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1. Affective state dependence and relative trait stability of perfectionism in sleep disturbances Dependência do estado afetivo e estabilidade relativa do traço do perfeccionismo nas perturbações de sono

Author

Berta R. Maia, Maria J. Soares, Ana T. Pereira, Mariana Marques, Sandra C. Bos, Ana Gomes, José Valente, Maria H. Azevedo, and António Macedo

Subjects
Avaliação, Sintomas afetivos, Estudante, Análise de variância, Transtornos do sono, Evaluation, Affective symptoms, Students, Analysis of variance, Sleep disorders, Psychiatry, RC435-571
Abstract

OBJECTIVE: To evaluate the degree of absolute change, relative stability and state dependence of trait perfectionism in sleep disturbances in a sample of university students. METHOD: Participants completed the Multidimensional Perfectionism Scale and two items concerning sleep difficulties. The mean age at T0 (baseline) was 19.59 years (SD = 1.61, range = 17-25) and 62.5% of the sample were female. RESULTS: Absolute changes in self-oriented and socially-prescribed perfectionism were found. Relative stability was found for all perfectionism dimensions. Prior and concurrent sleep disturbances explained a significant amount of variance in perfectionism. Controlling for the effects of sleep measures, prior self-oriented perfectionism and other-oriented perfectionism were the only significant predictors of subsequent self-oriented perfectionism and other-oriented perfectionism, at T1 and T2. Difficulties falling asleep at T1 and socially-prescribed perfectionism at T0 were significant predictors of socially-prescribed perfectionism at T1. CONCLUSION: Despite significant changes in perfectionism mean scores over the follow-up, the correlation analyses demonstrated that participants remained quite stable in regard to their relative levels of perfectionism. As concurrent difficulties initiating sleep also predicted concurrent socially-prescribed perfectionism, this seems to be one dimension of perfectionism with trait-state characteristics.OBJETIVOS: Avaliar o grau de mudança absoluta, de estabilidade relativa e dependência do estado do perfeccionismo nas perturbações de sono numa amostra de estudantes universitários. MÉTODO: Os sujeitos completaram a Escala Multidimensional do Perfeccionismo e dois itens sobre dificuldades em dormir. Os dados foram recolhidos em três momentos de avaliação, separados por um intervalo de um ano acadêmico. A idade média dos sujeitos no T0 era de 19,59 anos (DP = 1,61, variação = 17-25); 62,5% eram mulheres. RESULTADOS: Foram encontradas ao longo do follow-up mudanças absolutas para o perfeccionismo auto-orientado e para o perfeccionismo socialmente prescrito. Foi encontrada estabilidade relativa para todas as dimensões do perfeccionismo. As dificuldades de sono prévias e concorrentes explicaram significativamente a variância do perfeccionismo. Controlando o efeito das dificuldades em dormir, o perfeccionismo auto-orientado e o perfeccionismo orientado para o outro prévios foram os únicos preditores significativos de perfeccionismo auto-orientado e perfeccionismo orientado para o outro (T1 e T2). As dificuldades em iniciar o sono no T1 e o perfeccionismo socialmente prescrito prévio (T0) revelaram-se preditores significativos de perfeccionismo socialmente prescrito no T1. CONCLUSÃO: Apesar das mudanças significativas nas pontuações médias de perfeccionismo ao longo do follow-up, as análises de correlação demonstraram que os participantes permaneceram relativamente estáveis nos seus níveis de perfeccionismo. Uma vez que as dificuldades em iniciar o sono concorrentes se revelaram um preditor significativo de perfeccionismo socialmente prescrito, esta é a dimensão do perfeccionismo que possui características traço-estado.

Published
2011
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2. Overexpression of the Mitotic Checkpoint Genes BUB1 and BUBR1 is Associated with Genomic Complexity in Clear Cell Kidney Carcinomas

Author

Mafalda Pinto, Joana Vieira, Franclim R. Ribeiro, Maria J. Soares, Rui Henrique, Jorge Oliveira, Carmen Jerónimo, and Manuel R. Teixeira

Subjects
Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282, Cytology, QH573-671
Abstract

Background: A defective mitotic checkpoint has been proposed to contribute to chromosomal instability (CIN). We have previously shown that expression changes of the mitotic arrest deficiency (MAD) gene family plays a role in renal cell cancer (RCC) characterized by numerical chromosomal changes, namely papillary and chromophobe carcinomas, but nothing is known about the expression of mitotic checkpoint genes in the clear cell histotype (ccRCC).

Published
2008
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3. International distribution and age estimation of the Portuguese BRCA2 c.156_157insAlu founder mutation

Author

Maria J. Soares, Mauricio Magalhaes Costa, Ingrid Petroni Ewald, Rachel Kyle, Nelly Sabbaghian, Torben A Kruse, Leonor Gusmão, Mads Thomassen, Silvia Casadei, Annemarie H. van der Hout, Marc Tischkowitz, Patrícia Rocha, Ana Vega, Miguel de la Hoya, Patricia Ashton-Prolla, Lone Sunde, Sara Gutiérrez-Enríquez, Dirce Maria Carraro, Conxi Lázaro, Philippe Maillet, Maroulio Pertesi, Cindy Benson, Pedro Pinto, Alberto Gulino, Nancy Uhrhammer, Drakoulis Yannoukakos, William D. Foulkes, Lucie Cornil, Etienne Rouleau, Ana Peixoto, Ignacio Blanco, Gaelle Benais-Pont, Robert Royer, Mary Claire King, Montserrat Baiget, Thangarajan Rajkumar, María Dolores Miramar, Ana Rodriguez Valle, Maria Teresa Calvo, Judith Balmaña, Anne-Marie Gerdes, Rosette Lidereau, Giuseppe Giannini, Catarina Santos, Eladio Velasco, Maria Isabel Achatz, Dorthe G. Crüger, Luisa Mota-Vieira, Carmen Alonso, Orland Diez, Eitan Friedman, Manuela Pinheiro, Brigitte Bressac-de Paillerets, Yael Laitman, Steven A. Narod, Teresa Ramón y Cajal, Begoña Graña, António Amorim, Trinidad Caldés, Lídia Feliubadaló, Mercedes Durán, Bruno Pardo, Erik Teugels, Audrey Remenieras, Manuel R. Teixeira, Yves-Jean Bignon, and Ana Blanco

Subjects
Proband, Reading Frames, Cancer Research, Genes, BRCA2, Polymerase Chain Reaction, DISEASE, 0302 clinical medicine, BREAST/OVARIAN CANCER FAMILIES, skin and connective tissue diseases, Predictive testing, Sequence Deletion, founder mutation, c.156_157insalu brca2 mutation, hereditary breast/ovarian cancer, age estimation, c.156-157insalu brca2 mutation, Ovarian Neoplasms, Genetics, 0303 health sciences, education.field_of_study, medicine.diagnostic_test, REARRANGEMENT, Founder Effect, 3. Good health, Oncology, 030220 oncology & carcinogenesis, Mutation (genetic algorithm), GENETIC-HETEROGENEITY, Female, Population, Breast Neoplasms, Polymorphism, Single Nucleotide, 03 medical and health sciences, Breast cancer, medicine, Humans, Genetic Predisposition to Disease, Amino Acid Sequence, Genetic Testing, RNA, Messenger, Founder mutation, education, 030304 developmental biology, Genetic testing, Portugal, business.industry, Haplotype, medicine.disease, Genetics, Population, Mutation, Age estimation, c.156_157insAlu BRCA2 mutation, business, Hereditary breast/ovarian cancer, Microsatellite Repeats, Founder effect
Abstract

9 páginas, 4 figuras, 1 tabla.-- El pdf del artículo es la versión pre-print.-- et al., The c.156_157insAlu BRCA2 mutation has so far only been reported in hereditary breast/ovarian cancer (HBOC) families of Portuguese origin. Since this mutation is not detectable using the commonly used screening methodologies and must be specifically sought, we screened for this rearrangement in a total of 5,443 suspected HBOC families from several countries. Whereas the c.156_157insAlu BRCA2 mutation was detected in 11 of 149 suspected HBOC families from Portugal, representing 37.9% of all deleterious mutations, in other countries it was detected only in one proband living in France and in four individuals requesting predictive testing living in France and in the USA, all being Portuguese immigrants. After performing an extensive haplotype study in carrier families, we estimate that this founder mutation occurred 558 ± 215 years ago. We further demonstrate significant quantitative differences regarding the production of the BRCA2 full length RNA and the transcript lacking exon 3 in c.156_157insAlu BRCA2 mutation carriers and in controls. The cumulative incidence of breast cancer in carriers did not differ from that of other BRCA2 and BRCA1 pathogenic mutations. We recommend that all suspected HBOC families from Portugal or with Portuguese ancestry are specifically tested for this rearrangement., This study was supported by Ministério da Saúde (Project N8 15/2007) and Liga Portuguesa Contra o Cancro. IPATIMUP was funded by Fundaçáo para a Ciência e Tecnologia, through POCI (Programa Operacional Ciència e Inovaçáo 2010). MT and WDF are supported by the Susan G. Komen Foundation for the Cure, the Jewish General Hospital Weekend to End Breast Cancer and the Fonds de la Recherche en Santé du Québec. EAV and MD are supported by grants PI061102 (Ministerio de Ciencia e Innovación) and 200820I135 (CSIC).

Published
2010
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4. CSF1R copy number changes, point mutations, and RNA and protein overexpression in renal cell carcinomas

Author

Ana Teresa Martins, Rui Henrique, Nuno Cerveira, Maria J. Soares, Carmen Jerónimo, Ana Peixoto, Joana Vieira, Mafalda Pinto, Jorge Oliveira, and Manuel R. Teixeira

Subjects
Pathology, medicine.medical_specialty, Cell, DNA Mutational Analysis, Gene Dosage, Gene Expression, PDGFRB, Receptor, Macrophage Colony-Stimulating Factor, Biology, medicine.disease_cause, Gene dosage, Pathology and Forensic Medicine, Receptor, Platelet-Derived Growth Factor beta, Renal cell carcinoma, medicine, Biomarkers, Tumor, Humans, Point Mutation, RNA, Messenger, Carcinoma, Renal Cell, In Situ Hybridization, Fluorescence, Kidney, Reverse Transcriptase Polymerase Chain Reaction, medicine.disease, Molecular biology, Immunohistochemistry, Kidney Neoplasms, Clear cell renal cell carcinoma, medicine.anatomical_structure, Carcinogenesis, Clear cell
Abstract

Renal cell carcinomas comprise a heterogeneous group of tumors. Of these, 80% are clear cell renal cell carcinomas, which are characterized by loss of 3p, often with concomitant gain of 5q22qter. Although VHL is considered the main target gene of the 3p deletions, none has been identified as the relevant target gene for the 5q gain. We have studied 75 consecutive kidney tumors and paired normal kidney samples to evaluate at the genomic and expression levels the tyrosine kinase genes CSF1R and PDGFRB as potential targets in this region. Our findings show that RNA expression of CSF1R, but not of PDGFRB, was significantly higher in clear cell renal cell carcinomas than in normal tissue samples, something that was corroborated at the protein level by immunohistochemistry. The CSF1R staining pattern in clear cell renal cell carcinomas was clearly different from that observed in other renal cell carcinomas, suggesting its potential usefulness in differential diagnosis. FISH analysis demonstrated whole chromosomal gain and relative CSF1R/PDGFRB copy number gain in clear cell renal cell carcinomas, which might contribute to CSF1R overexpression. Finally, one polymorphism and two novel mutations were identified in CSF1R in clear cell renal cell carcinoma patients. Our data allow us to conclude that CSF1R plays a relevant role in clear cell renal cell carcinoma carcinogenesis and raise the possibility that CSF1R may represent a future valuable therapeutic target in these patients.

Published
2009

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