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Tests of the lateral and torsional stability are quite sensitive to the experimental conditions, such as support conditions and loading system. Controlling all of these conditions in a full-size test is a very challenging task. Therefore, in this paper, an experimental measurement method that can control the experimental conditions using a small-scale model was proposed to evaluate the lateral and torsional stability of beams. For this, a loading system was provided to maintain the vertical direction of the load applied to the beam, and a support frame was produced to satisfy the in-plane and out-of-plane support conditions. The experimental method using a small-scale model was applied successively to the lateral and torsional behavior and stability of I-shaped beams. The proposed experimental methods, which effectively accommodate the changes in the geometry and length of the beam, could contribute to further experimental studies regarding the lateral and torsional stability of flexural members. [ABSTRACT FROM AUTHOR]

Hedgehog (Hh) signaling is an essential pathway in embryonic development of prostate. Hh also plays roles in the proliferation of progenitor cells and cancer cells of adult prostate. However, how Hh signaling contributes to carcinogenesis of prostate is poorly understood. Stathmin1 is a microtubule-regulating protein that plays an important role in the assembly and disassembly of the mitotic spindle. Stathmin1 is expressed in normal developing mouse prostate and in prostate cancer. The expression pattern of stathmin1 is similar to that of Shh in prostate development and cancer, suggesting a connection between these two proteins. In this study, we examined the relationship between stathmin1 and Hh signaling. Here, we show that stathmin1 expression is regulated by Hh signaling in prostate cancer cells. Cyclopamine, a specific inhibitor of Hh signaling, reduced the expression of stathmin1 in prostate cancer cells. However, the Shh peptide induced stathmin1 expression. Overexpression of Gli1 further confirmed the relationship. Co-expression of stathmin1 and Patched 1, a receptor for Hh signaling was observed in prostate cancer tissues. Cyclopamine and stathmin1 siRNA both decreased proliferation of prostate cancer cells but did not produce an additive effect, suggesting a common pathway. These results suggest that Hh signaling regulates proliferation of prostate cancer cells by controlling stathmin1 expression. [ABSTRACT FROM AUTHOR]

Hedgehog signaling plays critical roles during embryonic development. It is also involved in tissue regeneration and carcinogenesis in various adult tissues. Moreover, it regulates the maintenance of cancer stem cells and adult stem cells. Although hedgehog signaling is important in gastric carcinogenesis, its role in gastric regeneration has not been previously examined. In the present study, we evaluated the expression and roles of hedgehog signaling during gastric regeneration. Gastric ulcers were induced by serosal application of an acetic acid solution in mice. Sham-operated mice served as controls. The proliferation of gastric progenitor cells was studied using bromodeoxyuridine (BrdU). The expression of hedgehog signaling molecules and the differentiation of gastric progenitor cells were examined by immunohistochemical staining and Western blotting. One day after the induction of gastric ulcer, the proliferation of gastric progenitor cells increased; however, the expression of hedgehog signaling molecules, including sonic hedgehog (Shh), Indian hedgehog (Ihh), desert hedgehog (Dhh), and patched (Ptch1) decreased at the ulcer margin. From 5 days after the induction of gastric ulcer, newly generated gastric glands and their differentiation were observed at the ulcer margin. The expression of hedgehog signaling molecules gradually increased in the newly generated gastric glands of the ulcer margin. Cyclopamine, a specific inhibitor of hedgehog signaling, significantly inhibited the differentiation of mucous cells and parietal cells during the gastric regeneration process. The above results suggest that hedgehog signaling is involved in the differentiation of gastric progenitor cells during the gastric ulcer repair process. [ABSTRACT FROM AUTHOR]

Ischemia-induced cerebral injury evolves over a longer period than previously believed through post-ischemic inflammation. Retinoic acid (RA) has been shown to exert cytoprotective effects on several cells, but its effects on ischemia-induced cerebral injury have been poorly characterized. The aim of the present study was to examine the effects of all- trans-RA on ischemia-induced cerebral injury and elucidate the underlying mechanism. All- trans-RA treatment reduced the size of the ischemia-induced cerebral infarct. To elucidate the underlying mechanism, ischemia-induced cerebral inflammation was studied by examination of expressions of interleukin 1β (IL-1β) and ED-1. RA treatment significantly reduced the cerebral inflammation. Moreover, cerebral ischemic induction of cyclooxygenase-2 (COX-2) and CCAAT/enhancer binding protein β (C/EBPβ), which binds to the COX-2 promoter, was also inhibited by RA. These results suggest that RA can reduce ischemia-induced cerebral injury by an anti-inflammatory action, which may be effected via inhibition of C/EBPβ-mediated COX-2 induction. [ABSTRACT FROM AUTHOR]

The receptor activator of nuclear factor (NF)-κB ligand (RANKL; also termed TRANCE/OPGL/ODF/TNFSF11), a new member of the tumor-necrosis factor (TNF) superfamily, was identified as a key cytokine involved in the differentiation of the immune system and the regulation of immunity as well as in bone metabolism. In particular, RANKL-deficient mice showed defects in the early differentiation of T lymphocytes, suggesting that RANKL is a novel regulator of early thymocyte development. Here, we describe the expression of RANKL during regeneration following acute involution induced by cyclophosphamide in the rat thymus. The present study demonstrates the presence and upregulated expression of the RANKL in thymic subcapsular, paraseptal, perivascular, and medullary epithelial cells during thymus regeneration. Our results suggest that the RANKL expressed in these thymic epithelial cells plays a role in the development of T cells during thymic regeneration. [ABSTRACT FROM AUTHOR]