Browsing by Author "Oliveira, C"
Now showing 1 - 10 of 14
Results Per Page
Sort Options
- Avaliação da Capacidade de Decisão em Psiquiatria de LigaçãoPublication . Vicente, F; Nascimento, M; Oliveira, C; Tomé, C; Vieira, C; Luis, AIntrodução: Entre as funções do psiquiatra de ligação, encontra-se a avaliação da capacidade de decidir. Esta envolve a capacidade de fazer escolhas de forma autónoma e surge de forma relevante na prática clínica diária como pré-condição ao consentimento informado. Objetivos: Os autores pretendem rever o processo subjacente à avaliação da capacidade de decisão, assim como outra informação relevante publicada a este respeito. Métodos: Revisão não sistemática da literatura através da pesquisa eletrónica nos motores de busca Medline/Pubmed. Resultados: A capacidade de decidir apenas pode ser avaliada relativamente a uma decisão em particular, sendo que o seu resultado não é necessariamente estável ao longo do tempo. Da mesma forma, não existe nenhum diagnóstico que permita concluir, por si só, pela incapacidade para decidir ou que possibilite prescindir da sua avaliação. Depende de vários fatores: conteúdo, forma do pensamento e funções cognitivas. Pode igualmente ser influenciada pelo nível de instrução do indivíduo, traços da personalidade, estados emocionais/mecanismos de coping ou fatores circunstanciais. Qualquer médico deverá estar habilitado para a realização desta avaliação. O psiquiatra de ligação deve ser envolvido perante a suspeita de doença mental capaz de prejudicar a capacidade de consentir ou perante a necessidade de validar uma avaliação já realizada. Appelbaum e Grisso propuseram uma avaliação sistematizada segundo os seguintes critérios: a) comunicação da escolha, b) compreensão, c) apreciação e d) processo de decisão racional/ raciocínio. Numa tentativa de minimizar diferenças entre avaliadores, foram desenvolvidos vários instrumentos de avaliação, entre os quais se destaca a MacArthur Competence Assessment Tool. Particularmente nos doentes com défice cognitivo, tem sido também utilizada o Mini Mental State Examination, surgindo propostas no sentido de correlacionar os scores obtidos com a presença de capacidade de decisão. Perante a incapacidade para decidir, deverá ser respeitado o melhor interesse do doente, sendo procurada uma “decisão de substituição”, no rigoroso respeito pela ética e pela lei. Conclusões: Um doente capaz de decidir deve apresentar: a) atenção focada no problema; b) capacidade de considerar as diferentes opções propostas; c) capacidade de avaliar os riscos e benefícios e d) capacidade de antecipar os seus possíveis resultados.
- CHARACTERIZATION OF THE POPULATION OF PREGNANT WOMEN ATTENDING A MENTAL HEALTH SERVICEPublication . Ferreira, T; Dehanov, S; Oliveira, C; Castro, S; Ribeiro, R; Maia, TIntroduction: Psychopathological symptoms are common during pregnancy and their detection and referral to specialized care is often suboptimal. The aim of this study was to perform a descriptive analysis of sociodemographic, mental health, and obstetric features of a population of pregnant women followed at Psychiatry consultation. Methodology: This was a cross-sectional, descriptive study of women followed both at Gynecology/Obstetrics and Psychiatry consultations of Hospital Prof. Doutor Fernando Fonseca between 2014 and 2016. A total of 76 women were included, for whom pre-defined features associated in the literature with risk of developing psychopathological symptoms during pregnancy were collected. Results and Discussion: Risk factors identified in the development of depressive symptoms included absence of an affective relationship during pregnancy (n=11; 14.5%), being first-generation immigrant (n=17; 22.4%), and substance use before (n=18; 23.7%) or during (n=10; 13.1%) pregnancy. Sample was divided into women with previous Psychiatry follow-up who became pregnant (n=44; 57.9%) and women referred to Psychiatry consultation during pregnancy (n=32; 42.1%). In the second group, 18.8% (n=6) of referrals were from primary health care, being relevant to understand whether this represents an under-referral. Prescription of 21 risk category D drugs was identified, alerting to the need of caution in pharmacological prescription and of considering non-pharmacological options (e.g., cognitive-behavioral therapy) for management of these cases. Conclusions: Risk factors identified in this study represent an opportunity to optimize clinical practice and improve these patients’ follow-up
- Estudo de utilização de albumina humana 20% no Hospital Fernando FonsecaPublication . Afonso, R; Costa, C; Elias, C; Fernandes, J; Ferreira, A; Jesus, S; Oliveira, C; Oliveira, I; Oliveira, MJ; Prata, A; Almeida, P
- Mutational mechanism for DAB1 (ATTTC)n insertion in SCA37: ATTTT repeat lengthening and nucleotide substitutionPublication . Loureiro, J; Oliveira, C; Mota, C; Castro, A; Costa, C, et al.Dynamic mutations by microsatellite instability are the molecular basis of a growing number of neuromuscular and neurodegenerative diseases. Repetitive stretches in the human genome may drive pathogenicity, either by expansion above a given threshold, or by insertion of abnormal tracts in nonpathogenic polymorphic repetitive regions, as is the case in spinocerebellar ataxia type 37 (SCA37). We have recently established that this neurodegenerative disease is caused by an (ATTTC)n insertion within an (ATTTT)n in a noncoding region of DAB1. We now investigated the mutational mechanism that originated the (ATTTC)n insertion within an ancestral (ATTTT)n . Approximately 3% of nonpathogenic (ATTTT)n alleles are interspersed by AT-rich motifs, contrarily to mutant alleles that are composed of pure (ATTTT)n and (ATTTC)n stretches. Haplotype studies in unaffected chromosomes suggested that the primary mutational mechanism, leading to the (ATTTC)n insertion, was likely one or more T>C substitutions in an (ATTTT)n pure allele of approximately 200 repeats. Then, the (ATTTC)n expanded in size, originating a deleterious allele in DAB1 that leads to SCA37. This is likely the mutational mechanism in three similar (TTTCA)n insertions responsible for familial myoclonic epilepsy. Because (ATTTT)n tracts are frequent in the human genome, many loci could be at risk for this mutational process.
- Mutational mechanism for DAB1 (ATTTC)n insertion in SCA37: ATTTT repeat lengthening and nucleotide substitutionPublication . Loureiro, J; Oliveira, C; Mota, C; Castro, A; Costa, C; Loureiro, J, et al.Dynamic mutations by microsatellite instability are the molecular basis of a growing number of neuromuscular and neurodegenerative diseases. Repetitive stretches in the human genome may drive pathogenicity, either by expansion above a given threshold, or by insertion of abnormal tracts in nonpathogenic polymorphic repetitive regions, as is the case in spinocerebellar ataxia type 37 (SCA37). We have recently established that this neurodegenerative disease is caused by an (ATTTC)n insertion within an (ATTTT)n in a noncoding region of DAB1. We now investigated the mutational mechanism that originated the (ATTTC)n insertion within an ancestral (ATTTT)n . Approximately 3% of nonpathogenic (ATTTT)n alleles are interspersed by AT-rich motifs, contrarily to mutant alleles that are composed of pure (ATTTT)n and (ATTTC)n stretches. Haplotype studies in unaffected chromosomes suggested that the primary mutational mechanism, leading to the (ATTTC)n insertion, was likely one or more T>C substitutions in an (ATTTT)n pure allele of approximately 200 repeats. Then, the (ATTTC)n expanded in size, originating a deleterious allele in DAB1 that leads to SCA37. This is likely the mutational mechanism in three similar (TTTCA)n insertions responsible for familial myoclonic epilepsy. Because (ATTTT)n tracts are frequent in the human genome, many loci could be at risk for this mutational process.
- Mutational mechanism for DAB1 (ATTTC)n insertion in SCA37: ATTTT repeat lengthening and nucleotide substitution.Publication . Loureiro, J; Oliveira, C; Mota, C; Castro, A; Costa, C, et al.Dynamic mutations by microsatellite instability are the molecular basis of a growing number of neuromuscular and neurodegenerative diseases. Repetitive stretches in the human genome may drive pathogenicity, either by expansion above a given threshold, or by insertion of abnormal tracts in nonpathogenic polymorphic repetitive regions, as is the case in spinocerebellar ataxia type 37 (SCA37). We have recently established that this neurodegenerative disease is caused by an (ATTTC)n insertion within an (ATTTT)n in a noncoding region of DAB1. We now investigated the mutational mechanism that originated the (ATTTC)n insertion within an ancestral (ATTTT)n . Approximately 3% of nonpathogenic (ATTTT)n alleles are interspersed by AT-rich motifs, contrarily to mutant alleles that are composed of pure (ATTTT)n and (ATTTC)n stretches. Haplotype studies in unaffected chromosomes suggested that the primary mutational mechanism, leading to the (ATTTC)n insertion, was likely one or more T>C substitutions in an (ATTTT)n pure allele of approximately 200 repeats. Then, the (ATTTC)n expanded in size, originating a deleterious allele in DAB1 that leads to SCA37. This is likely the mutational mechanism in three similar (TTTCA)n insertions responsible for familial myoclonic epilepsy. Because (ATTTT)n tracts are frequent in the human genome, many loci could be at risk for this mutational process.
- Mutational mechanism for DAB1 (ATTTC)n insertion in SCA37: ATTTT repeat lengthening and nucleotide substitution.Publication . Loureiro, J; Oliveira, C; Mota, C; Castro, A; Costa, C; Loureiro JL2, J, et al.5,6Dynamic mutations by microsatellite instability are the molecular basis of a growing number of neuromuscular and neurodegenerative diseases. Repetitive stretches in the human genome may drive pathogenicity, either by expansion above a given threshold, or by insertion of abnormal tracts in nonpathogenic polymorphic repetitive regions, as is the case in spinocerebellar ataxia type 37 (SCA37). We have recently established that this neurodegenerative disease is caused by an (ATTTC)n insertion within an (ATTTT)n in a noncoding region of DAB1. We now investigated the mutational mechanism that originated the (ATTTC)n insertion within an ancestral (ATTTT)n . Approximately 3% of nonpathogenic (ATTTT)n alleles are interspersed by AT-rich motifs, contrarily to mutant alleles that are composed of pure (ATTTT)n and (ATTTC)n stretches. Haplotype studies in unaffected chromosomes suggested that the primary mutational mechanism, leading to the (ATTTC)n insertion, was likely one or more T>C substitutions in an (ATTTT)n pure allele of approximately 200 repeats. Then, the (ATTTC)n expanded in size, originating a deleterious allele in DAB1 that leads to SCA37. This is likely the mutational mechanism in three similar (TTTCA)n insertions responsible for familial myoclonic epilepsy. Because (ATTTT)n tracts are frequent in the human genome, many loci could be at risk for this mutational process.
- Mutational mechanism for DAB1 (ATTTC)n insertion in SCA37: ATTTT repeat lengthening and nucleotide substitution.Publication . Loureiro, J; Oliveira, C; Mota, C; Castro, A; Costa, C; Loureiro, J, et al.Abstract Dynamic mutations by microsatellite instability are the molecular basis of a growing number of neuromuscular and neurodegenerative diseases. Repetitive stretches in the human genome may drive pathogenicity, either by expansion above a given threshold, or by insertion of abnormal tracts in nonpathogenic polymorphic repetitive regions, as is the case in spinocerebellar ataxia type 37 (SCA37). We have recently established that this neurodegenerative disease is caused by an (ATTTC)n insertion within an (ATTTT)n in a noncoding region of DAB1. We now investigated the mutational mechanism that originated the (ATTTC)n insertion within an ancestral (ATTTT)n . Approximately 3% of nonpathogenic (ATTTT)n alleles are interspersed by AT-rich motifs, contrarily to mutant alleles that are composed of pure (ATTTT)n and (ATTTC)n stretches. Haplotype studies in unaffected chromosomes suggested that the primary mutational mechanism, leading to the (ATTTC)n insertion, was likely one or more T>C substitutions in an (ATTTT)n pure allele of approximately 200 repeats. Then, the (ATTTC)n expanded in size, originating a deleterious allele in DAB1 that leads to SCA37. This is likely the mutational mechanism in three similar (TTTCA)n insertions responsible for familial myoclonic epilepsy. Because (ATTTT)n tracts are frequent in the human genome, many loci could be at risk for this mutational process.
- Mutational mechanism for DAB1 (ATTTC)n insertion in SCA37: ATTTT repeat lengthening and nucleotide substitution.Publication . Loureiro, JR; Oliveira, C; Mota, C; Castro, AF; Costa, C; Loureiro, J; Coutinho, P; Martins, S; Sequeiros, J; Silveira, IDynamic mutations by microsatellite instability are the molecular basis of a growing number of neuromuscular and neurodegenerative diseases. Repetitive stretches in the human genome may drive pathogenicity, either by expansion above a given threshold, or by insertion of abnormal tracts in nonpathogenic polymorphic repetitive regions, as is the case in spinocerebellar ataxia type 37 (SCA37). We have recently established that this neurodegenerative disease is caused by an (ATTTC)n insertion within an (ATTTT)n in a noncoding region of DAB1. We now investigated the mutational mechanism that originated the (ATTTC)n insertion within an ancestral (ATTTT)n . Approximately 3% of nonpathogenic (ATTTT)n alleles are interspersed by AT-rich motifs, contrarily to mutant alleles that are composed of pure (ATTTT)n and (ATTTC)n stretches. Haplotype studies in unaffected chromosomes suggested that the primary mutational mechanism, leading to the (ATTTC)n insertion, was likely one or more T>C substitutions in an (ATTTT)n pure allele of approximately 200 repeats. Then, the (ATTTC)n expanded in size, originating a deleterious allele in DAB1 that leads to SCA37. This is likely the mutational mechanism in three similar (TTTCA)n insertions responsible for familial myoclonic epilepsy. Because (ATTTT)n tracts are frequent in the human genome, many loci could be at risk for this mutational process.
- Prevalence of HLA antibodies in post pregnancies female blood donorsPublication . Barra, A; Barradas, A; Cardoso, E; Costa, C; Fontes, A; Gil, A; Oliveira, C; Ramalhete, L; Rodrigues, T; Sancho, MR; Silva, I; Simões, A; Trindade, HBackground: Transfusion related acute lung injury (TRALI) is known as transfusion hazard with high morbidity and mortality rate. Mainly HLA class II have been associated with TRALI. Preventive measures are in the exclusion of donor female as they carry any these antibodies. Aim: We study a group of female blood donor with prior history of two or more pregnancies (G2), one (G1) pregnancy and without any pregnancy (G0) for detection of HLA antibodies. Methods: We collected a total of 108 samples between September and December of 2010 (G2-56; G1-19 and G0-33 samples). For detection of HLA antibodies we used the LABScreen Mixed Assay which is multiplex technique that detects anti HLA Class I and II 1gG antibodies. Microparticles (beads) are coated with HLA antigens. Those beads have a combination of two dyes, and for each set of beads the dyes proportions are different so that the bead sets can be distinguished. Positivity was defined when the ratio is equal or higher than 4. Results: In the totality of the 108 study samples we found positivity for HLA class I antibodies in 22% (G2-32%, G1-26%, G0-3%) and for HLA class II antibodies in 17% of samples (G2-27%, G1-5%, and G0-6%). Positivity for both HLA class I and II antibodies was found only in G2 samples (18%) and G1 samples (5%). Our study also shows a 12% of positivity only for HLA class I antibodies (G2-14%, G1-21%, G0-3%) and a 6% of positivity only for HLA class II antibodies (G2-9%, G1-0%, G0-6%). Conclusions: Our study reveals higher prevalence of HLA class I and II antibodies in G2 population . Women with both positive HLA Class I and II antibodies have been excluded for blood donation in order to prevent TRALI in recipients. This study will continue with a higher number of samples. Idea was to test all this women to HLA class antibodies prior to each blood donation.