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At least 865 records · Page 48Linked to original sources
PubMed1992

Suppression of spreading depression of Leão in neocortex by an N-methyl-D-aspartate receptor antagonist.

Spreading depression has been implicated in the pathophysiology of a number of diseases such as migraine, stroke and epilepsy. The characteristics of this phenomenon were explored in neocortex of anesthetized rats. Spreading depression was produced in 10 of 15 animals using mechanical, electrical and chemical stimulation. Mean amplitude of the DC shift was -9.3 mV, mean duration at any one electrode 65 sec and rate of spread 2-5 mm/min. Spreading depression was facilitated by focal interictal spike activity induced by penicillin and completely blocked by the N-methyl-D-aspartate (NMDA) receptor antagonist, DL-2-aminophosphonovaleric acid (APV), providing further evidence that excitatory amino acid neurotransmission is a critical element in the development or propagation of the phenomenon.

2-Amino-5-phosphonovalerate↗
PubMedDate not supplied

[Migraine with a combination of aura symptoms as a clinical manifestation of cortical spreading depression].

The pathomechanism of the migraine aura remains unclear. The most probable cause of the aura is cortical spreading depression with associated hypoperfusion. Both the cortical spreading depression and hypoperfusion begin in the occipital lobes and spread forward slowly (2-3 mm/min) in a wave-like mode along the brain convolutions and cross territories of brain arteries. We present a 24-year-old female patient with a combination of aura symptoms. Each migraine attack began with a bright scintillating zig-zag, which crossed the visual field. It was followed by left sided hemiparesthesiae marching from the face to the hand. The last symptom of aura was motor aphasia. Later a unilateral, pulsating headache developed with associated photo- and phonophobia. The stable pattern and duration of aura symptoms in the presented case suggest that the cortical spreading depression plays an important role in the pathomechanism of migraine with aura.

Adult↗
PubMed1983

Glutamate and spreading depression in chick retina.

This work is centered on the involvement of glutamate in spreading depression. Chick eye cup preparations bathed with Ringer solution at 28 degrees C were used. For chemical stimulation KCl was increased and glutamate was added to the Ringer solution. The occurrence of spreading depression was detected by visual observation of the optical changes accompanying the phenomenon. Enzymatic method based on the fluorescence of the reduced form of nicotinamide adenine dinucleotide was used for glutamate dosage in the Ringer's samples. The investigations proceeded under six different experimental conditions, and the results were analysed by nonparametric statistical methods. No correlation was found between spreading depression and glutamate outflux. The glutamate hypothesis to account for spreading depression was discussed, and experimental situations involving glutamate, K+ and Cl- were indicated that proved unfavorable to the incidence of the reaction.

Animals↗
PubMed1994

Cortical point-spread function and long-range lateral interactions revealed by real-time optical imaging of macaque monkey primary visual cortex.

Processing of retinal images is carried out in the myriad dendritic arborizations of cortical neurons. Such processing involves complex dendritic integration of numerous inputs, and the subsequent output is transmitted to multiple targets by extensive axonal arbors. Thus far, details of this intricate processing remained unexaminable. This report describes the usefulness of real-time optical imaging in the study of population activity and the exploration of cortical dendritic processing. In contrast to single-unit recordings, optical signals primarily measure the changes in transmembrane potential of a population of neuronal elements, including the often elusive subthreshold synaptic potentials that impinge on the extensive arborization of cortical cells. By using small visual stimuli with sharp borders and real-time imaging of cortical responses, we found that shortly after its onset, cortical activity spreads from its retinotopic site of initiation, covering an area at least 10 times larger, in upper cortical layers. The activity spreads at velocities from 100 to 250 microns/msec. Near the V1/V2 border the direct activation is anisotropic and we detected also anisotropic spread; the "space constant" for the spread was approximately 2.7 mm parallel to the border and approximately 1.5 mm along the perpendicular axis. In addition, we found cortical interactions between cortical activities evoked by a small "center stimulus" and by large "surround stimuli" positioned outside the classical receptive field. All of the surround stimuli used suppressed the cortical response to the center stimulus. Under some stimulus conditions iso-orientation suppression was more pronounced than orthogonal-orientation suppression. The orientation dependence of the suppression and its dependency on the size of some specific stimuli indicate that at least part of the center surround inhibitory interaction was of cortical origin. This findings reported here raise the possibility that distributed processing over a very large cortical area plays a major role in the processing of visual information by the primary visual cortex of the primate.

Animals↗
PubMed2000

FGF-2 isoforms of 18 and 22.5 kDa differentially modulate t-PA and PAI-1 expressions on the pancreatic carcinoma cells AR4-2J: consequences on cell spreading and invasion.

Pancreatic tumors overexpress FGF-2 and t-PA, but the implication of the growth factor in t-PA synthesis and t-PA-dependent tumor invasion remains unknown. FGF-2 is present in different isoforms: The 18 kDa FGF-2 is secreted, while the 22.5 kDa one is nuclearized and exerts intracrine regulations bypassing cell-surface FGF receptors. Rat pancreatic carcinoma AR4-2J cells producing either the 18 or the 22.5 kDa FGF-2 after transfection with FGF-2 cDNAs have been used to analyze the role of FGF-2 in t-PA expression and t-PA-related cell spreading. The 22.5 kDa FGF-2 reduced t-PA and PAI-1 synthesis 2-fold. Addition of recombinant 18 kDa FGF-2 (rFGF-2) to cell cultures resulted in increased t-PA and decreased PAI-1 expression. By contrast, rFGF-2 did not significantly modify t-PA synthesis in cells producing the 22.5 kDa FGF-2. Cell spreading was t-PA-dependent. Furthermore, cells producing the 22.5 kDa FGF-2 migrated less than control cells and cells producing the 18 kDa FGF-2. Overall, our data show that secretory FGF-2 is involved in t-PA synthesis by pancreatic cancer cells and facilitates cell spreading. The 22.5 kDa FGF-2 exerts opposite effects by decreasing t-PA expression in basal conditions and during rFGF-2 stimulation. Since the expression of the 22.5 kDa FGF-2 is under specific controls, its up-regulation might have the potential to reduce spreading of pancreatic cancer cells.

Animals↗
PubMed1998

Using avidin-mediated binding to enhance initial endothelial cell attachment and spreading.

Binding between the protein avidin and the vitamin biotin was used as an extrinsic, high affinity receptor-ligand system to augment the intrinsic integrin-dependent cellular adhesion mechanism. Glass substrates were coupled with avidin receptors through an adsorbed film of biotinylated bovine serum albumin (b-BSA). The avidin-treated slides then were seeded with biotinylated bovine aortic endothelial cells (BAEC). A 3:1 ratio of BSA:b-BSA provided the best results in terms of specific cellular attachment, growth, and spreading. Control surfaces consisted of bare glass or glass with adsorbed BSA. Attachment of unmodified BAEC to glass decreased in the presence of anti-beta 1 integrin antibody. Adhesion of biotinylated BAEC to avidin-treated slides was not affected by anti-beta 1 integrin antibody, consistent with integrin-independent avidin-mediated adhesion. The initial rate of cell spreading was greatest for avidin-biotin-mediated adhesion (80.0 +/- 25.6 microns2/h), followed by integrin-dependent cellular adhesion on plain glass (35.7 +/- 7.7 microns2/h) and, finally, by adhesion on BSA-coated protein surfaces (10.2 +/- 0.3 microns2/h). Biotinylated and unmodified BAEC, cultured for 1 h in serum-containing media, were subjected to laminar flow in a variable-height flow chamber that provided a range of shear stresses from 0.2 to 75 dynes/cm2. The critical shear stress required to detach 50% of the cells in serum-containing media increased from 4.6 +/- 0.8 dynes/cm2 for integrin-dependent adhesion to 12.6 +/- 1.2 dynes/cm2 for avidin-biotin-mediated adhesion. Avidin-mediated attachment for biotinylated BAEC increased initial cellular spreading rates and strength of attachment (i.e., at 1 h) by a factor of two and three, respectively. These results support the hypothesis that integrin-mediated cell attachment and spreading can be enhanced using high affinity integrin-independent binding.

Animals↗
PubMed2000

Relationships among cell attachment, spreading, cytoskeletal organization, and migration rate for anchorage-dependent cells on model surfaces.

Many research and commercial applications use a synthetic substrate which is seeded with cells in a serum-containing medium. The surface properties of the material influence the composition of the adsorbed protein layer, which subsequently regulates a variety of cell behaviors such as attachment, spreading, proliferation, migration, and differentiation. In this study, we examined the relationships among cell attachment, spreading, cytoskeletal organization, and migration rate for MC3T3-E1 osteoblasts on glass surfaces modified with -SO(x), -NH(2), -N(+)(CH(3))(3), -SH, and -CH(3) terminal silanes. We also studied the relationship between cell spread area and migration rate for a variety of anchorage-dependent cell types on a model polymeric biomaterial, poly(acrylonitrile-vinylchloride). Our results indicated that MC3T3-E1 osteoblast behavior was surface chemistry dependent, and varied with individual functional groups rather than general surface properties such as wettability. In addition, cell migration rate was inversely related to cell spread area for MC3T3-E1 osteoblasts on a variety of silane-modified surfaces as well as for different anchorage-dependent cell types on a model polymeric biomaterial. Furthermore, the data revealed significant differences in migration rate among different cell types on a common polymeric substrate, suggesting that cell type-specific differences must be considered when using, selecting, or designing a substrate for research and therapeutic applications.

3T3 Cells↗
PubMed1998

Un-cross-linked fibrin substrates inhibit keratinocyte spreading and replication: correction with fibronectin and factor XIII cross-linking.

Wound repair is characterized by the presence of a fibrin-rich matrix, but the effect of fibrin on re-epithelialization remains unclear. In this study, we determined the effects of different fibrin matrices on cultured human neonatal keratinocytes. Using purified fibrinogen and fibrin gels generated by the enzymatic action of thrombin, batroxobin (it leads to retention of fibrinopeptide B), or Agkistrodon contortrix thrombin-like enzyme (ACTE; it leads to retention of fibrinopeptide A), we determined the effect of each of these matrices on keratinocyte morphology, attachment, spreading, and replication as compared to tissue culture plastic. Morphologically, keratinocytes seeded on fibrin surfaces were more rounded and formed three-dimensional structures. Specific cell attachment, as measured at either 37 degrees C or 4 degrees C, was not altered on the different fibrin substrates (P > .05) but was increased on fibrinogen and factor XIII cross-linked fibrin (P < .01). However, keratinocytes seeded on fibrin, regardless of the presence or absence of fibrinopeptides A or B, showed a marked decrease (up to 71%) in cell numbers by days 5 (P = .0357) and 10 (P = .0114). Keratinocyte spreading was decreased by 78.8% (P = .0006), 80.3% (P = .0001), and 89.2% (P = .0001) on thrombin-, batroxobin-, and ACTE-generated fibrin, respectively, but not on fibrinogen-coated dishes. However, either the addition of fibronectin or cross-linking of fibrin with factor XIII allowed full keratinocyte spreading to occur (P = .0002 and P = .0013, respectively). We conclude that fibrin inhibits keratinocyte spreading in the absence of other matrix or plasma proteins or cross-linking by factor XIII.

Cell Adhesion↗
PubMed1999

MHC class I-restricted epitope spreading in the context of tumor rejection following vaccination with a single immunodominant CTL epitope.

Epitope spreading is a process whereby epitopes distinct from and non-cross-reactive with an inducing epitope become targets of an evolving immune response. This phenomenon has been associated most notably with the progression of naturally occurring or experimentally induced chronic autoimmune diseases. We have investigated the potential occurrence of epitope spreading in the context of antitumor cytotoxic T cell (CTL) responses using chicken ovalbumin (OVA) as a model antigen. Our results indicate that following rejection of OVA-expressing EG.7 tumor cells effectuated by a CTL response which is induced against the MHC class I-restricted immunodominant epitope OVA257-264, there occurs intramolecular diversification of the CTL response to two additional OVA-derived epitopes, OVA176-183 and OVA55-62, as well as intermolecular spreading to other endogenous tumor-derived determinants. It seems that CTL-mediated tumor cell destruction in vivo favors cross-presentation of additional epitopes with the consequent activation of additional tumor-reactive lymphocytes. The process of epitope spreading in that context has obvious important implications for the design of antigen-specific antitumor immunotherapies.

Animals↗
PubMed1988

Computerized tomographic prediction of extraluminal spread and prognostic implications of lesion width in esophageal carcinoma.

The use of preoperative computed tomographic (CT) scans of the chest in carcinoma of the esophagus to associate preoperative staging with postoperative survival is controversial. Thirty-two patients who underwent esophagectomy and reconstruction were examined with respect to a variety of variables available on preoperative evaluation, including lesion width on CT scan, lesion length on CT scan, and barium esophagogram. Each variable was evaluated for its ability to predict the presence of extraesophageal spread of tumor, as determined pathologically by logistic regression analysis. Lesions greater than 3.0 cm in width by CT scan were associated with a significantly higher incidence of extraesophageal spread. Tumor location, gender, histologic grade, presence of in situ lesions, vascular invasion, eosinophilia, nodal metastases, and preoperative chemotherapy had no predictive value for survival. Duration of survival was affected by the presence of esophageal spread of disease and lesion width. These results indicate that preoperative CT scanning can predict extraesophageal spread of tumor, and this is associated with overall survival.

Actuarial Analysis↗
PubMed1990

Growth and spread of hepatocellular carcinoma. A review of 240 consecutive autopsy cases.

All 240 consecutive cases of hepatocellular carcinoma (HCC) that underwent autopsy at the National Cancer Center Hospital (Tokyo, Japan) between September 1962 and August 1986 were reviewed. Among these cases, 162, for which photographs of cut surfaces of the primary tumors were available, were grossly classified using a combination of both Eggel's classification and our own into three major types, i.e., nodular, massive, and diffuse as described by Eggel (Eggel H, Beitr Pathol Anat 1901; 30:506-604), and three subgroups of nodular type, i.e., single nodular type (type 1), single nodular type with extranodular growth (type 2), and contiguous multinodular type (type 3) by our classification (Kanai T et al., Cancer 1987; 60:810-819). Seventy-eight cases were classified as nodular type, comprising seven cases of type 1, 61 cases of type 2, and ten cases of type 3. Sixty-seven and 17 cases were classified as massive and diffuse type, respectively. Of the 78 nodular-type tumors, 59 measured less than 10 cm, whereas 64 of 67 massive-type tumors were 10 cm or more in size. The incidence of intrahepatic and extrahepatic tumor spread of HCC was significantly higher for tumors measuring more than 5 cm. As to the relationship between macroscopic type and tumor spread, the frequency of spread was lowest for type 1 tumors, and high for the other types. Intrahepatic metastasis was detected in 28.6% of type 1, 93.4% of type 2, 100% of type 3, and 98.5% of massive-type tumors. Lymph node metastasis was detected in 14.3% of type 1, 24.6% of type 2, 70% of type 3, 38.8% of massive-type and 52.9% of diffuse-type tumors. Hematogenous extrahepatic metastasis was detected in 14.3% of type 1, 47.5% of type 2, 70% of type 3, 74.6% of massive-type and 82.4% of diffuse-type tumors. It appears that not only primary tumor size but also its macroscopic type has an important influence on the growth and spread of HCC.

Adolescent↗
PubMed2000

Rho regulates T cell receptor ITAM-induced lymphocyte spreading in an integrin-independent manner.

T cell receptor (TCR) engagement increases integrin-mediated adhesion to APC, resulting in the stabilization of the T cell : APC interaction and the close apposition of the two cell membranes. Here we show that engagement of either the TCR or CD3 chimeras with immobilized antibodies causes the rapid spreading of T cells in an integrin-independent fashion. This effect concurs with the polymerization of the actin cytoskeleton and is dependent on the integrity of the immunoreceptor tyrosine-based activation motifs of the CD3 subunits. Expression of a dominant negative mutant of RhoA, as well as the Rho-specific inhibitor C3 toxin, abolished TCR-induced spreading. In contrast, constitutively active or dominant negative forms of Rac and Cdc42 did not affect cell spreading. We conclude that signals emanating from the TCR can directly induce T cell spreading, independently of integrins, and via a Rho-dependent reorganization of the actin cytoskeleton.

Actins↗
PubMed2000

Spreading waves of transient and prolonged decreases in water diffusion after subarachnoid hemorrhage in rats.

Diffusion-weighted MRI (DWI), which can detect cortical spreading depressions (SDs) as propagating waves of reduced apparent diffusion coefficient (ADC) of water, was used to investigate whether spreading depression occurs after subarachnoid hemorrhage (SAH) induced by endovascular perforation in the rat. Eleven rats underwent SAH while positioned in the magnet. The ADC measurements had a temporal resolution of 12 sec. Transient decreases in ADC to 74 +/- 5% of pre-SAH values were observed in three rats after SAH, which propagated over the cortex with an average speed of 4.2 +/- 0. 6 mm/min, consistent with an SD wave. Furthermore, in all 11 rats, a wavefront of reduced ADC, which did not resolve within the 12 min observation period, spread at a speed of 3.2 +/- 1.7 mm/min in the ipsilateral cortex, and again is consistent with the speed of SD propagation. Therefore, spreading depression-like cellular depolarization is a consequence of acute subarachnoid hemorrhage in rats. Magn Reson Med 44:110-116, 2000.

Animals↗
PubMed1988

Social networks of disease spread in the lower Illinois valley: a simulation approach.

This study illustrates the use of disease modeling and simulation techniques to the study of the spread of disease within and between social networks. A Reed-Frost type model of disease spread is used to construct a simulation of the spread of tuberculosis within three prehistoric populations of the Lower Illinois River Valley during Middle Woodland, Late Woodland, and Mississippian times. A high and low population size was modeled for each time period. Late Woodland model 2 (low population estimate) is the only model that experienced pathogen extinction with host survival. The rest of the models experienced rapid and severe host population decline. The results of the simulation suggest that a social network size of between 180 and 440 persons is required under the conditions of this model for host-pathogen coexistence (i.e., endemicity) to occur. The severe population decline experienced by these populations suggests that tuberculosis as modeled here could not have existed in these populations. Future refinements of modeling and simulation techniques can provide additional insights into how disease spreads among social contacts.

History, Ancient↗
PubMed1990

The effects of population structure on the spread of the HIV infection.

A model for the spread of human immunodeficiency virus (HIV) in a population of male homosexuals is presented. The population is divided into five groups on the basis of degree of sexual activity. Within each group, the individuals are classified as 1) susceptible; 2) infective; or 3) removed because of a lack of sexual activity associated with advanced acquired immunodeficiency disease (AIDS). The infective individuals are further subdivided into four stages of infection. Analyses of the model address two questions with regard to the spread of HIV: (1) What is the effect of level of sexual activity on an individual's risk for infection, and (2) What is the effect that assumptions about mixing between groups have on both individual risk and transmission throughout a population? Results from analyses using a number of different parameter estimates show that increased levels of sexual activity increase the likelihood that an individual will become infected. In addition, the initial spread of the disease is markedly affected by variation in the amount of contact among individuals from different subpopulations. The steady-state incidence of the disease is not markedly affected by variation in the contact patterns, but the size of the steady-state population and therefore the proportion of infected individuals in the population does vary significantly with changes in the degree of mixing among subpopulations. These results show clearly the sensitivity of model outcomes to variation in the patterns of contact among individuals and the need for better data on such interactions to aid in understanding and predicting the spread of HIV.

HIV Infections↗
PubMed1991

Organization of the membrane skeleton in spreading mouse blastomeres. I. Morphological analysis.

Differentiation in the mouse embryo begins at the 8-cell stage when the blastomeres spread against each other in a process called compaction. The spreading behavior of blastomeres on lectin-coated coverslips mimics that of blastomeres in the embryo, and we have utilized this model system to obtain an en face view of the membrane skeleton in the spreading blastomeres. Embryos were cultured on the coverslips for periods ranging from 20 sec to 6 hr, and the cells were disrupted to expose the cytoplasmic face of the adherent membranes and their associated filaments. The "membrane lawn" preparations were fixed, critical point dried, rotary shadowed, and the replicas examined by transmission electron microscopy. Using this technique we found that the plasmalemma of rounded blastomeres is associated with a lacy 3-dimensional filamentous meshwork that is transformed into a thin mat of densely woven filaments when the cells flatten. The overall organization of the membrane skeleton is similar in flattening 2- and 8-cell embryos, but there are significant differences in the time required for spreading to take place, in the means whereby the membrane skeletons are reorganized, and in the extent of maximal flattening. The significance of these observations for the compaction process is discussed.

Animals↗
PubMed2003

Effects of silkworm paralytic peptide on in vitro hematopoiesis and plasmatocyte spreading.

Bombyx mori paralytic peptide (BmPP), a multifunctional cytokine-like molecule, is expressed in the hematopoietic organ-wing imaginal disc complex, suggesting that BmPP is involved in both immune response and the hematopoietic process. We studied the effects of BmPP on plasmatocytes and hematopoietic organs of the silkworm. BmPP (1 microM) stimulated spreading of circulating plasmatocytes, but the percentage of spread plasmatocytes was only 20%. Over 10 nM of BmPP, however, elicited prominent spreading in 70% of young plasmatocytes discharged from cultured hematopoietic organs. Cells in hematopoietic organs that were enzymatically dispersed did not spread even after adding 100 nM of BmPP, indicating that plasmatocytes acquired BmPP-sensitivity immediately after discharge. When cultured in a medium containing larval plasma, hematopoietic organs grew markedly and discharged a large number of hemocytes, over 95% of which were morphologically plasmatocytes. The hemocyte discharge was blocked in the medium containing BmPP dose-dependently, although hematopoietic organ growth was not suppressed. These results suggest that BmPP plays important roles both in hematopoietic regulation and in the hemocyte immune reaction of the silkworm.

Animals↗
PubMed2002

Histologic indices in biopsy specimens for estimating the probability of extended local spread in patients with rectal carcinoma.

BACKGROUND: Although precise preoperative assessment of the extent of local cancer spread is important to determine the appropriate treatment strategy, imaging modalities have not been sufficient. The aim of this study was to establish effective preoperative indices that would predict the degree of local spread in patients with rectal carcinoma. METHODS: In specimens from 437 patients with advanced rectal carcinoma, the submucosal horizontal invasive frontal region was examined histologically with reference to three unfavorable characteristics: 1) tumor "budding", 2) poor differentiation, and 3) vascular invasion. In addition, a transanal submucosal biopsy, which targets the tumor edge, was performed on 85 patients to verify the utility of preoperative evaluation of these parameters. RESULTS: Multivariate logistic analysis showed that three unfavorable parameters had independent impact on the degree of nodal involvement. These parameters related significantly to the number of lymph nodes involved, the development of extranodal tumor deposits, circumferential surgical margin involvement, and lateral pelvic lymph node metastases. Regarding patients without unfavorable parameters as a standard, the odds ratio of pelvic recurrence was 1.8 (0.9-3.4) in patients with one unfavorable parameter and 5.3 (2.7-10.2) in patients with multiple unfavorable parameters. Based on the transanal biopsy, the submucosal invasive frontal region could be estimated in 73 patients (85.9%). Among these cases, the multiple unfavorable parameters were relevant to an increased risk of extensive local spread. In addition, pelvic recurrence developed in 36% of patients with multiple unfavorable parameters (no-risk patients, 5%; single-risk patients, 13%). CONCLUSION: Histology in the submucosal invasive frontal region reflects the extent of local spread and can be evaluated preoperatively by transanal biopsy, which should become a useful tool for therapy selection for patients with advanced rectal carcinoma.

Adult↗