Navegando por Palavras-chave "PPT"

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    Assessment of free fetal DNA concentration in maternal plasma during the first trimester of pregnancy: comparative study between EDTA and PPT tubes - pilot study
    (Informa Healthcare, 2015-01-01) Chadud, Carolina Schneider; Araujo Junior, Edward [UNIFESP]; Martinhago, Ciro Dresh; Mello Andari, Viviane Cristina; Tedesco, Giselle Darahem; Silva Bussamra, Luiz Claudio [UNIFESP]; Aoki, Tsutomu; Med Coll Sci Santa Casa São Paulo FCMSCSP; Universidade Federal de São Paulo (UNIFESP); RDO Med Diagnost
    Objective: To compare ethylenediamine tetraacetic acid (EDTA) tubes and plasma preparation tubes (PPT) for evaluating maternal plasma during the first trimester of pregnancy.Methods: A cross-sectional study was conducted on 24 male fetuses in women between 6 and 14 weeks of pregnancy. Blood samples (10 mL) were collected and stored in EDTA and PPT tubes. Subsequently, the samples were centrifuged and sent for free fetal DNA extraction by means of the polymerase chain reaction (PCR) technique. the reactions were performed in a real time PCR machine for detecting the amplification products. the genome region chosen for performing the PCR reactions was a target specific for the Y chromosome, in which the DYS-14 marker was amplified only when the DNA was of male sex. the free fetal DNA concentration was given by the threshold cycle (TC). To compare the tubes, the paired Student t-test was used.Results: the mean gestational age was 11.08 +/- 2.30 weeks (range: 6-14). the mean TC for PPT was 30.08 +/- 1.05 (range: 27.08-32.61) and for EDTA, 30.23 +/- 0.96 (range: 28.01-32.09), but without statistical significance (p = 0.357).Conclusion: We did not observe any statistically significant difference in free fetal DNA concentration between the EDTA and PPT tubes.
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    Estradiol-induced regulation of GLUT4 in 3T3-L1 cells: involvement of ESR1 and AKT activation
    (Bioscientifica Ltd, 2017) Campello, Raquel S.; Fatima, Luciana A.; Barreto-Andrade, Joao Nilton; Lucas, Thais F. [UNIFESP]; Mori, Rosana C.; Porto, Catarina S. [UNIFESP]; Machado, Ubiratan F.
    Impaired insulin-stimulated glucose uptake involves reduced expression of the GLUT4 (solute carrier family 2 facilitated glucose transporter member 4, SLC2A4 gene). 17 beta-estradiol (E-2) modulates SLC2A4/GLUT4 expression, but the involved mechanisms are unclear. Although E-2 exerts biological effects by binding to estrogen receptors 1/2 (ESR1/2), which are nuclear transcriptional factors
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    Estrogen Receptor 1 Agonist PPT Stimulates Slc2a4 Gene Expression and Improves Insulin-Induced Glucose Uptake in Adipocytes
    (Bentham Science Publ Ltd, 2012-10-01) Campello, R. S.; Alves-Wagner, A. B.; Lucas, T. F. [UNIFESP]; Mori, R. C.; Furuya, D. T.; Porto, Catarina Segreti [UNIFESP]; Machado, U. F.; Universidade de São Paulo (USP); Universidade Federal de São Paulo (UNIFESP)
    Type 2 diabetes mellitus is characterized by disruption in glycemic homeostasis, involving impaired insulin-induced glucose disposal. For that, reduced glucose transporter GLUT4, encoded by Slc2a4 gene, plays a fundamental role. Conversely, increase in Slc2a4/GLUT4 expression improves glycemic homeostasis. Recent studies have proposed that estradiol is able to modulate Slc2a4 expression, according to distinct effects upon estrogen receptors ESR1/ESR2. We hypothesize that ESR1-agonist effect could stimulate Slc2a4 expression; thus, increasing cellular glucose disposal, which could be beneficial to glycemic control. Differentiated 3T3-L1 adipocytes were treated (24 hours) with selective ESR1-agonist PPT 1,3,5-tris(4-hydroxyphenyl)-4- propyl-1H-pyrazole, selective ESR1-antagonist MPP 1,3-Bis(4-hydroxyphenyl)-4- methyl-5-[4-(2-piperidinylethoxy)phenol]-1H-pyrazole dihydrochloride, and selective ESR2 agonist DPN 2,3-bis(4-Hydroxyphenyl)-propionitrile, with/without 17 beta-estradiol (E2). We analyzed Slc2a4 mRNA (real time PCR) and GLUT4 protein (Western blotting) expression, transcriptional activity of the Slc2a4 repressor Nuclear Factor-kappa B (NF-kappa B) (electrophoretic mobility shift assay), and cellular glucose disposal (2-deoxi-D-[H-3]glucose uptake, 2-DG). ESR1-agonist PPT enhanced Slc2a4/GLUT4 expression (similar to 30%) in the absence or presence of 0.1 and 10 nmol/L E2, and decreased the NF-kappa B binding activity (similar to 50%). Conversely, ESR1-antagonist MPP, together with E2, decreased Slc2a4/GLUT4 expression (20-40%) and increased NF-kappa B binding activity (similar to 30%). Furthermore, treatment with ESR2-agonist DPN decreased Slc2a4/GLUT4 expression (20-50%). 2-DG uptake was modulated in parallel to that observed in GLUT4 protein. The present results reveal that ESR1 activity enhances, whereas ESR2 activity represses, Slc2a4/GLUT4 expression. These effects are partially mediated by NF-kappa B, and allow parallel changes in adipocyte glucose disposal. Furthermore, the data provide evidences that ESR1-agonist PPT, as a Slc2a4/GLUT4 enhancer, can be a promising coadjuvant d(r)ug for diabetes mellitus therapy.
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    Estrogen receptor ESR1 regulates the phospholipase C-inositol phosphate signaling in the hippocampus from rats in proestrous and estrous phases
    (Elsevier B.V., 2013-01-01) Maruyama, Nadia O.; Lucas, Thais F. G. [UNIFESP]; Porto, Catarina S. [UNIFESP]; Abdalla, Fernando M. F.; Inst Butantan; Universidade Federal de São Paulo (UNIFESP)
    The aim of the present study was to investigate the involvement of estrogen receptors in the activation of phospholipase C (PLC)-phosphoinositide hydrolysis in the hippocampus from rats in estrous and proestrous phases. 17 beta-Estradiol (E2) and ESR1 -selective agonist PPT, but not ESR2-selective agonist DPN, induced a rapid increase on total [H-3]-inositol phosphate accumulation in the hippocampus from both rats. These effects are mediated by PLC activation, since the inhibition of this protein decreased the total [H-3]-inositol phosphate accumulation. the pretreatment with ESR1 and ESR2 antagonist ICI 182,780, but not with GPER antagonist G-15, blocked the total [H-3]-inositol phosphate accumulation induced by E2 and PPT, confirming that ESR1 is upstream component regulating this rapid effect. SRC family of protein tyrosine kinases inhibitor PP2 blocked the total [H-3]-inositol phosphate accumulation induced by E2 and PPT in hippocampus, suggesting that ESR1 undergoes translocation from the nuclei to the plasma membrane region via SRC to activate rapid signaling pathways. Furthermore, the magnitude of the response to E2 and PPT was higher in hippocampus from rats in proestrous than in estrous. On the other hand, the expression of the ESR1 is higher in hippocampus from rats in estrous than in proestrous, indicating that the regulation of this receptor by estrous cycle does not play a role in the magnitude of the response to E2 and PPT in hippocampus. in conclusion, our results indicate that E2 activates SRC-mediated translocation of ESR1 to the plasma membrane, which results in the activation of PLC-inositol phosphate signaling pathway in rat hippocampus. Thus, these rapid estrogen actions in hippocampus might be a key step mediating cellular events important for learning and memory. (C) 2012 Elsevier Inc. All rights reserved.