Sickle Cell Trait Subjects
Mostrando 1-8 de 8 artigos, teses e dissertações.
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1. Perfil oxidativo e bioquímico em pacientes que apresentam anemia falciforme ou traço falciforme / Oxidative and biochemistry profile in sickle cell trait subjects and sickle cell anaemia patients
A Anemia Falciforme (AF) é uma doença autossômica recessiva e, dentre as hemoglobinopatias, é a mais comum das alterações hematológicas hereditárias conhecidas no homem. Sua distribuição é ampla, abrangendo todos os continentes. AF foi a primeira doença caracterizada em nível molecular. É causada por uma mutação no gene beta da globina, produ
Publicado em: 2008
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2. Efeito do ácido lipóico sobre parâmetros de estresse oxidativo em indivíduos traço falciformes ou pacientes falciformes / Alpha lipoic acid effect on oxidative stress parameters in sickle cell trait subjects and sickle cell patients
A anemia falciforme (AF) é causada por uma mutação (Glu6Val) no gene que codifica a b-globina gerando a hemoglobina S (HbS). A HbS tem a tendência a se polimerizar quando desoxigenada. Isto resulta em graves manifestações clínicas para o indivíduo homozigoto (HbSS). O traço falciforme (HbAS), geralmente assintomático, também pode apresentar dano o
Publicado em: 2008
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3. Mecanismos reguladores da sintese de globinas : avaliação funcional da região R/PYR e analise da expressão genica diferencial na persistencia hereditaria de hemoglobina fetal e na delta-beta talassemia / Regulatory mechanisms of globin syntheis : functional evaluation of R/PYR region and differential gene expression analysis in hereditary persistence of etal hemoglobin and delta-beta thalassemia
The genetic mechanisms underlying the continued expression of the ?-globin genes during the adult stage in deletional hereditary persistence of fetal hemoglobin (HPFH) and ??-thalassemias are not completely understood. For deletional HPFH, three main hypotheses were proposed to explain the relationship between these deletions and the non-suppression of ? -ge
Publicado em: 2006
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4. OXYGEN DISSOCIATION CURVES IN SICKLE CELL ANEMIA AND IN SUBJECTS WITH THE SICKLE CELL TRAIT
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5. Mild sickle-cell anaemia in Iran associated with high levels of fetal haemoglobin.
Sixteen subjects, with sickle-cell anaemia, all Iranians (ages 3 to 56 years), with very mild symptomatology are reported. Some of the subjects had been totally asymptomatic. Splenomegaly was noted in 9 cases. There was an increase in the mean level of fetal haemoglobin (18%); this is the probable explanation for the mild phenotype. In 29 subjects with sickl
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6. Frequency and clinical significance of erythrocyte genetic abnormalities in Omanis.
The frequencies of four malaria associated erythrocyte genetic abnormalities have been established in 1000 Omani subjects. They are: homozygous alpha+ thalassaemia (-alpha/-alpha) 0.45; high Hb A2 beta thalassaemia trait 0.015; sickle trait (Hb A/S) 0.061; and glucose 6 phosphate dehydrogenase deficiency (Gd-): males 0.27, females 0.11. From our data the alp
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7. Thalassaemia types and their incidence in Sardinia.
The frequency of thalassaemia syndromes in Sardinia was examined by a population survey. The data indicate that about 12.6% of the Sardinian subjects are carriers of beta-thalassaemia, while 6.9% of the population carries an alpha-thalassaemia gene, with a slight difference between the various provinces. These are among the highest frequencies of thalassaemi
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8. Molecular defect in the sickle erythrocyte skeleton. Abnormal spectrin binding to sickle inside-our vesicles.
Although functional abnormalities of the sickle erythrocyte membrane skeleton have been described, there is little quantitative data on the function of the proteins that compose the skeleton. We have examined the association of spectrin, the major skeletal protein, with ankyrin, its high-affinity membrane binding site, and found sickle erythrocytes to have m