Las casas-torre bajomedievales. Análisis sistémico de un proceso de reestructuración espacial/territorial

[ES] La torre banderiza es uno de los más relevantes elementos del patrimonio construido vasco. Diseminados por toda la geografía de la comunidad autónoma, se pueden encontrar ejemplos representativos de este tipo arquitectónico, característico de una convulsa etapa que se prolongó algo más allá del período de crisis bajomedieval (siglos XIV-XVI). Este trabajo pretende por un lado formular una propuesta interpretativa sistémica e integradora que, partiendo del análisis estratigráfico de las fábricas, muestre el peso específico de esta construcción como elemento de gestión de los recursos del territorio. Pero sobre todo, en las siguientes líneas se hace una decidida apuesta por una forma de entender la investigación histórico-arqueológica.

Serological and Genetic Evidence for Altered Complement System Functionality in Systemic Lupus Erythematosus: Findings of the GAPAID Consortium

Systemic lupus erythematosus is a chronic autoimmune disease with multifactorial ethiopathogenesis. The complement system is involved in both the early and late stages of disease development and organ damage. To better understand autoantibody mediated complement consumption we examined ex vivo immune complex formation on autoantigen arrays. We recruited patients with SLE (n = 211), with other systemic autoimmune diseases (n = 65) and non-autoimmune control subjects (n = 149). Standard clinical and laboratory data were collected and serum complement levels were determined. The genotype of SNP rs1143679 in the ITGAM gene was also determined. Ex vivo formation of immune complexes, with respect to IgM, IgG, complement C4 and C3 binding, was examined using a functional immunoassay on autoantigen microarray comprising nucleic acids, proteins and lipids. Complement consumption of nucleic acids increased upon binding of IgM and IgG even when serum complement levels were decreased due to consumption in SLE patients. A negative correlation between serum complement levels and ex vivo complement deposition on nucleic acid autoantigens is demonstrated. On the contrary, complement deposition on tested protein and lipid autoantigens showed positive correlation with C4 levels. Genetic analysis revealed that the non-synonymous variant rs1143679 in complement receptor type 3 is associated with an increased production of anti-dsDNA IgG antibodies. Notwithstanding, homozygous carriers of the previously reported susceptible allele (AA) had lower levels of dsDNA specific IgM among SLE patients. Both the non-synonymous variant rs1143679 and the high ratio of nucleic acid specific IgG/IgM were associated with multiple organ involvement. In summary, secondary complement deficiency in SLE does not impair opsonization of nucleic-acid-containing autoantigens but does affect other antigens and potentially other complement dependent processes. Dysfunction of the receptor recognizing complement opsonized immune complexes promotes the development of class-switched autoantibodies targeting nucleic acids.

Biscaytel Sociedad Cooperativa Pequeña: El reto de dirigir una pequeña empresa recién creada

Duración (en horas): De 21 a 30 horas. Nivel educativo: Grado

Procesos de prociclidad crediticia e impacto de la provisión estadística en España

Códigos JEL: G21, E32, E44

Una aproximación al origen de la crisis financiera internacional

Este artículo es una adaptación de la conferencia titulada “Génesis de la crisis financiera”, que fue impartida en el Curso de Verano “Diez años del euro: 1999-2009”, celebrado los días 25 y 26 de junio de 2009 en el marco de los XXVIII Cursos de Verano de la UPV/EHU

Modelo de dinámica de sistemas para la implantación de tecnologías de la información en la gestión estratégica universitaria

394 p.

Una aproximación psicosocial al conflicto vasco. Construyendo la paz en espacio abierto

450 p.

La evaluación de los úrsidos en medios karsticos de la Cornisa Cantábrica

681 p.

LDLR and PCSK9 Are Associated with the Presence of Antiphospholipid Antibodies and the Development of Thrombosis in aPLA Carriers

Introduction The identification of the genetic risk factors that could discriminate non-thrombotic from thrombotic antiphospholipid antibodies (aPLA) carriers will improve prognosis of these patients. Several human studies have shown the presence of aPLAs associated with atherosclerotic plaque, which is a known risk factor for thrombosis. Hence, in order to determine the implication of atherosclerosis in the risk of developing thrombosis in aPLA positive patients, we performed a genetic association study with 3 candidate genes, APOH, LDLR and PCSK9. Material & Methods For genetic association study we analyzed 190 aPLA carriers -100 with non-thrombotic events and 90 with thrombotic events-and 557 healthy controls. Analyses were performed by chi(2) test and were corrected by false discovery rate. To evaluate the functional implication of the newly established susceptibility loci, we performed expression analyses in 86 aPLA carrier individuals (43 with thrombotic manifestations and 43 without it) and in 45 healthy controls. Results Our results revealed significant associations after correction in SNPs located in LDLR gene with aPLA carriers and thrombotic aPLA carriers, when compared with healthy controls. The most significant association in LDLR gene was found between SNP rs129083082 and aPLA carriers in recessive model (adjusted P-value = 2.55 x 10(-3); OR = 2.18; 95% CI = 1.49-3.21). Furthermore, our work detected significant allelic association after correction between thrombotic aPLA carriers and healthy controls in SNP rs562556 located in PCSK9 gene (adjusted P-value = 1.03 x 10(-2); OR = 1.60; 95% CI = 1.24-2.06). Expression level study showed significantly decreased expression level of LDLR gene in aPLA carriers (P-value < 0.0001; 95% CI 0.16-2.10; SE 0.38-1.27) in comparison to the control group. Discussion Our work has identified LDLR gene as a new susceptibility gene associated with the development of thrombosis in aPLA carriers, describing for the first time the deregulation of LDLR expression in individuals with aPLAs. Besides, thrombotic aPLA carriers also showed significant association with PCSK9 gene, a regulator of LDLR plasma levels. These results highlight the importance of atherosclerotic processes in the development of thrombosis in patients with aPLA.