The role of graphite layers in gravitational deformation of pelitic schist

Deep-seated landslides in pelitic schists are common in many countries, but are poorly investigated and understood. In this study we present the first detailed examination and modelling of landslide mechanisms in these materials. We found that pelitic schist commonly contains black, graphite-rich layers on a scale of millimeters to centimeters thickness that are typically weaker than neighboring layers. By examining microscopic textures in borehole samples obtained from landslide masses of pelitic schist, we find that ductile gravitational shearing commonly occurs within these weaker layers, accompanied by brittle fracture in the surrounding layers. To investigate this mechanisms, we have performed high-precision direct shear tests, using a novel back-pressured shearbox, on artificial rock samples both with and without graphite layers placed between pre-cut shear surfaces. The tests used normal stresses up to 800 kPa (equivalent to 32 m depth of burial). We found that the coefficients of friction for samples with graphite layers embedded in the artificial rock samples (0.30, representing an angle of internal friction of 16.7°) were much lower than those without graphite layers on the pre-cut surface (0.85). The shear strength of the artificial rocks with embedded layers of graphite decreased abruptly with increasing areal extent of the graphite layer along the shear surface, from which it can be inferred that the continuity of a graphite layer in natural pelitic schist has a considerable effect on shear resistance. These results suggest that even comparatively low dip angles of schistosity in pelitic schist could initiate microscopic slip along the graphite-rich layers

Shiga toxin activates p38 MAP kinase through cellular Ca2+ increase in Vero cells

AbstractWe examined whether the mitogen-activated protein kinase (MAPK) pathway is involved in Shiga toxin (Stx)-induced Vero cell injury. Consonant with cell injury, Stx caused a transient extracellular signal-regulated kinase1/2 (ERK1/2) and a sustained p38 MAPK phosphorylation. p38 MAPK inhibitors (SB 203580 and PD 169316), but not an ERK1/2 kinase inhibitor (PD 98059), partially inhibited the Stx-induced cell death. BAPTA-AM, a Ca2+ chelator, reduced both cell injury and p38 MAPK phosphorylation. Antioxidants reduced Stx1-induced p38 MAPK phosphorylation. These data indicate that Stx activates p38 MAPK through an increase in intracellular Ca2+ and reactive oxygen species, and this signaling is involved in Stx-induced cell death

Alpha lipoic acid selectively inhibits proliferation and adhesion to fibronectin of v-H-ras-transformed 3Y1 cells

Here, we focused on the effects of racemic α-lipoic acid on proliferation and adhesion properties of 3Y1 rat fibroblasts and the v-H-ras-transformed derivative, HR-3Y1-2 cells. Racemic α-lipoic acid inhibited proliferation of HR-3Y1-2 but not 3Y1 cells at 0.3 and 1.0 mM. R-(+)-α-lipoic acid also inhibited proliferation of HR-3Y1-2 cells equivalent to that of racemic α-lipoic acid. In addition, racemic α-lipoic acid decreased intracellular reactive oxygen species levels in HR-3Y1 cells but not 3Y1 cells. Next, we evaluated the effects of racemic α-lipoic acid on cell adhesion to fibronectin. The results indicated that racemic α-lipoic acid decreased adhesive ability of HR-3Y1-2 cells to fibronectin-coated plates. As blocking antibody experiment revealed that β1-integrin plays a key role in cell adhesion in this experimental system, the effects of racemic α-lipoic acid on the expression of β1-integrin were examined. The results indicated that racemic α-lipoic acid selectively downregulated the expression of cell surface β1-integrin expression in HR-3Y1-2 cells. Intriguingly, exogenous hydrogen peroxide upregulated cell surface β1-integrin expression in 3Y1 cells. Taken together, these data suggest that reduction of intracellular reactive oxygen species levels by α-lipoic acid could be an effective means of ameliorating abnormal growth and adhesive properties in v-H-ras transformed cells