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At least 433 records · Page 24Linked to original sources
PubMed1984

Step-by-step analysis of adhesion of human platelets to a collagen-coated surface defect in initial attachment and spreading of platelets in von Willebrand's disease.

Adhesion of platelets from the platelet-rich plasma (PRP) of patients with von Willebrand's disease (vWD) and healthy donors has been studied in a simple model system - wells of multiwell tissue culture plates coated with fibrillar calf skin collagen (CSC). This model is characterized by: (i) the presence of only one constituent of the vessel wall connective tissue matrix (collagen), (ii) the absence of surface-bound aggregates and thrombi, (iii) absence of overlapping of neighbouring spread platelets. A morphometric quantitation of adhesion by scanning electron microscopy (SEM) has been carried out. It allows to subdivide this process into three stages: 1) initial attachment of unspread platelets to the substrate, 2) platelet spreading on the substrate, and 3) attachment of unspread platelets to the upper surface of spread platelets. It was established that the PRP of vWD patients, compared to that of healthy donors, is characterized by a decreased total adhesion of platelets to a CSC-coated surface, which is manifested in the impairment of both the initial attachment and subsequent spreading of platelets. Addition of platelet-free plasma from healthy donors to the vWD PRP completely restores platelet spreading on collagen but little affects the initial attachment. These experiments performed on isolated collagen preparations provide further evidence for the initial attachment and spreading of platelets on collagenous constituents of the subendothelium being factor VIII/von Willebrand factor (FVIII/vWF)-dependent. In contrast to the adhesion on the collagen substrate, the adhesion of platelets from vWD PRP to a foreign surface, polystyrene plastic of uncoated wells, is the same as that of the normal PRP and, thus, FVIII/vWF-independent.

Collagen↗
PubMed1985

Extrauterine spread in endometrial carcinoma clinically confined to the uterus.

From July 1975 to April 1983, 237 patients had primary treatment for endometrial cancer at the Long Island Jewish-Hillside Medical Center. Included in this study were 74 of these patients with Stage I and 20 with Stage II endometrial carcinoma who underwent laparotomy without preoperative radiation. The purpose of the study was to determine the prevalence of extrauterine spread in endometrial carcinoma clinically confined to the uterus and to correlate risk variables with this spread. The parameters assessed were retroperitoneal nodal metastases, adnexal involvement, peritoneal implants and peritoneal cytology. The overall prevalence of extrauterine spread was 23.4% (Stage I, 18.9%; Stage II, 40.0%). The rate of nodal metastasis, adnexal involvement, peritoneal implant, and positive peritoneal cytology were 18.7, 7.4, 4.3, and 8.5%, respectively. No positive relationship was demonstrated between surface spread and risk variables. There was positive correlation between surface spread and peritoneal cytology (87.5%). Direct correlations were found between positive nodes and tumor growth over more than one-third of the endometrial surface (P less than 0.001), gross cervical involvement (P less than 0.001), deep myometrial invasion (p less than 0.001), length of uterine cavity, grade 3 tumor, papillary adenocarcinoma (40%), and stage of disease. Five-year survival rate of Stage I and Stage II in this small series was 77.8 and 55.6%. Complications of 16 radical hysterectomies in Stage II were minimal and transient. Because of frequent extrauterine spread in endometrial carcinoma clinically confined to the uterus, and exploratory laparotomy and peritoneal cytology may be desirable in Stage I and II disease before definitive treatment.

Actuarial Analysis↗
PubMed1989

Long-term suppression of the cerebral spread of a memory: effects of idazoxan and clonidine.

Bitemporal injections of puromycin consistently induce amnesia of aversive maze-learning in mice when administered within 3 days of training. These bitemporal puromycin injections lose their amnestic effectiveness if the latency between training and injection is extended beyond 6 days. Consistent with other evidence, we believe that memory (in our task) "spreads" during the 6 days following training. Since previous experiments have indicated that the central noradrenergic system is involved in this process of "memory spread," we have examined the effect of stimulation or blockade of the alpha 2-receptor. To this end, we administered a single dose of the alpha 2-adrenoceptor antagonist, idazoxan, or the alpha 2-agonist, clonidine. Idazoxan (1 mg/kg, SC) had no effect on engram spread. Clonidine (25 micrograms-125 ng/kg, SC), by contrast, suppressed engram spread for at least 30 days after treatment. When mice were tested at 60 and 90 days after treatment, spontaneous recovery (i.e., engram spread) was evident in only about 50% of the clonidine treated mice. Coadministration of idazoxan with clonidine blocked the effects of clonidine on "memory spread."

Animals↗
PubMed1990

Extent of mesorectal spread and involvement of lateral resection margin as prognostic factors after surgery for rectal cancer.

The extent of tumour growth beyond the muscularis propria (mesorectal spread) was measured in specimens from 167 consecutive patients with rectal cancer. The 5-year survival was significantly greater in patients with slight mesorectal spread (4 mm or less) than in those with more extensive mesorectal spread (55% [95% confidence interval 42-66%] vs 25% [13-38%]). The prognostic value for survival of mesorectal spread was independent of the presence of lymphnode metastases. There were also significant differences in survival between patients with slight and extensive mesorectal spread among patients with Dukes' stage B tumours (66% [41-82%] vs 37% [14-60%]) and those with Dukes' stage C tumours (30% [12-52%] vs 18% [6-34%]). Thus mesorectal spread of rectal cancer is an important determinant of survival, and its accurate measurement may serve to subdivide Dukes' B and C cases. In this study tumour involvement of the lateral resection margin was not a useful predictor of local recurrence, but it did correlate with poor prognosis.

Actuarial Analysis↗
PubMed1989

Regulation of RAW264 macrophage morphology and spreading: studies with protein kinase C activators, inhibitors and a cyclic AMP analog.

Protein kinases C and A probably play important roles in membrane signal transduction. To test the role of protein kinases in macrophage spreading, we have measured cell perimeters in the absence and presence of protein kinase C activators, inhibitors and a cAMP analog. Scanning electron microscopy indicated that macrophages spread extensively in the presence of protein kinase C activators. In contrast, protein kinase C inhibitor and dbcAMP (N6-2'-O-di-butyryladenosine 3':5'-cyclic monophosphate AMP) promote a round cell morphology with many surface folds. Quantitative optical microscopy experiments showed that the maximal effects of these reagents were achieved within 30 min. The protein kinase C activators dioctonylglycerol (3 microM), phenylephrine (1 microM), and phorbol myristate acetate (1 micrograms/ml) increased macrophage spreading. Similarly, the calcium ionophore A23187 (1 microgram) increased spreading. In contrast, the protein kinase C inhibitors chlorpromazine (30 microM), sphingosine (10 microM), trifluoroperazine (10 microM), and H-7 (10 microM) significantly reduce macrophage spreading. The analog dibutyryl cAMP (30 microM) abrogates the effects of protein kinase C activators. These data suggest that protein kinase C participates in the regulation of macrophage spreading. Furthermore, the protein kinase A activator dibutyryl cAMP can inhibit the effects of protein kinase C activators.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1994

Invasion and spread of single glycoprotein deleted mutants of Aujeszky's disease virus (ADV) in the trigeminal nervous pathway of pigs after intranasal inoculation.

The purpose of the study was to evaluate the role which non-essential envelope glycoproteins play in the neuroinvasion and neural spread of ADV. The invasion and spread in the trigeminal nervous pathway with the Ka strain of ADV and its single deletion mutants Ka gI-, Ka gp63- and Ka gIII- were examined after intranasal inoculation in neonatal pigs by virus isolation and immunocytochemistry. Evaluation was performed in the nasal mucosa, trigeminal ganglion (1st neuronal level), ponsmedulla (2nd neuronal level) and thalamus-cerebellum (3rd neuronal level). The Ka gIII- mutant invaded up to the 3rd neuronal level of the trigeminal pathway and spread in a similar way to the parental Ka strain. The Ka gp63- mutant invaded up to the 3rd neuronal level but the spread of this mutant was impaired at all the neuronal levels. The Ka gI- mutant was least neuroinvasive and reached only up to the 2nd neuronal level. The results showed that glycoproteins gI and gp63 play a role in the invasion and spread of ADV in the nervous system. However, the gI glycoprotein appears to be the most important for neuroinvasion and neural spread of ADV in pigs. Therefore, gI deleted vaccines may be considered to be safer with respect to the neuroinvasion than vaccines carrying single deletions of other non-essential envelope glycoproteins.

Animals↗
PubMed2006

Activated c-Fms recruits Vav and Rac during CSF-1-induced cytoskeletal remodeling and spreading in osteoclasts.

Colony-stimulating factor-1 (CSF-1) induces osteoclast spreading that requires activation of c-Src and phosphatidyl inositol 3-kinase (PI3-K), both of which are recruited to activated c-Fms, the CSF-1 receptor. The present report provides evidence that the hemopoietic guanine nucleotide exchange factor (GEF), Vav, and its target GTPase, Rac, lie downstream from this initial signaling complex. CSF-1 treatment of osteoclast-like cells induced translocation of Vav to the plasma membrane, an increase in its phosphotyrosine content, and a concomitant decline in the amount of phosphoinositol 4,5-bisphosphate bound to Vav, changes known to induce Vav's GEF activity. CSF-1 induced the association of Vav and Rac and increased Rac's GTPase activity. CSF-1 also induced rapid translocation of Rac to the periphery of spreading neonatal rat osteoclasts where it co-localized primarily with Vav3 and to a lesser extent with Vav1. Wortmannin, an inhibitor of PI3-K, blocked CSF-1-induced Rac translocation and prevented CSF-1-induced spreading and actin reorganization in osteoclasts. CSF-1-induced osteoclast spreading was not significantly reduced in osteoclasts isolated from Vav1 knock-out mice and Vav1 knock-out mice had normal bone density. Microinjection of constitutively active Rac, but not constitutively active Cdc42 or RhoA, induced lamellipodia formation and osteoclast spreading, mimicking the effects of CSF-1. Dominant-negative Rac blocked CSF-1-induced osteoclast spreading, whereas neither dominant-negative Cdc42 nor C3, an inhibitor of RhoA, affected the response to CSF-1. These data demonstrate that Vav and Rac lie downstream from activated PI3-K in CSF-1-treated osteoclasts and that Rac is required for CSF-1-induced cytoskeletal remodeling in these cells.

Actins↗
PubMed2006

Cytoplasmic pH-dependent spreading of polymorphonuclear leukocytes: regulation by pH of PKC subcellular distribution and F-actin assembly.

Cytoplasmic pH (pHi) plays an important role in the regulation of polymorphonuclear leukocyte (PMN) spreading, but the molecular mechanisms involved have long been obscure. In the present study, we investigated the pH-dependence of phorbol myristate acetate (PMA)-induced PMN spreading. A change in pHi alone did not induce spreading, but cytoplasmic alkalinization promoted the spreading induced by PMA, whereas acidification inhibited it. To further investigate the mechanism by which pHi affects cell spreading, we employed subcellular fractionation and immunoblot analyses to evaluate the effect of pH on the subcellular distribution of protein kinase C (PKC) and assembly of the actin cytoskeleton. We found that cytoplasmic alkalinization enhanced PKC membrane distribution and quantitatively up-regulated the actin cytoskeleton. On the other hand, cytoplasmic acidification was found to have effects on these signaling molecules that were opposite to those of cytoplasmic alkalinization. These results may provide a potential explanation for the pH-regulation of the PMA-induced PMN spreading.

Actins↗
PubMed2004

T cell epitope spreading to myelin oligodendrocyte glycoprotein in HLA-DR4 transgenic mice during experimental autoimmune encephalomyelitis.

Epitope spreading has been implicated in the pathogenesis of experimental autoimmune encephalomyelitis (EAE) and human multiple sclerosis (MS). T cell epitope spreading has been demonstrated in rodents for myelin basic protein (MBP) and proteolipid protein (PLP) determinants, but not for myelin oligodendrocyte glycoprotein (MOG), another important myelin antigen. Moreover, the role of human autoimmunity-associated MHC molecules in epitope spreading, including HLA-DR2 and DR4, has not been formally examined. To address these questions, we investigated epitope spreading to MOG determinants in HLA-DR4 (DRB1*0401) transgenic mice during EAE. The data show that upon induction of EAE in HLA-DR4 transgenic mice with the immunodominant HLA-DR4-restricted MOG peptide 97-108 (MOG(97-108); TCFFRDHSYQEE), the T cell response diversifies over time to MOG(181-200) (core: MOG(183-191); FVIVPVLGP) and MBP. The spreading epitope MOG(181-200) binds with high affinity to HLA-DRB1*0401 and is presented by human HLA-DRB1*0401+antigen presenting cells. Moreover, this epitope is encephalitogenic in HLA-DRB1*0401 transgenic mice. This study demonstrates intra- and intermolecular epitope spreading to MOG and MBP in "humanized" HLA-DR4 transgenic mice.

Animals↗
PubMed2006

MRI findings and spreading patterns of necrotizing external otitis: is a poor outcome predictable?

AIM: To evaluate spreading patterns of necrotizing external otitis (NEO) by magnetic resonance imaging (MRI) and to identify spreading patterns related to a poor outcome. MATERIALS AND METHODS: Fourteen patients with NEO were divided into good and poor outcome groups according to their final clinical outcomes. Initial MRI images were retrospectively reviewed for regional abnormalities, and follow-up MRI images were reviewed for ICA flow void abnormality and for the following five spreading patterns: medial, crossed, anterior, intracranial, and combined. The frequencies of the abnormal flow void or spreading patterns were compared between the good and poor response groups. RESULTS: Seven (50%) and seven (50%) patients were respectively allocated to the good and poor outcome groups. Retrocondylar fat infiltration was the most commonest finding on initial MRI images (93%). The frequencies of the abnormal flow void and spreading patterns in the good and poor groups, respectively, were: abnormal flow void, 0 and four (57%); anterior, two (29%) and three (43%); medial, six (86%) and seven (100%); crossed, six (86%) and seven (100%); intracranial middle cranial fossa, one (14%) and four (57%); intracranial posterior cranial fossa, four (57%) and six (86%); intracranial foramen magnum, one (14%) and six (86%). CONCLUSIONS: NEO almost always involves the retrocondylar fat and spreads via various pathways to extracranial or intracranial spaces. The presence of an abnormal flow void and intracranial dural enhancement, particularly in the middle cranial fossa and foramen magnum, may indicate a poor prognosis.

Aged↗
PubMed2006

Coculture with endothelial cells enhances vascular smooth muscle cell adhesion and spreading via activation of beta1-integrin and phosphatidylinositol 3-kinase/Akt.

The interactions between endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) play significant roles in the homeostasis of the blood vessel during vascular remodeling. Cell adhesion and spreading are an essential process for VSMC migration, survival and proliferation in the events of vascular physiology and pathophysiology. However, effects of ECs on adhesion and spreading of VSMCs have not been characterized yet. Here, the interaction of ECs and VSMCs on adhesion and spreading of VSMCs were investigated by using a coculture system. The results showed that VSMCs cocultured with ECs exhibited a significant increase in the number of adherent and spreading cells, and much more mRNA (twofold, P<0.01) and protein (threefold, P<0.05) expression of beta(1)-integrin comparing to the control, i.e., VSMCs cultured alone. Furthermore, the enhanced functional activity of beta(1)-integrin expression was confirmed by FACS. A beta(1)-integrin blocking antibody (P5D2) could inhibit the EC-induced VSMC adhesion and spreading. It was demonstrated that in correspondence with enhanced cell adhesion, ECs also prompted focal adhesion complex assembly and stress fiber formation of VSMCs. The phosphatidylinositol 3-kinase (PI3K)/Akt pathway was more pronouncedly activated in response to VSMC attachment. Our results for the first time show that coculture with ECs enhances VSMC adhesion and spreading by up-regulating beta(1)-integrin expression and activating the PI3K/Akt pathway, suggesting that the interaction between ECs and VSMCs serves an important role in vascular homeostasis and remodeling.

Cell Adhesion↗
PubMed2005

Experimental investigation of fluid drop spreading on heterogeneous and anisotropic porous media.

Study of spreading phenomena on porous substrates is important from theoretical as well as applications point of view. An example of such applications is composite processing, where operations involve displacement of air/volatiles by polymeric fluids through porous media composed of fibers. In this work, dynamics of drop spreading was investigated on fibrous porous substrates used in composite processing. These porous media are heterogeneous and anisotropic. Spreading front of silicon oil drops was tracked on borosilicate glass, quartz, and two different kinds of glass fiber mats: woven fabric and unidirectional. For the woven fabric, spreading front was observed to progress in steps of increasing and decreasing rate. For the unidirectional mat, the spreading front progressed with decreasing rate. The dynamics of spreading were fitted to power law in order to compare results with other porous substrates.

Journal Article↗
PubMed2006

Flux-assisted wetting and spreading of Al on TiC.

The effect of a K-Al-F-based flux on the spreading of Al on TiC, at temperatures up to 900 degrees C, in Ar and in air has been studied. Whilst obtuse contact angles were observed without flux, the flux facilitated rapid spreading to a perfect wetting condition, in both Ar and in air. The atmosphere was found to have a weak effect on the spreading kinetics as the liquid flux provides a locally protective atmosphere by spreading over the TiC surface and also on the solid surface of Al. The flux dissolves the aluminium oxide, covering Al, so that when Al melts, and the oxide layer has been removed or weakened, intimate contact occurs between liquid Al and the TiC substrate facilitating spontaneous spreading and instantaneous wetting of liquid Al on TiC. Since flux-assisted spreading is very rapid and occurs without the formation of a reaction layer at the Al/TiC interface, this process is very different to the reactive wetting behaviour previously reported in the Al-TiC system.

Journal Article↗
PubMed2006

Vaccination with a HER2/neu peptide induces intra- and inter-antigenic epitope spreading in patients with early stage breast cancer.

BACKGROUND: We are conducting clinical vaccine trials with the HER2/neu peptide, E75, in patients with breast cancer. The purpose of this study was to demonstrate clonal expansion of E75-specific CD8(+) T cells and to identify intra- and interantigenic epitope spreading. METHOD: Pre- and postvaccination peripheral blood leukocyte samples (24 node positive [NP] and 20 node negative [NN]) from 44 vaccinated patients were analyzed. HLA-A2:Ig dimer molecules were loaded with the HER2 peptides, E75 or GP2, and were used with anti-TcR and CD8 antibodies to stain peripheral blood leukocyte immediately ex vivo and were analyzed with flow cytometry. In 8 randomly selected patients, dimers were loaded with the folate binding protein peptide E41 to evaluate for interantigenic epitope spreading. RESULTS: All patients with NP and 95% of the patients with NN showed E75-specific clonal expansion. Patients with NN showed more robust expansion. All patients with NP and 85% of the patients with NN showed evidence of intra-antigenic epitope that was spreading to GP2. However, patients with NN showed only moderate expansion to this subdominant epitope, which was not included in the immunizing mix. The degree of HER2/neu expression and disease stage impacted the ability to expand clonally E75- and GP2-specific CD8(+) T cells. Evidence of interantigenic epitope spreading to E41 was shown in 63% of the patients who were tested. CONCLUSION: Our data provide evidence for the induction of intra- and interantigenic epitope spreading that results from a single HER2/neu peptide vaccine even in early staged patients. The ability to raise immunity to multiple tumor antigens depends on both the degree of HER2/neu expression and the extent of disease. Epitope spreading is an essential element for the success of a peptide vaccine strategy.

Antigens, Neoplasm↗
PubMed2001

Apolipoprotein AI and HDL(3) inhibit spreading of primary human monocytes through a mechanism that involves cholesterol depletion and regulation of CDC42.

The objective of the current study was to characterize the influence of high density lipoproteins (HDL) on processes related to the vascular recruitment of human monocytes, which may contribute to the anti-atherogenic properties of these lipoproteins. We show that HDL(3) and apo AI inhibit the following processes in primary human monocytes: (1) M-CSF induced cell spreading; (2) M-CSF stimulated expression of surface molecules involved in adhesion, migration, and scavenging; (3) fMLP induced chemotaxis. These processes are obviously modulated by the regulation of cellular cholesterol pools as indicated by the following findings. In Tangier monocytes with defective apo AI induced cholesterol efflux, apo AI had no influence on the spreading response. In control cells, stimulation of cholesterol efflux by p-cyclodextrin mimicked the effect of apo AI and HDL(3) on spreading and chemotaxis, whereas cholesterol loading with enzymatically modified LDL (E-LDL) showed the opposite effect. Finally, a similar inverse regulation by E-LDL and apo AI/HDL(3) was also observed in regard to the surface expression of beta(1)- and beta(2)-integrins as well as the hemoglobin/haptoglobin scavenger receptor CD163 and the Fcgamma-IIIaR CD16. CDC42 was identified as a potential downstream target linking changes in cellular cholesterol content to monocyte spreading and chemotaxis. Thus, CDC42 antisense markedly reduced spreading and, in parallel with their influence on monocyte spreading, HDL(3), apo AI and p-cyclodextrin down-regulated CDC42 expression while E-LDL had the inverse effect. The apo AI induced decrease of CDC42 protein expression was paralleled by the reduction of active GTP-bound CDC42. In summary, we provide evidence that HDL(3) and apo AI are able to inhibit processes in primary human monocytes, which are related to the recruitment of monocytes into the vessel wall and probably involve regulation of cellular cholesterol pools and CDC42 function.

Apolipoprotein A-I↗
PubMed2003

Spreading of aqueous SDS solutions over nitrocellulose membranes.

Experimental investigations were carried out on the spreading of small drops of aqueous SDS solutions over dry thin porous substrates (nitrocellulose membranes) in the case of partial wetting. The time evolution was monitored of the radii of both the drop base and the wetted area inside the porous substrate. The total duration of the spreading process was subdivided into three stages: the first stage: the drop base expands until the maximum value of the drop base is reached, the contact angle rapidly decreases during this stage; the second stage: the radius of the drop base remains constant and the contact angle decreases linearly with time; the third stage: the drop base shrinks and the contact angle remains constant. The wetted area inside the porous substrate expends during the whole spreading process. Appropriate scales were used with a plot of the dimensionless radii of the drop base, of the wetted area inside the porous substrate and the dynamic contact angle on the dimensionless time. Our experimental data show: the overall time of the spreading of drops of SDS solution over dry thin porous substrates decreases with the increase of surfactant concentration; the difference between advancing and hydrodynamic receding contact angles decreases with the surfactant concentration increase; the constancy of the contact angle during the third stage of spreading has nothing to do with the hysteresis of contact angle, but determined by the hydrodynamic reasons. It is shown using independent spreading experiments of the same drops on nonporous nitrocellulose substrate that the static receding contact angle is equal to zero, which supports our conclusion on the hydrodynamic nature of the hydrodynamic receding contact angle on porous substrates.

Collodion↗
PubMed1997

Additive effect of luminance and color cues in generation of neon color spreading.

A series of experiments were designed to examine how luminance and color cues influence the occurrence of neon color spreading for the Ehrenstein pattern plus the cross pattern. The proportion of "see" responses for color spreading was obtained for different combinations of the luminance and color of the pattern components. The following were obtained. (1) Increase in the luminance of the inducing pattern and/or the color difference between the cross and the inducing pattern raised the proportion of "see" responses for color spreading. This implies that luminance and color signals additively contribute to the generation of the color spreading, but in different ways. (2) The "iso-spreading contours" for the generation of color spreading were determined on the two-dimensional isoluminant plane composed of the L-M and S-(L+M) axes. The contours were approximately described by rotated quadratic or ellipse functions. The additive interaction within the chromatic systems [the L-M system and the S-(L+M) system] was less significant than that across the luminance and chromatic systems. (3) The pattern of the experimental results could not be explained straightforwardly by existing models.

Color Perception↗
PubMed2004

Endpoint-attached heparin blocks neutrophil sticking and spreading.

Neutrophils adhere to polymer surfaces by partly unknown mechanisms. Heparin-coating of such surfaces is employed to improve biocompatibility of extracorporeal circulation. The aim of the study was to investigate mechanisms for interactions between neutrophils and uncoated versus heparin-coated surfaces. Isolated human neutrophils were incubated in tissue culture plates. Uncoated plates induced sticking and spreading of unstimulated neutrophils. Heparin-coating reduced sticking by approximately 75%, and adherent cells were less spread (p<0.001). Experiments in plates coated with modified heparins showed that sticking and spreading were not related to anticoagulatory ability or surface charge. Unstimulated neutrophil sticking was unchanged whether the media contained divalent cations or 1mM ethylenediaminetetraacetic acid (EDTA). Spreading on uncoated plates was greater in the presence of Ca(2+) and/or Mg(2+) than with EDTA. Spreading of unstimulated neutrophils on heparin-coated plates varied little with different media. Pre-incubation with anti-CD11b/CD18 antibodies did not significantly influence adhesion to heparin-coated plates. There were no differences in expression of the antiadhesive receptor CD43 (leukosialin) on adherent neutrophils on uncoated and heparin-coated plates, and pre-incubation with anti-CD43 antibody had little effect on neutrophil sticking. These data indicate an adhesive mechanism independent of selectins, integrins, and leukosialin, and inhibition of sticking and spreading by heparin-coating.

Antigens, CD↗