Human T-cell leukemia virus type I infects human lung epithelial cells and induces gene expression of cytokines, chemokines and cell adhesion molecules

<p>Abstract</p> <p>Background</p> <p>Human T-cell leukemia virus type I (HTLV-I) is associated with pulmonary diseases, characterized by bronchoalveolar lymphocytosis, which correlates with HTLV-I proviral DNA in carriers. HTLV-I Tax seems to be involved in the development of such pulmonary diseases through the local production of inflammatory cytokines and chemokines in T cells. However, little is known about induction of these genes by HTLV-I infection in lung epithelial cells.</p> <p>Results</p> <p>We tested infection of lung epithelial cells by HTLV-I by coculture studies in which A549 alveolar and NCI-H292 tracheal epithelial cell lines were cocultured with MT-2, an HTLV-I-infected T-cell line. Changes in the expression of several cellular genes were assessed by reverse transcription-polymerase chain reaction, enzyme-linked immunosorbent assay and flow cytometry. Coculture with MT-2 cells resulted in infection of lung epithelial cells as confirmed by detection of proviral DNA, HTLV-I Tax expression and HTLV-I p19 in the latter cells. Infection was associated with induction of mRNA expression of various cytokines, chemokines and cell adhesion molecule. NF-κB and AP-1 were also activated in HTLV-I-infected lung epithelial cells. <it>In vivo </it>studies showed Tax protein in lung epithelial cells of mice bearing Tax and patients with HTLV-I-related pulmonary diseases.</p> <p>Conclusion</p> <p>Our results suggest that HTLV-I infects lung epithelial cells, with subsequent production of cytokines, chemokines and cell adhesion molecules through induction of NF-κB and AP-1. These changes can contribute to the clinical features of HTLV-I-related pulmonary diseases.</p

Legionella pneumophila infection induces programmed cell death, caspase activation, and release of high-mobility group box 1 protein in A549 alveolar epithelial cells: inhibition by methyl prednisolone

<p>Abstract</p> <p>Background</p> <p><it>Legionella pneumophila </it>pneumonia often exacerbates acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Apoptosis of alveolar epithelial cells is considered to play an important role in the pathogenesis of ALI and ARDS. In this study, we investigated the precise mechanism by which A549 alveolar epithelial cells induced by <it>L. pneumophila </it>undergo apoptosis. We also studied the effect of methyl prednisolone on apoptosis in these cells.</p> <p>Methods</p> <p>Nuclear deoxyribonucleic acid (DNA) fragmentation and caspase activation in <it>L. pneumophila</it>-infected A549 alveolar epithelial cells were assessed using the terminal deoxyribonucleotidyl transferase-mediated triphosphate (dUTP)-biotin nick end labeling method (TUNEL method) and colorimetric caspase activity assays. The virulent <it>L. pneumophila </it>strain AA100jm and the avirulent <it>dotO </it>mutant were used and compared in this study. In addition, we investigated whether methyl prednisolone has any influence on nuclear DNA fragmentation and caspase activation in A549 alveolar epithelial cells infected with <it>L. pneumophila</it>.</p> <p>Results</p> <p>The virulent strain of <it>L. pneumophila </it>grew within A549 alveolar epithelial cells and induced subsequent cell death in a dose-dependent manner. The avirulent strain <it>dotO </it>mutant showed no such effect. The virulent strains of <it>L. pneumophila </it>induced DNA fragmentation (shown by TUNEL staining) and activation of caspases 3, 8, 9, and 1 in A549 cells, while the avirulent strain did not. High-mobility group box 1 (HMGB1) protein was released from A549 cells infected with virulent <it>Legionella</it>. Methyl prednisolone (53.4 μM) did not influence the intracellular growth of <it>L. pneumophila </it>within alveolar epithelial cells, but affected DNA fragmentation and caspase activation of infected A549 cells.</p> <p>Conclusion</p> <p>Infection of A549 alveolar epithelial cells with <it>L. pneumophila </it>caused programmed cell death, activation of various caspases, and release of HMGB1. The dot/icm system, a major virulence factor of <it>L. pneumophila</it>, is involved in the effects we measured in alveolar epithelial cells. Methyl prednisolone may modulate the interaction of <it>Legionella </it>and these cells.</p

Impulse Control in Finance: Numerical Methods and Viscosity Solutions

The goal of this thesis is to provide efficient and provably convergent numerical methods for solving partial differential equations (PDEs) coming from impulse control problems motivated by finance. Impulses, which are controlled jumps in a stochastic process, are used to model realistic features in financial problems which cannot be captured by ordinary stochastic controls. The dynamic programming equations associated with impulse control problems are Hamilton-Jacobi-Bellman quasi-variational inequalities (HJBQVIs) Other than in certain special cases, the numerical schemes that come from the discretization of HJBQVIs take the form of complicated nonlinear matrix equations also known as Bellman problems. We prove that a policy iteration algorithm can be used to compute their solutions. In order to do so, we employ the theory of weakly chained diagonally dominant (w.c.d.d.) matrices. As a byproduct of our analysis, we obtain some new results regarding a particular family of Markov decision processes which can be thought of as impulse control problems on a discrete state space and the relationship between w.c.d.d. matrices and M-matrices. Since HJBQVIs are nonlocal PDEs, we are unable to directly use the seminal result of Barles and Souganidis (concerning the convergence of monotone, stable, and consistent numerical schemes to the viscosity solution) to prove the convergence of our schemes. We address this issue by extending the work of Barles and Souganidis to nonlocal PDEs in a manner general enough to apply to HJBQVIs. We apply our schemes to compute the solutions of various classical problems from finance concerning optimal control of the exchange rate, optimal consumption with fixed and proportional transaction costs, and guaranteed minimum withdrawal benefits in variable annuities

Elsberg Syndrome with Eosinophilic Meningoencephalitis Caused by Angiostrongylus cantonensis

A 42-year-old man was admitted to our hospital with a history of fever, headache and disorientation. His cerebrospinal fluid revealed eosinophilia and his serum had an antibody against Angiostrongylus cantonensis (A. cantonensis). Then, he was diagnosed as eosinophilic meningoencephalitis caused by A. cantonensis. He was treated with repeated lumbar punctures and oral prednisolone. Although a symptom he had been suffering from at the time of his admission was urinary retention, this symptom disappeared as his general condition improved. Therefore his case was considered to be Elsberg syndrome with eosinophilic meningoencephalitis caused by A. cantonensis