HERALDO POSSOLO DE SOUZA

(Fonte: 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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  • 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.
  • article 11 Citação(ões) na Scopus
    PGC-1 beta regulates HER2-overexpressing breast cancer cells proliferation by metabolic and redox pathways
    (2016) VICTORINO, Vanessa Jacob; BARROSO, W. A.; ASSUNCAO, A. K. M.; CURY, V.; JEREMIAS, I. C.; PETRONI, R.; CHAUSSE, B.; ARIGA, S. K.; HERRERA, A. C. S. A.; PANIS, C.; LIMA, T. M.; SOUZA, H. P.
    Breast cancer is a prevalent neoplastic disease among women worldwide which treatments still present several side effects and resistance. Considering that cancer cells present derangements in their energetic homeostasis, and that peroxisome proliferator-activated receptor- gamma coactivator 1 (PGC-1) is crucial for cellular metabolism and redox signaling, the main objective of this study was to investigate whether there is a relationship between PGC-1 expression, the proliferation of breast cancer cells and the mechanisms involved. We initially assessed PGC-1 beta expression in complementary DNA (cDNA) from breast tumor of patients bearing luminal A, luminal B, and HER2-overexpressed and triple negative tumors. Our data showed that PGC-1 beta expression is increased in patients bearing HER2-overexpressing tumors as compared to others subtypes. Using quantitative PCR and immunoblotting, we showed that breast cancer cells with HER2-amplification (SKBR-3) have greater expression of PGC-1 beta as compared to a non-tumorous breast cell (MCF-10A) and higher proliferation rate. PGC-1 beta expression was knocked down with short interfering RNA in HER2-overexpressing cells, and cells decreased proliferation. In these PGC-1 beta-inhibited cells, we found increased citrate synthase activity and no marked changes in mitochondrial respiration. Glycolytic pathway was decreased, characterized by lower intracellular lactate levels. In addition, after PGC-1 beta knockdown, SKBR-3 cells showed increased reactive oxygen species production, no changes in antioxidant activity, and decreased expression of ERR alpha, a modulator of metabolism. In conclusion, we show an association of HER2overexpression and PGC-1 beta. PGC-1 beta knockdown impairs HER2-overexpressing cells proliferation acting on ERR alpha signaling, metabolism, and redox balance.
  • 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.
  • 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.
  • conferenceObject
    URINARY BIOMARKER NGAL IN PATIENTS WITH CIRRHOSIS AND BACTERIAL INFECTIONS: ACCURACY STUDY IN ACUTE KIDNEY INJURY PREDICTION DEFINED BY KDIGO CRITERIA
    (2016) XIMENES, R. O.; HELOU, C.; DINIZ, M.; BARBEIRO, D.; SOUZA, H.; D'ALBUQUERQUE, L. A.; CARRILHO, F.; FARIAS, A.
  • article 6 Citação(ões) na Scopus
    Proteomic profiling identifies N-acetylmuramoyl-L-alanine amidase as a novel biomarker of sepsis
    (2016) SILVA, Fabiano Pinheiro da; CATALDI, Thais Regiani; LIMA, Thais Martins de; STARZYNSKI, Paulo Nogueira; BARBEIRO, Hermes Vieira; LABATE, Monica Teresa Veneziano; MACHADO, Marcel Cerqueira Cesar; SOUZA, Heraldo Possolo de; LABATE, Carlos Alberto
    Aim: Sepsis is a critical condition that leads to high mortality and is the most common cause of death in intensive care units. Despite exhaustive efforts by the scientific community, a reliable biomarker for diagnosis, evolution and prognosis of sepsis is still lacking. Results & methodology: Here, using high-throughput proteomics, we describe N-acetylmuramoyl-L-alanine amidase as a novel candidate for differentiating infectious and noninfectious inflammatory syndromes. Discussion & conclusion: This is the first description of N-acetylmuramoyl-L-alanine amidase as a biomarker that can be used alone or in conjunction with other biomarkers to facilitate the diagnosis of sepsis in the critically ill.
  • article 6 Citação(ões) na Scopus
    Preventive and therapeutic moderate aerobic exercise programs convert atherosclerotic plaques into a more stable phenotype
    (2016) CARDINOT, Themis M.; LIMA, Thais M.; MORETTI, Ana I. S.; KOIKE, Marcia K.; NUNES, Valeria S.; CAZITA, Patricia M.; KRIEGER, Marta H.; BRUM, Patricia C.; SOUZA, Heraldo P.
    The mechanisms by which exercise affects atherosclerotic plaque stability remain incompletely understood. We evaluated the effects of two training protocols on both atherosclerotic plaque structure and the signaling pathways involved in plaque rupture. Methods: Male low-density lipoprotein (LDL) receptor knockout mice were fed a high-fat, high-cholesterol diet (HFD). One group was subjected to moderate exercise using a treadmill for 14 weeks (preventive protocol). The other group started an exercise regimen after 16 weeks of the HFD (therapeutic group). Atherosclerotic plaques within the aorta were evaluated for lipid and collagen contents, as well as for inflammatory markers. Plasma cholesterol and cytokine levels were also determined. Results: The mice receiving a HFD developed hypercholesterolemia and atherosclerotic plaques within the aorta. The aortas from the animals in the preventive protocol exhibited smaller lipid cores and higher collagen content. These animals also exhibited lower CD40 expression within the plaques. The aortas of the mice in the therapeutic group exhibited higher collagen content, but no differences in either lipid core size or plaque size were noted. No differences in blood pressure, plasma cholesterol, cytokine levels, plaque size or metalloproteinase 9 expression were observed in the trained animals compared with the sedentary animals. Conclusion: Moderate aerobic exercise modified atherosclerotic plaque characteristics and converted the plaques into a more stable phenotype, increasing the collagen content in response to both exercise programs. Furthermore, moderate aerobic exercise reduced the animals' fat content and decreased the activity of the CD40-CD40L signaling pathway in the preventive group.