Shear Behavior Models of Steel Fiber Reinforced Concrete Beams Modifying Softened Truss Model Approaches.

Recognizing that steel fibers can supplement the brittle tensile characteristics of concrete, many studies have been conducted on the shear performance of steel fiber reinforced concrete (SFRC) members. However, previous studies were mostly focused on the shear strength and proposed empirical shear strength equations based on their experimental results. Thus, this study attempts to estimate the strains and stresses in steel fibers by considering the detailed characteristics of steel fibers in SFRC members, from which more accurate estimation on the shear behavior and strength of SFRC members is possible, and the failure mode of steel fibers can be also identified. Four shear behavior models for SFRC members have been proposed, which have been modified from the softened truss models for reinforced concrete members, and they can estimate the contribution of steel fibers to the total shear strength of the SFRC member. The performances of all the models proposed in this study were also evaluated by a large number of test results. The contribution of steel fibers to the shear strength varied from 5% to 50% according to their amount, and the most optimized volume fraction of steel fibers was estimated as 1%-1.5%, in terms of shear performance.

Heme oxygenase-1 mediates cytoprotection against nitric oxide-induced cytotoxicity via the cGMP pathway in human pulp cells.

OBJECTIVE: This study examined the effects of exogenous nitric oxide (NO) on human pulp cells and the involvement of cyclic 3',5'-monophosphate (cGMP) in pulpal protection induced by heme oxygenase-1 (HO-1) against NO-induced cytotoxicity. STUDY DESIGN: This study investigated cytotoxicity and HO-1 induction in pulp cells induced by the NO donor S-nitroso-N-acetyl-D,L-penicillamine (SNAP), by using Western blotting and a cell viability assay. It also investigated whether HO-1 contributes to the cytoprotective effect against the cytotoxicity caused by NO and the relationship between HO-1 and cGMP in the signaling pathway. RESULTS: S-nitroso-N-acetyl-D,L-penicillamine decreased cell viability, but increased HO-1 expression in a concentration- and time-dependent manner in human pulp cells. NO-induced cytotoxicity was inhibited in the presence of hemin (inducer of HO-1), whereas it was enhanced in the presence of zinc protoporphyrin IX (ZnPP IX, HO-1 inhibitor); therefore, the NO-induced cytotoxicity was correlated with HO-1 expression. Pretreatment with a membrane-permeable cGMP analog, 8-bromo-cGMP, restored cell death and enhanced the HO-1 protein expression induced by SNAP. By contrast, 1 mM SNAP inhibited guanylate cyclase in pulp cells pretreated with 1H-[1,2,4]oxadiazole[4,3-alpha]quinoxalin-1-one (ODQ), resulting in marked cytotoxicity. CONCLUSION: These findings of a link between HO-1, regulated via the cGMP system and NO-induced cytotoxicity in human pulp cells, suggest a protective role for HO-1 in pulpal inflammation.