Electrochemical behavior of Ti/Al2O3 interfaces produced by diffusion bonding

In the field of biomedical applications a special interest exists regarding the study of the physicochemical and mechanical behaviour of materials, with special focus on the electrochemical degradation of metal/ceramic interfaces. In fact, etal/ceramic interfaces may be present in several biomedical devices, ranging from external or implantable sensors, to dental implants. Diffusion bonding represents an important technique since, in opposition to other production technologies, such as active metal brazing, avoid the possible liberation of certain chemical components harmful to health. The aim of this work is to study the electrochemical degradation of the interface formed between commercially pure Ti and Al2O3 produced by diffusion bonding, in contact with a physiological solution. The present approach included the evaluation of the contribution of individual and pairs of interfacial layers on the global degradation processes. For this propose d.c. electrochemical techniques were used to monitor the open-circuit potential, and to perform potentiodynamic polarization and galvanic corrosion evaluation. Also, electrochemical impedance spectroscopy was used as a complementary technique of the corrosion behaviour of the interface. Chemical composition and morphology of samples and corrosion products were evaluated by SEM and EDS analysis. According to experimental results, two principal reaction layers were formed in the interface: TiAl and Ti3Al. The TiAl layer appears to be the responsible for the strong increase in corrosion rate of the interface.Fundação para a Ciência e Tecnologia -POCTI/CTM/33384/2000; SFRH/BPD/ 5518/2001

Prevalence Of α-thalassemia 3.7 Kb Deletion In The Adult Population Of Rio Grande Do Norte, Brazil

α-Thalassemia, arising from a defect in α-globin chain synthesis, is often caused by deletions involving one or both of the α-genes on the same allele. With the aim of investigating the prevalence of α-thalassemia 3.7 kb deletion in the adult population of Rio Grande do Norte, 713 unrelated individuals, between 18 and 59 years-of-age, were analyzed. Red blood cell indices were electronically determined, and A 2 and F hemoglobins evaluated by HPLC. PCR was applied to the molecular investigation of α-thalassemia 3.7 kb deletion. Eighty (11.2%) of the 713 individuals investigated presented α-thalassemia, of which 79 (11.1%) were heterozygous (-α 3.7/αα) deletions and 1 (0.1%) homozygous (-α 3.7/-α 3.7). Ethnically, heterozygous deletions were higher (24.8%) in Afro-Brazilians. Comparison of hematological parameters between individuals with normal genotype and those with heterozygous α +-thalassemia showed a statistically significant difference in the number of erythrocytes (p < 0.001), MCV (p < 0.001), MCH (p < 0.001) and Hb A 2 (p = 0.007). This study is one of the first dedicated to investigating α-thalassemia 3.7 kb deletion in the population of the State Rio Grande do Norte state. Results obtained demonstrate the importance of investigating this condition in order to elucidate the causes of microcytosis and hypochromia. © 2012, Sociedade Brasileira de Genética. Printed in Brazil.353594598Adorno, E.V., Couto, F.D., Moura Neto, J.P., Menezes, J.F., Rêgo, M., Reis, M.G., Gonçalves, M.S., Hemoglobinopathies in newborns from Salvador, Bahia, Northeast Brazil (2005) Cad Saúde Pública, 21, pp. 292-298Bezerra, C.M., Meissner, R.V., Diagnóstico molecular da talassemia alfa + (deleção-( 3.7) em indivíduos com microcitose e/ou hipocromia atendidos no Hemocentro Dalton Barbosa Cunha em Natal, Rio Grande do Norte (2010) Rev Bras Hematol Hemoter, 32, pp. 90-91. , (Abstract in English)Borg, J., Georgitsi, M., Aleporou-Marinou, V., Kollia, P., Patrinos, G.P., Genetic recombination as a major cause of mutagenesis in the human globin gene clusters (2009) Clin Biochem, 42, pp. 1839-1850Borges, E., Wenning, M.R.S.C., Kimura, E.M., Gervásio, S.A., Costa, F.F., Sonati, M.F., High prevalence of alpha-thalassemia among individuals with microcytosis and hypochromia without anemia (2001) Braz J Med Biol Res, 34, pp. 759-762Cascudo, L.C., (1984) História do Rio Grande do Norte, p. 524. , 2 edition. Fundação José Augusto, NatalCouto, F.D., Albuquerque, A.B.L., Adorno, E.V., Moura Neto, J.P., Freitas, A.L., Oliveira, J.L.B., Reis, M.G., Gonçalves, M.S., Alpha-thalassemia-2, 3.7 kb deletion and hemoglobin AC heterozygosity in pregnancy: A molecular and hematological analysis (2003) Clin Lab Haematol, 25, pp. 29-34Dacie, J.V., Lewis, S.M., (1995) Practical Haematology., p. 608. , Churchill Livingstone, EdinburghDodé, C., Krishnamoorthy, R., Lamb, J., Rochette, J., Rapid analysis of-α 3.7 thalassaemia and ttt anti3.7 triplication by enzymatic amplification analysis (1992) Br J Haematol, 83, pp. 105-111Harteveld, L.C., Higgs, D.R., H-thalassaemia (2010) Orphanet J Rare Dis, 5, pp. 1-21Higgs, D.R., H-Thalassaemia (1993) Baillière's Clin Haematol, 6, pp. 117-150Higgs, D.R., The pathopysiology and clinical features of H thalassemia (2009) Disorders of Hemoglobin, pp. 266-295. , In: Steinberg MH, Forget BG, Higgs DR and Weatherall DJ (eds) 2 nd edition. Cambridge University Press, New YorkHiggs, D.R., Weatherall, D.J., The alpha thalassaemias (2009) Cell Mol Life Sci, 66, pp. 1154-1162Mouélé, R., Pambou, O., Feingold, J., Galactéros, F., M-thalassemia in Bantu population from Congo-Brazzaville: Its interaction with sickle cell anemia (2000) Hum Hered, 50, pp. 118-125Peres, M.J., Romão, L., Carreiro, H., Picanço, I., Batalha, L., Magalhães, H.A., Martins, M.C., Lavinha, J., Molecular basis of H-thalassemia in Portugal (1995) Hemoglobin, 19, pp. 343-352Rahim, F., Microcytic hypochromic anemia patients with thalassemia: Genotyping approach (2009) J Med, 63, pp. 101-108Sankar, V.H., Arya, V., Tewari, D., Gupta, U.R., Pradhan, M., Genotyping of alpha-thalassemia in microcytic hypochromic anemia patients from North India (2006) Indian J Med Res, 47, pp. 391-395Sonati, M.F., Farah, S.B., Ramalho, A.S., Costa, F.F., High prevalence of alpha-thalassemia in a black population of Brazil (1991) Hemoglobin, 15, pp. 309-311Souza, A.E.S., Takanashi, S.Y.L., Cardoso, G., Guerreiro, J.F., S-thalassemia (3.7 kb deletion) in a population from the Brazilian Amazon region: Santarém, Pará State (2009) Genet Mol Res, 8, pp. 477-481Steinberg, M.H., Nagel, R.L., Hemoglobins of the embryo, fetus and adult (2009) Disorders of Hemoglobin, pp. 119-135. , In: Steinberg MH, Forget BG, Higgs DR and Weatherall DJ (eds) 2 nd edition. Cambridge University Press, New YorkWagner, S.C., Castro, S.M., Gonzalez, T.P., Santin, A.P., Filippon, L., Zaleski, C.F., Azevedo, L.A., Hutz, M., Prevalence of common c-thalassemia determinants in south Brazil: Importance for the diagnosis of microcytic anemia (2010) Genet Mol Biol, 33, pp. 641-645Weatherall, D.J., Clegg, J.B., Inherited haemoglobin disorders: An increasing global health problem (2001) Bull World Health Organ, 79, pp. 704-71