1,401 research outputs found
Pia Sebastiani, piano (Argentina)
Concierto interpretado por Pia Sebastiani. Esta pianista y compositora nació en Buenos Aires, donde estudió con la orientación de los maestros Lalewicz, Gilardi y Baldi. Merced a los numerosos premios y becas nacionales y extranjeros obtenidos en el comienzo de su carrera, viajó más tarde a Europa y los Estados Unidos, donde se perfeccionó con los maestros Marquerite Long, Magda Tagliaferro, Olivier Messiaen, Darius Milhaud y Aaron Copland. Así, esta artista egresó del Conservatorio Nacional de París y del "Berhshire Music Center" (Tanglewood). Desde entonces realizó ininterrumpidamente giras por los más importantes centros musicales de Europa, Latinoamérica y los Estados Unidos.
En este concierto interpretó obras de D. Scarlatti, J. Brahms, C. Debussy, G. Faure y A. Ginastera
[The current outlook in the therapy of autoimmune diseases]
Recent advances in immunology and molecular biology have contributed to a much greater understanding of the pathogenetic mechanisms of the autoimmune diseases and thus to the development of new rationally-based therapies. Most of the immunosuppressive agents that have been tried in autoimmune disease patients nonspecifically suppress the immune response, often causing various side effects. Autoimmune diseases result from the activation of self-reactive T cells that recognize autoantigens or foreign antigens cross-reactive with an autoantigen coupled with major histocompatibility complex (MHC) products on an antigen presenting cell. It appears possible to modulate T cell activation by interfering with the interaction between T cell receptor and the peptide-MHC molecule complex. A number of sites are potential targets for immunologic intervention, such as MHC molecules, T cell receptor, CD4 and CD3 molecules, adhesion molecules, cytokines and cytokine receptors. In the present review the most important new therapeutic approaches to autoimmune conditions, which appear to be more selective in overcoming the limitations of non-specific treatments, are summarized. They include monoclonal antibodies, cytokines and cytokine-inhibitors, peptides interacting with MHC molecules and T cell vaccination
Hepatic iron overload is common in chronic hepatitis B and is more severe in patients coinfected with hepatitis D virus.
Immunogenetic studies on systemic lupus erythematosus
Understanding the pathogenesis of systemic lupus erythematosus (SLE) remains a considerable challenge. Multiple abnormalities of both the innate and adaptive immune system have been described and, furthermore, immunological dysfunction precedes clinical presentation by many years. There is a strong genetic basis to SLE, which means that genetic studies can play a key role in furthering our understanding of this disease. Because susceptibility variants are present from birth and are unaffected by the course of the disease, or by its treatment, genetic analysis is, perhaps uniquely, capable of identifying fundamental, causative, disease mechanisms. In this article, we review our SLE immunogenetic studies performed in collaboration with the European Working Party on Systemic Lupus Erythematosus. By considering the results of our research and the recent advances obtained by genome-wide associations' studies, we can begin to understand how dysregulation at a number of key immunological steps may predispose to the development of SLE
Infection-genetics relationship in systemic lupus erythematosus
Genetic, environmental, and hormonal factors contribute to disease susceptibility in systemic lupus erythematosus. Among environmental factors, infectious agents play a major role. When considering the complex relationship between genetic predisposition and infections in the pathogenesis of systemic lupus erythematosus, we have to consider that infectious agents can interact with the immune system in several ways. For example, molecular mimicry, altered apoptosis of the host cells, exposure of as yet masked antigens to the immune system by a given microorganism, and direct viral invasion of immunocompetent cells are all mechanisms that may give rise to dysfunction of the immune system; in addition, some genetically determined deficit of the immune system, such as complement deficiency or deficit of mannose binding lectine, may cause insufficient clearance of infectious agents, whose persistence in the host may determine autoimmunity. Finally, evidence has been emerging suggesting that the production of autoantibodies, by infected B-lymphocytes, may be drawn by altered expression of particular microRNA in these cells. In this paper, we review some of the distinct scenarios that can account for the role of infectious agents, acting on a genetically prone host, in determining systemic lupus erythematosus
Function of the HLA class I and II molecules: Relationship with autoimmunity [Funzione delle molecole HLA di classe I e II: correlazioni con l'autoimmunità]
Major histocompatibility complex (HLA in humans) encodes membrane proteins which play a very important role in the activation of the immune system. Besides the well known class I molecules (HLA-A, B, C) and class II molecules (HLA-DR, DQ, DP), loci have been discovered whose products are involved in antigen processing and presentation, such as the 'peptide transporter genes' and the 'proteasomes'. In addition, MHC-encoded heat shock proteins may be involved in delivering peptides to class II molecules and to membrane transport proteins which pump peptides into the endoplasmic reticulum for coupling with class I molecules, and the regulatory promotor regions of HLA class II molecules influence the transcriptional levels of the structural genes. MHC is equivalent to an eukaryotic operon encoding a complete kit for the processing and presentation of antigens to T lymphocytes. This kit includes various sets of genes for molecules with distinct functions. Various degrees of polymorphism exist in all these classes of genes. These polymorphisms could contribute to the disease associations at present attributed to the MHC glycoproteins
Capillary microscopy: Association of two distinct patterns of capillary alterations in an overlap syndrome
Evaluation of Plasma Levels of Soluble HLA-G and HLA-G Genotypes in Kidney Transplant Recipients
In the field of transplantation, expression of HLA-G, a nonclassical HLA molecule with immunosuppressive functions and limited gene polymorphism, is considered beneficial for graft acceptance; various studies have aimed to demonstrate this role in transplantation. Recently, in other clinical conditions, it has been observed that insulin resistance was associated with HLA-G14bpins/del polymorphism, the most studied regulatory polymorphism of this molecule. In the present study, plasma levels of the soluble form of HLA-G (sHLA-G) were analyzed in kidney transplant recipients (n = 103) with different HLA-G14bpins/del genotypes. In a group of 26 recipients, sHLA-G was detected before and after transplantation (1 year) to evaluate early variations. In 77 recipients, sHLA-G was detected after transplantation (3-24 years) and correlated with occurrence of long-term post-transplant morbidity (diabetes mellitus, hyperlipidemia, hypertension, obesity, etc.). Methods: Levels of sHLA-G were measured in plasma with an enzyme-linked immunosorbent assay; HLA-G14bpins/del and HLA-G+3142C>G genotypes were assessed using direct polymerase chain reaction. Results: Plasma levels of sHLA-G significantly decreased during the first year after transplantation (P =.019); no significant correlations were found with genotypes or early post-transplant events. Lower levels of sHLA-G were found in recipients with post-transplant diabetes mellitus or obesity carrying the HLA-G14bpins/ins (P =.006 and P =.003, respectively) or HLA-G+3142G/G genotypes. Conclusions: A complex modulation of HLA-G, which includes both immunologic and metabolic effects, could affect the risk for long-term post-transplant morbidity in kidney transplant recipients. Associations of HLA-G, diabetes, and obesity deserve to be investigated by deeply exploring HLA-G regulatory variants
Pneumocystis carinii pneumonia complicating selective CD4 T cell depletion induced by corticosteroid therapy in a patient with systemic lupus erythematosus
Grain morphology and strength-dilatancy of sands
The presented experimental study, from micro to macro scale, assesses the effects of grain shape on the strength-dilatancy behaviour and physical properties of seven natural sands of different origins and mineralogical composition. The micro-scale has been characterized by processing 2D image of grains, using the fractal analysis of particle contour to define their shape. The macroscopic material properties are evaluated performing direct shear tests at three different normal stresses, and measuring void ratios limit and angles of repose. An innovative method to interpret the experimental data obtained has pinpointed interesting relationships linking the morphological features of grains to the mechanical and physical properties of sands. Data confirm that the increase in grain shape irregularity produces an increase in all the variables investigated: void ratios limit, friction angles and dilatancy parameters
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