EDWIN ROGER PARRA CUENTAS

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  • article 39 Citação(ões) na Scopus
    Expression of Acetylcholine and Its Receptor in Human Sympathetic Ganglia in Primary Hyperhidrosis
    (2013) MOURA JUNIOR, Nabor B. de; DAS-NEVES-PEREIRA, Joao C.; OLIVEIRA, Flavio R. G. de; JATENE, Fabio B.; PARRA, Edwin R.; CAPELOZZI, Vera L.; WOLOSKER, Nelson; CAMPOS, Jose R. M. de
    Background. The pathophysiologic characteristics of primary hyperhidrosis are not well understood and seem to be related to a sympathetic nervous system dysfunction. The resection of thoracic sympathetic chain ganglia is the most effective treatment for hyperhidrosis; however sympathetic ganglia function in normal individuals and in patients with hyperhidrosis is unknown. Methods. A cross-sectional study, in which 2 groups of 20 subjects were analyzed: the hyperhidrosis group (HYP), comprised of patients with hyperhidrosis who were eligible for thoracic sympathectomy, and the control group (CON) comprised of brain-dead organ donors without a history of hyperhidrosis. For each subject, the following were performed: resection of the third left sympathetic ganglion, measurement of the ganglion's diameter, and immunohistochemical evaluation by quantification of strong and weak expression areas of primary antibodies against acetylcholine and alpha-7 neuronal nicotinic receptor subunit. Results. The presence of a strong alpha-7 subunit expression area was 4.85% in patients with primary hyperhidrosis and 2.34% in controls (p < 0.001), whereas the presence of a weak expression area was 11.48% in the HYP group and 4.59% in the CON group (p < 0.001). Strong acetylcholine expression was found in 4.95% of the total area in the HYP group and in 1.19% in the CON group (p < 0.001), whereas weak expression was found in 18.55% and 6.77% of the HYP and CON groups, respectively (p < 0.001). Furthermore, diameter of the ganglia was 0.71 cm in the HYP group and 0.53 cm in the CON group (p < 0.001). Conclusions. There is a higher expression of acetylcholine and alpha-7 neuronal nicotinic receptor subunit in the sympathetic ganglia of patients with hyperhidrosis. Furthermore, the diameter of the thoracic sympathetic chain ganglia is larger in such patients. (Ann Thorac Surg 2013;95:465-71) (c) 2013 by The Society of Thoracic Surgeons
  • article 7 Citação(ões) na Scopus
    Morphometric evaluation of nitric oxide synthase isoforms and their cytokine regulators predict pulmonary dysfunction and survival in systemic sclerosis
    (2013) PARRA, E. R.; AGUIAR, A. C. Junior; SILVA, L. O.; SOUZA, H. S. P.; ESPINOZA, J. D.; CAPELOZZI, V. L.
    Because histopathological changes in the lungs of patients with systemic sclerosis (SSc) are consistent with alveolar and vessel cell damage, we presume that this interaction can be characterized by analyzing the expression of proteins regulating nitric oxide (NO) and plasminogen activator inhibitor-1 (PAI-1) synthesis. To validate the importance of alveolar-vascular interactions and to explore the quantitative relationship between these factors and other clinical data, we studied these markers in 23 cases of SSc nonspecific interstitial pneumonia (SSc-NSIP). We used immunohistochemistry and morphometry to evaluate the amount of cells in alveolar septa and vessels staining for NO synthase (NOS) and PAI-1, and the outcomes of our study were cellular and fibrotic NSIP, pulmonary function tests, and survival time until death. General linear model analysis demonstrated that staining for septal inducible NOS (iNOS) related significantly to staining of septal cells for interleukin (IL)-4 and to septal IL-13. In univariate analysis, higher levels of septal and vascular cells staining for iNOS were associated with a smaller percentage of septal and vascular cells expressing fibroblast growth factor and myofibroblast proliferation, respectively. Multivariate Cox model analysis demonstrated that, after controlling for SSc- NSIP histological patterns, just three variables were significantly associated with survival time: septal iNOS (P=0.04), septal IL-13 (P=0.03), and septal basic fibroblast growth factor (bFGF; P=0.02). Augmented NOS, IL-13, and bFGF in SSc-NSIP histological patterns suggest a possible functional role for iNOS in SSc. In addition, the extent of iNOS, PAI-1, and IL-4 staining in alveolar septa and vessels provides a possible independent diagnostic measure for the degree of pulmonary dysfunction and fibrosis with an impact on the survival of patients with SSc.
  • 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
    Collagen V activation and matrix extracellular remodeling mediated pulmonary fibrosis in experimental models of bleomycin and 3-5-di-tert-4-hidroxitoluene
    (2013) LOPES, Deborah; MARTINS, Vanessa; TEODORO, Walcy; ROGER, Edwin; CAPELOZZI, Vera Luiza
  • conferenceObject
    Side effects of tacrolimus upon airway epithelial tissue
    (2013) SILVA, Maristela Prado e; SOTO, Sonia; ALMEIDA, Francine; LIMONETE, Tatiana; PARRA, Edwin; PEGO-FERNANDES, Paulo; JATENE, Fabio; PAZETTI, Rogerio
  • 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.
  • article 6 Citação(ões) na Scopus
    Avaliação imuno-histoquímica e morfométrica de COX-1 e COX-2 no remodelamento pulmonar na fibrose pulmonar idiopática e na esclerose sistêmica
    (2013) PARRA, Edwin Roger; LIN, Flavia; MARTINS, Vanessa; RANGEL, Maristela Peres; CAPELOZZI, Vera Luiza
    Objective: To study the expression of COX-1 and COX-2 in the remodeled lung in systemic sclerosis (SSc) and idiopathic pulmonary fibrosis (1PF) patients, correlating that expression with patient survival. Methods: We examined open lung biopsy specimens from 24 SSc patients and 301PF patients, using normal lung tissue as a control. The histological patterns included fibrotic nonspecific interstitial pneumonia (NS1P) in SSc patients and usual interstitial pneumonia (UP) in 1PF patients. We used immunohistochemistry and histomorphometry to evaluate the expression of COX-1 and COX-2 in alveolar septa, vessels, and bronchioles. We then correlated that expression with pulmonary function test results and evaluated its impact on patient survival. Results: The expression of COX-1 and COX-2 in alveolar septa was significantly higher in 1PF-U1P and SSc-NS1P lung tissue than in the control tissue. No difference was found between 1PF-UIP and SSc-NS1P tissue regarding COX-1 and COX-2 expression. Multivariate analysis based on the Cox regression model showed that the factors associated with a low risk of death were younger age, high DLCO/alveolar volume, 1PF, and high COX-1 expression in alveolar septa, whereas those associated with a high risk of death were advanced age, low DLCO/alveolar volume, SSc (with NS1P), and low COX-1 expression in alveolar septa. Conclusions: Our findings suggest that strategies aimed at preventing low COX-1 synthesis will have a greater impact on SSc, whereas those aimed at preventing high COX-2 synthesis will have a greater impact on 1PF. However, prospective randomized clinical trials are needed in order to confirm
  • 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.
    Background: 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
    Epithelial mesenchymal transition in fibroblastic foci of different fibrosing lung diseases: Repair or remodeling?
    (2013) FABRO, Alexandre Todorovic; HALBWEDL, Iris; PARRAS, Edwin Roger; CAPELOZZI, Vera Luiza; POPPER, Helmut
  • conferenceObject
    Collagen V Maintains Experimental Pulmonary Fibrosis In Il17-dependent And -Independent Pathways
    (2013) FABRO, A. T.; SILVA, P. Q.; ZOCOLARO, W. S.; ALMEIDA, M. S.; MINATEL, I. O.; PRANDO, E. C.; RAINHO, C. A.; VELOSA, A. P.; TEODORO, W. R.; PARRA-CUENTAS, E. R.; POPPER, H. H.; CAPELOZZI, V. L.