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PubMed1987

Effects of aging on parathyroid hormone stimulated ionic fluxes in rat parotid cell aggregates.

The effects of aging on parathyroid hormone stimulated calcium and phosphate efflux from isolated rat parotid cell aggregates differed from that of epinephrine stimulated calcium efflux in magnitude, chronology, and ionic dependence. Parathyroid stimulated ionic fluxes were maximal at 1-3 months of age, declined until 12 months and remained constant thereafter. Epinephrine stimulated calcium efflux remained maximal between 3 and 12 months and declined until at least 24 months. Absolute stimulation of calcium efflux over basal levels was maximal at 4-8% while phosphate efflux was 20-30%.

Aging↗
PubMed1978

The effects of orally administered L-arginine HCl on the development of myeloma tumors in BABL/C mice following the injection of single cell suspensions, cell aggregates or tumor fragments; and on the growth of two ascites tumour cell lines.

When arginine-HCl was added to the drinking water of Balb/c mice the formation of subcutaneous tumours following the injection of single cell suspensions of MPC-11 cells was prevented, however, tumours did develop after injecting tumour fragments or aggregates of suspension-cultured cells. Arginine-HCl had no inhibitory effect upon the production of Krebs II and 6C3HED lymphoma ascites tumours in Balb/c and C3H mice respectively.

Administration, Oral↗
PubMed1980

Junctional resistance and action potential delay between embryonic heart cell aggregates.

Spheroidal aggregates of embryonic chick ventricle cells were brought into contact and allowed to synchronize their spontaneous beats. Action potentials were recorded with both intracellular and extracellular electrodes. The degree of electrical interaction between the newly apposed aggregates was assessed by measuring the delay or latency (L) between the entrained action potentials, and by determining directly interaggregate coupling resistance (Rc) with injected current pulses. Aggregate size, contact area between the aggregates, and extracellular potassium concentration (Ko+) were important variables regulating the time-course of coupling. When these variables were controlled, L and Rc were found to be linearly related after beat synchrony was achieved. In 4.8 mM Ko+ L/Rc = 3.7 ms/M omega; in 1.3 mM Ko+ L/Rc = 10.1 ms/M omega. We conclude that action potential delay between heart cell aggregates can be related quantitatively to Rc.

Action Potentials↗
PubMed1985

Effect of leukocyte activation on the formation of heterotypic tumor-cell aggregates in vitro.

Walker tumor cell (1 x 10(6) cells/ml) were incubated at 37 degrees C in a stirred cuvette with rat peritoneal exudate cells (9 x 10(6) cells/ml) with or without the synthetic leukocyte chemo-attractant fMLP (2 x 10(6) M) or biologically active concentrations of the major endogenous chemo-attractant, C5a. Aggregation, induced by the chemo-attractants, was detected after 3 min by a platelet aggregometer and by studying cytocentrifuge preparations. The response was amplified in the presence of cytochalasin B (5 micrograms/ml). Tumor cells could be identified in the aggregates by their morphology or by autoradiography after labeling with 3H-thymidine. Although tumor cells were incorporated into the leukocyte aggregates, there was no appreciable change in the number of aggregates formed between tumor cells themselves. Levine III human breast tumor cells (1 x 10(6)/ml) in heparinized human blood were incorporated into leukocyte aggregates within 30 min of adding 50 U cobra venom factor to activate complement. Aggregation correlated with a decrease in complement hemolytic activity (CH50). The aggregation reaction was not cytotoxic to tumor cells when evaluated by Trypan blue exclusion or by 51Cr release. We conclude that local tumor cells can be incorporated into aggregates formed when leukocytes are stimulated by chemo-attractants. We postulate that intravascular activation of neutrophils might affect the localization of circulating tumor cells by incorporating them into microembolic cell aggregates and by causing damage to the pulmonary endothelium.

Animals↗
PubMed1974

The colony forming efficiency of single cells and cell aggregates from a spontaneous mouse mammary tumour using the lung colony assay.

Single cell suspensions of spontaneous C3H mammary tumours did not produce colonies in the lungs of syngeneic mice after intravenous injection whereas cell aggregates obtained from similar tumours did. The number of colonies formed after the injection of aggregates was related to aggregate size and was proportional to the number injected.Single cells grew in an intramuscular site and in vitro and it was also found that if spontaneous tumours were passaged in vivo a few times single cells would grow in the lung.

Animals↗
PubMed1992

Recognition and prevention of two cases of erroneous haemocytometry counts due to platelet and white blood cell aggregation. The use of acid citrate dextrose as an auxiliary anticoagulant.

Two cases of anticoagulant-induced platelet-white blood cell aggregation are described, which resulted in erroneous haemocytometry counts. Aggregation was avoided by the use of acid citrate dextrose (ACD) as an auxiliary anticoagulant, thus enabling quantification of platelets and white blood cells.

Anticoagulants↗
PubMed2004

C-reactive protein and red cell aggregation correlate with late venous function after acute deep venous thrombosis.

OBJECTIVE: Risk factors leading to development and subsequent progression of chronic venous insufficiency after acute deep venous thrombosis (DVT) are only partially identified. Inflammation and rheologic abnormalities might have a causative role. The purpose of this study was to investigate C-reactive protein (CRP), D -dimer, and blood rheologic parameters in patients after acute DVT in relation to clinical outcome. SUBJECTS AND METHODS: Patients with a history of acute proved DVT underwent clinical examination and duplex ultrasound scanning of the veins, and Venous Clinical Severity Score (VCSS) and Venous Segmental Disease Score (VSDS) were calculated. Further, CRP, D -dimer, and several rheologic parameters were determined and related to outcome as assessed with venous scores. RESULTS: Forty-three patients were examined 28 (median) months after the index event. Patients had higher CRP ( P < .001), D -dimer ( P < .001), red blood cell aggregation ( P < .01), fibrinogen concentration ( P < .01), and leukocyte count ( P < .05) than did healthy control subjects. CRP and red blood cell aggregation were positively correlated with VCSS ( r = 0.42 and P < .01, and r = 0.30 and P < 0.05, respectively). Multivariate regression analysis showed that the relation between CRP and VCSS was independent of other laboratory and rheologic parameters and of age, total thrombus load, duration of compression therapy after the index event, recurrence, recanalization, and presence of comorbid conditions ( P < .05). CONCLUSIONS: CRP is independently related to the severity of venous dysfunction in patients after acute DVT. Chronic inflammation as well as changes in blood rheologic parameters may be causally involved in the development of chronic venous insufficiency occurring in the medium-term and long-term course after acute DVT.

Acute Disease↗
PubMed1984

A new simple method for measuring red cell aggregation.

A viscometric technique is outlined for the measurement of red cell aggregation (RCA). Samples are submitted to a constant shear rate of 2,4 s-1. The resulting time dependent torque signal reaches a peak soon after starting the rotation and falls within seconds to a constant baseline, thereby describing an area "F" with the baseline. The shear history of the sample being strictly controlled, "F" is reproducible and shows a direct, positive correlation with RCA as determined for instance in the "aggregometer".

Blood Viscosity↗
PubMed2000

The mechanics of heterotypic cell aggregates: insights from computer simulations.

Finite element-based computer simulations are used to investigate a number of phenomena, including tissue engulfment, cell sorting, and checkerboard-pattern formation, exhibited by heterotypic cell aggregates. The simulations show that these phenomena can be driven by a single equivalent force, namely a surface (or interfacial) tension, that results from cytoskeletal components and cell-cell adhesions. They also reveal that tissue engulfment, cell sorting, and checkerboard-pattern formation involve several discernible mechanical features or stages. With the aid of analytical arguments, we identify the conditions necessary for each of these phenomena. These findings are consistent with previous experimental investigations and computer simulations, but pose significant challenges to current theories of cell sorting and tissue engulfment.

Biomechanical Phenomena↗
PubMed2006

Discriminating in vitro cell fusion from cell aggregation by flow cytometry combined with fluorescence resonance energy transfer.

Expression of fusion proteins in the plasma membrane enables cells to bind and fuse with surrounding cells to form syncytia. Cell fusion can have important functional outcomes for the interacting cells, as syncytia formation does in AIDS pathogenesis. Studies on cell fusion would be facilitated by a quantitative method able to discriminate between cellular aggregates and bona fide fused cells in a cell population. Flow cytometry with fluorescence resonance energy transfer is applied here for analyzing fusion of HIV-1 envelope-expressing cells with CD4+ Jurkat cells. Fusion partners were labeled with the vital lipophilic fluorescent probes DiO (green) and DiI (red) and FRET is manifested by an enhancement of the DiI red fluorescence intensity in double fluorescent cells, thus allowing discrimination between fused and aggregated cells. The inhibitory effect of anti-CD4 monoclonal antibodies and the inhibitory peptide T-20 upon cell fusion were readily quantified by this technique. This method allows the distinction of fused and aggregated cells even when they are at low frequencies.

CD4-Positive T-Lymphocytes↗
PubMedDate not supplied

In vitro estimation of red blood cells' aggregation using ultrasound Doppler techniques.

Aggregation of red blood cells (RBCs) is one of the principal hemorheological factors which plays an important role in capillary circulation. In order to study RBC's aggregation, an ultrasound Doppler in vitro technique, using pulsed wave monoelement pencil 4 MHz probes, was designed. A hydraulic pump system has been implemented, using an electric step motor that establishes in a certain distance, a laminar blood flow profile into a rectangular cross-section plexiglass tube. Blood coming from blood collection bags was used and following certain typical measuring protocols, red blood cells' samples of various parameters and conditions were acquired. Adding dextrans to the blood samples, red blood cells aggregation was achieved and observed for various hematocrit values. Both the emitted and the backscattered signals were driven to a system containing a multi-channel digital oscilloscope--of high sampling rate and processing capabilities--and a powerful PC with a high acquisition A/D card and special control software. The estimation of mean aggregates size--by measuring the mean ultrasonic intensity scattered by the blood sample--led us to a qualitative, in vitro ultrasonic method.

Dextrans↗
PubMed2000

Detection of red cell aggregation by low shear rate viscometry in whole blood with elevated plasma viscosity.

The viscosity of whole blood measured at low shear rates is determined partly by shear resistance of the red cell aggregates present, stronger aggregation increasing the viscosity in the absence of other changes. Effects of cell deformability can confound interpretation and comparison in terms of aggregation, however, particularly when the plasma viscosity is high. We illustrate the problem with a comparison of hematocrit-adjusted blood from type 1 diabetes patients and controls in which it is found the apparent and relative viscosities at a true shear rate of 0.20 s-1 are lower in the patient samples than age matched controls, in spite of reports that aggregation is increased in such populations. Because the plasma viscosities of the patients were higher on average than controls, we performed a series of experiments to examine the effect of plasma protein concentration and viscosity on normal blood viscosity. Dilution or concentration by ultrafiltration of autologous plasma and viscosity measurements at low shear on constant hematocrit red cell suspensions showed (a) suspension viscosity at 0.25 and 3 s-1 increased monotonically with plasma protein concentration and viscosity but (b) the relative viscosity increased, in concert with the microscopic aggregation grade, up to a viscosity of approximately 1.25 mPa-s but above this the value the relative viscosity no longer increased as the degree of aggregation increased in concentrated plasmas. It is suggested that in order to reduce cell deformation effects in hyperviscous pathological plasmas, patient and control plasmas should be systematically diluted before hematocrit is adjusted and rheological measurements are made. True shear rates should be calculated. Comparison of relative viscosities at low true shear rates appears to allow the effects of red cell aggregation to be distinguished by variable shear rate viscometry in clinical blood samples.

Adult↗
PubMed1995

Heparan sulfate-mediated cell aggregation. Syndecans-1 and -4 mediate intercellular adhesion following their transfection into human B lymphoid cells.

Because syndecans are present at sites of cell-cell contact in vivo it has been hypothesized that they play a role in mediating cell-cell adhesion. However, there has been no direct evidence to support this notion. To address this question, B lymphoid (ARH-77) cells were transfected with the cDNA for murine syndecan-1. Unlike the parental cells, the transfectants form large multicellular aggregates in suspension cultures and stain intensely for syndecan-1 at sites of cell-cell contact. Using rotation-mediated aggregation assays, we find that aggregation of syndecan-1-transfected cells is dependent on divalent cations and is inhibited by the following: (i) addition of heparin and heparin-like glycosaminoglycans, (ii) removal of heparan sulfate from the cell surface, or (iii) addition of exogenous purified syndecan-1. Mixing of syndecan-1-transfected and control-transfected cells results in aggregates containing both cell types indicating that aggregation occurs through a heterophilic adhesion mechanism in which heparan sulfate chains bind to a counter-receptor present on these cells. Importantly, syndecan-4-transfected cells also aggregate in a heparan sulfate-dependent manner, while in contrast, betaglycan-transfected cells aggregate poorly. Thus, syndecans may be important mediators of cell-cell adhesion, but this function may not be common to all transmembrane heparan sulfate-bearing proteoglycans.

Animals↗
PubMed1981

Cell aggregation of the marine sponge Geodia cydonium. Identification of lectin-producing cells.

A D-galactose-specific lectin, purified from the marine sponge Geodia cydonium, is present on the cell surface of mucoid cells, free choanocytes and choanocyte clusters, as revealed first, by the adhesion assay which is based on the formation of "rosettes" with erythrocytes, and second, by immunofluorescence studies. Using the same techniques no lectin could be identified on the surface of archaeocytes. Rosette formation was inhibited in the presence of 20 mM D-lactose as well as after preincubation of erythrocytes with purified lectin. Titration experiments in a hemagglutination assay showed that the highest level of extractable lectin (5% of the total protein) is found in mucoid cells, lower concentrations are determined in choanocyte clusters (0.07%), free choanocytes (0.05%) and archaeocytes (0.01%). Only the mucoid cells were found to synthesize lectin which is secreted and subsequently transferred to the cell surface of other cell types. As one consequence of the binding of the lectin to the cell surface of aggregation-deficient choanocytes or archaeocytes, the conversion of these cells to aggregation-susceptible ones is observed. These results support previous evidence that the lectin is involved in the reaggregation process of single cells in the homologous biological system.

Animals↗
PubMed2001

Ethanol-induced cell aggregation (flocculation) and its physiological background in Schizosaccharomyces pombe rive 4-2-1.

Cell aggregation (flocculation) of the yeast Schizosaccharomyces pombe strain RIVE 4-2-1 developed in glucose-containing medium, but only in the presence of ethanol. Cell surface proteins which participated in cell to cell interactions were characterised by the susceptibility of flocculation to different proteolytic enzymes, heat treatment, denaturing and thiol compounds and by the inhibition of flocculation by sugars and derivatives. It was shown that a galactose-specific lectin was involved in this new type of flocculation.

Carbohydrates↗
PubMed2004

Cannabinoid-mediated neuroprotection following interferon-gamma treatment in a three-dimensional mouse brain aggregate cell culture.

Multiple sclerosis is increasingly recognized as a neurodegenerative disease which is triggered by inflammation in the central nervous system (CNS). Demyelination-associated axonal or neuronal damage is a primary cause of disability and has thus far not been successfully targeted by available drug therapies. The neuroprotective properties of both endogenous and administered cannabinoids have been shown in in vivo and in vitro models of CNS damage following excitotoxic, oxidative, traumatic and ischaemic insults, with a predominantly apoptotic effector mechanism. In this study a foetal mouse telencephalon aggregate cell culture system was developed to compare tissue from cannabinoid receptor 1 knockout mice with wildtype counterparts. Aggregate formation and neurofilament/myelin basic protein accumulation were dependent on the age of foetal dissection and species used. Following treatment with interferon-gamma, levels of myelin basic protein, neurofilament, neuronal dephosphorylation and caspase 3 activation were assessed in telencephalon tissue in vitro. Cytokine treatment resulted in significant loss of the neuronal marker neurofilament-H in cannabinoid receptor 1 knockout cultures but not in wildtypes, indicating that presence of the cannabinoid receptor 1 gene can be neuroprotective. Caspase 3 activation was higher in cultures from knockout animals, indicating an apoptotic mechanism of cell death. Dephosphorylated neurofilament levels were significantly elevated in knockout mice, lending support to the premise that neurofilament dephosphorylation is a marker for neuronal damage. Taken together, these results indicate that neuroprotection could be elicited through the cannabinoid receptor 1, and point towards a potential therapeutic role for cannabinoid compounds in demyelinating conditions such as multiple sclerosis.

Animals↗
PubMed1995

Cell aggregation and apoptosis induced by hemodialysis membranes.

During hemodialysis, circulating mononuclear cells can be stimulated to different degrees, depending on membrane biocompatibility. Cell activation usually leads to aggregation and proliferation. It may also result in apoptosis if cells are subjected to abnormal activation. This may be the case of cells exposed to bioincompatible hemodialysis membranes. The study presented here evaluates the effects of two hemodialysis membranes, with different degrees of biocompatibility, (Cuprophan (CU; Lundia IC 5N; GAMBRO, Sweden) and polyacrylonitrile (AN69; Biospal 3000S, Hospal, France)) on aggregation and apoptosis of circulating human mononuclear cells and the human mononuclear cell line (THP-1). The results showed that 2-h incubation with CU, a bioincompatible membrane, produces cell aggregation of both peripheral mononuclear cells and THP-1 cells (35% and 54%, respectively). After 48 h of incubation with a CU membrane, apoptotic death was observed in 32% of THP-1 cells and in 45% of normal peripheral mononuclear cells. Neither cell aggregation nor apoptosis was observed after incubation with the AN69 membrane. CU membrane-induced apoptosis was inhibited by Staurosporrin (Sigma, St. Louis, MO) a protein kinase C (PKC)-inhibitor, suggesting that cell apoptosis induced by the CU membrane is mediated by a PKC-dependent cell activation. Furthermore, cell prestimulation with phorbol 12-myristate 13-acetate, an activator of PKC, results in a increase in the percentage of THP-1 cell death by apoptosis after CU exposure (53%). Our study indicates that CU membranes induce mononuclear cell activation, leading to cell apoptosis.

Acrylic Resins↗