ALEXANDRE TELES GARCEZ

(Fonte: Lattes)
Índice h a partir de 2011
7
Projetos de Pesquisa
Unidades Organizacionais
Instituto do Câncer do Estado de São Paulo, Hospital das Clínicas, Faculdade de Medicina
LIM/43 - Laboratório de Medicina Nuclear, Hospital das Clínicas, Faculdade de Medicina

Resultados de Busca

Agora exibindo 1 - 4 de 4
  • article 14 Citação(ões) na Scopus
    The contributions of dipeptidyl peptidase IV to inflammation in heart failure
    (2016) SALLES, Thiago de Almeida; ZOGBI, Camila; LIMA, Thais Martins de; CARNEIRO, Camila de Godoi; GARCEZ, Alexandre Teles; BARBEIRO, Hermes Vieira; ANTONIO, Ednei Luiz; SANTOS, Leonardo dos; PEREIRA, Alexandre da Costa; TUCCI, Paulo Jose Ferreira; FARIA, Daniele de Paula; SORIANO, Francisco Garcia; GIRARDI, Adriana Castello Costa
    Circulating dipeptidyl peptidase IV (DPPIV) activity correlates with cardiac dysfunction in humans and experimental heart failure (HF) models. Similarly, inflammatory markers are associated with poorer outcomes in HF patients. However, the contributions of DPPIV to inflammation in HF remain elusive. Therefore, this study aimed to investigate whether the cardioprotective effects of DPPIV inhibition after myocardial injury are accompanied by reduced cardiac inflammation, whether circulating DPPIV activity correlates with the levels of systemic inflammatory markers in HF patients, and whether leukocytes and/or splenocytes may be one of the sources of circulating DPPIV in HF. Experimental HF was induced in male Wistar rats by left ventricular myocardial injury after radiofrequency catheter ablation. The rats were divided into three groups: sham, HF, and HF + DPPIV inhibitor (sitagliptin). Six weeks after surgery, cardiac function, perfusion and inflammatory status were evaluated. Sitagliptin treatment improved cardiac function and perfusion, reduced macrophage infiltration, and diminished the levels of inflammatory biomarkers including TNF-alpha, IL-1 beta, and CCL2. In HF patients, serum DPPIV activity correlated with CCL2, suggesting that leukocytes may be the source of circulating DPPIV in HF. Unexpectedly, DPPIV release was higher in splenocytes from HF rats and similar in HF circulating mononuclear cells compared with those from sham, suggesting an organ-specific modulation of DPPIV in HF. Collectively, our data provide new evidence that the cardioprotective effects of DPPIV inhibition in HF may be due to suppression of inflammatory cytokines. Moreover, they suggest that a vicious circle between DPPIV and inflammation may contribute to HF development and progression.
  • article 9 Citação(ões) na Scopus
    Evaluation of GX1 and RGD-GX1 peptides as new radiotracers for angiogenesis evaluation in experimental glioma models
    (2016) OLIVEIRA, Erica Aparecida de; FAINTUCH, Bluma Linkowski; TARGINO, Roselaine Campos; MORO, Ana Maria; MARTINEZ, Raquel Chacon Ruiz; PAGANO, Rosana Lima; FONOFF, Erich Talamoni; CARNEIRO, Camila de Godoi; GARCEZ, Alexandre Teles; FARIA, Daniele de Paula; BUCHPIGUEL, Carlos Alberto
    Gliomas are the most common type among all central nervous system tumors. The aggressiveness of gliomas is correlated with the level of angiogenesis and is often associated with prognosis. The aim of this study is to evaluate the novel GX1 peptide and the heterodimer RGD-GX1 radiolabeled with technetium-99m, for angiogenesis detection in glioma models. Radiolabeling and radiochemical controls were assessed for both radioconjugates. In vitro binding studies in glioma tumor cells were performed, as well as biodistribution in SCID mice bearing tumor cells, in order to evaluate the biological behavior and tumor uptake of the radiocomplexes. Blocking and imaging studies were also conducted. MicroSPECT/CT images were acquired in animals with experimentally implanted intracranial tumor. Open field activity was performed to evaluate behavior, as well as perfusion and histology analysis. The radiochemical purity of both radiotracers was greater than 96 %. In vitro binding studies revealed rather similar binding profi le for each molecule. The highest binding was for RGD-GX1 peptide at 120 min in U87MG cells (1.14 +/- A 0.35 %). Tumor uptake was also favorable for RGD-GX1 peptide in U87MG cells, reaching 2.96 +/- A 0.70 % at 1 h p.i. with 47 % of blocking. Imaging studies also indicated better visualization for RGD-GX1 peptide in U87MG cells. Behavior evaluation pointed brain damage and histology studies confirmed actual tumor in the uptake site. The results with the angiogenesis seeking molecule Tc-99m-HYNIC-E-[c(RGDfk)-c(GX1)] were successful, and better than with Tc-99m-HYNIC-PEG(4)-c(GX1). Future studies targeting angiogenesis in other glioma and nonglioma tumor models are recommended.
  • article 1014 Citação(ões) na Scopus
    The Brazilian Zika virus strain causes birth defects in experimental models
    (2016) CUGOLA, Fernanda R.; FERNANDES, Isabella R.; RUSSO, Fabiele B.; FREITAS, Beatriz C.; DIAS, Joao L. M.; GUIMARAES, Katia P.; BENAZZATO, Cecilia; ALMEIDA, Nathalia; PIGNATARI, Graciela C.; ROMERO, Sarah; POLONIO, Carolina M.; CUNHA, Isabela; FREITAS, Carla L.; BRANDAO, Wesley N.; ROSSATO, Cristiano; ANDRADE, David G.; FARIA, Daniele de P.; GARCEZ, Alexandre T.; BUCHPIGEL, Carlos A.; BRACONI, Carla T.; MENDES, Erica; SALL, Amadou A.; ZANOTTO, Paolo M. de A.; PERON, Jean Pierre S.; MUOTRI, Alysson R.; BELTRAO-BRAGA, Patricia C. B.
    Zika virus (ZIKV) is an arbovirus belonging to the genus Flavivirus (family Flaviviridae) and was first described in 1947 in Uganda following blood analyses of sentinel rhesus monkeys(1). Until the twentieth century, the African and Asian lineages of the virus did not cause meaningful infections in humans. However, in 2007, vectored by Aedes aegypti mosquitoes, ZIKV caused the first noteworthy epidemic on Yap Island in Micronesia(2). Patients experienced fever, skin rash, arthralgia and conjunctivitis(2). From 2013 to 2015, the Asian lineage of the virus caused further massive outbreaks in New Caledonia and French Polynesia. In 2013, ZIKV reached Brazil, later spreading to other countries in South and Central America3. In Brazil, the virus has been linked to congenital malformations, including microcephaly and other severe neurological diseases, such as Guillain-Barre syndrome(4,5). Despite clinical evidence, direct experimental evidence showing that the Brazilian ZIKV (ZIKVBR) strain causes birth defects remains absent(6). Here we demonstrate that ZIKVBR infects fetuses, causing intrauterine growth restriction, including signs of microcephaly, in mice. Moreover, the virus infects human cortical progenitor cells in vitro, leading to an increase in cell death. We also report that the infection of human brain organoids results in a reduction of proliferative zones and disrupted cortical layers. These results indicate that ZIKVBR crosses the placenta and causes microcephaly by targeting cortical progenitor cells, inducing cell death by apoptosis and autophagy, and impairing neurodevelopment. Our data reinforce the growing body of evidence linking the ZIKVBR outbreak to the alarming number of cases of congenital brain malformations. Our model can be used to determine the efficiency of therapeutic approaches to counteracting the harmful impact of ZIKVBR in human neurodevelopment.
  • article 7 Citação(ões) na Scopus
    SUV Normalized by Skeletal Volume on F-18-Fluoride PET/CT Studies
    (2016) CARVALHO, Giovanna; MARIN, Jose Flavio Gomes; GARCEZ, Alexandre Teles; DUARTE, Paulo Schiavom; SAPIENZA, Marcelo Tatit; BUCHPIGUEL, Carlos Alberto
    Objective: To propose a technique for SUV normalization on F-18-fluoride PET/CT (F-18-NaF) studies based on skeletal volume and to compare the SUVs normalized by this technique with the ones normalized by body weight. Methods: SUVs were obtained in volumes of interest (VOIs) in proximal diaphyseal regions of the right humerus (HD) and right femur (FD) in 12 selected F-18-NaF studies. The 12 studies presented both regions considered normal by visual examination on PET and CT and were performed in patients presenting body weight below 50 kg (B50) or above 90 kg (A90) (6 patients in each group). The maximum SUVs were calculated in these 2 bone regions in both groups of patients using body weight (SUV BW) and skeletal volume (SUV SV) methodologies. The total skeletal volume for each patient was estimated based on whole skeletal VOIs automatically defined on the CT component of the PET/CT study. The maximum SUVs calculated using the 2 methodologies were compared. Results: The maximum SUVs BW were statistically higher in the group A90 in both regions, with a P < 0.001 and P < 0.008 for FD and HD, respectively. The maximum SUVs SV in the 2 regions were not statistically different between the groups B50 and A90, P values of 0.27 and 0.87 for FD and HD, respectively. Conclusions: The SUVs normalized by skeletal volume present similar results in groups of patients with extremes of body weight. Therefore, this methodology could be more adequate than the one normalized by body weight to semiquantitatively analyze F-18-NaF studies.