Slurry Seal Maintenance Applications

A slurry seal mixture consists of graded fine aggregate (normally minus 3/8-inch material), mixing grade emulsified asphalt (SS-1 or SS-lH), and water. The water is added to aid in mixing and to provide a free-flowing consistency so that the mixture can be spread in thin layers on the surface of an existing pavement. After the mixture is spread, the water evaporates and the remaining material, aggregate and base asphalt, forms a thin seal on the pavement surface which resembles a fine-grained asphaltic-concrete surface. As a result of the free-flowing consistency and the fineness of the aggregate, a slurry mixture readily fills cracks, voids, small depressions, and will form a thin seal over the entire pavement surface

Comparison of Contained Rock Asphalt Mat (CRAM) with Conventional Asphaltic Concrete Pavements

A brochure proposing the use of Contained Rock Asphalt Mat (CRAM) provided a comparison of stress distributions throughout a CRAM structure (Figure 1) as compared to a conventional pavement (Figure 2). Experience has indicated that stress distributions do not always present the most sensitive or appropriate analysis of a pavement structure. Distributions of strains, and more particularly work , are better indicators of load distributions throughout a pavement structure and subsequent performance

Rat Urinary Bladder Carcinogenesis by Dual-Acting PPARα + γ Agonists

Despite clinical promise, dual-acting activators of PPARα and γ (here termed PPARα+γ agonists) have experienced high attrition rates in preclinical and early clinical development, due to toxicity. In some cases, discontinuation was due to carcinogenic effect in the rat urothelium, the epithelial layer lining the urinary bladder, ureters, and kidney pelvis. Chronic pharmacological activation of PPARα is invariably associated with cancer in rats and mice. Chronic pharmacological activation of PPARγ can in some cases also cause cancer in rats and mice. Urothelial cells coexpress PPARα as well as PPARγ, making it plausible that the urothelial carcinogenicity of PPARα+γ agonists may be caused by receptor-mediated effects (exaggerated pharmacology). Based on previously published mode of action data for the PPARα+γ agonist ragaglitazar, and the available literature about the role of PPARα and γ in rodent carcinogenesis, we propose a mode of action hypothesis for the carcinogenic effect of PPARα+γ agonists in the rat urothelium, which combines receptor-mediated and off-target cytotoxic effects. The proposed mode of action hypothesis is being explored in our laboratories, towards understanding the human relevance of the rat cancer findings, and developing rapid in vitro or short-term in vivo screening approaches to faciliate development of new dual-acting PPAR agonist compounds