Alimentary consumption of women active and physically inactive in postmenopausal period

El objetivo del presente estudio fue observar el consumo alimenticio y la prevalencia del síndrome metabólico en mujeres activas e inactivas físicamente en la post-menopausia. La muestra fue compuesta de 83 mujeres, pertenecientes al municipio de Natal (Río Grande do Norte) de Brasil; pertenecientes al programa “Natal Activa”, con edad media de 59,7 ± 8,08 años. Se aplicó un cuestionario para analizar la frecuencia del consumo alimenticio, un cuestionario de actividad física, una anamnesis clínica, una evaluación antropométrica, exámenes bioquímicos y un diagnóstico del Síndrome Metabólico. Los resultados mostraron que las mujeres activas consumen más alimentos protectores que las mujeres inactivas. La prevalencia del síndrome metabólico en las mujeres inactivas fue mayor que en las mujeres activas, además, existe la necesidad de cambiar dichos hábitos en esta población, pudiéndose alcanzar así mayores cambios corporales y metabólicos, minimizando la incidencia del síndrome metabólico en los dos gruposThe aim of this study was to observe the dietary intake and the prevalence of metabolic syndrome in physically active and inactive women in the postmenopause. The sample was composed of 83 women, from the municipality of Natal (Rio Grande do Norte) in Brazil; from the "Natal Active" program, with an average age of 59.7 ± 8.08 years old. A questionnaire to analyze the frequency of food consumption, physical activity questionnaire, a clinical anamnesis, anthropometric evaluation, biochemical tests and a diagnosis of metabolic syndrome was applied. The results showed that active women consume more protective foods than inactive women. The prevalence of metabolic syndrome in inactive women was higher than in active women, in addition, there is a need to change those habits in this population, being able thus to achieve greater physical and metabolic changes, minimizing the incidence of metabolic syndrome in both group

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

Cytotoxicity Of Dehydrocrotonin (a Nor-clerodane From Croton Cajucara) On Human Lymphocytes

Trans-Dehydrocrotonin, a 19-nor-clerodane, is the major norditerpene obtained from Croton cajucara, a Brazilian medicinal plant which presents important biological effects, such as antineoplastic and antiulcerogenic activities. In this work, we analyzed the effect of this sesquiterpene lactone on normal human lymphocytes. The cell viability was verified after treatment for 24 and 72 h with trans-dehydrocrotonin, in the presence and absence of phytohemagglutin (specific mitogen for this cell), through three end-points to assess cytotoxicity in vitro: MTT reduction (mitochondrial function), protein quantification (cell number) and phosphatase activity (cell metabolism). When the cells were treated with dehydrocrotonin in the presence of mitogen, no toxic effect was observed. Nevertheless, in the absence of mitogen, the IC50 was 450 μM for MTT reduction and phosphatase activity. Moreover, in this condition, trans-dehydrocrotonin caused stimulation of protein content from 100 μM. Our results suggest that phytohemagglutin protects human lymphocytes against the trans-dehydrocrotonin toxic effect.276914917Cho, J.Y., Baik, K.U., Jung, J.H., Park, M.H., (2000) Eur. J. Pharmacol, 398, pp. 399-407Hiruma-Lima, C.A., Gracioso, J.S., Rodriguez, J.A., Haun, M., Nunes, D.S., Brito, A.R.M.S., (2000) J. Ethnopharmacol, 69, pp. 229-234Costa, A.M.L., Silva, J.C.R., Rao, V.S.N., Maciel, M.A.M., Pinto, A.C., (1990) Phytother. Res, 13, pp. 689-691Grynberg, N.F., Echevarria, A., Lima, J.E., Pamplona, S.S.R., Pinto, A.C., Maciel, M.A.M., (1999) Planta Med, 65, pp. 687-689Costa, M.P., Magalhaes, N.S.S., Gomes, F.E.S., (2007) Braz. J. Pharm, 17, pp. 275-286Maciel, M.A.M., Aoyama, H., Melo, P.S., Granjeiro, P.A., Haun, M., Ferreira, C.V., (2000) Pharm. Pharmacol. Comm, 6, pp. 331-334Lemos, T.M.A., Miranda, M.A., Cavagis, A.D.M., Aoyama, H., Ferreira, C.V., (2008) Lat. Am. J. Pharm, 27, pp. 436-439Ferreira, C.V., Justo, G.Z., Souza, A.C.S., Queiroz, K.C.S., Zambuzzi, W.F., Aoyama, H., Peppelenbosch, M.P., (2006) Biochem, 8, pp. 1859-1873Harrison, S., Page, C.P., Spina, D., (1999) Gen. Pharmacol, 32, pp. 287-298Zhang, Z.-Y., (2001) Curr. Oppin. Chem. Biol, 5, pp. 416-423Szamel, M., Ebel, U., Uciechowski, P., Kaever, V., Resch, K., (1997) Biochim. Biophys. Acta, 1356, pp. 217-248Queiroz, K.C.S., Zambuzzi, W.F., Souza, A.C.S., Silva, R.A., Machado, D., Justo, Z., Carvalho, H.F., Ferreira, C.V., (2007) Cancer Lett, 258, pp. 126-134Souza-Brito, A.R.M., Rodriguez, J.A., Hiruma-Lima, C.A., Haun, M., Nunes, D.S., (1998) Planta Med, 64, pp. 126-129Maciel, M.A.M., Pinto, A.C., Brabo, S.N., Silva, M.N., (1998) Phytochemistry, 49, pp. 823-828Denizot, F., Lang, R., (1986) J. Immunol. Meth, 89, pp. 271-277Hartree, E.F., (1972) Anal. Biochem, 48, pp. 422-427Loveland, B.E., Johns, T.G., Mackay, I.R., Vaillant, F., Wang, Z.X., Hertzog, P., (1992) Assays Biochem. Internat, 27, pp. 501-510Nieper, H., Müller, H., (1998) Virol. Meth, 72, pp. 153-162Narasimhan, T.R., Harindranath, N., Premlata, S., Kesava Murthy, B.S., Subba Rao, P.V., (1985) Planta Med, 14, pp. 194-197Jodynis-Liebert, J., Murias, M., Bloszyk, E., (2000) Planta Med, 66, pp. 199-20

Kinectic Characterization And Flavonoid Effect On Human Lymphocyte Protein Tyrosyne Phosphatase

The aim of this work was to determine the kinetic properties and evaluate the effect of some flavonoids oh human lymphocyte protein tyrosine phosphatase. Tyrosine-, serine- and threonine-phosphate were hydrolyzed by this phosphatase 60%, 20% and 10%, respectively. In the kinetic studies the enzymatic activity was determined by using p-nitrophenylphosphate (pNPP) as substrate. The enzyme presented optimum pH around 5.0 and was inhibited by 100 μM p-chloromercuribenzoate (pCMB) (80%), 10 mM fluoride (35%), 10 mM vanadate (100%), and 5mM Cu +2 (85%). The enzyme was also strongly inhibited by a tyrosine phosphatase inhibitor cocktail, but was unaffected by okadaic acid. These results confirm that the major phosphatase activity in human lymphocytes is a protein tyrosine phosphatase. Among the bioflavonoids tested only fisetin showed an inhibitory effect in order of 80% on the enzymatic activity.273436439Ferreira, C.V., Justu, G.Z., Souza, A.C.S., Queiroz, K.C.S., Zambuzzi, W.F., Aoyama, H., Peppelenbosch, M.P., (2006) Biochem, 88, pp. 1859-1873Jia, Z., (1997) Biochem. Cell Biol, 75, pp. 17-26Cantley, L.C., Auger, K.R., Carpenter, C., Duckworth, B., Graziani, A., Kapeller, R., Soltoff, S., (1991) Cell, 64, pp. 281-302Taylor, S.I., Cama, A., Accili, D., Barbetti, R., Quon, M.J., Sierra, M., Suzuli, Y., Wertheimer, E., (1992) Endocrinol. Review, 13, pp. 566-595Parnetti, L., Senin, U., Meccoci, P., (1997) Drugs, 53, pp. 752-768Zhang, Z.-Y., (2001) Curr. Opin. Chem. Biol, 5, pp. 416-423Casagrande, F., Darbon, J.M., (2001) Biochem. Pharmacol, 61, pp. 1205-1215Aoyama, H., Melo, P.S., Granjeiro, P.A., Haun, M., Ferreira, C.V., (2000) Pharm. Pharmacol. Comm, 6, pp. 331-334Ben-Arie, A., Hagay, Z., Bem-Hurt, H., Open, M., Dgani, R., (1999) Eur. J. Obs. Gyn. Rep. Biol, 86, pp. 69-7