Aggregate Spreading Research Articles

Study on Fracture Toughness of Cement Treated Aggregate

In order to investigate the effect of curing period and cement content of the specimen on fracture toughness of cement treated aggregate, a series of parametric tests have been conducted. By means of three-point bending method, the fracture toughness of cement treated aggregate was measured. In this study, four specimen curing periods (14 d, 28 d, 60 d and 90 d) and four different cement contents (4%, 5%, 6% and 7%) were used. The results indicate that the fracture toughness of cement treated aggregate is increasing with the increase of specimen curing period. Besides, with the increase of cement content, there is a tendency to decrease in the fracture toughness of cement treated aggregate. The higher cement content will be adverse to prevent the fine fissure inside cement treated aggregate base layer spreading further.

Spreading dynamics and wetting transition of cellular aggregates

We study the spreading of spheroidal aggregates of cells, expressing a tunable level of E-cadherin molecules, on glass substrates decorated with mixed fibronectin and polyethylene glycol. We observe the contact area by optical interferometry and the profile by side-view microscopy. We find a universal law of aggregate spreading at short times, which we interpret through an analogy with the spreading of viscoelastic droplets. At long times, we observe either partial wetting or complete wetting, with a precursor film of cells spreading around the aggregate with two possible states. In strongly cohesive aggregates this film is a cellular monolayer in the liquid state, whereas in weakly cohesive aggregates, cells escape from the aggregate, forming a 2D gas. The escape of isolated cells is a physical mechanism that appears also to be present in the progression of a noninvasive tumor into a metastatic malignant carcinoma, known as the epithelial-mesenchymal transition.

Optimizing Rolling Patterns for Chip Seals Using Laboratory Aggregate Loss Performance Tests on Field Fabricated Samples

This paper presents a study to determine the optimal rolling patterns for chip seals based on aggregate retention performance. Chip seal sections composed of single seals of granite 78M and CRS-2 emulsion are constructed using five different rolling patterns with two or three rollers. Both pneumatic tire and combination rollers are used in developing these patterns. Chip seal samples are obtained from the sections for laboratory testing. The aggregate retention performance is evaluated using the flip-over test, Vialit test, and the third-scale model mobile loading simulator. It is found that the time delay between aggregate spreading and rolling is an important parameter for the aggregate retention performance. The laboratory aggregate retention test results are used along with typical roller speeds and the maximum allowable time delay between aggregate spreading and rolling to develop optimal rolling patterns for two and three rollers.

Contact Inhibition of Cell Spreading: A Mechanism for the Maintenance of Thyroid Cell Aggregation in Vitro

When freshly isolated porcine thyroid cells are stimulated with thyrotropin (TSH) they organize to form functional follicles in conventional substrate-adherent culture. Cell aggregation is essential for follicular reorganization and is likely to be influenced by the balance between cell-cell adhesion (promoting aggregation) and cell-substrate adhesion (favoring spreading and monolayer formation). Recently we observed that TSH potentiated cell-cell adhesion and in the present study we have sought evidence that TSH might also regulate cell-substrate adhesion. Two parameters of cell-substrate adhesion, namely, cell attachment to collagen and cell spreading upon collagen, were measured using preparations of isolated single cells and of multicellular aggregates. TSH had no effect upon the attachment or spreading of single cells, but inhibited aggregate spreading without affecting aggregate attachment. The possibility that cell-cell contact modulated the response to TSH in aggregates, but not in single cells, was confirmed using a cell-free membrane preparation which inhibited the spreading of single cells but not their rate of attachment. Moreover, TSH potentiated the inhibitory effect of membranes on the spreading of single cells. Heparin also specifically inhibited the spreading of both single cells and cell aggregates, suggesting that a heparin-sensitive adhesive mechanism might be recruited as thyroid cells spread. We conclude that thyroid cell-substrate adhesion is regulated by a synergistic interaction between cell-cell contact and TSH which preferentially inhibited cell spreading but not attachment. Such contact-dependent inhibition of cell spreading is predicted to preserve cell aggregates and hence contribute to the maintenance of thyroid follicular differentiation in vitro.