RESUMO
Performance and load normalized coefficients, deriving from an experimental campaign of measurements conducted at the large scale wind tunnel of the Politecnico di Milano (Italy), are presented with the aim of providing useful benchmark data for the validation of numerical codes. Rough data, derived from real scale measurements on a three-bladed Troposkien vertical-axis wind turbine, are manipulated in a convenient form to be easily compared with the typical outputs provided by simulation codes. The here proposed data complement and support the measurements already presented in "Wind Tunnel Testing of the DeepWind Demonstrator in Design and Tilted Operating Conditions" (Battisti et al., 2016) [1].
RESUMO
AIMS: Extrafollicular activation of B cells is rarely observed in human lymph nodes. The aim of this study was to extensively analyse the expression of surface molecules and transcription factors in four such cases, comparing them with follicular B cells and medullary cord plasma cells. METHODS AND RESULTS: Various combinations of B-cell-related surface markers and transcription factors were studied by triple immunofluorescence. While in the germinal centre, reactive immunoglobulin production occurred exclusively in non-proliferating cells, in extrafollicular activation proliferation of B cells and immunoglobulin production coexisted. In two of these cases proliferating cells were mainly IgG+CD27+, i.e. derived from class-switched postgerminal centre memory B cells. Some of these cells expressed CD30. In the other two cases, immunoglobulin-forming cells were non-class-switched IgM+CD27- B cells, representing a primary expansion of naive B cells. CONCLUSIONS: Extrafollicular B-cell activation is the morphological correlate of rapid B-cell responses that do not involve the germinal centres. It is pathogenetically heterogeneous, comprising primary responses that occur prior to, or independent of, germinal centre reaction or memory cell activation in recall responses.
Assuntos
Linfócitos B/química , Ativação Linfocitária , Antígenos CD/análise , Antígenos CD20/análise , Linfócitos B/imunologia , Antígenos CD79 , Proteínas de Ligação a DNA/análise , Imunofluorescência/métodos , Centro Germinativo/imunologia , Centro Germinativo/patologia , Humanos , Hiperplasia , Imunoglobulina G/análise , Fatores Reguladores de Interferon , Antígeno Ki-1/análise , Antígeno Ki-67/análise , Linfonodos/imunologia , Linfonodos/patologia , Glicoproteínas de Membrana/análise , Modelos Biológicos , Neprilisina/análise , Fator de Transcrição PAX5 , Fator 1 de Ligação ao Domínio I Regulador Positivo , Proteoglicanas/análise , Proteínas Proto-Oncogênicas/análise , Proteínas Proto-Oncogênicas c-bcl-6 , Receptores de Antígenos de Linfócitos B/análise , Proteínas Repressoras/análise , Sindecanas , Transativadores/análise , Fatores de Transcrição/análise , Membro 7 da Superfamília de Receptores de Fatores de Necrose Tumoral/análiseRESUMO
Pancreatic serous microcystic adenomas (SCAs) are rare, benign tumors with a striking female preference. Virtually no information is available about chromosomal or genetic anomalies in this disease. We performed extensive molecular characterization of 21 cases of formalin-fixed, paraffin-embedded sporadic SCAs consisting in genome-wide allelic loss analysis with 79 microsatellite markers covering all 22 autosomes, assessment of microsatellite instability, and mutational analysis of the VHL, K-ras, and p53 genes in nine cases for which frozen tissue was available. Although no case showed microsatellite instability of the type seen in mismatch repair-deficient tumors, a relatively low fractional allelic loss of 0.08 was found. Losses on chromosome 10q were the most frequent event in SCAs (50% of cases), followed by allelic losses on chromosome 3p (40% of cases). Moderately frequent losses (>25% of cases) were found on chromosomes 1q, 2q, and 7q. The VHL gene, located on chromosome 3p, had somatic inactivating mutations in two of nine cases (22%), whereas no mutations were found in either K-ras or p53, in agreement with the finding that all 21 cases stained negative for p53 by immunohistochemistry. Our study indicates that the involvement of chromosomal arms 10q and 3p is characteristic of SCAs and that the VHL gene is involved in a subset of sporadic cases.