HERALDO POSSOLO DE SOUZA

(Fonte: Lattes)
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Lattes
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Departamento de Clínica Médica, Faculdade de Medicina - Docente
Instituto Central, Hospital das Clínicas, Faculdade de Medicina - Médico
LIM/02 - Laboratório de Anatomia Médico-Cirúrgica, Hospital das Clínicas, Faculdade de Medicina
LIM/51 - Laboratório de Emergências Clínicas, Hospital das Clínicas, Faculdade de Medicina

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Autor e Coautores FMUSP-HC Normalizados: DENISE FREDIANI BARBEIRO ×

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Agora exibindo 1 - 10 de 23
  • conferenceObject
    URINARY BIOMARKER NGAL IN PATIENTS WITH HEPATORENAL SYNDROME: ACCURACY STUDY IN PREDICTION OF NO RESPONSE TO THERAPY WITH ALBUMIN AND TERLIPRESSIN
    (2016) XIMENES, R. O.; HELOU, C.; DINIZ, M.; BARBEIRO, D.; SOUZA, H.; D'ALBUQUERQUE, L. A.; CARRILHO, F.; FARIAS, A.
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    Intestinal Barrier Dysfunction in Ageing Animals With Acute Pancreatitis: Increased Intestinal Inflammation?
    (2015) MACHADO, Marcel C.; SILVA, Fabiano Pinheiro da; CUNHA, Debora G.; BARBEIRO, Denise F.; COELHO, Ana Maria M.; SOUZA, Heraldo P.
  • article 31 Citação(ões) na Scopus
    High-fat diet inhibits PGC-1 alpha suppressive effect on NF kappa B signaling in hepatocytes
    (2018) BARROSO, Wermerson Assuncao; VICTORINO, Vanessa Jacob; JEREMIAS, Isabela Casagrande; PETRONI, Ricardo Costa; ARIGA, Suely Kunimi Kubo; SALLES, Thiago A.; BARBEIRO, Denise Frediani; LIMA, Thais Martins de; SOUZA, Heraldo Possolo de
    The peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1 alpha) regulates the expression of genes implicated in fatty acid oxidation and oxidative phosphorylation. Its role in liver steatosis is well established, since mice with liver-specific deletion of PGC-1 alpha exhibit lipid accumulation and high-fat diet reduces hepatic PGC-1 alpha expression in mice. In this study, we investigated the role of PGC-1 alpha in the inflammatory changes observed in steatohepatitis induced by high-fat diet. C57black/6 mice were fed a high-fat diet containing 30% fat for 10 weeks. After euthanasia, liver morphology was examined by HE staining and inflammation was determined by IL-6, TNF-alpha, and IL-1 beta quantification. Liver gene expression of PGC-1 isoforms was evaluated by real-time PCR and p65 NF kappa B nuclear translocation by Western blotting. HepG2 cells were treated with linoleic acid overload for 72 h to create an in vitro model of steatohepatitis. RNA interference (RNAi) was used to evaluate the involvement of PGC-1 alpha on inflammatory mediators' production by hepatocytes. The high-fat diet led to a state of nonalcoholic steatohepatitis, associated with increased deposits of intra-abdominal fat, hyperglycemia and hyperlipidemia. Mice liver also exhibited increased proinflammatory cytokines' levels, decreased PGC-1 alpha expression, and marked increase in p65 NF kappa B nuclear translocation. Linoleic acid treated cells also presented increased expression of proinflammatory cytokines and decreased PGC-1 alpha expression. The knockdown of PGC-1 alpha content caused an increase in IL-6 expression and release via enhanced I kappa B alpha phosphorylation and subsequent increase of p65 NF kappa B nuclear translocation. High-fat diet induces liver inflammation by inhibiting PGC-1 alpha expression and its suppressive effect in NF kappa B pathway.
  • article 2 Citação(ões) na Scopus
    Sodium Taurocholate Induced Severe Acute Pancreatitis in C57BL/6 Mice
    (2021) SERRA, Mariana B.; KOIKE, Marcia K.; BARBEIRO, Denise F.; MACHADO, Marcel C. C.; SOUZA, Heraldo P. de
    Biliary acute pancreatitis induction by sodium taurocholate infusion has been widely used by the scientific community due to the representation of the human clinical condition and reproduction of inflammatory events corresponding to the onset of clinical biliary pancreatitis. The severity of pancreatic damage can be assessed by measuring the concentration, speed, and volume of the infused bile acid. This study provides an updated checklist of the materials and methods used in the protocol reproduction and shows the main results from this acute pancreatitis (AP) model. Most of the previous publications have limited themselves to reproducing this model in rats. We have applied this method in mice, which provides additional advantages (i.e., the availability of an arsenal of reagents and antibodies for these animals along with the possibility of working with genetically modified strains of mice) that may be relevant to the study. For acute pancreatitis induction in mice, we present a systematic protocol, with a defined dose of 2.5% sodium taurocholate at an infusion speed 10 mu L/min for 3 min in C57BL/6 mice that reaches its maximal level of severity within 12 h of induction and highlight results with outcomes that validate the method. With practice and technique, the total estimated time, from the induction of anesthesia to the completion of the infusion, is 25 min per animal.
  • article 15 Citação(ões) na Scopus
    Septic shock in older people: a prospective cohort study
    (2013) SILVA, Fabiano Pinheiro da; ZAMPIERI, Fernando Godinho; BARBEIRO, Denise Frediani; BARBEIRO, Hermes Vieira; GOULART, Alessandra Carvalho; TORGGLER FILHO, Francisco; VELASCO, Irineu Tadeu; CRUZ NETO, Luiz Monteiro da; SOUZA, Heraldo Possolo de; MACHADO, Marcel Cerqueira Cesar
    Background: Septic shock is the first cause of death in Intensive Care Units. Despite experimental data showing increased inflammatory response of aged animals following infection, the current accepted hypothesis claims that aged patients are immunocompromised, when compared to young individuals. Results: Here, we describe a prospective cohort study designed to analyze the immune profile of this population. Conclusion: Older people are as immunocompetent as the young individual, regarding the cytokines, chemokines and growth factors response to devastating infection.
  • conferenceObject
    Inflammatory and antioxidant response in obese septic shock patients
    (2013) VICTORINO, Vanessa Jacob; BARBEIRO, Hermes Vieira; BARBEIRO, Denise Frediani; SILVA, Fabiano Pinheiro; SOUZA, Heraldo Possolo
    There is no consensus about the influence of obesity on sepsis. Hence, we evaluated the inflammatory and antioxidant response in obese patients (body mass index > 30) with septic shock compared to non-infected obese and non-obese septic patients. Blood samples were obtained from 27 critically ill patients admitted to ICUs in Clinics Hospital, Universidade de Sao Paulo. Cytokines were measured by ELISA Milliplex and antioxidant activity by colorimetric methods. There are small differences in the cytokine profiles in obese septic patients (n=6), compared to obese non-infected ones (n=10). Only FGF2, TGF-α, IFN-α2, IFN-{gamma}, IL-10, MCP-3, IL-13 and IL-15 presented significantly higher levels in septic patients. Interestingly, there was a marked increase in superoxide dismutase (SOD) and catalase (CAT) activity in erythrocytes from the septic group. Compared to their non-obese septic counterparts, septic obese patients presented significantly lower levels of FGF2, IL-4, TNF-β and VEGF. SOD activity was higher in this group, compared to non-obese patients. We concluded that obese patients with septic shock maintain cytokine levels similar to the ones observed in their non-obese counterparts, while increasing their antioxidant activity.
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    Effect of low level laser therapy on lung mechanics and inflammatory response
    (2013) CURY, Vivian; LIMA, Thais; ARIGA, Suely; BARBEIRO, Denise; PINHEIRO, Nathalia; PRADO, Carla Maximo; MORETTI, Ana Iochabel; SOUZA, Heraldo Possolo
  • article 14 Citação(ões) na Scopus
    Low level laser therapy reduces acute lung inflammation without impairing lung function
    (2016) CURY, Vivian; LIMA, Thais Martins de; PRADO, Carla Maximo; PINHEIRO, Nathalia; ARIGA, Suely K. K.; BARBEIRO, Denise F.; MORETTI, Ana I.; SOUZA, Heraldo P.
    Acute lung injury is a condition characterized by exacerbate inflammatory reaction in distal airways and lung dysfunction. Here we investigate the treatment of acute lung injury (ALI) by low level laser therapy (LLLT), an effective therapy used for the treatment of patients with inflammatory disorders or traumatic injuries, due to its ability to reduce inflammation and promote tissue regeneration. However, studies in internal viscera remains unclear. C57BL/6 mice were treated with intratracheal lipopolysaccharide (LPS) (5 mg/kg) or phosphate buffer saline (PBS). Six hours after instillation, two groups were irradiated with laser at 660 nm and radiant exposure of 10 J/cm(2). Intratracheal LPS inoculation induced a marked increase in the number of inflammatory cells in perivascular and alveolar spaces. There was also an increase in the expression and secretion of cytokines (TNF-alpha, IL-1 beta, IL-6,) and chemokine (MCP-1). The LLLT application induced a significant decrease in both inflammatory cells influx [GRAPHICS] and inflammatory mediators secretion. These effects did not affect lung mechanical properties, since no change was observed in tissue resistance or elastance. In conclusion LLLT is able to reduce inflammatory reaction in lungs exposed to LPS without affecting the pulmonary function and recovery.
  • article 20 Citação(ões) na Scopus
    Sorafenib prevents liver fibrosis in a non-alcoholic steatohepatitis (NASH) rodent model
    (2015) STEFANO, J. T.; PEREIRA, I. V. A.; TORRES, M. M.; BIDA, P. M.; COELHO, A. M. M.; XERFAN, M. P.; COGLIATI, B.; BARBEIRO, D. F.; MAZO, D. F. C.; KUBRUSLY, M. S.; D'ALBUQUERQUE, L. A. C.; SOUZA, H. P.; CARRILHO, F. J.; OLIVEIRA, C. P.
    Liver fibrosis occurring as an outcome of non-alcoholic steatohepatitis (NASH) can precede the development of cirrhosis. We investigated the effects of sorafenib in preventing liver fibrosis in a rodent model of NASH. Adult Sprague-Dawley rats were fed a choline-deficient high-fat diet and exposed to diethylnitrosamine for 6 weeks. The NASH group (n=10) received vehicle and the sorafenib group (n=10) received 2.5 mg.kg(-1).day(-1) by gavage. A control group (n=4) received only standard diet and vehicle. Following treatment, animals were sacrificed and liver tissue was collected for histologic examination, mRNA isolation, and analysis of mitochondrial function. Genes related to fibrosis (MMP9, TIMP1, TIMP2), oxidative stress (HSP60, HSP90, GST), and mitochondrial biogenesis (PGC1 alpha) were evaluated by real-time quantitative polymerase chain reaction (RT-qPCR). Liver mitochondrial oxidation activity was measured by a polarographic method, and cytokines by enzyme-linked immunosorbent assay (ELISA). Sorafenib treatment restored mitochondrial function and reduced collagen deposition by nearly 63% compared to the NASH group. Sorafenib upregulated PGC1 alpha and MMP9 and reduced TIMP1 and TIMP2 mRNA and IL-6 and IL-10 protein expression. There were no differences in HSP60, HSP90 and GST expression. Sorafenib modulated PGC1 alpha expression, improved mitochondrial respiration and prevented collagen deposition. It may, therefore, be useful in the treatment of liver fibrosis in NASH.
  • conferenceObject
    Urinary NGAL biomarker predicts non response to therapy with albumin and terlipressin in patients with hepatorenal syndrome
    (2016) XIMENES, Rafael O.; HELOU, Claudia; BARBEIRO, Denise F.; SOUZA, Heraldo; MIGITA, Beatriz; D'ALBUQUERQUE, Luiz C.; CARRILHO, Flair J.; FARIAS, Alberto O.