. All of these findings indicate that protection against systemic spread in CP(+) plants is caused by one or more mechanisms that, in correlation with the protection against initial infection upon inoculation, result in a phenotype of resistance to TMV.

Capsid↗
PubMed1995

Rapid spreading and mature hemidesmosome formation in HaCaT keratinocytes induced by incubation with soluble laminin-5r.

HaCaT cells, an immortalized keratinocyte line, incubated in plastic wells in the presence of conditioned medium from 804G cells adhered and spread rapidly in less than 30 min. In contrast, cells plated in fibroblast or keratinocyte conditioned medium adhered poorly and remained rounded at 30 min. Immunodepletion of 804G conditioned medium with polyclonal antisera to laminin-5r, but not control antisera, abolished rapid cell spreading. Electron microscopy of HaCaT cells spread by incubation in 804G conditioned medium, but not control medium, revealed mature hemidesmosomes after 24 h. Rapid spreading was also observed in wells precoated with 804G conditioned medium or 804G cell-deposited matrix, but not with fibronectin, vitronectin, or laminin-1. Immunoblotting of 804G conditioned medium with anti-laminin-5r antibodies unveiled polypeptides of 150, 140, 135, and 100 kDa, identical by electrophoretic mobility to immunoreactive polypeptides in 804G deposited matrix. Our results suggest that addition of laminin-5r in a soluble form is sufficient to promote rapid spreading and hemidesmosome assembly in keratinocytes. The mechanism of soluble laminin-5r action may include efficient surface "priming" for cell adhesion. Soluble laminin-5r may have a physiologic role in morphogenesis and repair of the epidermis and may be of use for therapeutic applications.

Animals↗
PubMed1987

Coepibolin, the activity of human serum that enhances the cell spreading properties of epibolin, associates with albumin.

Earlier studies have shown that epibolin, a glycoprotein in human plasma, identical to preparations from other laboratories referred to as serum spreading factor and vitronectin, requires a second plasma activity in order to support maximal primary epidermal cell spreading. This plasma fraction, referred to as coepibolin, alone supports no cell spreading but potentiates the activity of epibolin by at least 5-10 times. Studies reported here indicate that coepibolin activity associates with one plasma fraction, it cannot be substituted by commercial preparations of ovalbumin, soybean trypsin inhibitor, or hemoglobin, but it can be substituted by commercial bovine or human serum albumin. The activity purified to electrophoretic homogeneity comigrates with, and shows antigenic properties of albumin. Under the assay conditions coepibolin affects the extent and morphology of cell spreading: in the presence of epibolin plus coepibolin cells assume a more polar orientation than in epibolin alone. For its maximal effect coepibolin must be present continuously in the early phases of cell spreading.

Alkalies↗
PubMed2004

Projecting rates of spread for invasive species.

All else being equal, the faster an invading species spreads, the more dangerous its invasion. The projection of spread rate therefore ought to be a central part of the determination of invasion risk. Originally formulated in the 1970s to describe the spatial spread of advantageous alleles, integrodifference equation (IDE) models have since been co-opted by population biologists to describe the spread of populations. More recently, they have been modified to include population structure and environmental variability. We review how IDE models are formulated, how they are parameterized, and how they can be analyzed to project spread rates and the sensitivity of those rates to changes in model parameters. For illustrative purposes, we apply these models to Cytisus scoparius, a large shrub in the legume family that is considered a noxious invasive species in eastern and western North America, Chile, Australia, and New Zealand.

Algorithms↗
PubMed2004

Increased intake of fruit and vegetables and a low-fat diet, with and without low-fat plant sterol-enriched spread consumption: effects on plasma lipoprotein and carotenoid metabolism.

BACKGROUND: Regular intake of plant sterol (phytosterol)-enriched foods enhances the cholesterol lowering effect of diets. One side effect associated with plant sterol consumption is a modest reduction in plasma carotenoid concentrations. This study investigated the effect of consuming a low-fat National Cholesterol Education Programme (NCEP) Step 1 diet, including a low-fat plant sterol ester (PSE)-enriched spread on cholesterol metabolism to determine if specific dietary advice to increase daily fruit and vegetable intake could prevent reduced plasma carotenoid concentrations. MATERIALS AND METHODS: In this randomised, crossover double-blind trial, 48 hypercholesterolaemic men received 21 g day(-1) of a low-fat PSE-enriched spread or placebo for 3 weeks, interrupted by 3 weeks washout. Individuals also adhered to a NCEP Step 1 diet and repeated 3-day food diaries monitored adherence. Specific advice was provided to increase dietary fruit and vegetable intakes. Fasting blood samples were collected at pre- and post-intervention for lipoprotein and carotenoid analysis. RESULTS: Plasma total and low-density lipoprotein (LDL) cholesterol concentrations were significantly (P <0.05) reduced, by 4.6 and 7.1%, respectively, after the PSE-enriched low-fat spread. Plasma apo B concentrations were significantly (P <0.0005) lower after the PSE spread. PSE consumption was also associated with significantly (P <0.05) lower total plasma beta-carotene concentrations, but this change was not significant after lipid standardisation. PSE consumption had no effect on retinol, alpha-carotene, gamma-tocopherol, alpha-tocopherol, lutein, zeaxanthin, beta-crypyoxanthin or lycopene concentrations. CONCLUSION: Dietary advice to increase daily fruit and vegetable consumption may be effective in preventing a reduction in plasma carotenoid concentrations previously associated with PSE consumption. Further, PSE incorporated in a low-fat spread and consumed as part of a NCEP Step 1 diet are effective in reducing total and LDL cholesterol.

Adult↗
PubMed1995

Identification of a novel virulence gene, virA, on the large plasmid of Shigella, involved in invasion and intercellular spreading.

A novel virulence gene (virA) was identified upstream of the virG gene on the large plasmid of Shigella flexneri 2a YSH6000. Characterization of virA mutants infecting MK2 epithelial cell monolayers revealed that their invasive capacity was decreased to less than one fifth of the wild-type level. Nevertheless, the bacteria were capable of expressing and secreting IpaB, IpaC and IpaD proteins. The virA mutants were also impaired in their ability to spread intercellularly, since the bacteria gave rise to a small number of foci in a focus-plaque-forming test with MK2 cells. Although virG expression was slightly decreased in the virA mutants, introduction of a cloned virG gene into a virA mutant, N1945, failed to restore spreading ability. Although, introduction of a cloned virA gene into N1945 restored invasiveness and spreading ability, the reduced virG transcription level was not affected, indicating that the reduced virG expression in virA mutants does not play a major role in defective intercellular spreading. The nucleotide sequence of the virA region revealed that the virA gene was located 528 bp upstream of the virG gene, in the opposite orientation. The deduced amino acid sequence of the VirA protein indicated a 44.7 kDa protein with no homology to known proteins. The VirA protein was secreted into the culture supernatant, a process that required the Mxi and Spa loci. The expression of virA was under the control of the virB gene, the positive regulator of the ipa, mxi and spa operons. These results indicate that virA is a new member of the invasion regulon directed by virB and that the VirA function is involved in invasion and intercellular spreading.

Amino Acid Sequence↗
PubMed2004

Mutual antagonism of ethylene and jasmonic acid regulates ozone-induced spreading cell death in Arabidopsis.

Ethylene (ET) and jasmonic acid (JA) have opposite effects on ozone (O(3))-induced spreading cell death; ET stimulates, and is required for the spreading cell death, whereas JA protects tissues. We studied the underlying molecular mechanisms with the O(3)-sensitive, JA-insensitive jasmonate resistant 1 (jar1), and the O(3)-tolerant, ET-insensitive ethylene insensitive 2 (ein2) mutants. Blocking ET perception pharmacologically with norbornadiene (NBD) in jar1, or ET signaling genetically in the jar1 ein2 double mutant prevented the spread of cell death. This suggests that EIN2 function is epistatic to JAR1, and that the JAR1-dependent JA pathway halts oxidative cell death by directly inhibiting ET signaling. JAR1-dependent suppression of the ET pathway was apparent also as increased EIN2-dependent gene expression and ET hypersensitivity of jar1. Physiological experiments suggested that the target of JA is upstream of Constitutive Triple Response 1 (CTR1), but downstream of ET biosynthesis. Gene expression analysis of 1-aminocyclopropane-1-carboxylic acid (ACC)-treated and O(3)-exposed ein2 and jar1 revealed reciprocal antagonism: the EIN2-mediated suppression of the JA pathway. The results imply that the O(3)-induced spreading cell death is stimulated by early, rapid accumulation of ET, which can suppress the protecting function of JA thereby allowing cell death to proceed. Extended spreading cell death induces late accumulation of JA, which inhibits the propagation of cell death through inhibition of the ET pathway.

Arabidopsis↗
PubMed1990

The effect of removal of cerebrospinal fluid on cephalad spread of spinal analgesia with 0.5% plain bupivacaine.

Increased intraabdominal pressure is well known to cause higher cephalad spread of spinal analgesia. The reason for this is believed to be a decrease in the cerebrospinal fluid (CSF) volume. If this mechanism is correct, then the cephalad spread of local anesthetic solutions should also be facilitated when the CSF volume is intentionally reduced without increasing the intraabdominal pressure. Sixty-six patients without evidence of increased intraabdominal pressure and undergoing urological procedures were randomly allocated to three groups. All received 10 mg 0.5% bupivacaine for spinal anesthesia. In Group I, the anesthetic was injected after free drops of CSF. In Groups II and III, three and five ml were removed, respectively, before injecting bupivacaine. Mean cephalad spread of analgesia 20 min after injection in the three groups was T10.2 +/- 2.0, T9.4 +/- 1.8 and T7.0 +/- 2.1, respectively. When CSF was reduced by 5 ml, the level of spread not only showed a statistically significant difference from that of the control group, but also from that of Group II (P less than 0.05). Our results show that higher cephalad spread of spinal anesthetic is possible by reducing the CSF volume without evidence of increased intraabdominal pressure.

Abdomen↗
PubMed1997

Morphogenesis and development of superficial spreading tumor of the colon and rectum.

The aim of this study was to clarify the morphogenesis and mechanism of a wide intramucosal extension of a superficial spreading (epithelial) tumor (SST; defined as an epithelial tumor with wide intramucosal spreading involving a diameter of 30 mm or more) in the colon and rectum. For this purpose favorable sites, histological components, and histological growth patterns were compared between 95 cases of SST (16 adenomas and 79 carcinomas) and 2356 non-SST cases, which served as controls. The frequency of SST was significantly higher in the cecum and rectum, and lower in the sigmoid colon when compared to the locations of the control. Among the SST cases, 82.3% of superficial spreading carcinoma (SSC) had an adenomatous component and 96.2% had a cytologically low-grade carcinoma (CAL). In intramucosal SSC, the adenomatous and/or CAL component was predominant, and the proportion of high-grade carcinoma (CAH) was significantly smaller in intramucosal SSC in comparison with the control group. In the mucosal spreading area of SST, 78.9% were tubulovillous in histological type and 86.3% showed a replacing growth pattern. These results indicate that an SST initially develops as an adenoma in at least 85.3% of cases and CAL in 14.7% cases at most; spreads superficially in the mucosa by a replacing growth mechanism that forms a tubulovillous and villous structure; and is affected by intestinal peristalsis less than non-SST.

Adenoma↗
PubMed1997

Oligodendrocyte-type 2 astrocyte progenitors use a metalloendoprotease to spread and migrate on CNS myelin.

Oligodendrocyte-type 2 astrocyte (O-2A) progenitors are highly motile cells which migrate in the developing and adult central nervous system (CNS). Adult CNS myelin, however, contains inhibitory proteins, the neurite growth inhibitors NI 35/250, which block neurite outgrowth and spreading of many different cell types, such as astrocytes and fibroblasts. In the present study we investigated the spreading of dissociated cells and migration out of aggregates ('spheres') of primary O-2A cultures and of a glial precursor cell line (CG-4) on purified CNS myelin and on CNS tissue. Primary O-2A progenitors and CG-4 cells quickly attached to and spread on CNS myelin-coated culture dishes, showing no inhibition by the neurite growth inhibitors. CG-4 cells migrated with a velocity of 30 microns/h on a CNS myelin protein extract and at 5.7 microns/h on adult spinal cord tissue. Both cell spreading and migration on a CNS substrate could be specifically blocked by metalloprotease blockers like o-phenanthroline and the tetrapeptide carbobenzoxy-phe-ala-phe-tyr-amide, whereas blockers of the serine, aspartyl and cysteine proteases had no effect. On differentiation to astrocytes, the O-2A progenitors lost their ability to spread on CNS myelin. These results suggest the crucial involvement of a metalloprotease in the mechanism of migration on a CNS substrate. In vivo, migration of oligodendrocyte progenitors may be an important aspect of myelin repair following local traumatic, inflammatory or toxin-induced myelin loss.

Animals↗
PubMedDate not supplied

Human hippocampal seizure spread studied by depth and subdural recording: the hippocampal commissure.

Eleven patients had seizures with unilateral temporal lobe onset recorded with simultaneous bilateral medial temporal depth electrodes and neocortical (subdural) electrodes at least on the side of seizure onset. Of a total of 55 seizures, four had simultaneous onset in neocortex and hippocampus, and 51 had onset in unilateral hippocampus. None originated solely in temporal neocortex. Three reproducible patterns of seizure spread from hippocampus were defined in which seizures spread initially to ipsilateral neocortex (32 seizures), spread first to contralateral hippocampus (13 seizures), or spread simultaneously to ipsilateral neocortex and contralateral hippocampus. Although the region of hippocampus in which seizures arose was constant, patterns of spread sometimes varied in the same patient. When contralateral neocortical involvement occurred, it was after or with contralateral hippocampus but never before. These results suggest the existence of an operational hippocampal commissure in humans.

Electroencephalography↗
PubMed2001

Clinicopathological features of superficial spreading and nonspreading squamous cell carcinoma of the esophagus.

OBJECTIVES: Superficially spreading carcinoma of the esophagus, consisting mainly of intraepithelial carcinoma, is not as rare as was previously thought. Despite the surgical significance of this entity, no general definition has been established, and the clinical features of this disease remain to be clarified. METHODS: A total of 54 patients with superficial carcinoma of the esophagus (defined as carcinoma limited to the epithelium or superficially invading the lamina propria or submucosa) were classified into two groups according to the longitudinal extent of the lesion. A total of 13 patients with superficially spreading carcinoma (defined as a superficial carcinoma measuring >5 cm and consisting mainly of intraepithelial carcinoma) were compared to 41 patients with nonspreading esophageal carcinoma. RESULTS: One patient with superficially spreading carcinoma had a positive resection margin because of multiple cancerous lesions. The only significant difference in the clinical and pathological features of the two groups was a higher prevalence of associated multiple cancerous lesions in patients with the superficially spreading type. CONCLUSIONS: Superficially spreading carcinoma of the esophagus is often associated with multiple cancerous lesions. For endoscopists and esophageal surgeons, it is important to define the proximal extent of intraepithelial cancer and the presence of multiple cancerous lesions to perform curative resection.

Carcinoma in Situ↗
PubMed1996

Attachment, spreading and migration of melanoma cells on vitronectin. The rôle of alpha V beta 3 and alpha V beta 5 integrins.

Recent in situ studies suggest the alpha V beta 3 integrin is a tumour progression marker in melanoma. We analyzed 5 human melanoma cell lines for their expression of the vitronectin binding alpha V beta 3 and alpha V beta 5 integrins using flow cytometry. The role of these receptors in cell attachment, spreading and migration was investigated using attachment assays, video time lapse spreading and migration assays and with function blocking monoclonal antibodies. Cell lines derived from later stages of tumor progression exhibited high levels of alpha V beta 3 expression, whereas no similar correlation with alpha V beta 5 expression was identified. Cell attachment, spreading and migration response on vitronectin correlated well with the expression level of the alpha V beta 3 but not the alpha V beta 5 vitronectin receptor. Blocking of the alpha V beta 3 integrin resulted in a significant decrease in cell attachment, spreading and motility whereas the function blocking antibody against the alpha V beta 5 integrin only inhibited cell attachment in cell lines with the highest level of expression of this integrin. Taken together, our study indicates that the level of expression of the alpha V beta 3 and alpha V beta 5 integrins is heterogeneous in melanoma cell lines and that the alpha V beta 5 integrin, if present, may function only during the initial cell attachment whereas the alpha V beta 3 plays an important role in cell spreading and cell migration as well.

Antibodies, Blocking↗