Mild gestational hyperglycaemia as a risk factor for metabolic syndrome in pregnancy and adverse perinatal outcomes

Objective The aims of this study were to evaluate the prevalence of metabolic syndrome (MS) in a cohort of pregnant women with a wide range of glucose tolerance, pre-pregnancy risk factors for MS during pregnancy and the effects of MS in the occurrence of adverse perinatal outcomes.Research Design and Methods One hundred and thirty six women with positive screening for gestational diabetes (GDM) were classified by two diagnostic methods: glycaemic profile and 100 g oral glucose tolerance test (OGTT) as normoglycaemic, mild gestational hyperglycaemic, GDM, and overt GDM. Markers of insulin resistance were measured between 24-28 and 36th week of gestation, and 6 weeks after delivery.Results The prevalence of MS was 0; 20.0; 23.5 and 36.4% in normoglycaemic, mild hyperglycaemic, GDM and overt GDM groups, respectively. Previous history of GDM with or without insulin use, body mass index (BMI) >= 25, hypertension, family history of diabetes in first-degree relatives, non-Caucasian ethnicity, history of prematurity and polyhydramnios were statistically significant pre-pregnancy predictors for MS in the index pregnancy, that by its turn increased the occurrence of adverse perinatal outcomes (p = 0.01).Conclusions The prevalence of MS increases with the worsening of glucose tolerance and is an independent predictor of adverse perinatal outcomes; impaired glycaemic profile identifies pregnancies with important metabolic abnormalities that are linked to the occurrence of adverse perinatal outcomes even in the presence of a normal OGTT, in patients that are not currently classified as having GDM. Copyright (C) 2008 John Wiley & Sons, Ltd.

Studies on the Expression of Fibroblast Growth Factor-2 from Odontoblast-like Cells

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Cyclosporin but not tacrolimus significantly increases salivary cytokine contents in rats

Background: Cyclosporin (CsA) and tacrolimus (FK-506) are immunosuppressive drugs that specifically inhibit T-cell activation via calcineurin inhibition. Gingival overgrowth is a common side effect following the administration of CsA. The severity of gingival overgrowth seen in patients taking FK-506 is less than that observed with CsA. Little is known about the involvement of saliva in drug-induced gingival overgrowth. The purpose of this study was to investigate the salivary contents of tumor growth factor β1 (TGF-β1), epidermal growth factor (EGF), and interleukin-6 (IL-6) as well as the hystometry of gingival tissue obtained from rats treated with either FK-506 or CsA. Methods: For 30 or 60 days rats received daily subcutaneous injection doses of either CsA or FK-506 (10 mg/kg). The concentrations of TGF-β1, EGF, and IL-6 in saliva were determined by enzyme-linked immunosorbent assay, and after histological processing, the oral epithelium and connective tissue were assessed at the region of the lower first molars. Results: The levels of TGF-β1, EGF, and IL-6 in saliva were not significantly altered by any of the treatments after 30 days. After 60 days of treatment with CsA, gingival overgrowth and significant increase in salivary TGF-β1, EGF, and IL-6 concentrations were observed; no statistically significant changes were induced by FK-506. Conclusion: Within the limits of this experimental study, it can be concluded that CsA, but not FK-506, induced gingival overgrowth associated with an increase of the salivary levels of the cytokines TGF-β1, EGF, and IL-6.

Le(a-b-) phenotype: potential risk factor for infection by the RH strain of Toxoplasma gondii in pregnancy

The Lewis histo-blood group system is characterized by the expression of the Lea and Le(b) antigens in the gastrointestinal tract, whose synthesis results in interactions between alpha 2-L-fucosyltransferase (FUTII) and alpha 3/4-L-fucosyltransferase (FUTIII) enzymes coded by the FUT2 (19q. 13.3) and FUT3 (19p13.3) genes. FUTII and FUTIII fucosylate the type 1 oligosaccharide precursor (Gal beta 1 -> 3NAcGlc beta 1 -> 3-R) at distinct positions to form H type 1 (Fuc alpha 1. 2Gal beta 1. 3NAcGlc beta 1 -> 3-R) and Le(a) (Gal beta 1 -> 3[Fuc alpha 1 -> 4] NAcGlc beta 1 -> 3-R) antigens, respectively. The fucosylation of H type 1 antigens by FUTIII results in the Leb antigen (Fuc alpha 1. 2Gal beta 1. 3[Fuca1. 4] NAcGlc beta 1. 3-R). Thus, the presence of the FUTII and FUTIII enzymes leads to the expression of the Le(a+b+) phenotype, while the presence of only FUTIII allows the expression of the Le(a+b-) phenotype. The absence of the FUTIII enzyme leads to the expression of the Le(a-b-) phenotype, independent of the presence or absence of FUTII. Point mutations in FUT2 and FUT3 genes change the activity of these enzymes, impair the synthesis of Le(a) and Le(b) antigens, and contribute to the variability of Lewis phenotypes in the gastrointestinal tract. Toxoplasma gondii, an apicomplexan parasite that infects a large proportion of the world's population, utilizes the gastrointestinal tract as an infection route and seems to adhere to glycosylated molecules to invade human cells. These apparently independent events may be related. The aim of this study was to test the hypothesis that there is an association between the Lewis histo-blood group system and infection by T. gondii. Two hundred and nine serum samples collected from pregnant women were submitted to screening tests to detect anti-T. gondii antibodies, employing the indirect hemagglutination method. ELISA was utilized to identify IgG class anti-T. gondii antibodies specific for the RH strain. A hundred and ninety-five samples with concordant results for both methods were selected to form two groups: seropositive (G1) and seronegative (G2). The G428A mutation of the FUT2 gene, and T202C and C314T of the FUT3 gene, which allow inference of the gastrointestinal tract Lewis phenotypes, were identified using PCR-RFLP and PCR-SSP methods, respectively. Among the 195 samples selected, 116 (59.5%) were seropositive and 79 (40.5%) were seronegative. In G1, 68 (58.6%) were classified as Le(a+b+), 30 (25.9%) as Le(a+b-), and 18 (15.5%) as Le(a-b-), and in G2, 67 (84.8%) were classified as Le(a+b+), 12 (15.2%) as Le(a+b-), and 0 (0%) as Le(a-b-) (P < 0.0001). The Le(a-b-) phenotype is associated with a high risk of RH strain T. gondii infection when compared with the Le(a+b+) [P = 0.0001; OR = 36,460; 95%CI = 2.152-617,680] and Le(a+b-) phenotypes [P = 0.0118; OR = 15,165; 95%CI = 0.8463-271,710]. The Le(a+b-) phenotype showed a higher risk compared to the Le(a+b+) phenotype [P = 0.0206; OR = 2463; 95%CI = 2463-5214]. The results suggest that the Le(a-b-) phenotype is strongly associated with a greater risk of infection by the RH strain of T. gondii compared to the other phenotypes. It is possible that the absence of fucosylation of the type 1 oligosaccharide precursor as well as the variations in the structures of the Le(a) and Le(b) antigens influence susceptibility to infection by this parasite.

Purificação, imobilização e caracterização bioquímica de lipase produzida por Penicillium sect. Gracilenta CBMAI 1583 em cultivo submerso

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)