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The electronic structure of an electroactive polyaniline and its derivatives was investigated using an ab initio quantum chemical method based on the density functional theory. Calculations indicated the association of the real space distribution of the unpaired-electron spin-density and the polymerizability of the aniline derivatives. Species that exhibited polymerization showed a similarity in the net spin populations of the nitrogen atom and the ring carbon atom when it is in the para position.

Objectives: Objectives were 1) to determine whether a correlation exists between facial pain or headache and sinus disease severity by computed tomography (CT) scan in patients with rhinosinusitis and 2) to compare disease severity and pain perception in two geographically diverse North American patient populations. Study Design: Prospective patient questionnaire before CT scan of the paranasal sinuses. Methods: Patients with refractory rhinosinusitis were recruited at the University of Texas Medical Branch (Galveston, TX) and the University of Alberta (Edmonton, Alberta, Canada). Before CT scanning, patients completed a pain questionnaire. All scans were interpreted by one neuroradiologist and were scored using the Lund-McKay, Harvard, and Kennedy staging systems for rhinosinusitis. Results: Fifty-one patients completed questionnaires (27 were Canadian). There was no correlation between pain severity and disease severity reflected by any of the three staging systems used (P >.05). The mean pain score for the U.S. patients was 7.3, and for Canadian patients, 5.2. The mean CT scores for U.S. versus Canadian patients were as follows: Lund-McKay, 2.6 versus 6.6; Harvard, 0.7 versus 1.0; and Kennedy, 1.4 versus 2.2. The Canadian patients had more severe disease on CT scan (Lund-McKay, P Conclusions: There was no correlation between pain severity and disease severity by sinus CT scan as graded by the Lund-McKay, Harvard, or Kennedy staging system. Facial pain and headache, although frequent complaints of patients with rhinosinusitis, are not useful predictors of sinus disease severity. There appears to be a difference in pain perception between the two North American populations. [ABSTRACT FROM AUTHOR]

The discovery of tumor-associated antigens recognized by T lymphocytes opens the possibility of vaccinating cancer patients with defined antigens. However, one of the major limitation of peptide-based vaccines is the low immunogenicity of antigenic peptides. Interestingly, if these epitopes are directly delivered into the cytoplasm of antigen presenting cells, they can be efficiently presented via the direct MHC class I presentation pathway. To improve antigen entry, one promising approach is the use of cell penetrating peptides (CPPs). However, most studies use a covalent binding of the CPP with the antigen. In the present study, we focused on the C-terminal domain of Vpr which was previously demonstrated to efficiently deliver plasmid DNA into cells. We provide evidence that the peptides Vpr55-91 and Vpr55-82 possess the capacity of delivering proteins and epitopes into cell lines as well as into human primary dendritic cells, without the necessicity for a chemical linkage. Moreover, immunization of HLA-A2 transgenic mice with Vpr55-91 as the sole adjuvant is able to induce antigen-specific cytotoxic T lymphocytes against multiple tumor epitopes. [ABSTRACT FROM AUTHOR]

Dystrophin-based gene therapy treatments aimed at correcting the Duchenne muscular dystrophy phenotype require stable expression of normal dystrophin (DYST) protein in myocytes without immune responses, which would compromise long-term expression. To predict cytotoxic T-cell-mediated responses elicited by transgenes, we used here H-2-negative HLA-A*0201 transgenic mice and identified human DYST epitopes, which elicit HLA-A*0201-restricted cytotoxic T cell activities. Among a series of eight peptides predicted from the human DYST sequence, not shared with the endogenous mouse DYST sequence, four of them were able to bind to HLA-A*0201 molecules and to induce cytotoxic T lymphocyte (CTL) responses. After human DYST DNA transfer in muscle of HLA-A*0201 mice, only the human DYST1281 epitope, located in the spectrin-like repeat 9 domain, induced strong CD8+ CTL responses. Using the corresponding human DYST1281 peptide/HLA-A*0201 tetramer, we detected human DYST1281-specific CD8+ T cells in peripheral lymphoid organs and blood of HLA-A*0201 mice injected with human DYST DNA. Our results demonstrate that muscle injection with human DYST DNA systematically triggers CTL responses against this HLA-A*0201-restricted human DYST1281 peptide, which is present in long human DYST isoforms. Identification of such immunodominant human DYST epitopes and use of peptide/HLA tetramers will allow the immunomonitoring of CTL responses in HLA-phenotyped Duchenne muscular dystrophy patients undergoing gene therapy. Finally, the knowledge of HLA-A*0201-restricted human DYST peptides will be of importance to test, in mouse models, new immunomodulatory interventions allowing long-term engraftment of human dystrophin. [Copyright &y& Elsevier]

CD8+ cytotoxic T cells are critical for viral clearance from the lungs upon influenza virus infection. The contribution of antigen cross-presentation by DCs to the induction of anti-viral cytotoxic T cells remains controversial. Here, we used a recombinant influenza virus expressing a nonstructural 1-GFP (NS1-GFP) reporter gene to visualize the route of antigen presentation by lung DCs upon viral infection in mice. We found that lung CD103+ DCs were the only subset of cells that carried intact GFP protein to the draining LNs. Strikingly, lung migratory CD103+ DCs were not productively infected by influenza virus and thus were able to induce virus-specific CD8+ T cells through the cross-presentation of antigens from virally infected cells. We also observed that CD103+ DC resistance to infection correlates with an increased anti-viral state in these cells that is dependent on the expression of type I IFN receptor. These results show that efficient cross-priming by migratory lung DCs is coupled to the acquisition of an anti-viral status, which is dependent on the type I IFN signaling pathway. [ABSTRACT FROM AUTHOR]