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Articles by M Teixeira
Total Records ( 3 ) for M Teixeira
  N Bettencourt , J Rocha , M Carvalho , D Leite , A. M Toschke , B Melica , L Santos , A Rodrigues , M Goncalves , P Braga , M Teixeira , L Simoes , S Rajagopalan and V. Gama

Background— Multislice computed tomography (MSCT) has shown high negative predictive value in ruling out obstructive coronary artery disease. Preliminary studies in patients with valvular heart disease (VHD) have demonstrated the potential of MSCT angiography (CTA) in such patients, precluding need for invasive angiography (XA). However, larger prospectively designed studies, including patients with atrial fibrillation and incorporating dose reduction algorithms, are needed.

Methods and Results— To evaluate the clinical utility of 64-slice CT in the preoperative assessment in patients with VHD, we prospectively studied 452 consecutive patients undergoing routine cardiac catheterization for eligibility. Two hundred thirty-seven patients underwent both MSCT and XA. Segment-based, vessel-based, and patient-based agreement between CTA and XA was estimated assuming that "nonevaluable" segments were positive for significant coronary stenosis. In a patient-based analysis, sensitivity, specificity, positive predictive value, and negative predictive values of CTA were 95%, 89%, 66%, and 99%, respectively; in vessel-based analysis, 90%, 92%, 48%, and 99%, respectively; and in segment-based analysis, 89%, 97%, 38%, and 100%, respectively. No significant differences were found between patients with or without atrial fibrillation. A CAC value of 390 was the best cutoff for the identification of patients with positive or inconclusive CTA (which would not be exempted from XA in the clinical setting).

Conclusions— In the preoperative assessment of patients with predominant VHD, the diagnostic accuracy of 64-slice CTA for ruling out the presence of significant coronary artery disease is very good even when including patients with irregular heart rhythm. Using this approach, CAC quantification before CTA can be successfully used to identify patients who should be referred directly to XA, sparing unnecessary exposure to radiation.

  S Viengchareun , P Kamenicky , M Teixeira , D Butlen , G Meduri , N Blanchard Gutton , C Kurschat , A Lanel , L Martinerie , S Sztal Mazer , M Blot Chabaud , E Ferrary , N Cherradi and M. Lombes

Aldosterone effects are mediated by the mineralocorticoid receptor (MR), a transcription factor highly expressed in the distal nephron. Given that MR expression level constitutes a key element controlling hormone responsiveness, there is much interest in elucidating the molecular mechanisms governing MR expression. To investigate whether hyper- or hypotonicity could affect MR abundance, we established by targeted oncogenesis a novel immortalized cortical collecting duct (CCD) cell line and examined the impact of osmotic stress on MR expression. KC3AC1 cells form domes, exhibit a high transepithelial resistance, express 11β-hydroxysteroid dehydrogenase 2 and functional endogenous MR, which mediates aldosterone-stimulated Na+ reabsorption through the epithelial sodium channel activation. MR expression is tightly regulated by osmotic stress. Hypertonic conditions induce expression of tonicity-responsive enhancer binding protein, an osmoregulatory transcription factor capable of binding tonicity-responsive enhancer response elements located in MR regulatory sequences. Surprisingly, hypertonicity leads to a severe reduction in MR transcript and protein levels. This is accompanied by a concomitant tonicity-induced expression of Tis11b, a mRNA-destabilizing protein that, by binding to the AU-rich sequences of the 3'-untranslated region of MR mRNA, may favor hypertonicity-dependent degradation of labile MR transcripts. In sharp contrast, hypotonicity causes a strong increase in MR transcript and protein levels. Collectively, we demonstrate for the first time that optimal adaptation of CCD cells to changes in extracellular fluid composition is accompanied by drastic modification in MR abundance via transcriptional and posttranscriptional mechanisms. Osmotic stress-regulated MR expression may represent an important molecular determinant for cell-specific MR action, most notably in renal failure, hypertension, or mineralocorticoid resistance.

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