In this paper, we present the result of analytical investigation pertaining to the structural behavior of steel-concrete composite plate girder with arch-type web stiffener. In the arch-type web stiffener located in the compression side of web, infill concrete is cast to strengthen the arch-type stiffener and also to exert resisting force against compression force. This type of composite steel-concrete plate girder bridge is built and is in service. To understand the behavior thoroughly, analytical parametric study was conducted by using the finite element method. As a result it was found that the effect of arch-type stiffener with infill concrete is considerable for the design of such type composite girder bridge.

In this paper, we present the result of investigations pertaining to the elastic buckling of simply supported columns with various cross-sectional dimensions but the same length and volume. In the investigations the accuracy of the analysis methods is studied and it was found that the result obtained by the successive approximations technique is the most accurate. In addition, the elastic buckling loads of columns with variable cross-section dimensions are obtained by the theoretical and numerical methods. From the results, it was found that the buckling loads obtained by the numerical methods are close to the buckling loads obtained by the successive approximations technique for the practical standpoints. Moreover, the buckling load of column with convexity in its middle is the highest while the buckling load of the tapered column is the lowest as expected.

Previous work demonstrated that an ethanol extract (HS0608) of a mixture of three medicinal plants of Curcuma longae radix, Phellinus linteus, and Scutellariae radix markedly inhibits Aβ (25-35)-induced neurotoxicity. The present study was performed to further verify the neuroprotective effect of HS0608 on oxidative and ischemic cerebral injury using cultured rat cortical neurons and rats. Exposure of cultured cortical neurons to 100 μM hydrogen peroxide (H2O2) induced neuronal apoptotic death. At 10-100μg/ml, HS0608 inhibited neuronal death, elevation of intracellular calcium concentration ([Ca2+]i), and generation of reactive oxygen species (ROS) induced by H2O2 in primary cultures of rat cortical neurons. In vivo, HS0608 prevented cerebral ischemic injury induced by 2-h middle cerebral artery occlusion (MCAO) and 24-h reperfusion. The ischemic infarct and edema were significantly reduced in rats that received HS0608 (200 mg/kg). These results suggest that the anti-oxidative properties of HS0608 may be responsible for its neuroprotective effect against focal cerebral ischemic injury and that HS0608 may have a therapeutic role in neurodegenerative diseases such as stroke.