674 resultados para Lupus nephritis
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El arte de la negociación es una estrategia fundamental en la toma de decisiones y un proceso mediante el cual las partes, en todas las áreas de la vida y en todas las disciplinas y profesiones, intentan resolver conflictos y llegar acuerdos, compatiblemente con sus necesidades e intereses. De una forma más sencilla, la negociación podría definirse como: “…cualquier comunicación entre dos o más personas con la intención de influenciar o persuadir” (R. Bordone, Harvard Law School, MA). Todos estos elementos destacan la importancia de desarrollar destrezas y competencias que fortalezcan este tipo de habilidad y la necesidad de conocer las reglas del juego de esta poderosa herramienta. Según la Escuela de Harvard, la forma más exitosa y provechosa de negociar es la recogida por el modelo integrativo-cooperativo, el que se base sobre premisas muy diferentes del tradicional modelo distributivo. Este último responde a nuestra forma de negociar más espontánea y lamentablemente desacertada, es decir, una forma de negociar que se reduce a un simple reparto de lo que haya sobre la mesa, sin visualizar, analizar posibles opciones negociadoras más allá de este simple reparto. Es un esquema que responde a una negociación “dura”, que se fundamenta en una concepción adversarial de las relaciones humanas (homo homini lupus, T. Hobbes), en donde hay un ganador y un perdedor, sin tintes intermedios. Al contrario, la idea con el modelo que propone la Escuela de Harvard, -el modelo integrativo-cooperativo-es uno por el que una negociación exitosa es aquella que “crea valor sobre la mesa” y que genera beneficios para todas las partes, no solo una de ellas. En otras palabras, el enfoque no es aquel por el que si uno pierde, el otro gana sino uno en el que la otra parte debe alcanzar un razonable nivel de satisfacción en sus requerimientos y demandas. Este modelo crea valor sobre la mesa inclusive más allá de los posibles beneficios que puedan conseguirse a partir de un determinado acuerdo; por ejemplo, ataja el conflicto y preserva las relaciones humanas, las que a menudo, en base al modelo tradicional (ganarperder) quedan perjudicadas. Finalmente, el modelo cooperativo es uno que abre la puerta a la empatía, la escucha activa, la transparencia y confianza; todos elementos que sin lugar a dudas facilitan las complejas relaciones interpersonales.
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Genetic association analyses of family-based studies with ordered categorical phenotypes are often conducted using methods either for quantitative or for binary traits, which can lead to suboptimal analyses. Here we present an alternative likelihood-based method of analysis for single nucleotide polymorphism (SNP) genotypes and ordered categorical phenotypes in nuclear families of any size. Our approach, which extends our previous work for binary phenotypes, permits straightforward inclusion of covariate, gene-gene and gene-covariate interaction terms in the likelihood, incorporates a simple model for ascertainment and allows for family-specific effects in the hypothesis test. Additionally, our method produces interpretable parameter estimates and valid confidence intervals. We assess the proposed method using simulated data, and apply it to a polymorphism in the c-reactive protein (CRP) gene typed in families collected to investigate human systemic lupus erythematosus. By including sex interactions in the analysis, we show that the polymorphism is associated with anti-nuclear autoantibody (ANA) production in females, while there appears to be no effect in males.
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We introduce a procedure for association based analysis of nuclear families that allows for dichotomous and more general measurements of phenotype and inclusion of covariate information. Standard generalized linear models are used to relate phenotype and its predictors. Our test procedure, based on the likelihood ratio, unifies the estimation of all parameters through the likelihood itself and yields maximum likelihood estimates of the genetic relative risk and interaction parameters. Our method has advantages in modelling the covariate and gene-covariate interaction terms over recently proposed conditional score tests that include covariate information via a two-stage modelling approach. We apply our method in a study of human systemic lupus erythematosus and the C-reactive protein that includes sex as a covariate.
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Background 29 autoimmune diseases, including Rheumatoid Arthritis, gout, Crohn’s Disease, and Systematic Lupus Erythematosus affect 7.6-9.4% of the population. While effective therapy is available, many patients do not follow treatment or use medications as directed. Digital health and Web 2.0 interventions have demonstrated much promise in increasing medication and treatment adherence, but to date many Internet tools have proven disappointing. In fact, most digital interventions continue to suffer from high attrition in patient populations, are burdensome for healthcare professionals, and have relatively short life spans. Objective Digital health tools have traditionally centered on the transformation of existing interventions (such as diaries, trackers, stage-based or cognitive behavioral therapy programs, coupons, or symptom checklists) to electronic format. Advanced digital interventions have also incorporated attributes of Web 2.0 such as social networking, text messaging, and the use of video. Despite these efforts, there has not been little measurable impact in non-adherence for illnesses that require medical interventions, and research must look to other strategies or development methodologies. As a first step in investigating the feasibility of developing such a tool, the objective of the current study is to systematically rate factors of non-adherence that have been reported in past research studies. Methods Grounded Theory, recognized as a rigorous method that facilitates the emergence of new themes through systematic analysis, data collection and coding, was used to analyze quantitative, qualitative and mixed method studies addressing the following autoimmune diseases: Rheumatoid Arthritis, gout, Crohn’s Disease, Systematic Lupus Erythematosus, and inflammatory bowel disease. Studies were only included if they contained primary data addressing the relationship with non-adherence. Results Out of the 27 studies, four non-modifiable and 11 modifiable risk factors were discovered. Over one third of articles identified the following risk factors as common contributors to medication non-adherence (percent of studies reporting): patients not understanding treatment (44%), side effects (41%), age (37%), dose regimen (33%), and perceived medication ineffectiveness (33%). An unanticipated finding that emerged was the need for risk stratification tools (81%) with patient-centric approaches (67%). Conclusions This study systematically identifies and categorizes medication non-adherence risk factors in select autoimmune diseases. Findings indicate that patients understanding of their disease and the role of medication are paramount. An unexpected finding was that the majority of research articles called for the creation of tailored, patient-centric interventions that dispel personal misconceptions about disease, pharmacotherapy, and how the body responds to treatment. To our knowledge, these interventions do not yet exist in digital format. Rather than adopting a systems level approach, digital health programs should focus on cohorts with heterogeneous needs, and develop tailored interventions based on individual non-adherence patterns.
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Mycoplasmal lipid-associated membrane proteins (LAMPs) and Mycoplasma arthritidis mitogen (MAM superantigen) are potent stimulators of the immune system. The objective of this work was to detect antibodies to MAM and LAMPs of Mycoplasma hominis and M. fermentans in the sera of patients affected by rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) to identify mycoplasmal products that can be involved in the etiopathogenesis of these autoimmune diseases. Serum samples from female RA and SLE patients and controls, recombinant MAM, and LAMPs of M. hominis PG21 and M. fermentans PG18 were used in Western blot assays. A similar frequency of sera from patients and controls reactive to MAM was detected. A larger number of M. hominis and M. fermentans LAMPs were recognized by sera from RA patients than controls, but no differences were detected between sera from SLE patients and controls. Among the LAMPs recognized by IgG antibodies from RA patients, proteins of molecular masses in a range of < 49 and a parts per thousand yen20 KDa (M. hominis) and < 102 and a parts per thousand yen58 KDa (M. fermentans) were the most reactive. These preliminary results demonstrate the strong reactivity of antibodies of RA patients with some M. hominis and M. fermentans LAMPs. These LAMPs could be investigated as mycoplasmal antigens that can take part in the induction or amplification of human autoimmune responses.
Autolytic Mycobacterium leprae Hsp65 fragments may act as biological markers for autoimmune diseases
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Investigating the proteolytic activity of the recombinant Mycobacterium leprae Heat Shock Protein of 65 kDa (rHsp65), chaperonin 2 (cpn2), we observed that it displays high instability. The fragmentation process starts at the C-terminus followed by progressive degradation of the N-terminus, which leads to a stable fragment comprising the middle region of the molecule. Urea was able to prevent autolysis, probably due to its denaturing action, while EDTA increased degradation levels indicating the need for metal ions. Peptides originated from autolysis were purified and analyzed by mass spectrometry, generating a continuous map. Since the bacteria and mammalian Hsp60 are known to be targets of the immune response and have been implicated in autoimmune diseases and chronic inflammation, the in vivo effect of rHsp65 peptides was evaluated in the spontaneous Systemic Lupus Erythematosus (SLE) model developed by the (NZB/NZW)F(1) mouse hybrids, and their individual anti-rHsp65 IgG2a/IgG1 antibody titer ratio was determined. The results showed orientation toward a T(H)1 responsiveness, and the treatment with the rHsp65 peptides diminished the environmental variance of the survival time of treated animals. These results outline the fact that environmental factors may also act through the modified stability expression of Heat Shock Proteins intervening during autoimmune processes. (C) 2011 Elsevier Ltd. All rights reserved.
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Common Variable Immunodeficiency (CVID) is a primary immunodeficiency disease characterized by defective immunoglobulin production and often associated with autoimmunity. We used flow cytometry to analyze CD4(+)CD25(HIGH)FOXP3(+) T regulatory (Treg) cells and ask whether perturbations in their frequency in peripheral blood could underlie the high incidence of autoimmune disorders in CVID patients. In this study, we report for the first time that CVID patients with autoimmune disease have a significantly reduced frequency of CD4(+)CD25(HIGH)FOXP3(+) cells in their peripheral blood accompanied by a decreased intensity of FOXP3 expression. Notably, although CVID patients in whom autoimmunity was not diagnosed had a reduced frequency of CD4(+)CD25(HIGH)FOXP3(+) cells, FOXP3 expression levels did not differ from those in healthy controls. In conclusion, these data suggest compromised homeostasis of CD4(+)CD25(HIGH)FOXP3(+) cells in a subset of CVID patients with autoimmunity, and may implicate Treg cells in pathological mechanisms of CVID. (C) 2009 Elsevier Inc. All rights reserved.
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The range of the Gray Wolf (Canis lupus), once covering most of North America, has been drastically reduced by an estimated 95% due to habitat loss and extermination by humans. The wolf was extirpated from Maine in the 1800’s. Wolf reintroductions have been suggested for Maine, but there is some debate about how much land is suitable for wolves. I developed a wolf habitat suitability analysis using ArcGIS and data from the Maine Office of GIS and the United States National Atlas. The model incorporates land cover, presence of major roads and railways, conservation land, industrial, non-industrial, and public woodlot ownership, distance from major points of population, deer population, and slope. The model results show areas of high and low wolf suitability in Maine. The model suggests that the best potential habitat for wolves in Maine is situated in the northwest of the state. Possible future reintroductions or natural colonization from other areas would have the highest likelihood of survival in these areas.
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The eastern timber wolf (Canis lupus lycaon) once inhabited Maine, as well as the rest of the eastern United States and southern Canada. As a result of human land use and widespread extermination campaigns, wolf numbers dramatically decreased, and by the early twentieth century, no wolves remained in Maine. As large carnivorous and territorial mammals, wolves require contiguous undeveloped areas with abundant prey. This project is a feasibility study that identifies the areas in Maine that are suitable for the reintroduction of wolves. We used GIS modeling to identify contiguous forested areas over 1,000 km2, calculate road and population density, and map the presence or absence of prey throughout the state. These variables were combined in a habitat suitability model to determine the location and amount of suitable wolf habitat in Maine. The northwestern part of the state appears most suitable for wolf reintroduction as it is relatively undeveloped with low road and population densities. There is also a smaller isolated area in Washington County that might be suitable, but further investigation is required.
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A S100B é uma proteína ligante de cálcio, de massa molecular de 21kDa, expressa principalmente por astrócitos. Esta proteína tem sido implicada em atividades funcionais tanto intra quanto extracelulares. Muitos estudos têm sugerido que intracelularmente ela está envolvida na modulação de proteínas do citoesqueleto e na regulação do ciclo celular. A proteína S100B pode ser secretada pelos astrócitos e desenvolver atividades extracelulares, que parecem depender de sua concentração. Em concentração nanomolar ela atua como fator trófico às células neurais, enquanto que em concentrações micromolar ela pode ser neurotóxica. A quantificação da proteína S100B no sangue e líquor se correlaciona com a extensão e intensidade do dano ao sistema nervoso central (SNC) o que permite sua utilização em estudos como marcador bioquímico de dano ou disfunção cerebral. Esta tese está dividida em três partes. A primeira parte propõe a utilização clínica da proteína S100B em patologias com envolvimento do SNC como a síndrome de Down, mielopatia associada ao vírus HTLV-I, lupus eritematoso sistêmico, epilepsia secundária a neurocisticercose e, além disso demonstramos a curva de ontogenia da S100B no sangue. Na segunda parte descrevemos uma atividade de nucleotidases presente em líquor de ratos, e finalmente, na terceira parte abordamos as perspectivas para futuros trabalhos. Os resultados obtidos pelo nosso grupo e por outros grupos internacionais relatam que a proteína S100B é um marcador inespecífico para evidenciar dano ou disfunção em doenças agudas e crônicas com envolvimento do SNC. Apesar de ser um marcador inespecífico, medidas dos níveis da proteína S100B tem grande sensibilidade para detectar uma resposta celular cerebral inespecífica. Além disso, demonstramos que estudos clínicos com esta proteína necessitam controles pareados por idade e sexo. A atividade nucleotidásica descrita no líquor de ratos hidrolisa preferencialmente o GDP e UDP comparado aos outros nucleotídeos. Nas perspectivas, os resultados mostrados são referentes a experimentos preliminares o que torna prematuro qualquer tipo de conclusão.
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