Evaluation of Seismic Rupture Models for the 2011 Tohoku-Oki Earthquake Using Tsunami Simulation

Developing a realistic, three-dimensional rupture model of the large offshore earthquake is difficult to accomplish directly through band-limited ground-motion observations. A potential indirect method is using a tsunami simulation to verify the rupture model in reverse because the initial conditions of the associated tsunamis are caused by a coseismic seafloor displacement correlating to the rupture pattern along the main faulting. In this study, five well-developed rupture models for the 2011 Tohoku-Oki earthquake were adopted to evaluate differences in simulated tsunamis and various rupture asperities. The leading wave of the simulated tsunamis triggered by the seafloor displacement in Yamazaki et al. (2011) model resulted in the smallest root-mean-squared difference (~0.082 m on average) from the records of the eight DART (Deep-ocean Assessment and Reporting of Tsunamis) stations. This indicates that the main seismic rupture during the 2011 Tohoku earthquake should occur in a large shallow slip in a narrow range adjacent to the Japan trench. This study also quantified the influences of ocean stratification and tides which are normally overlooked in tsunami simulations. The discrepancy between the simulations with and without stratification was less than 5% of the first peak wave height at the eight DART stations. The simulations, run with and without the presence of tides, resulted in a ~1% discrepancy in the height of the leading wave. Because simulations accounting for tides and stratification are time-consuming and their influences are negligible, particularly in the first tsunami wave, the two factors can be ignored in a tsunami prediction for practical purposes

Apical membrane rupture and backward bile flooding in acetaminophen-induced hepatocyte necrosis

Morphological changes of hepatocyte death have so far only been described on cells in culture or in tissue sections. Using a high-resolution and high-magnification multiphoton microscopic system, we recorded in living mice serial changes of acetaminophen (APAP)-induced hepatocyte necrosis in relevance to metabolism of a fluorogenic bile solute. Initial changes of hepatocyte injury included basal membrane disruption and loss of mitochondrial membrane potential. An overwhelming event of rupture at adjacent apical membrane resulting in flooding of bile into these hepatocytes might ensue. Belbs formed on basal membrane and then dislodged into the sinusoid circulation. Transmission electron microscopy disclosed a necrotic hepatocyte depicting well the changes after apical membrane rupture and bile flooding. Administration of the antidote N-acetylcysteine dramatically reduced the occurrence of apical membrane rupture. The present results demonstrated a hidden but critical step of apical membrane rupture leading to irreversible APAP-induced hepatocyte injury

Nitrogen-Functionalized Graphene Nanoflakes (GNFs:N): Tunable Photoluminescence and Electronic Structures

This study investigates the strong photoluminescence (PL) and X-ray excited optical luminescence observed in nitrogen-functionalized 2D graphene nanoflakes (GNFs:N), which arise from the significantly enhanced density of states in the region of {\pi} states and the gap between {\pi} and {\pi}* states. The increase in the number of the sp2 clusters in the form of pyridine-like N-C, graphite-N-like, and the C=O bonding and the resonant energy transfer from the N and O atoms to the sp2 clusters were found to be responsible for the blue shift and the enhancement of the main PL emission feature. The enhanced PL is strongly related to the induced changes of the electronic structures and bonding properties, which were revealed by the X-ray absorption near-edge structure, X-ray emission spectroscopy, and resonance inelastic X-ray scattering. The study demonstrates that PL emission can be tailored through appropriate tuning of the nitrogen and oxygen contents in GNFs and pave the way for new optoelectronic devices.Comment: 8 pages, 6 figures (including toc figure

Is the drug-induced hypersensitivity syndrome (DIHS) due to human herpesvirus 6 infection or to allergy-mediated viral reactivation? Report of a case and literature review

<p>Abstract</p> <p>Background</p> <p>Drug-Induced Hypersensitivity Syndrome (DIHS) is a severe and rare systemic reaction triggered by a drug (usually an antiepileptic drug). We present a case of DISH and we review studies on the clinical features and treatment of DIHS, and on its pathogenesis in which two elements (Herpesvirus infection and the drug) interact with the immune system to trigger such a syndrome that can lead to death in about 20% of cases.</p> <p>Case presentation</p> <p>We report the case of a 26-year old woman with fever, systemic maculopapular rash, lymphadenopathy, hepatitis and eosinophilic leukocytosis. She had been treated with antibiotics that gave no benefit. She was taking escitalopram and lamotrigine for a bipolar disease 30 days before fever onset. Because the patient's general condition deteriorated, betamethasone and acyclovir were started. This treatment resulted in a mild improvement of symptoms. Steroids were rapidly tapered and this was followed with a relapse of fever and a worsening of laboratory parameters. Human herpesvirus 6 (HHV-6) DNA was positive as shown by PCR. Drug-Induced Hypersensitivity Syndrome (DIHS) was diagnosed. Symptoms regressed on prednisone (at a dose of 50 mg/die) that was tapered very slowly. The patient recovered completely.</p> <p>Conclusions</p> <p>The search for rare causes of fever led to complete resolution of a very difficult case. As DIHS is a rare disease the most relevant issue is to suspect and include it in differential diagnosis of fevers of unknown origin. Once diagnosed, the therapy is easy (steroidal administration) and often successful. However our case strongly confirms that attention should be paid on the steroidal tapering that should be very slow to avoid a relapse.</p