New physics and the tau polarization vector in b→cτνˉτb\to c \tau \bar\nu_\tau decays

For a general $H_b\to H_c\tau\bar\nu_\tau$ decay we analyze the role of the $\tau$ polarization vector ${\cal P}^\mu$ in the context of lepton flavor universality violation studies. We use a general phenomenological approach that includes, in addition to the Standard Model (SM) contribution, vector, axial, scalar, pseudoscalar and tensor new physics (NP) terms which strength is governed by, complex in general, Wilson coefficients. We show that both in the laboratory frame, where the initial hadron is at rest, and in the center of mass of the two final leptons, a $\vec {\cal P}$ component perpendicular to the plane defined by the three-momenta of the final hadron and the $\tau$ lepton is only possible for complex Wilson coefficients, being a clear signal for physics beyond the SM as well as time reversal (or CP-symmetry) violation. We make specific evaluations of the different polarization vector components for the $\Lambda_b\to\Lambda_c$, $\bar B_c\to\eta_c,J/\psi$ and $\bar B\to D^{(*)}$ semileptonic decays, and describe NP effects in the complete two-dimensional space associated with the independent kinematic variables on which the polarization vector depends. We find that the detailed study of ${\cal P}^\mu$ has great potential to discriminate between different NP scenarios for $0^-\to 0^-$ decays, but also for $\Lambda_b \to \Lambda_c$ transitions. For this latter reaction, we pay special attention to corrections to the SM predictions derived from complex Wilson coefficients contributions.Comment: 34 latex pages, 10 figures, 1 table. Enlarged and modified discussion. New references and one new figure adde

The Pathogenesis Of Tropical Spastic Paraparesis/human T-cell Leukemia Type I-associated Myelopathy

Tropical spastic paraparesis/human T-cell leukemia type I-associated myelopathy (TSP/HAM) is caused by a human T-cell leukemia virus type I (HTLV-I) after a long incubation period. TSP/HAM is characterized by a chronic progressive paraparesis with sphincter disturbances, no/mild sensory loss, the absence of spinal cord compression and seropositivity for HTLV-I antibodies. The pathogenesis of this entity is not completely known and involves a multivariable phenomenon of immune system activation against the presence of HTLV-I antigens, leading to an inflammatory process and demyelination, mainly in the thoracic spinal cord. The current hypothesis about the pathogenesis of TSP/HAM is: 1) presence of HTLV-I antigens in the lumbar spinal cord, noted by an increased DNA HTLV-I load; 2) CTL either with their lytic functions or release/production of soluble factors, such as CC-chemokines, cytokines, and adhesion molecules; 3) the presence of Tax gene expression that activates T-cell proliferation or induces an inflammatory process in the spinal cord; 4) the presence of B cells with neutralizing antibody production, or complement activation by an immune complex phenomenon, and 5) lower IL-2 and IFN-γ production and increased IL-10, indicating drive to a cytokine type 2 pattern in the TSP/HAM subjects and the existence of a genetic background such as some HLA haplotypes. All of these factors should be implicated in TSP/HAM and further studies are necessary to investigate their role in the development of TSP/HAM.331213951401Aboulafia, D.M., Clinical implications of human T-cell leukemia virus type I/II-associated diseases (1995) AIDS Reader, 5, pp. 118-125Uchiyama, T., Yodoi, J., Sagawa, K., Takatsuki, K., Uchino, H., Adult T-cell leukemia: Clinical and hematologic features of 16 cases (1977) Blood, 50, pp. 481-492Osame, M., Janssen, R., Kubota, H., Nishitani, H., Igata, A., Nagataki, S., Mori, M., Khabbaz, R., Nationwide survey of HTLV-I-associated myelopathy in Japan: Association with blood transfusion (1990) Annals of Neurology, 28, pp. 50-56Gessain, A., Barin, F., Vernant, J.C., Gout, O., Maurs, L., Calender, A., De The, G., Antibodies to human T-lyrnphotropic virus type-I in patients with tropical spastic paraparesis (1985) Lancet, 2, pp. 407-410Osame, M., Usuku, J., Izumo, S., Ijichi, N., Amitani, H., Igata, A., Matsumoto, M., Tara, M., HTLV-I-associated myelopathy: A new clinical entity (1985) Lancet, 1, pp. 1031-1032Gessain, A., Gout, O., Chronic myelopathy with human T-lymphotropic virus type I (HTLV-I) (1992) Annals of Internal Medicine, 117, pp. 933-946Iwasaki, Y., Pathology of chronic myelopathy associated with HTLV-I infection (TSP/HAM) (1990) Journal of Neurological Sciences, 96, pp. 103-123Seiki, M., Hattori, S., Hirayama, Y., Yoshida, M., Human adult T-cell leukemia virus: Complete nucleotide sequence of the provirus genome integrated in leukemia cell DNA (1983) Proceedings of the National Academy of Sciences, USA, 80, pp. 3618-3622Murphy, E.L., Blattner, W.A., HTLV-I-associated leukemia: A model for chronic retroviral diseases (1988) Annals of Neurology, 23, pp. S174-S180Piccardo, P., Ceroni, M., Rodgers-Johnson, P., Mora, C., Asher, D.M., Char, G., Gibbs C.J., Jr., Gajdusek, D.C., Pathological and immunological observations on tropical spastic paraparesis in patients from Jamaica (1988) Annals of Neurology, 23, pp. 156-160Azizuki, S., Nakasato, O., Higuchi, Y., Tanabe, K., Setoguchi, M., Yoshida, S., Miyazaki, Y., Okajima, T., Necropsy findings in HTLV-I associated myelopathy (1987) Lancet, 1, pp. 156-157Tendler, G.L., Greenberg, S.J., Blattner, W.A., Manns, A., Murphy, E., Fleisher, T., Hanchard, B., Waldmann, T.A., Transactivation of mterleukin 2 and its receptor induces immune activation in human T-cell lymphotropic virus type I-associated myelopathy: Pathogenic implications and a rationale for immunotherapy (1990) Proceedings of the National Academy of Sciences, USA, 87, pp. 5218-5222Cheng, H., Tranok, J., Parks, W.P., Human immunodeficiency virus type 1 genome activation induced by human T-cell leukemia virus type 1 tax protein is through cooperation of NF-kB and tat (1998) Journal of Virology, 72, pp. 6911-6916Gessain, A., Saal, F., Gout, O., Daniel, M.T., Flandrin, G., De The, G., Peries, J., Sigaux, F., High human T-cell lymphotropic virus type I proviral DNA load with polyclonal integration in peripheral blood mononuclear cells of French West Indian, Guianese, and African patients with tropical spastic paraparesis (1990) Blood, 75, pp. 428-433Nagai, M., Usuku, K., Matsumoto, W., Kodama, D., Takenouchi, T.M., Hashiguchi, S., Ichinose, M., Osame, M., Analysis of HTLV-I proviral load in 202 TSP/HAM patients and 243 asymptomatic HTLV-I carriers: High proviral load strongly predisposes to TSP/HAM (1998) Journal of Neurovirology, 4, pp. 586-593Manns, A., Miley, J.W., Wilks, J.R., Morgan, O.C., Hanchard, B., Warfe, G., Cranston, B., Waters, D., Quantitative proviral DNA and antibody levels in the natural history of HTLV-I infection (1999) Journal of Infectious Diseases., 180, pp. 1487-1493Hara, H., Autoimmune mechanism in TSP/HAM (1994) Nippon Rinsho, 52, pp. 2919-2925Levin, M.C., Krichavsky, M., Berk, J., Foley, S., Rosenfeld, M., Dalmau, J., Chang, G., Jacobson, S., Neuronal molecular mimicry in immune-mediated neurologic disease (1998) Annals of Neurology, 44, pp. 87-98Hoffman, T.L., Doms, R.W., Chemokines and coreceptors in HIV/SIV-host interactions (1998) AIDS, 12 (SUPPL. A), pp. S17-S26Copeland, K.F.T., Heeney, J.L., T helper cell activation and human retroviral pathogenesis (1996) Microbiological Reviews, 60, pp. 722-742Oliva, A., Kinter, A.L., Vaccarezza, M., Rubbert, A., Catanzaro, A., Mo'r, S., Monaco, J., Fauci, A.S., Natural killer cells from human immunodeficiency virus (HIV)-in-fected individuals are an important source of CC-chemokines and suppress HIV-1 entry and replication in vitro (1998) Journal of Clinical Investigation, 102, pp. 223-231Umehara, F., Izumo, S., Takeya, M., Takahashi, K., Sato, E., Osame, M., Expression of adhesion molecules and monocyte chemcattractant protem-1 (MCP-1) in the spinal cord lesions in HTLV-I-associated myelopathy (1996) Acta Neuropathologica, 91, pp. 343-350Giraudon, P., Buart, S., Bernard, A., Belin, M.F., Cytokines secreted by glial cells infected with HTLV-I modulate the expression of matrix metalloproteinases (MMPs) and their natural inhibitor (TIMPs): Possible involvement in neurodegenerative processes (1997) Molecular Psychiatry, 2, pp. 107-110Greten, T.F., Slansky, J.E., Kubota, R., Soldan, S.S., Jaffee, E.M., Leist, T.P., Pardoll, D.M., Schneck, J.P., Direct visualization of antigen-specific T cells: HTLV-1 Taxi11-19-specific CD8(+) T cells are activated in peripheral blood and accumulate in cerebrospinal fluid from TSP/ HAM patients (1998) Proceedings of the National Academy of Sciences, USA, 95, pp. 7568-7573Biddison, W.E., Kubota, R., Kawanishi, T., Taub, D.D., Cruikshank, W.W., Center, D.M., Connor, E.W., Jacobson, S., Human T cell leukemia virus type I (HTLV-I)-specific CD8+ CTL clones from patients with HTLV-I-associated neurologic disease secrete proinflammatory cytokines, chemokmes, and matrix metalloproteinase (1997) Journal of Immunology, 159, pp. 2018-2025Hoffman, P.M., Dhib-Jalbut, S., Mikovits, J.A., Robbins, D.S., Wolf, A.L., Bergey, G.K., Lohrey, N.C., Ruscetti, F.W., Human T-cell leukemia virus type I infection of monocytes and microglial cells in primary human cultures (1992) Proceedings of the National Academy of Sciences, USA, 89, pp. 11784-11788Fox, R.J., Levin, M.C., Jacobson, S., Tumor necrosis factor alpha expression in the spinal cord of human T-cell lymphotrophic virus type I associated myelopathy/tropical spastic paraparesis patients (1996) Journal of Neurovirology, 2, pp. 323-329Nagai, M., Ijichi, S., Hall, W.W., Osame, M., Differential effect of TGF-beta 1 on the in vitro activation of HTLV-I and the proliferates response of CDS+ T lymphocytes in patients with HTLV-I-associated myelopathy (TSP/HAM) (1995) Clinical Immunology and Immunopathology, 77, pp. 324-331Saarloos, M.N., Koenig, R.E., Spear, G.T., Elevated levels of iC3b and C4d, but not Bb, complement fragments from plasma of persons infected with human T cell leukemia virus HTLVI with HTLV-I-associated myelopathy/tropical spastic paraparesis (1995) Journal of Infectious Diseases, 172, pp. 1095-1097Lira, J., Nakamura, M., Sawada, Y., Ohori, N., Itoyama, Y., Yamamoto, N., Sakaki, Y., Goto, I., Antibody titers to HTLV-Ip40tax protein and gag-env hybrid protein in HTLV-I-associated myelopathy/tropical spastic paraparesis: Correlation with increased HTLV-I proviral DNA load (1992) Journal of Neurological Sciences, 107, pp. 98-104Usuku, K., Sonoda, S., Osame, M., Yashiki, S., Takahashi, K., Matsumoto, M., Sawada, T., Igata, A., HLA haplotype-linked high immune responsiveness against HTLV-I in HTLV-I-associated myelopathy: Comparison with adult T-cell leukemia/lymphoma (1988) Annals of Neurology, 23, pp. 143-150Godoy, A.J., Itoyama, Y., Tokunaga, K., Hara, H., Kawaga, Y., Kiyokawa, H., Maeda, Y., Goto, I., Allolymphocytotoxic antibodies in sera from HTLV-I-associated myelopathy/tropical spastic paraparesis patients-putative anti-HLA antibodies (1994) Journal of Neurological Sciences, 125, pp. 62-69Uchiyama, T., Human T cell leukemia virus type I (HTLV-I) and human diseases (1997) Annual Review of Immunology, 15, pp. 15-37Manns, A., Hanchard, B., Morgan, O.S., Wilks, R., Cranston, B., Nam, J.M., Blank, M., Sonoda, S., Human leukocyte antigen class II alleles associated with human T-cell lymphotropic virus type I infection and adult T-cell leukemia/ lymphoma in a Black population (1998) Journal of the National Cancer Institute, 90, pp. 617-622Jeffery, K.J.M., Usuku, K., Hall, S.E., Matsumoto, W., Taylor, G.P., Procter, J., Bunce, M., Bangham, C.R.M., HLA alleles determine human T-lymphotropic virus-I (HTLV-I) proviral load and the risk of HTLV-I-associated myelopathy (1999) Proceedings of the National Academy of Sciences, USA, 96, pp. 3848-3853Bangham, C.R.M., Kermode, A.L., Hall, S.E., Daenke, S., The cytotoxic T-lymphocyte response to HTLV-I: The main determinant of disease? (1996) Seminars in Virology, 7, pp. 41-48Höllsberg, P., Pathogenesis of chronic progressive myelopathy associated with human T-cell lymphotropic virus type I (1997) Acta Neurologica Scandinavica, 169 (SUPPL.), pp. 86-93Elovaara, I., Koenig, S., Brewah, A.Y., Woods, R.M., Lehky, T., Jacobson, S., High human T cell lymphotropic virus type 1 (HTLV-1)-specific precursor cytotoxic T lymphocyte frequencies in patients with HTLV-1-associated neurological disease (1993) Journal of Experimental Medicine, 177, pp. 1567-1573Casseb, J., Hong, M.A., Salomão, S., Duarte, A.J.S., Gallo, D., Hendry, R.M., Comfection with human immunodeficiency virus and human T-cell lymphotropic virus type I: Reciprocal activation with clinical and immunological consequences (1997) Clinical Infectious Diseases, 25, pp. 1259-1260Casseb, J., Is HTLV-I more clever than HIV-I? (1998) Clinical Infectious Diseases, 27, pp. 1309-131

Estructura cristalina y molecular de la 2-Cloro Isonitroacetanilida

En este trabajo se presenta la estructura cristalina y molecular de la 2-cloro isonitrosoacetanilida, derivado de la isonitrosoacetanilida, serie que constituye una línea de investigación de la Sección de Cristalografía del C.S.I.C. de Barcelona. La estructura ha sido resuelta por difracción de rayos-X. Las dimensiones de la celda elemental son: (...

Estructura cristalina y molecular de la dihidrazida malonica anhidra

[ES] En este trabajo se presenta la estructura cristalina y molecular de la hidracida malónica anhidra. La estructura cristalina ha sido resuelta por difracción de Rayos X. Las dimensiones de la celda elemental son: a = 6.986Å, b0 = 4.828Å, c0 = 17.619Å, β = 93.490, V = 593.19Å y su grupo espacial es el P21/c, Z = 4.[EN] In this paper, the crystal and molecular structure of the nalonic dihydrazide has been solved by means of the X-Ray difraction and the direct methods. The unit cell dimensions are: a = 6.986Å, b0 = 4.828Å, c0 = 17.619Å, β = 93.490, V = 593.19Å y su grupo espacial es el P21/c, Z = 4.Peer reviewe

‘The International Teacher Leadership project,’ a case of international action research.

Copyright CARNThe paper arises from the International Teacher Leadership project, a research and development project involving researchers and practitioners in 14 European countries. The paper provides a conceptual exploration of the idea of teacher leadership and its role in educational reform, central to which is the idea that teachers, regardless of their level of power and organisational position, can engage in the leadership of enquiry-based development activity aimed at influencing their colleagues and embedding improved practices in their schools. The paper provides an outline of the project’s methodology which builds on that used in the Carpe Vitam Leadership for Learning project (Frost, 2008a). It is a form of collaborative action research which is highly developmental and discursive. It seeks to identify principles, strategies and tools that can be applied in a range of cultural settings. The paper includes a thematic analysis of the cultural contexts and policy environments of the participating countries in order to identify the obstacles to teacher leadership and to inform the nature of the support strategies employed

A Two-Phase Innate Host Response to Alphavirus Infection Identified by mRNP-Tagging In Vivo

A concept fundamental to viral pathogenesis is that infection induces specific changes within the host cell, within specific tissues, or within the entire animal. These changes are reflected in a cascade of altered transcription patterns evident during infection. However, elucidation of this cascade in vivo has been limited by a general inability to distinguish changes occurring in the minority of infected cells from those in surrounding uninfected cells. To circumvent this inherent limitation of traditional gene expression profiling methods, an innovative mRNP-tagging technique was implemented to isolate host mRNA specifically from infected cells in vitro as well as in vivo following Venezuelan equine encephalitis virus (VEE) infection. This technique facilitated a direct characterization of the host defense response specifically within the first cells infected with VEE, while simultaneous total RNA analysis assessed the collective response of both the infected and uninfected cells. The result was a unique, multifaceted profile of the early response to VEE infection in primary dendritic cells, as well as in the draining lymph node, the initially targeted tissue in the mouse model. A dynamic environment of complex interactions was revealed, and suggested a two-step innate response in which activation of a subset of host genes in infected cells subsequently leads to activation of the surrounding uninfected cells. Our findings suggest that the application of viral mRNP-tagging systems, as introduced here, will facilitate a much more detailed understanding of the highly coordinated host response to infectious agents