150 research outputs found

    Convergence of simple adaptive Galerkin schemes based on h − h/2 error estimators

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    We discuss several adaptive mesh-refinement strategies based on (h − h/2)-error estimation. This class of adaptivemethods is particularly popular in practise since it is problem independent and requires virtually no implementational overhead. We prove that, under the saturation assumption, these adaptive algorithms are convergent. Our framework applies not only to finite element methods, but also yields a first convergence proof for adaptive boundary element schemes. For a finite element model problem, we extend the proposed adaptive scheme and prove convergence even if the saturation assumption fails to hold in general

    Quasi-Optimal Convergence Rate for an Adaptive Finite Element Method

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    Evaluation of a functional epigenetic approach to identify promoter region methylation in phaeochromocytoma and neuroblastoma

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    The molecular genetics of inherited phaeochromocytoma have received considerable attention, but the somatic genetic and epigenetic events that characterise tumourigenesis in sporadic phaeochromocytomas are less well defined. Previously, we found considerable overlap between patterns of promoter region tumour suppressor gene (TSG) hypermethylation in two neural crest tumours, neuroblastoma and phaeochromocytoma. In order to identify candidate biomarkers and epigenetically inactivated TSGs in phaeochromocytoma and neuroblastoma, we characterised changes in gene expression in three neuroblastoma cell lines after treatment with the demethylating agent 5-azacytidine. Promoter region methylation status was then determined for 28 genes that demonstrated increased expression after demethylation. Three genes HSP47, homeobox A9 (HOXA9) and opioid binding protein (OPCML) were methylated in >10% of phaeochromocytomas (52, 17 and 12% respectively). Two of the genes, epithelial membrane protein 3 (EMP3) and HSP47, demonstrated significantly more frequent methylation in neuroblastoma than phaeochromocytoma. These findings extend epigenotype of phaeochromocytoma and identify candidate genes implicated in sporadic phaeochromocytoma tumourigenesis

    Corantes de batata doce roxa para uso em alimentos.

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    Um processo de preparo de produtos corantes a partir da batata doce roxa, Ipomoea batatas, Lam., Convulvolaceae, de polpa roxa, foi desenvolvida visando seu emprego como aditivo corante em alimentos. Os produtos corantes resultaram da solubilização do amido, constituinte principal da batata doce, que se atingiu por meio de hidrólise acida com ácidos minerais, como os ácidos clorídrico ou sulfúrico, ou por meio de hidrólises enzimáticas. Hidrólises ácidas seguidas de hidrólises enzimáticas com amiloglicosidase e hidrólises enzimáticas com amilase seguida de amiloglicosidase foram consideradas mais efetivas. Produtos concentrados líquidos viscosos de 72 Brix e produtos em pó obtidos por liofilização e secagem por "spray" foram preparados, cujo teor em antocianinas foi de 0,24%, 0,15% e 0,12% respectivamente. Ensaios de intensidade de cor e conservação dos corantes em função do meio forma feitos. O processo de obtenção dos corantes de batata doce roxa, desenvolvido no CTAA, constitui-se em processo inovador tanto no que se refere a mateira prima empregada quanto ao processamento e um pedido de privilegio de inovação foi redigido para avaliação no INPI.bitstream/item/65377/1/CTAA-DOCUMENTOS-9-CORANTES-DE-BATATA-DOCE-ROXA-PARA-USO-EM-ALIMENTOS-FL-06785.pd

    The first Dutch SDHB founder deletion in paraganglioma – pheochromocytoma patients

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    Contains fulltext : 81280.pdf (publisher's version ) (Open Access)BACKGROUND: Germline mutations of the tumor suppressor genes SDHB, SDHC and SDHD play a major role in hereditary paraganglioma and pheochromocytoma. These three genes encode subunits of succinate dehydrogenase (SDH), the mitochondrial tricarboxylic acid cycle enzyme and complex II component of the electron transport chain. The majority of variants of the SDH genes are missense and nonsense mutations. To date few large deletions of the SDH genes have been described. METHODS: We carried out gene deletion scanning using MLPA in 126 patients negative for point mutations in the SDH genes. We then proceeded to the molecular characterization of deletions, mapping breakpoints in each patient and used haplotype analysis to determine whether the deletions are due to a mutation hotspot or if a common haplotype indicated a single founder mutation. RESULTS: A novel deletion of exon 3 of the SDHB gene was identified in nine apparently unrelated Dutch patients. An identical 7905 bp deletion, c.201-4429_287-933del, was found in all patients, resulting in a frameshift and a predicted truncated protein, p.Cys68HisfsX21. Haplotype analysis demonstrated a common haplotype at the SDHB locus. Index patients presented with pheochromocytoma, extra-adrenal PGL and HN-PGL. A lack of family history was seen in seven of the nine cases. CONCLUSION: The identical exon 3 deletions and common haplotype in nine patients indicates that this mutation is the first Dutch SDHB founder mutation. The predominantly non-familial presentation of these patients strongly suggests reduced penetrance. In this small series HN-PGL occurs as frequently as pheochromocytoma and extra-adrenal PGL

    Association of Serum Ferritin Levels Before Start of Conditioning With Mortality After alloSCT - A Prospective, Non-interventional Study of the EBMT Transplant Complications Working Party

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    Elevated serum ferritin levels occur due to iron overload or during inflammation and macrophage activation. A correlation of high serum ferritin levels with increased mortality after alloSCT has been suggested by several retrospective analyses as well as by two smaller prospective studies. This prospective multicentric study aimed to study the association of ferritin serum levels before start of conditioning with alloSCT outcome. Patients with acute leukemia, lymphoma or MDS receiving a matched sibling alloSCT for the first time were considered for inclusion, regardless of conditioning. A comparison of outcomes between patients with high and low ferritin level was performed using univariate analysis and multivariate analysis using cause-specific Cox model. Twenty centers reported data on 298 alloSCT recipients. The ferritin cut off point was determined at 1500 mu g/l (median of measured ferritin levels). In alloSCT recipients with ferritin levels above cut off measured before the start of conditioning, overall survival (HR = 2.5, CI = 1.5-4.1, p = 0.0005) and progression-free survival (HR = 2.4, CI = 1.6-3.8, p <0.0001) were inferior. Excess mortality in the high ferritin group was due to both higher relapse incidence (HR = 2.2, CI = 1.2-3.8, p = 0.007) and increased non-relapse mortality (NRM) (HR = 3.1, CI = 1.5-6.4, p = 0.002). NRM was driven by significantly higher infection-related mortality in the high ferritin group (HR = 3.9, CI = 1.6-9.7, p = 0.003). Acute and chronic GVHD incidence or severity were not associated to serum ferritin levels. We conclude that ferritin levels can serve as routine laboratory biomarker for mortality risk assessment before alloSCT.Peer reviewe
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