EDWIN ROGER PARRA CUENTAS
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conferenceObject Combining Inhibitor of DNA - Binding Proteins and Angigenic Markers Expression Predict Long Term Survival of Patients with Non-Small Cell Lung Cancer(2013) ANTONANGELO, L.; TUMA, T. S.; VARGAS, F. S.; PARRA, E. R.; TERRA, R. M.; ACENCIO, M.; CAPELOZZI, V. L.Background: Inhibitor of DNA binding (Id) proteins is an emerging promise as biologic marker on oncogenic transformation, cancer progression and tumor angiogenesis, the last, by the regulation of vascular endothelial growth factor (VEGF) expression. Design: We evaluated Ids (1, 2 and 3), VEGF expression and microvessel density (CD34+) in tumor and stromal cells and their impact on survival of 85 patients with surgically excised lung squamous cell carcinoma and adenocarcinoma. Immunohistochemistry and morphometry were used for the quantitation and Kaplan-Meyer survival curves and Cox regression for the statistical analyses. Results: It was found that high Id-1 and VEGF expression and high microvessel density were associated with worse prognosis (Log Rank Test, p<0.001). The Cox model controlled for histological type, age, lymph node stage, Ids, VEGF and microvessel density demonstrated that age, lymph node stage, Id1 and Id3 expression and vascular density were significantly associated with overall survival. A point at the median for Id1, Id3 and vascular density divided patients into 2 groups of different prognosis. Those with higher expression of Id1, Id3 and vascular density had a higher risk of death than those with lower Id-1, Id-3 and microvessel density. Conclusions: Inhibitor of DNA binding (Id) proteins and vascular density are strongly related to prognosis, suggesting that treatment strategies aimed for preventing high Ids synthesis, or local responses to angiogenesis may have impact on NSLC survival.conferenceObject Elastic-Collagen Profile in Emphysematous Airspaces from Different Chronic Fibrosing Lung Disorders(2013) MARCAL, L. J.; ANTONANGELO, L.; PARRA, E. R.; VARGAS, F. S.; TEODORO, W. R.; NASCIMENTO, E. C. T.; CAPELOZZI, V. L.Background: Parenchyma elastic and collagen components of chronic fibrosing lung disorders has been exhaustively investigated, but little attention has been aimed at the emphysematous airspaces present in bullous disease, smoking-related interstitial disease and usual interstitial pneumonia. The aim of this study was to evaluate whether elastic deposition accompanies collagen deposition in the repairing process of emphysematous airspaces in chronic fibrosing lung injuries. Design: The elastic and collagen fibers distribution were evaluated in emphysematous airspaces of bullous type I and II disease, smoking-related interstitial fibrosis and of usual interstitial pneumonia (UIP). Lung specimens obtained by surgical lung biopsy or by bullectomy divided the patients into four groups: 1) type I bullous disease (SPT-I; n=7); 2) type II bullous disease (SPT-II; n=12); 3) smoking-related interstitial pneumonia (SRIP; n=5) and 4) usual interstitial pneumonia/idiopathic pulmonary fibrosis (UIP/IPF; n=5). Collagen and elastic fibers were identified respectively by Picrosirius-polarization and Weigert's resorcin-fucsin staining and quantified by image analysis.The results were expressed in percentual area. Descriptive ResultsStaining Disease Mean Std. Deviation Std. Error Minimum Maximum Picro-sirius STP-I 40.71 15.87 6.00 18.56 61.67 Picro-sirius STP-II 40.58 15.95 4.60 15.67 63.35 Picro-sirius SRIP 30.18 9.23 4.13 25.31 46.64 Picro-sirius UIP/IPF 40.99 13.99 6.26 24.76 60.07 Resorcina STP-I 19.97 10.63 4.02 3.71 33.76 Resorcina STP-II 18.42 6.17 1.78 10.19 26.70 Resorcina SRIP 11.86 9.72 4.35 1.87 25.62 Resorcina UIP/IPF 18.49 9.95 4.45 12.43 35.77 Results: The proportion of collagen fibers was two times higher when compared with the elastic component in the four groups. In addition, a lower percentage of elastic and collagen fibers were observed in SRIP when compared with UIP/IPF, SPT-I and SPT-II. Table 1. Conclusions: A smaller amount of elastic and collagen fibers accompanies the remodeling of the emphysematous airspaces in smoking-related interstitial pneumonia when compared to the other fibrosing diseases, suggesting a different remodeling spectrum in chronic fibrosing lung diseases.conferenceObject Down Regulation of Angiotensin II Receptor Type 1 (AGTR1) Contrast with Up Regulation of Type 2 (AGTR2) in Idiopathic Pulmonary Fibrosis(2013) PARRA, E. R.; RUPPERT, A. D. P.; RANGEL, M. P.; CAPELOZZI, V. L.Idiopathic pulmonary fibrosis (IPF) is the most common form of idiopathic interstitial pneumonia. IPF represents a progressive and lethal disorder and is of major concern due to its unresolved pathogenesis and limited responsiveness to currently available therapies. IPF is characterized by alveolar injury, fibroblast proliferation and extracellular matrix (ECM) accumulation with severe loss of respiratory function. Angiotensin II (ANGII) signaling, mediated via angiotensin II receptor type 1 (AGTR1) or type 2 (AGTR2), controls tissue remodeling in fibrosis, but the relevance of AGTR2 and AGTR1 remains elusive. Design: Twenty-seven patients with biopsy-proven IPF disease with pulmonary evaluation by high-resolution computed tomography (HRCT) and pulmonary function tests were studied. Ten normal lung tissues (NLT) were included with controls. AGTR1 and AGTR2 in lung parenchyma were detected by immunohistochemistry and quantified by histomorphometry. Results: Quantitative analysis revealed a significant increase of AGTR2 expression in epithelial, endothelial and fibroblastic cells from patients with IPF when compared to NLT group. In contrast, AGTR1 expression levels are decreased in these cells from patients with IPF when compared with NTL. Pulmonary function tests no showed correlation with expression of AGTR1 or AGTR2. The median follow-up was 42.70 months. Ten patients were still alive, 17 died from causes related to IPF. Kaplan Meier curve, showed that the 5-year survival rate in patients with <0.05% of AGTR1 levels was 58.20% versus 24.66% in the group with ≥ 0.05% of AGTR1 levels (p < 0.05). Conclusions: In summary, we demonstrated increased expression of AGTR2 and decreased expression of AGTR1 in lung tissues from patients with IPF suggesting that they may be promising markers of prognosis in these patients.conferenceObject COLVa2 a Biomarker of Vasculopathy in Scleroderma?(2013) MORAIS, J.; MARTIN, P.; CAMARGO, I. C.; KATAYAMA, M. L.; CARRASCO, S.; GOLDEINSTEIN-SCHAINBERG, C.; PARRAS, E. R.; BARRENCE, F.; VELOSA, A. P.; CAPELOZZI, V. L.; TEODORA, W. R.conferenceObject Bleomycin and Paraquat Mediated Pulmonary Fibrosis Is IL-17 Independent(2012) FABRO, A. T.; PARRA, E. R.; RAGEL, M. P.; TEODORO, W. R.; POPPER, H. H.; CAPELOZZI, V. L.Background: Pulmonary fibrosis is a destructive process that in many cases are of unknown cause such as idiopathic pulmonary fibrosis. Better characterization of the immunological mechanisms of pulmonary fibrosis is needed to identify new therapeutic modalities for these diseases. The aim of the current study was to characterize the mechanisms of pulmonary fibrosis in the late phase and to determine whether IL-17A plays an important regulatory role. Design: The pulmonary fibrosis was induced in distinct animal models, including Bleomycin (B-BLM) and Paraquat (B-PQ) in Balb/c mice. Additionally, IL17-RA Knockout (IL17KO) and wild C57 mice (C-BLM) were included. We used the picrosirius-polarization method and weigert’s resorcin-fuchsin stain tomorphometric study the peribronchiolar collagen and elastic fibers, respectively. By immunohistochemistry, we evaluate TGF-β, IL-21, IL-6, CD83, IL-17, IL-23, IL-13,STAT3, PDGF, FGF, TNF-α and limphocytic markers expression, using stereology method. The sacrifice of mice was performed 21 day after induction. Results: We report here that late PQ and BLM-mediated peribronchiolar fibrosis is IL-17 independent, as IL17-RA -/- mice developed similar peribronchiolar fibrosis after induction when compared to B-BLM, B-PQ and C-BLM (Fig left). We found that only B-BLM and B-PQ presented increase of elastic fibers and they show apositive correlation with the deposition of collagen fibers. In IL-17KO group TGF and collagen correlated. The B-BLM showed marked increase in dendritic cells (CD83) and T lymphocytes (CD3), but the IL-17 axis is suppressed by low expression of IL-23, IL-13 and IL-17 (tendency). In contrast, the mice without IL-17A receptor (IL17KO) showed overexpression of IL-17 axis by high expression of IL-17, IL-6, IL-21, STAT3 and CD8+ T cell. The B-PQ group has only increased FGF-β. Conclusions: Bleomycin and paraquat-mediated peribronchiolar fibrosis is IL-17 independent in the late phase. However, distinct mechanisms of peribronchiolar fibrosis may be involved, such as IL-17 response in C57 mice and presentation and processing of antigens in Balb/c mice. More studies are necessary to validate the regulatory role of IL-17 on pulmonary fibrosis process.conferenceObject Hyaluronan and Its Impact as New Biochemical Marker on Diagnosis and Prognosis of Lung Cancer(2012) RANGEL, M. P.; SA, V. K. de; MARTINS, J. R. M.; PARRA, E. R.; MENDES, A.; OLIVIERI, E.; CARRARO, D. M.; CAPELOZZI, V. L.