VERA LUIZA CAPELOZZI

(Fonte: Lattes)
Índice h a partir de 2011
31
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Patologia, Faculdade de Medicina - Docente
LIM/03 - Laboratório de Medicina Laboratorial, Hospital das Clínicas, Faculdade de Medicina

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Agora exibindo 1 - 10 de 388
  • article 2 Citação(ões) na Scopus
    A more gradual positive end-expiratory pressure increase reduces lung damage and improves cardiac function in experimental acute respiratory distress syndrome
    (2022) FERNANDES, Marcos V. S.; ROCHA, Nazareth N.; FELIX, Nathane S.; RODRIGUES, Gisele C.; SILVA, Luisa H. A.; COELHO, Mariana S.; FONSECA, Ana Carolina F.; TEIXEIRA, Ana Carolina G. M.; CAPELOZZI, Vera L.; PELOSI, Paolo; SILVA, Pedro L.; MARINI, John J.; ROCCO, Patricia R. M.
    Increases in positive end-expiratory pressure (PEEP) or recruitment maneuvers may increase stress in lung parenchyma, extracellular matrix, and lung vessels; however, adaptative responses may occur. We evaluated the effects of PEEP on lung damage and cardiac function when increased abruptly, gradually, or more gradually in experimental mild/moderate acute respiratory distress syndrome (ARDS) induced by Escherichia coli lipopolysaccharide intratracheally. After 24 h, Wistar rats (n = 48) were randomly assigned to four mechanical ventilation strategies according to PEEP levels: 1) 3 cmH(2)O for 2 h (control); 2) 3 cmH(2)O for 1 h followed by an abrupt increase to 9 cmH(2)O for 1 h (no adaptation time); 3) 3 cmH(2)O for 30 min followed by a gradual increase to 9 cmH(2)O over 30 min then kept constant for 1 h (shorter adaptation time); and 4) more gradual increase in PEEP from 3 cmH(2)O to 9 cmH(2)O over 1 h and kept constant thereafter (longer adaptation time). At the end of the experiment, oxygenation improved in the shorter and longer adaptation time groups compared with the no-adaptation and control groups. Diffuse alveolar damage and expressions of interleukin-6, club cell protein-16, vascular cell adhesion molecule-1, amphiregulin, decorin, and syndecan were higher in no adaptation time compared with other groups. Pulmonary arterial pressure was lower in longer adaptation time than in no adaptation (P = 0.002) and shorter adaptation time (P = 0.025) groups. In this model, gradually increasing PEEP limited lung damage and release of biomarkers associated with lung epithelial/endothelial cell and extracellular matrix damage, as well as the PEEP-associated increase in pulmonary arterial pressure. NEW & NOTEWORTHY In a rat model of Escherichia coli lipopolysaccharide-induced mild/moderate acute respiratory distress syndrome, a gradual PEEP increase (shorter adaptation time) effectively mitigated histological lung injury and biomarker release associated with lung inflammation, damage to epithelial cells, endothelial cells, and the extracellular matrix compared with an abrupt increase in PEEP. A more gradual PEEP increase (longer adaptation time) decreased lung damage, pulmonary vessel compression, and pulmonary arterial pressure.
  • conferenceObject
    In Situ Evidence Of Pulmonary Endothelial Activation In Patients With Granulomatosis With Polyangiitis And Systemic Sclerosis
    (2015) KAWANO-DOURADO, L.; AB'SABER, A. M.; CAPELOZZI, V.; BARBAS, C. S. V.
  • article 29 Citação(ões) na Scopus
    A long-term prospective randomized controlled study of non-specific interstitial pneumonia (NSIP) treatment in scleroderma
    (2011) DOMICIANO, Diogo S.; BONFA, Eloisa; BORGES, Claudia T. L.; KAIRALLA, Ronaldo A.; CAPELOZZI, Vera L.; PARRA, Edwin; CHRISTMANN, Romy Beatriz
    The association of cyclophosphamide (CYC) and prednisone (PRED) for the treatment of lung fibrosis in systemic sclerosis (SSc) was only evaluated in uncontrolled studies, although in idiopathic interstitial lung disease (ILD) this association seems to be beneficial in patients with non-specific interstitial pneumonia (NSIP). Objectives: To treat SSc-ILD in a prospective open-label controlled study based on lung pattern during 12 months of treatment. Methods: A 3-year analysis was also performed. Twenty-four consecutive patients with SSc and ILD were submitted to an open lung biopsy. Eighteen patients (NSIP) were randomized in two groups: CYC versus CYC + PRED during 12 months. Lung function tests (diffusion lung capacity of monoxide carbone corrected for hemoglobin concentration (DLCO-Hb), forced vital capacity (FVC), total lung capacity) and Modified Rodnan Skin Score (MRSS) were performed before, after one of treatment and after 3 years from the end of the treatment. Results: Pulmonary function tests were similar in both groups on baseline. After 1 year of treatment, FVC% was comparable between CYC groups (p = 0.72) and in CYC + PRED (p = 0.40). Three years after the end of treatment, FVC% values (p = 0.39 in group CYC and p = 0.61 in CYC + PRED and p = 0.22 in CYC + PRED) and DLCO-Hb (p = 0.54 in CYC and p = 0.28 in CYC + PRED) were similar compared to 1 year of treatment. We observed a reduction of the MRSS in the CYC + PRED group after 1 year of treatment (p = 0.02); although after 3 years, MRSS values remained stable in both groups. Conclusions: CYC was effective to stabilize lung function parameters in NSIP lung pattern of SSc disease for 3 years after the end of a 1-year therapy.
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    MODELING INFLAMMATORY MEDIATORS AND APOPTOSIS BY PLEURAL MESOTHELIAL CELLS EXPOSED TO TALC PARTICLES
    (2014) ACENCIO, Milena Marques Pagliarelli; TEIXEIRA, Lisete Ribeiro; CAPELOZZI, Vera Luiza; SILVA, Bruna Rocha; ALVARENGA, Vanessa Adelia; SILVA, Carlos Rocha; VARGAS, Francisco Suso; MARCHI, Evaldo
  • 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
  • conferenceObject
    Proliferative biomarkers in Idiopathic pulmonary fibrosis: Clinical, radiological and functional significance
    (2012) PARRA, E. R.; CORNATI, M.; CAPELOZZI, V. L.
    Introduction: The natural course of idiopathic pulmonary fibrosis (IPF) could be predicted by proliferative markers of the fibrotic process, such as myofibroblasts and interleukins (IL)-13 and IL14. Our primary aim was to determine whether these proliferative markers influence the course of IPF measured by a radiological/functional score. Materials and Methods: Twenty-eight patients with biopsy-proven IPF, who underwent pulmonary evaluation by high-resolution computed tomography (HRCT) fibrosis score and pulmonary function tests, were included in the study. Five normal lung tissues (NLT) were included. Biomarkers in lung tissue were detected by immuno-histochemistry and quantified by histomorphometry for myofibroblasts including alpha-smooth muscle actin (a-SMA), anti-interleukin (IL)-4 and IL-13. Results: Myofibrobalst amount, IL-4 and IL-13 expression were higher in IPF than in NLT (P < 0.01). Myofibroblast expression of a-SMA was positively correlated to IL-14 and IL-13 expression. Lung tissue from patients with high HRCT fibrosis scores expressed significantly greatera-SMA+, IL-4 and IL-13 when compared to patients with low HRCT fibrosis scores (P < 0.05). Negative correlations were found between myofibroblasta-SMA+, vital capacity and diffusing capacity of the lung for carbon monoxide. Conclusions: Proliferative markers, detected by immunohistochemistry, in lung tissue allowed the recognition of a dichotomous distribution of HRCT fibrosis course and influenced pulmonary function tests, suggesting that they may be promising markers of prognosis in these patients.
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    Time-Controlled Adaptive Ventilation Versus Volume-Controlled Ventilation Under Similar Levels of Positive End-Release Pressure and Mean Respiratory System Pressure in Experimental Pneumonia
    (2020) SILVA, P. L.; MAGALHAES, R. F.; CRUZ, D. G.; ANTUNES, M. A.; FERNANDES, M. V. S.; OLIVEIRA, M. V. de; BRAGA, C. L.; SATALIN, J.; ANDREWS, P.; HABASHI, N.; NIEMAN, G.; GONGALVES-DE-ALBUQUERQUE, C.; SILVA, A. R.; RIBEIRO, R. V.; CAPELOZZI, V. L.; CRUZ, F. F.; SAMARY, C. S.; ROCCO, P. R.
  • 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.
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    Increased decorin and type V collagen in SSc pulmonary fibrosis
    (2012) TEODORO, W.; VELOSA, A. P.; MARCELINO, A.; MARTIN, P.; CARRASCO, S.; GOLDENSTEIN-SCHAINBERG, C.; PARRA, E.; YOSHINARI, N.; CAPELOZZI, V.
    Objective: To evaluate COL V and decorin expression in pulmonary tissue and to characterize biochemical profile of COLV from lung fibroblasts culture from SSc patients. Method: We evaluated COL V and decorin expression and tridimensional reconstruction (3D) of 6 patients with SSc without pulmonary hypertension that underwent surgical lung biopsy and as control was obtained lung fragments from 6 normal individuals who died from trauma. COL V amount in lung sections was evaluated with immunofluorescence. To biochemical characterization of COL V from lung fibroblasts culture was used quantitative immunoblot. Results: It was found that the structure of COLV fibers was distorted and strongly thickened in lung tissue from SSc patients compared with thin fibers pattern in the healthy controls. Decorin was distributed around COL V fibrils in the bronchovascular interstitium and vascular walls. Histomorphometric analysis of SSc lung demonstrated increased expression of both COL V and decorin when compared to the control (p<0.01). The semiquantitative imunoblot detected an increased high molecular weight COLV fraction in patients when compared to the control. Conclusion: The over expression and unusual organization of COLV fibers with biochemical changes associated to increased decorin indicates that matrix signalization pathway is involved in COLV fibrillogenesis process in SSc pulmonary fibrosis.
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    Intrapleural Target Therapies (anti-VEGF And Anti-EGFR) Reduce Malignant Pleural Effusion And Morbidity In An Experimental Model
    (2016) TEIXEIRA, L. R.; ACENCIO, M. M. P.; ALVARENGA, V. A.; PUKA, J.; LEITE, H. F. Z.; MILSONI, P. F.; FERNEZLIAN, S. M.; SANTOS, A. B. G.; MEDEIROS, M. C. R.; MARCHI, E.; CAPELOZZI, V. L.