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PubMed1997

An in vitro model of traumatic neuronal injury: loading rate-dependent changes in acute cytosolic calcium and lactate dehydrogenase release.

We developed a new in vitro model of neuronal injury using NT2-N cells to examine the effects of hydrodynamic loading rate on intraneuronal calcium dynamics and lactate dehydrogenase (LDH) release. Our apparatus consisted of a parallel disk viscometer which induced fluid shear stress with well-defined magnitudes and loading rates to cultured cells. We found that the deformation response of the cells was dependent on the severity of the insult, with increased cellular strains generated for higher shear stresses at a constant loading rate. Peak intracellular free calcium concentration correlated with strain, suggesting that mechanical deformation may regulate calcium response. Slowly applied fluid shear stress elicited no response, whereas high loading rates resulted in peak calcium increases 2.9 to 3.6 times baseline values as injury severity was increased. LDH release measured within 5 min after the insult correlated with loading rate. In addition, LDH release continued to increase out to 24 h following high loading rate conditions, demonstrating that the application of fluid shear stress led to prolonged cell damage. The acute response in NT2-N cells subjected to an insult with the CSID is dependent on the loading rate, and these results suggest that initial membrane deformation may trigger subsequent events.

Brain Injuries↗
PubMed1993

A novel in vitro model for the study of human keratinocyte/leucocyte interactions under autologous conditions.

Keratinocyte/leucocyte interactions have become an area of intense investigations in the last decade. However, few convenient in vitro models are available at present. We have therefore designed a novel in vitro system for autologous human keratinocyte/leucocyte co-culture. Non-invasive epidermal cell sampling was achieved by using outer root sheath cells from hair follicles. After one passage, pure keratinocyte cultures (no Langerhans cells or melanocytes) were obtained. Co-culture experiments were performed on a Transwell system: keratinocytes were grown on the porous cupula, and then laid on to wells containing leucocytes. Alternatively, leucocytes can be added to the cupula when contact interactions between the two cell types are to be investigated. Using this system, we demonstrated that Phaesolus vulgaris phytohaemagglutinin-activated T lymphocytes (with 10% monocytes) in the lower compartment induced intercellular adhesion molecule 1 (ICAM-1) and HLA-DR expression, and inhibited methyl-3H-thymidine incorporation in normal human autologous keratinocytes cultured on the cupula. These changes were mediated by soluble factors (no cell contacts between keratinocytes and leucocytes), and required lymphocyte activation. This is the first direct in vitro evidence for leucocyte-induced ICAM-1 and HLA-DR expression on keratinocytes. This system is a potential tool for the study of keratinocyte/leucocyte interactions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1975

Study of the mechanism of thyroid hormone secretion in an in vitro model system: indirect evidence for fusion of lysosomes with thyroglobulin liposomes.

The interaction between [131I]-thyroglobulin liposomes and thyroidal lysosomes was used as an in vitro model system for analyzing the relation of colloid droplets to lysosomes in follicular cells. The rates of hydrolysis of [131I]-thyroglobulin in a liposome-lysosome system (Lipo-Lyso system) and a thyroglobulin-lysosome system (TG-Lyso system) were compared. Hydrolysis of thyroglobulin in the Lipo-Lyso system increased hyperbolically and was greater than that in the TG-Lyso system for about 10 h. Liposomal thyroglobulin was not degraded by the 20,000 X g supernatant obtained on disruption of the lysosomal fraction. On varying the pH of the incubation medium, the highest activity was observed under acidic conditions in both systems. Under neutral or weakly alkaline conditions, the Lipo-Lyso system still showed 50% of the maximal hydrolytic activity, while the TG-Lyso system showed no activity. ATP and anaerobic conditions had no effect on either system. Cysteine (5 X 10-2M) and p-chloromercuribenzene sulfonic acid (PCMBS, 10-3 M) had not influence on hydrolysis in the Lipo-Lyso system, but in the TG-Lyso system cysteine greatly increased, and PCMBS significantly reduced the rate of hydrolysis. Dibutyryl cyclic AMP had no effect. Chlorpromazine (Cpz) decreased liposomal thyroglobulin hydrolysis in a concentration-dependent manner. In the TG-Lyso system, concentrations of 10-4M Cpz had no effect. These results strongly suggest that liposomes rapidly fused with lysosomes, providing optimal conditions for hydrolysis of thyroglobulin.

Adenosine Triphosphate↗
PubMed1996

Endometrial cell adhesion in an in vitro model using intact amniotic membranes.

OBJECTIVE: To study adhesion between endometrial tissue and peritoneum using intact amniotic membranes as an in vitro model. DESIGN: A cell biologic and immunohistochemical study. SETTING: Tertiary-care university medical center. PATIENTS: Ten patients with regular and ovulatory cycles. INTERVENTIONS: Mechanically dissected tissue fragments from endometrial biopsies were cultured on either side of intact amniotic membranes. Also, the carcinoma cell lines RL95-2 and AN3CA were used. MAIN OUTCOME MEASURES: The adhesion of endometrial fragments and of endometrial carcinoma cell lines to amniotic membrane was studied in vitro and evaluated using frozen sections. The composition of the extracellular matrix and the presence of intermediate filament proteins of amniotic membrane were determined using immunohistochemistry and compared with those of normal peritoneum. RESULTS: Peritoneum and amniotic membrane were similar with respect to expression of cytokeratins in epithelial lining and of extracellular matrix (ECM) components. The endometrial fragments did not adhere to the intact epithelial side of the amniotic membrane. In contrast, adhesion did occur to the nonepithelial side of the amnion. The carcinoma cell lines RL95-2 and AN3CA adhered to either side of intact amniotic membranes. CONCLUSIONS: An intact epithelial lining prevents adhesion of endometrial fragments to the ECM of amniotic membranes in vitro. An intact epithelium could be important defense mechanism in preventing initial adhesion of retrogradely shed endometrium fragments to peritoneum.

Amnion↗
PubMed2000

Progression of head and neck cancer in an in vitro model.

OBJECTIVE: To identify alterations in angiogenesis and cell cycle regulation as preneoplastic cells progress to cancer in an in vitro model of head and neck tumor progression. METHODS: Immortal human gingival keratinocyte (IHGK) cells (preneoplastic) were derived from normal oral keratinocytes and were immortalized with human papillomavirus 16. Transformation of IHGK cells with a carcinogen (NNK, 4-[methylnitrosamino]-1-[3-pyridyl]-1-butanone) gave rise to IHGKN cells. We determined the growth rates, cell cycle phase, expression of cell cycle regulators, and expression of vascular endothelial growth factor along with the organotypic features of these cells and compared them with characteristics of head and neck cancer cells. RESULTS: IHGK and IHGKN cells grown in raft culture were morphologically similar to severe dysplasia and carcinoma, respectively. The proportion of cells in G(0)/G(1) was similar between IHGK and IHGKN. However, the proportion of IHGK cells was 35% greater in S phase as compared with the IHGKN cells, while a greater percentage (40%) of IHGKN cells were in G(2)/M. The expression of the other cell cycle regulators tested was unchanged. IHGK cells secreted less vascular endothelial growth factor on day 1 when compared with IHGKN (50.6 vs 245.6 pg/mL), along with a lower overall production rate (79% vs 133%). CONCLUSIONS: Transformation of IHGK cells resulted in the activation of vascular endothelial growth factor associated with angiogenesis. Inactivation of the G(1) cell cycle regulation occurred during immortalization and before transformation, and was sustained after carcinogen exposure. These alterations correspond to changes observed in patients with head and neck squamous cell carcinoma. This model can be useful in testing novel therapeutic and preventive strategies.

Blotting, Western↗
PubMed2002

A hole in the skull distorts substantially the distribution of extracranial electrical fields in an in vitro model.

The purpose of this study was to quantify the distortion of electrical fields by skull foramina using an in vitro model. Extracranial voltage generated by current dipoles located inside a human calva immersed in saline were measured when a 4-mm hole was open and when it was blocked with paraffin wax. Dipoles were located either along the internal surface of the bone (superficial dipoles) or at increasing distances from the bone (deep dipoles). With the hole open, extracranial signals had a substantially greater amplitude than with the hole blocked. The locations of the largest voltage values recorded outside the skull depended on the distance of the recording electrode from the hole rather than on the location of the internal dipole. For superficial dipoles, voltage values with the hole open were as much as 116 times greater than when the hole was blocked. Furthermore, when the hole was open, the largest extracranial signals were seen at the hole even when the dipole was 5 to 6 cm away from the hole. The effects of skull holes were less prominent for deep dipoles than for superficial dipoles. Skull discontinuities can be major determinants for the distribution of extracranial EEG signals. These results have implications for EEG interpretation and for source localization.

Electric Conductivity↗
PubMed2005

V.A.C. instillation: in vitro model. Part 1.

The reproducibility of a V.A.C. (Vacuum Assisted Closure) instillation system was investigated by means of an in vitro model. The relation between the volume of a delivered solution and its removal from the system was studied in foams of various size. The relationship of instillation time periods and the volume of delivered solution was determined.

Anti-Bacterial Agents↗
PubMed2006

Brave little world: spheroids as an in vitro model to study tumor-immune-cell interactions.

Multicellular tumor spheroids (MCTS) are a well-established 3-D in vitro model system that reflects the pathophysiological in vivo situation in tumor microregions and of avascular micrometastatic sites. Because monocytes and other immune cells infiltrate into MCTS of different origin, such spheroid cocultures are a valuable, still underestimated tool to systematically study heterologous interactions between tumor and immune cells. The present article gives a brief overview on work that has been published on tumor-immune cell interactions in MCTS and also summarizes mechanisms of immune suppression in the tumor milieu focussing on myeloid cells. Using the coculture model, we recently demonstrated that tumor-derived lactic acid is a potent modulator of human monocyte as lactic acid inhibited the differentiation of monocytes (MO) into dendritic cells (DC) and also impaired antigen presentation. We show herein, that the capacity of various tumor cells in MCTS to secrete lactic acid differs up to tenfold, suggesting that this capacity is dependent on the tumor cell type. It is further demonstrated that lactic acid disturbs the migration of MO into MCTS as infiltration could be increased by blocking lactic acid production. We therefore discuss lactic acid which accumulates in many tumors and tumor microregions as a potent immune suppressor for MO/DC in the tumor milieu and conclude that these data are highly relevant for adoptive immunotherapy protocols with DC.

Cell Culture Techniques↗
PubMed1999

Hyperlactaemia without acidosis - an investigation using an in vitro model.

OBJECTIVE: To use an in vitro dilutional blood model to simulate aerobic hyperlactaemia, and to question whether base excess and anion gap distinguish aerobic from anaerobic lactate production. METHODS: Cooled fresh blood was diluted (3:1) with nine different crystalloid solutions, each with a sodium concentration of 140 mmol/L but with strong ion difference values ranging from -5 mEq/L to 40 mEq/L due to varying concentrations of Cl(-), HCO(3)(-) and lactate anions. Normocapnic pH and base excess values post-dilution were determined by gas equilibration. Strong ion difference and anion gap values were measured. RESULTS: There was close correlation between the normocapnic pH and both the diluent strong ion difference and the final strong ion difference of the diluted specimens (R(2) = 0.96 and 0.89 respectively). This was independent of lactate concentrations in diluent or in post-dilution plasma. Where lactate-containing crystalloid was added, base excess, normocapnic pH and anion gap were strongly correlated with the final plasma lactate concentrations (R(2) >or= 0.99). However, only at final lactate concentrations of approximately 10 - 15 mmol/L did values of base excess, normocapnic pH or anion gap indicate metabolic acidosis. CONCLUSIONS: Hyperlactaemia from any source reduces strong ion difference and base excess and increases the anion gap, but values may remain in the normal range until hyperlactaemia is severe. Abnormal base excess and anion gap values do not distinguish aerobic from anaerobic lactate production. Normal values merely reflect low sensitivity to small lactate elevations (aerobic or otherwise).

Journal Article↗
PubMed1991

Antibacterial activity of ciprofloxacin administered intravenously in a pharmacodynamic in vitro model.

The antibacterial activity of ciprofloxacin against Gram-positive and Gram-negative bacteria was evaluated in an in vitro model by simulating its pharmacokinetics following a single 100 or 200 mg administration intravenously. The one compartment open model described by Grasso and coworkers was used for these experiments. Ciprofloxacin concentrations in the model were reproduced by calculations based on the concentration-time curve in human volunteers as reported by Wise and others. The maximum reduction of viable cell count for Enterococcus faecalis and Staphylococcus aureus was from two-to three-orders of magnitude; for Pseudomonas aeruginosa and Enterobacter cloacae from four to seven orders. A rapid killing was recorded both for Gram-positive and Gram-negative bacteria, but the initial killing was more prolonged and more pronounced for the higher dosage. The last did not interfere with regrowth that occurred for all strains after eight hours.

Bacteria↗
PubMed1999

Lubeluzole shows neuroprotective effects in an "in-vitro"-model for neuronal lesions in the chicken retina.

In this study, the isolated chicken retina was used as an "in-vitro"-model for investigation of neuronal lesions to show the neuroprotective effects of lubeluzole. Lubeluzole is a neuroprotective compound that has been shown to stereoselectively rescue sensorimotor function and reduce infarct size in photochemical stroke models in rats. In the retina, the typical cell swelling of a developing lesion is accompanied by a very strong intrinsic optical signal (IOS), occurring simultaneous with the electrical signal which is based on changes in light scattering. In the presented model, lesions were elicited electrically with a tungsten microelectrode (0.1 MOmega). The degree of damage was evaluated with optical methods by measuring area and brightness of the affected tissue. Lubeluzole was much more effective in reducing the growth of the lesions than its R-isomer. However, both compounds enhanced the possibility of the neuronal tissue to recover after excitotoxic stimuli.

Animals↗
PubMed2002

Mast cells induce upregulation of P-selectin and intercellular adhesion molecule 1 on carotid endothelial cells in a new in vitro model of mast cell to endothelial cell communication.

It is suggested that mast cells contribute to cell recruitment in inflammation through the upregulation of endothelial adhesion molecules. P-selectin and intercellular adhesion molecule(ICAM)-1 are two key adhesion molecules that have been associated indirectly with mast cell activity. The canine C2 mastocytoma cell line and primary cultures of canine carotid endothelial cells were used to establish a new in vitro model to help study the interaction between mast cells and endothelial cells. Carotid endothelial cells were incubated with mast cell mediators to uncover their effect on endothelial ICAM-1 and P-selectin expression. To assess the relative contributions of tumour necrosis factor (TNF)-alpha and histamine to such effect, an H1 antihistamine and a TNF-alpha blocking antibody were used. Prior to activation by mast cell mediators, P-selectin was expressed only within the cytoplasm, and ICAM-1 was constitutively expressed on the surface of the canine carotid endothelial cells. Both adhesion molecules were enhanced significantly and strongly upon mast cell activation at various time points. Unstored TNF-alpha was fully responsible for ICAM-1 upregulation. P-selectin was up-regulated by both preformed and newly synthesized mast cell mediators, but neither histamine nor TNF-alpha accounted for such an effect. Therefore,a new model is proposed in which the pro-inflammatory effect of mast cells on endothelial cells can be studied in vitro. In this model, it has been demonstrated that only TNF-alpha accounts for the overexpression of ICAM-1 induced by mast cells, and that mast cells up-regulate P-selectin expression through a histamine-independent mechanism.

Animals↗
PubMed1997

Evaluation of a human corneal epithelial cell line as an in vitro model for assessing ocular irritation.

A human corneal epithelial cell line, 10.014 pRSV-T (HCR-T cells), has been used to develop a three-dimensional in vitro model of the human corneal epithelium (HCE-T model). HCE-T cells form a stratified culture when grown at the air-liquid interface on a collagen membrane in serum-free medium. This model served as the basis for assays which supported the ocular irritancy assessment of water-soluble test substances. Cellular alterations in the HCE-T model were measured following 5-min topical exposures to 20 chemicals [listed in the European Center for Ecotoxicology and Toxicology of Chemicals (ECETOC) Reference Chemicals Data Bank] and 25 surfactant-based product formulations [utilized in the Cosmetic, Toiletry, and Fragrance Association (CTFA) Alternatives Program Phase III]. In vitro assays used were transepithelial permeability to sodium fluorescein (TEP) and transepithelial electrical resistance (TER). These measured alterations in the barrier function of this corneal epithelial equivalent. Barrier function is a well-developed property in the HCE-T model that supports the mechanistic relevance of these assays. In vitro data, averaged from replicate assays, were compared to respective Draize rabbit eye irritation data from the publicly available ECETOC and CTFA databases using linear regression with Pearson's correlation analysis. For chemicals, Pearson's correlation coefficients, r, from comparisons of Draize maximum average scores (MAS) to TEP and TER data were 0.71 and 0.55, respectively. For product formulations, Pearson's correlation coefficients from comparisons of Draize MAS to TEP and TER data were 0.86 and 0.80, respectively. Data indicated that barrier function alterations in the HCE-T model correlated with ocular irritancy and corneal toxicity. While the irritancy of the chemicals tested was effectively assessed only by the TEP assay, that for the surfactant-based product formulations was effectively assessed by both the TEP and TER assays. Results also suggested that the HCE-T TEP and TER assays vary in their effectiveness for evaluating specific classes of test materials.

Animals↗
PubMed1989

An in vitro model of wound healing in the CNS: analysis of cell reaction and interaction at different ages.

We have developed an in vitro model in which cells responding to trauma in the immature and mature CNS can be isolated, placed into serum-free culture, and characterized. By implanting nitrocellulose filters into the brains of neonatal and adult rats under different conditions, we are able to harvest populations of cells responding to trauma in the neonate (critical period implant), in the adult (scar implant), and in implants that have remained in vivo past the critical period (postcritical period implant). Upon placement in culture, we have found that astrocytes represent the majority of cells occupying both the critical period and postcritical period implants, whereas fibroblasts and macrophages represent the majority of cells in the glial-fibroblastic scar. The morphologies of the astrocytes on the surface of the different implants, after 3 days in culture, differs markedly--the critical period astrocytes exhibiting a more ordered distribution compared to the haphazard arrangement of astrocyte processes on the surface of the postcritical and scar implants. After migration from the implant, critical period astrocytes assume an epithelioid morphology and cluster together setting up definite boundaries between themselves and the endothelial cells. In contrast, postcritical period astrocytes exhibit a more elongated morphology under the same culture conditions and appear to be randomly dispersed among the endothelial cells. The scar astrocytes exhibit a wide range of morphologies and, although they tend to cluster, do not exhibit the ordered association seen with the critical period astrocytes. We propose that the plasticity of the neonatal astrocytes and the rapid and ordered cellular response seen in vitro reflect the ability of the immature CNS in vivo to respond to injury without the formation of a glial-fibroblastic scar.

Aging↗
PubMed1991

In vitro models differentiating between direct and indirect effects of ischemia on astrocytes.

Mouse astrocytes in primary cultures were subjected to an in vitro model of ischemia (hypoxia combined with substrate deprivation, excess potassium, or elevated glutamate) and examined with the light (phase) and electron microscope. Three hours of hypoxia alone or in combination with the other insults had little effect upon the morphology of astrocytes but did cause disaggregation of polyribosomes. With reoxygenation, polyribosomes reformed and many mitochondria changed from the orthodox to the condensed configuration. Notably, there was little swelling. Excess (50 mM) potassium, added (as KCl) to a normal isotonic medium, also caused no swelling. However, when 50 mM potassium was substituted for a similar amount of sodium, marked astrocyte swelling did occur. A morphologically similar swelling was seen when glutamate (50 microM to 1 mM) was added to the culture medium, both with or without hypoxia with or without substrate deprivation. Potassium or glutamate-induced swelling was reversible with 1 h of recovery in normal medium. These results show that alterations in postischemic astrocytic morphology in vivo to a large extent can be reproduced in astrocytes in primary cultures. In addition, they suggest that postischemic astrocyte swelling is related to alterations in extracellular milieu, including accumulation of glutamate and/or alterations in the potassium/sodium ratios with increased potassium and decreased sodium. In contrast, morphologic alterations in polyribosomes and in mitochondria appear to be a direct response to ischemia itself.

Animals↗
PubMed1997

Development of an in vitro model to study the response of saphenous vein endothelium to pulsatile arterial flow and circumferential deformation.

OBJECTIVES: To develop an in vitro model of human saphenous vein bypass to facilitate study of the early adaptive responses of venous endothelium to arterial flow conditions. DESIGN MATERIAL AND METHODS: Segments of human saphenous vein (with or without external polytetrafluoroethylene (PTFE) stents to limit circumferential and radial deformation) were mounted in a bypass circuit and subjected to pulsatile flow with oxygenated Krebs solution to simulate arterial or venous flow conditions for a period of 90 min. The viability of the vein was assessed by the tissue ATP concentration and vasomotor responses to phenylephrine, sodium nitroprusside and bradykinin (endothelium-dependent). Immunohistochemistry was used to assess both endothelial preservation (CD31) and the expression of proteins involved in leukocyte adhesion: E-selectin, P-selectin and ICAM-1. Freshly excised veins were used as controls. RESULTS: The concentration of ATP was 320 +/- 11 nmol/g in freshly excised vein (n = 8) and following exposure to the arterial flow circuit increased to 566 +/- 60 nmol/g (n = 8, paired t-test, p = 0.003) in unstented veins and to 421 +/- 49 nmol/g (n = 8, paired t-test, p = 0.002) in externally stented veins (with PTFE). Both endothelium-dependent and sodium nitroprusside-induced vasodilatation responses were preserved after veins were exposed to the arterial flow circuit, but the sensitivity to phenylephrine was increased: EC50 decreasing from 9 microM, p = 0.008. There was a 5-10% decrease in staining area for CD31 after veins, stented or unstented, were exposed to the arterial flow circuit. However, after exposure to the arterial flow circuit, the staining area ratio for ICAM-1/CD31, which remained unchanged in externally stented veins, increased two-fold in unstented veins, p > 0.01: there were no changes in the staining area ratio P-selectin/CD31 and no staining for E-selectin was observed. CONCLUSION: Vasomotor responses and tissue ATP concentration indicate that the viability of saphenous vein can be maintained for up to 90 min in an ex vivo flow circuit and the CD31 staining indicated endothelial preservation. This opens up the possibility of investigating the early changes in saphenous vein endothelium following exposure to arterial pressure, as at bypass surgery. First results suggest that there is rapid upregulation of the leukocyte adhesion molecule ICAM-1, which can be prevented by limiting the circumferential deformation of the vein with an external PTFE stent.

Adaptation, Physiological↗
PubMed1992

Amikacin, ceftazidime, and flucloxacillin against suspended and adherent Pseudomonas aeruginosa and Staphylococcus epidermidis in an in vitro model of infection.

Bacterial inocula were exposed as suspended cultures or as adherent biofilms on glass beads in a novel in vitro model of infection to oscillating drug concentrations mimicking human serum kinetics during clinical treatment. Amikacin was given once or thrice daily alone or in combination with ceftazidime or flucloxacillin against Pseudomonas aeruginosa or Staphylococcus epidermidis. Killing of adherent bacteria was significantly reduced during single-drug treatment compared with suspended bacteria (P less than .001), and beta-lactams were more active than amikacin against both suspended and adherent bacteria (P less than .01). Amikacin-beta-lactam combinations killed the inocula more rapidly and were consistently bactericidal against both suspended and adherent pathogens (P less than .05). Once-daily dosing of amikacin produced greater initial killing than thrice daily dosing (P less than .05), but both regimens were similarly effective after 48 h. The differences in antibiotic activity against suspended and adherent bacteria may relate to clinical failures in the treatment of foreign-body infections by bacteria sensitive to the administered antibiotics, as determined by standard susceptibility tests.

Amikacin↗
PubMed1991

Single daily dosing of amikacin in an in-vitro model.

The pharmacodynamics of amikacin given as a single daily dose was compared with standard divided dosing in an in-vitro model of infection. This model allows the exposure of log phase bacteria to changing concentrations of antibiotics that simulate the kinetics of the drugs in human patients. Two strains of Pseudomonas aeruginosa, one sensitive and one resistant to azlocillin were studied (MICs for amikacin were 16 and 8 mg/l respectively). Simulated drug regimens included: amikacin 400 mg q 8 h; amikacin 1.2 g q 24 h; and azlocillin 4 g q 12 h. Each regimen alone and both combinations of amikacin plus azlocillin were studied. With both amikacin regimens initial rapid killing was followed by regrowth of resistant subpopulations. Azlocillin alone produced minimal killing of the resistant strain and moderate killing with ultimate bacteriostasis of the susceptible strain. Bacterial regrowth was prevented with both combination regimens with the single daily dose of amikacin plus azlocillin producing the most rapid and complete killing, especially of the azlocillin resistant strain. These data support further clinical studies of single daily dosing of aminoglycosides.

Amikacin↗