Neuroesquistossomose mansônica: aspectos clínicos, laboratoriais e terapêuticos

Submitted by Ana Maria Fiscina Sampaio ([email protected]) on 2014-05-05T18:28:22Z No. of bitstreams: 1 Andrade Filho AS Neuroesquistossomose Mansonica....pdf: 730449 bytes, checksum: 7a8a49d368d9c1e69c3e7aa5428793a9 (MD5)Made available in DSpace on 2014-05-05T18:28:22Z (GMT). No. of bitstreams: 1 Andrade Filho AS Neuroesquistossomose Mansonica....pdf: 730449 bytes, checksum: 7a8a49d368d9c1e69c3e7aa5428793a9 (MD5) Previous issue date: 1996Hospital Universitário Professor Edgard Santos. Universidade Federal da Bahia. Salvador, BA, BrasilFundação Oswaldo Cruz. Centro de Pesquisa Gonçalo Moniz. Salvador, BA, BrasilHospital Universitário Professor Edgard Santos. Universidade Federal da Bahia. Salvador, BA, BrasilHospital Universitário Professor Edgard Santos. Universidade Federal da Bahia. Salvador, BA, BrasilHospital Universitário Professor Edgard Santos. Universidade Federal da Bahia. Salvador, BA, BrasilHospital Universitário Professor Edgard Santos. Universidade Federal da Bahia. Salvador, BA, BrasilHospital Universitário Professor Edgard Santos. Universidade Federal da Bahia. Salvador, BA, BrasilHospital Universitário Professor Edgard Santos. Universidade Federal da Bahia. Salvador, BA, BrasilHospital Universitário Professor Edgard Santos. Universidade Federal da Bahia. Salvador, BA, BrasilHospital Universitário Professor Edgard Santos. Universidade Federal da Bahia. Salvador, BA, BrasilHospital Universitário Professor Edgard Santos. Universidade Federal da Bahia. Salvador, BA, BrasilOs autores relatam 16 casos de pacientes com forma meningomielorradicular da neuroesquistossomose mansônica, diagnosticados segundo critérios clínicos, laboratoriais e de imagem, acompanhados no Ambulatório de Neurologia-HUPES-UFBA no período de abril/91 a dezembro/93. Eles foram tratados com praziquantel associado a corticoterapia. O objetivo foi avaliar o grau de eficácia e de segurança da droga na regressão dos sinais e sintomas neurológicos.The authors report 16 patients bearing the meningomyeloradicular form of Mansonic neuroschistosomiasis diagnosed according to clinical, laboratorial and image criteria. Patients have been observed at the Neurology Ambulatory of the Federal University of Bahia, within the period of April/91 to December/93. They have been treated with praziquantel, associated to corticosteroids. The aim has been to evaluate the drug's efficiency and safety in decreasing the neurological signs and symptoms

Polimorfismos do gene IRF6 em pacientes brasileiros com fenda labial não sindrômica com ou sem fenda palatina

Non-syndromic orofacial clefts have a complex etiology due to the contribution from both genetic and environmental risk factors, as well as the interaction between them. Among the more than 15 susceptibility loci for non-syndromic orofacial clefts with considerable statistical and biological support, the IRF6 is the most validated gene by the majority of studies. Nonetheless, in genetically heterogeneous populations such as Brazilian, the confirmation of association between non-syndromic orofacial clefts and IRF6 common variants is not a consolidated fact and unrecognized IRF6 variants are poorly investigated. Objective: The aim of this study was to investigate the association of IRF6 polymorphisms with non-syndromic orofacial clefts development in a population from northeast Brazil. Methods: Blood samples of 186 non-syndromic orofacial clefts patients and 182 controls from Rio Grande do Norte, Brazil, were obtained to analyze IRF6 polymorphisms (rs2235371, rs642961, rs2236907, rs861019, and rs1044516) by real-time polymerase chain reaction. Non-syndromic orofacial clefts patients were classified in cleft lip and palate, cleft palate only and cleft lip only groups. Results: The genotype and allele frequencies of single nucleotide polymorphism rs2235371 in IRF6 showed significant differences in patients with cleft palate when compared to the controls, whereas no association was shown between rs642961, rs2236907, rs861019, and rs1044516 and non-syndromic orofacial clefts. Conclusion: The association found between rs2235371 and isolated cleft palate should be interpreted with caution due to the low number of individuals investigated, and more studies with larger sample size are needed to confirm these association. In addition, there is a lack of association of the rs642961, rs2236907 and rs861019 polymorphisms with non-syndromic orofacial clefts susceptibilityCONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO - CNPQ477608/2011-6As fendas orofaciais não sindrômicas possuem uma etiologia complexa devido à contribuição de fatores de risco genéticos e ambientais, assim como a interação entre eles. Dentre os mais de 15 loci de susceptibilidade para as fendas orofaciais não sindrômicas com considerável suporte estatístico e biológico, o IRF6 é o gene mais validado pela maioria dos estudos. Apesar disso, em populações geneticamente heterogêneas como a brasileira, a confirmação da associação entre as fendas orofaciais não sindrômicas e as variantes mais comuns do IRF6 ainda não é um fato consolidado e outras variantes não tão conhecidas IRF6 são pouco investigadas. Objetivo O objetivo deste estudo foi investigar a associação de variados polimorfismos do IRF6 com o desenvolvimento das fendas orofaciais não sindrômicas em uma população do nordeste do Brasil. Método Amostras de sangue de 186 pacientes com fendas orofaciais não sindrômicas e 182 controles do estado do Rio Grande do Norte, Brasil, foram obtidas para analisar os polimorfismos do IRF6 (rs2235371, rs642961, rs2236907, rs861019 e rs1044516) por reação em cadeia da polimerase em tempo real. Os pacientes com fendas orofaciais não sindrômicas foram classificados em fenda labiopalatina, fenda palatina isolada e fenda labial isolada. Resultados As frequências genotípica e alélica do polimorfismo de único nucleotídeo rs2235371 no IRF6 mostraram-se significativamente diferentes em pacientes com fenda palatina isolada quando comparadas as dos controles, enquanto que nenhuma associação foi encontrada entre rs642961, rs2236907, rs861019 e rs1044516 e risco para o desenvolvimento das fendas orofaciais não sindrômicas. Conclusão A associação encontrada entre rs2235371 e fenda palatina isolada deve ser interpretada com cautela devido ao baixo número de indivíduos investigados, sendo necessários mais estudos com um tamanho amostral maior para confirmar essa associação. Além disso, não foram encontradas associações significativas entre os demais polimorfismos do IRF6 rs642961, rs2236907, rs861019 e rs1044516 e a susceptibilidade às fendas orofaciais não sindrômica

The low-density lipoprotein receptor-related protein 5 (LRP5) 4037C>T polymorphism: candidate for susceptibility to type 1 diabetes mellitus

ABSTRACT Objective: The present study has investigated the association between low-density lipoprotein receptor-related protein 5 (LRP5) 4037C>T polymorphism and type 1 diabetes mellitus (T1DM) susceptibility in a Brazilian population. Subjects and methods: A total number of 134 T1DM patients and 180 normoglycemic individuals (NG) aged 6-20 years were studied. Glycated hemoglobin and glucose levels were determined. Genotyping of LRP5 4037C>T (rs3736228) was performed. Results: T1DM patients showed poor glycemic control. Genotypes in the codominant (CT: OR = 2.99 [CI 95%: 1.71-5.24], p T may represent a candidate for T1DM susceptibility, as well as poor glycemic control

Relationship between glycemic control and OPG gene polymorphisms with lower bone mineral density in patients with type 1 Diabetes mellitus

<div><p>ABSTRACT The aim of the present study was to investigate the bone mineral density (BMD) of patients with type 1 Diabetes mellitus (T1DM). We also assessed the association between osteoprotegerin (OPG) genetic polymorphisms and BMD. Genotyping was performed for 1181G>C and 163A>G OPG polymorphisms by allelic discrimination in 119 patients with T1DM and 161 normoglycemic (NG) individuals, aged 6 to 20 years old. Glycemic control, serum parameters of bone metabolism and BMD were evaluated. T1DM patients showed low BMD, poor glycemic control and decreased total calcium values when compared to controls (p < 0.05). For all the polymorphisms studied, the genotype and allele frequencies in patients with T1DM were not significantly different from the controls. In patients with T1DM, carriers of OPG 1181CC showed higher concentrations of ionized calcium compared to patients with GG+GC genotypes. These results suggest that low BMD is associated with poor glycemic control in T1DM. Despite the lack of a detected association between OPG polymorphisms and BMD in these patients, the increased ionized calcium in those carrying OPG 1181CC suggests a possible increase in osteoclastogenesis, a conclusion that may be supported by the lower BMD observed in these subjects.</p></div

Histomorphometric analyses of structural bone architecture.

<p>Trabecular separation (TbSP, μm) (A), trabecular width (TbWi, μm) (B), and trabecular bone area (BAr, %) (C) of control, type 1 diabetes mellitus (T1DM), and T1DM plus zinc supplementation (T1DMS) rats. All data are shown as means ± SEM. Comparisons between groups were analyzed with Kruskal-Wallis ANOVA on Ranks and Dunn’s post-hoc. <i>p</i> < 0.01*^/## vs. control group; <i>p</i> < 0.001*^/### vs. control group; <i>p</i> < 0.05 **^/# vs. T1DM group; <i>p</i> < 0.001**^/### vs. T1DM group.</p

Relative mRNA expression quantification.

<p><i>RANKL</i> (A), <i>OPG</i> (B), <i>OC</i> (C), <i>COL1A</i> (D), <i>MMP-2</i> (E), and <i>MMP-9</i> (F) mRNA expression in bone tissue of control, type 1 diabetes mellitus (T1DM), and T1DM plus zinc supplementation (T1DMS) rats. All data are expressed as fold-change vs. control group values, normalized to <i>GAPDH</i>. Comparisons between groups were analyzed with Kruskal-Wallis ANOVA on Ranks and Dunn’s post-hoc. <i>p</i> < 0.05*^/# vs. control group; <i>p</i> < 0.01*^/## vs. control group.</p

Assessment of collagen deposition by picrosirius red staining.

<p>Tibia staining for collagen content (picrosirius red). Total collagen (A), collagen type I (B), and collagen type III (C) contents of the control, type 1 diabetes mellitus (T1DM), and T1DM plus zinc supplementation (T1DMS) groups. All data are shown as means ± SEM. Comparisons between groups were analyzed with Kruskal-Wallis ANOVA on Ranks and Dunn’s post-hoc. <i>p</i> < 0.05 *^/# vs. control group.</p

Tibia biomechanical parameters of control, diabetic, and diabetic plus zinc supplementation groups.

<p>T1DM, type 1 diabetes mellitus; T1DMS, T1DM plus zinc supplementation. All data are shown as means ± SEM. Comparisons between groups were analyzed with Kruskal-Wallis ANOVA on Ranks and Dunn’s post-hoc.</p><p>*^/#<i>p</i> < 0.05 vs. control group;</p><p>*^/##<i>p</i> < 0.01 vs. control group.</p><p>Tibia biomechanical parameters of control, diabetic, and diabetic plus zinc supplementation groups.</p