This paper reports internal structures of a bedding-parallel fault in Permian limestone at Xiaojiaqiao outcrop that was moved by about 0.5 m during the 2008 MW7.9 Wenchuan earthquake. The fault is located about 3 km to the south from the middle part of Yingxiu-Beichuan fault, a major fault in the Longmenshan fault system that was moved during the earthquake. The outcrop is also located at Anxian transfer zone between the northern and central segments of Yingxiu-Beichuan fault where fault system is complex. Thus the fault is an example of subsidiary faults activated by Wenchuan earthquake. The fault has a strike of 243 • or N63 • E and a dip of 38 • NW and is nearly optimally oriented for thrust motion, in contrast to high-angle coseismic faults at most places. Surface outcrop and two shallow drilling studies reveal that the fault zone is several centimeters wide at most and that the coseismic slip zone during Wenchuan earthquake is about 1 mm thick. Fault zone contains foliated cataclasite, fault breccia, black gouge and yellowish gouge. Many clasts of foliated cataclasite and black gouge contained in fault breccia indicate multiple slip events along this fault. But fossils on both sides of fault do not indicate clear age difference and overall displacement along this fault should not be large. We also report results from high-velocity friction experiments conducted on yellowish gouge from the fault zone using a rotary shear low to high-velocity frictional testing apparatus. Dry experiments at normal stresses of 0.4 to 1.8 MPa and at slip rates of 0.08 to 1.35 m/s reveal dramatic slip weakening from the peak friction coefficient of around 0.6 to very low steady-state friction coefficient of 0.1-0.2. Slip weakening parameters of this carbonate fault zone are similar to those of clayey fault gouge from Yingxiu-Beichuan fault at Hongkou outcrop and from Pingxi fault zone. Our experimental result will provide a condition for triggering movement of subsidiary faults or off-fault damage during a large earthquake.
We previously reported that the generation of reactive oxygen species (ROS) is the initial event in cell death induced by 6-hydroxydopamine (6-OHDA), an experimental model of Parkinsonism. Since recent studies suggested the important role of antioxidant activity of alpha-lipoic acid (LA) in the suppression of apoptosis of various types, we studied the effect on 6-OHDA-induced apoptosis of PC12 cells. Biochemical analysis revealed that LA suppressed the 6-OHDA-induced ROS generation, increase of caspase-like activity and chromatin condensation. The suppression of 6-OHDA-induced apoptosis by LA required pre-incubation of PC12 cells with LA for 12-24 h. LA increased the intracellular levels of heme oxygenase-1 (HO-1) and glutathione (GSH) and stimulated the expression of GSH synthesis-related genes such as cystine/glutamate antiporter and gamma-glutamylcysteine synthetase (gamma-GCS). However, Sn-mesoporphyrin IX, an inhibitor of HO-1, did not attenuate the LA-induced suppression of apoptosis. In contrast, buthionine sulfoximine, an inhibitor of gamma-GCS, attenuated the LA-induced suppression of ROS generation and chromatin condensation. In addition, a transcription factor Nrf2, which regulates the expression of antioxidant enzymes such as gamma-GCS, translocated to the nucleus by LA. These results suggested that LA suppressed the 6-OHDA induced-apoptosis by the increase in cellular glutathione through stimulation of the GSH synthesis system but not by the expression of HO-1.
3-Nitropropionic acid (3NP) functions as an irreversible inhibitor of succinic acid dehydrogenase (complex II) and induces neuronal disorders in rats similar to those in patients with Huntington's disease. It is well known that L-carnitine (LC), a carrier of long chain fatty acid into the mitochondrial matrix, attenuates the neuronal degeneration in 3NP-treated rats. From these findings it has been suggested that 3NP induces certain neuronal cell death through mitochondrial dysfunction and that LC preserves the neurons against the dysfunction of mitochondria caused by 3NP. However, the detailed mechanism of cell death by 3NP and the protective actions of LC against the mitochondrial dysfunction have not been fully elucidated yet. Thus, we studied the molecular mechanism of the effects of 3NP and LC on isolated rat liver mitochondria. 3NP inhibited succinate respiration and the decreased respiratory control ratio of isolated mitochondria without affecting oxidative phosphorylation. 3NP induced a membrane permeability transition (MPT), which plays an important role in the mechanism of apoptotic cell death. 3NP stimulated Ca 2þ release from mitochondria, decreased membrane potential, induced mitochondrial swelling, and stimulated cytochrome c release from mitochondria. 3NP-induced swelling was suppressed by bovine serum albumin, inhibitors of phospholipase A 2 and by an inhibitor of classic MPT, cyclosporin A. Furthermore, LC suppressed the changes brought about by 3NP in mitochondrial functions in the presence of ATP. These results suggest that MPT underlies the mechanism of 3NP-induced cell death, and that LC attenuates mitochondrial MPT by decreasing long chain fatty acids generated by phospholipase A 2 .
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